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“The loss appears to be due to chlorine exposure, to which fish are especially sensitive,” school officials said in a statement. Aug. 12, 2022, 3:05 PM UTC / Source: Associated PressDAVIS, Calif. — About 21,000 fish died of possible chlorine exposure at a University of California, Davis research and care facility, school officials said Thursday.The university is investigating a “catastrophic failure” at the UC Davis Center for Aquatic Biology and Aquaculture, according to a statement. Officials didn’t say what kind of fish were killed.“The loss appears to be due to chlorine exposure, to which fish are especially sensitive,” the statement said.UC Davis has also initiated an independent external review to determine where systems failed and any potential risks at similar facilities, officials said.Scientists and students at the aquaculture center address “problems associated with California’s cultured and wild aquatic biological resources,” according to its website.“We know that many researchers, regulatory agencies, Native American tribes and other partners trust us to care for their aquatic species,” the university statement read. “We will work hard to earn that trust by conducting a thorough review of our facilities, holding ourselves accountable for what happened, and taking steps to prevent it from happening ever again.” | Biology |
Ian C Haydon/ UW Institute for Protein Design
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AI similar to the kind used to make images is now being used to design synthetic proteins. Scientists say its radically sped up their research.
Ian C Haydon/ UW Institute for Protein Design
AI similar to the kind used to make images is now being used to design synthetic proteins. Scientists say its radically sped up their research.
Ian C Haydon/ UW Institute for Protein Design
Susana Vazquez-Torres is a fourth-year graduate student at the University of Washington who wants to someday invent new drugs for neglected diseases.
Lately, she's been thinking a lot about snake bites: Around a hundred thousand people die each year from snake bites, according to the World Health Organization — and yet, she says, "the current therapeutics are not safe and are very expensive."
Part of the problem is that developing new drugs for things like snake bites has been a slow and laborious process. In the past, Torres says, it might have taken years to come up with a promising compound.
But recently, a new tool in her laboratory has rapidly sped up that timeline: Artificial intelligence. Torres started her current project in February and already has some candidate drugs lined up.
"It's just crazy that we can come up with a therapeutic in a couple of months now," she says.
Artificial intelligence is promising to upend the knowledge economy. It can already code computer programs, draw pictures and even take notes for doctors. But perhaps nowhere is the promise of AI closer to realization than the sciences, where technically-minded researchers are eager to bring its power to bear on problems ranging from disease to climate change.
On Thursday, the U.S. National Academies convened a two-day meeting on the potential for AI to change science. "AI scientists can really be more systematic, more comprehensive and not make errors," says Yolanda Gil, director of AI and data science initiatives at the Information Sciences Institute at the University of Southern California, who is attending the event.
Rather than using AI to do all science, she envisions a future in which AI systems plan and execute experiments, in collaboration with their human counterparts. In a world facing increasingly complex technical challenges, "there's not enough humans to do all this work," she says.
Proteins by Design
At the University of Washington, Vazquez-Torres is one of about 200 scientists working in a laboratory to design new therapies using proteins. Proteins are molecules that do much of the day-to-day work in biology: They build muscles and organs, they digest food, they fight off viruses.
Proteins themselves are built of simpler compounds known as amino acids. The problem is that these amino acids can be combined in a nearly infinite number of ways to make a nearly infinite number of proteins.
In the past, researchers had to systematically test many thousands of possible designs to try and find the right one for a particular job. Imagine being given a bucketful of keys to open a door — without knowing which one will actually work. You'd end up "just trying them out one at a time, to see what fits the best," says David Baker, the senior scientist who runs the lab.
AI has changed all that.
"Rather than having to make a bunch of possible structures on the computer and try them one by one, we can build one that just fits perfectly from scratch," he says.
The particular type of AI being used is known as diffusion modeling. It's the same technology used by popular AI image generators, like DALL-E or Midjourney. The system starts with a field of random pixels, essentially white noise, and then slowly tweaks each one until it creates what the user has asked for. In the case of an AI image generator that might be a picture of a flower. In the case of this lab's AI, it's a protein with a specific shape.
The shape of a protein often determines how well it will work, so this kind of AI is particularly well-suited for the job, Baker says. The AI also requires examples to learn from, and luckily, scientists have spent decades and billions of dollars developing a massive database full of proteins that it can study.
"There really aren't many places in science that have databases like that," Baker says.
And that's part of the reason that it's not yet clear whether every field will benefit equally from AI. Maria Chan is at Argonne National Laboratory in Illinois. She's working on developing new materials for the renewable economy — things like batteries and solar panels.
She says, unlike the field of proteins, there just isn't that much research on the sorts of materials she's studying.
"There hasn't been enough sort of measurements or calculations — and also that data is not organized in a way that everybody can use," she says.
Moreover, materials are different from proteins. Their properties are determined by interactions on many different scales — from the molecular all the way up to large scales.
Ian C Haydon/UW Institute for Protein Design
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Researchers at the University of Washington are using AI to design new kinds of proteins. Then they make them in the lab to see if they'll actually work.
Ian C Haydon/UW Institute for Protein Design
Researchers at the University of Washington are using AI to design new kinds of proteins. Then they make them in the lab to see if they'll actually work.
Ian C Haydon/UW Institute for Protein Design
The lack of data and complexity of materials make them harder to study using AI, but Chan still thinks it can help. Just about anything is better than the way scientists in the field worked prior to the computer revolution.
"The previous hundred years of science has to do with a lot of serendipity, and a lot of trial and error," she says. She believes AI will be needed to drive research forward — especially when it comes to the climate crisis, one of the most complicated problems in modern times.
Materials and proteins are far from the only fields working with AI in various ways. Systems are being actively developed in genetics, climate studies, particle physics, and elsewhere. The goal in many cases is to spot new patterns in vast quantities of scientific data — such as whether a genetic variation will cause a harmful abnormality.
Hypothesis hunters
But some researchers believe that AI could take a more fundamental role in scientific discovery. Hannaneh Hajishirzi, who works at the Allen Institute for Artificial Intelligence in Seattle, wants to develop new AI systems similar to ChatGPT for science. The goal would be a system that could crunch all the scientific literature in a field and then use that knowledge to develop new ideas, or hypotheses.
Because the scientific literature can span thousands of papers published over the course of decades, an AI system might be able to find new connections between studies and suggest exciting new lines of study that a human would otherwise miss.
Amr Nabil/AP
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Some researchers hope that AI could be used to find new materials for things like solar cells. There's limited data on these materials, and it's not stored centrally, so results are not guaranteed.
Amr Nabil/AP
Some researchers hope that AI could be used to find new materials for things like solar cells. There's limited data on these materials, and it's not stored centrally, so results are not guaranteed.
Amr Nabil/AP
"I would argue that at some point AI would be a really good tool for us to make new scientific discoveries," she says. Of course, it would still take human researchers to figure out if the scientific ideas the AI wanted to pursue were worthwhile.
Yolanda Gil at the University of Southern California wants to develop AI that can do all of science. She envisions automated systems that can plan and carry out experiments by themselves. That will likely mean developing entirely new kinds of AI that can reason better than the current models — which are notorious for fabricating information and making mistakes.
But if it could work, Gil believes the AI scientists could have a huge impact on research. She envisions a world in which AI systems can continuously reanalyze data, and update results on diseases or environmental change as it's happening.
"Why is it that the paper that was published in 2012 should have the definite answer to the question?" she asks. "That should never be the case."
Gil also thinks that AI scientists could also reduce errors and increase reproducibility, because the systems are automated. "I think it would be a lot more trustworthy; I think it could also be more systematic," she says.
But if AI scientists are the future, Susana Vazquez-Torres at the University of Washington doesn't seem worried about it. She and her labmates are attacking a wide swath of problems using their designer proteins — everything from new drugs, to vaccines, to improving photosynthesis in plants and finding new compounds to help break down plastics.
Vazquez-Torres says there are so many problems that need to be solved, and that many exciting discoveries lie ahead thanks to AI. "We can just make drugs right now so easily with these new tools," she says. Job security isn't a worry at all. "For me, it's the opposite — it's exciting." | Biology |
Study improves understanding of how bacteria benefit plant growth
Plants form alliances with microbes in the soil in which they grow. Legumes, for example, benefit from a symbiotic relationship with microbes that inhabit nodules in their roots and "fix" nitrogen in the atmosphere to make it available to promote the legumes' growth. But are microbes always beneficial to plants? Or does competition between strains for plant access degrade the service the bacteria ultimately provide?
A team led by scientists at the University of California, Riverside, set up experiments to answer these questions and better understand the competition process. The researchers used a native California plant with nodules, Acmispon strigosus, and a set of eight compatible nitrogen-fixing bacterial strains.
They infected some plants with each of the eight strains to directly measure their ability to infect the plants and provide benefits. They then infected other plants with pairs of bacterial strains to assess the competitive ability of each strain and the effect on plant performance.
The researchers found that competition between strains of beneficial bacteria in the soil degrades the service that the bacteria provide to their hosts. The study, "Competitive interference among rhizobia reduces benefits to hosts, " appears in the journal Current Biology.
"More specifically, we found interstrain competition that occurs in the soil before the bacteria infect the plant causes fewer of the bacteria to colonize the plant, resulting in the plant gaining smaller benefits in the end," said Joel Sachs, a professor of evolution, ecology, and organismal biology, who led the research team.
"To understand symbiosis, we often use sterile conditions where one strain of bacteria is 'inoculated' or introduced into an otherwise sterile host. Our experiments show that making that system slightly more complex—simply by using two bacterial strains at a time—fundamentally shifts the balance of benefits that the hosts receive, reshaping our understanding of how symbiosis works."
Sachs explained that a core challenge in agriculture is leveraging the services that microbes can provide to crops by promoting growth in a sustainable way, without the environmental costs of chemical fertilizers. His lab studies rhizobia—bacteria that promote plant growth.
Rhizobial competition is a longstanding problem for sustainable agriculture. Rhizobia form root nodules on legumes, within which the bacteria fix nitrogen for the plant in exchange for carbon from photosynthesis. Growers have long sought to leverage rhizobia to sustainably fertilize staple legume crops such as soybean, peanuts, peas, and green beans.
"One might think using rhizobia as inoculants should allow growers to minimize the use of chemical nitrogen, which is environmentally damaging," said Sachs, who chairs the Department of Evolution, Ecology, and Organismal Biology. "But such rhizobial inoculation is rarely successful. When growers inoculate their crops with high-quality rhizobia—strains that fix a lot of nitrogen—these 'elite' strains get outcompeted by indigenous rhizobia that are already in the soil and provide little or no benefit to hosts."
In their experiments, Sachs and his colleagues used bacterial strains whose genomes they had already sequenced. They also characterized the strains, which ranged from highly beneficial to ineffective at nitrogen fixation, to know exactly how beneficial they were to the target plant species. The researchers sequenced the contents of more than 1,100 nodules, each of which was from a plant that was inoculated with one of 28 different strain combinations.
Next, the researchers developed mathematical models to predict how much benefit co-inoculated plants would gain based on expectations from plants that were "clonally infected" (infected with one strain). This allowed the researchers to calculate the growth deficit that was specifically caused by interstrain competition.
"Our models showed that co-inoculated plants got much lower benefits from symbiosis than what could be expected from the clonal infections," said Arafat Rahman, a former graduate student in Sachs' lab and the first author of the research paper. "While beneficial bacteria work well in the lab, they get out-competed in the natural environment. Ultimately, we want to find a strain of bacteria—or a set of them—that gives maximum benefit to the host plant and is competitive against bacterial strains that are already in the soil."
Sachs explained that to discover and develop a bacterial strain that is highly beneficial to plants, scientists need to conduct experiments under very clean conditions.
"Ultimately, we want to use beneficial bacteria in agriculture," he said. "To identify these bacteria, we would, typically, add one bacterial strain to a plant in the lab and show that the plant grows much better with the strain than without. In the field, however, that plant is covered in microbes, complicating the story. In our experiments, we advanced from using one strain to a pair of strains to see what impact that has on plant growth. Interestingly, with just two strains, many of our predictions fell apart."
Rahman stressed that while experiments are needed to ascertain how beneficial a bacterial strain is, experiments that test how competitive the strain is against a panel of other bacterial strains are also needed.
"Both steps are crucial," he said. "Our work found some of the best strains can be highly beneficial to plant growth but as soon as you pair them with any other strain, that benefit is greatly reduced. Further, it is important to know at which stage the interstrain competition takes place: before the bacteria interact with the plant or after? Our work suggests it's the former and provides a useful guide to designing future experiments aimed at discovering strains that are better for delivery in crops."
Sachs said that in a lot of current experimental designs the focus is on the benefit to plants.
"It's important, however, to keep in mind that bacteria are shaped by natural selection," he said. "Some of them may be highly competitive in entering the nodule to infect the plant but not be very beneficial to the plant and that could be a trait that wins out in nature. If we are to leverage microbial communities for the services they can provide to plants and animals, we need to understand interstrain dynamics in these communities."
According to Sachs and Rahman, sustainable growth practices need to be a critical aspect of new agriculture to feed a growing population on a limited resource base.
"This will require moving past polluting methods such as adding huge amounts of chemical nitrogen to soil," Sachs said. "Understanding how to efficiently deliver beneficial microbes to a target host is a central challenge in medicine, agriculture, and livestock science. By revealing that interstrain dynamics can reduce the benefits of symbiosis, our work has opened new avenues of research to improve sustainable agricultural practices."
Sachs and Rahman were joined in the study by Max Manci, Cassandra Nadon, Ivan A. Perez, Warisha F. Farsamin, Matthew T. Lampe, Tram H. Le, and Lorena Torres Martínez of UCR, and Alexandra J. Weisberg and Jeff H. Chang of Oregon State University. Rahman plans to join Oregon State University as a postdoctoral researcher.
More information: Joel L. Sachs, Competitive interference among rhizobia reduces benefits to hosts, Current Biology (2023). DOI: 10.1016/j.cub.2023.06.081. www.cell.com/current-biology/f … 0960-9822(23)00867-9
Journal information: Current Biology
Provided by University of California - Riverside | Biology |
It may seem that your cat has an uncanny ability to sniff out treats.
Now, scientists have discovered the secret to felines' finesse at tracking down food.
Research reveals cats have noses that act like high-tech chemical analysis equipment usually found in the lab.
A complex collection of tightly coiled bony airway structures are behind their great sense of smell, and work in a similar way to parallel coiled gas chromatographs – laboratory equipment used to analyse the chemical makeup of substances.
Scientists from Ohio State University created a 3D computer model of a cat nose and simulated how an inhalation of air containing common cat food odours would flow through the coiled structures.
They found that the air separates into two flow streams.
One stream of air is cleansed and humidified before being sent to the lungs, while the other delivers the odour quickly and efficiently to the system responsible for smelling, also known as the olfactory region.
This allows cats to smell very quickly, rather than waiting for air to filter through the respiratory zone used for breathing, the team said.
The air that is sent down the tube for 'smell' is then recirculated in channels when it gets there.
Senior author Kai Zhao said: 'It's like you take a sniff, the air is shooting back there and then is being processed for a much longer time.
'It's a very good design if you think about it.
'For mammals, olfaction is very important in finding prey, identifying danger, finding food sources and tracking the environment.
'Simulation of air and odour flow through the virtual cat nose showed that it appears to function similarly to a parallel coiled gas chromatograph, in which the efficiency of the basic technique is boosted by the use of multiple tubes branching off of one high-speed gas stream.'
The findings were published in the journal Plos Computational Biology. | Biology |
This is the second in a three-part series on the obesity crisis. Part one tackles a complicated question â why does the obesity rate keep rising despite our efforts to stop it? -- and can be found here. Part three shows how doctors and patients can make treatment better and can be found here. [link TK]
July 5, 2023 -- In the mid-1980s, Louis Aronne strolled into a lab at Rockefeller University where a colleague was breeding mice. âI will never forget what he showed me,â said Aronne, now the director of obesity research and treatment at Weill Cornell Medicine in New York City. âHe had a cage with 10 mice, one severely obese and the others normal weight. He took blood from one of the thin mice and gave it to the fat mouse.â
When Aronne returned 3 days later, that obese mouse had turned thin.Â
It was proof of something Aronne already suspected: Obesity had biological causes and wasnât just a failure of willpower.
Years later, in 1994, that research led to the discovery of leptin, a hormone released from fat cells thatâs involved in the regulation of body weight. It was a watershed moment in obesity research.Â
Since then, Aronne and others have worked to build the clinical field of obesity medicine, attempting to shift the public and medical view of obesity from a purely behavioral issue to a disease worthy of medical treatment.Â
All the while, the U.S. obesity rate soared.Â
Now, another watershed moment: We finally have highly effective obesity drugs. The hype is real, and so are the weight loss results.Â
âIâve been saying for 30 years that when we find treatments that really work, people arenât going to believe the results,â Aronne says. âIt took longer than I expected, but itâs gratifying now to see.â
All this excitement raises a crucial question: Will the new drugs finally end the obesity crisis? Experts have their doubts.
The Big Question
The emerging class of obesity medications known as GLP-1 agonists is indeed a game changer. The weight loss drug semaglutide (Ozempic, Wegovy) showed groundbreaking results, and studies suggest a parade of even more impressive drugs are on the way.
Yes, the drugs offer new hope to millions with obesity complications. But to truly turn the tide on our 42% obesity rate, much more work remains to be done, researchers said, including answering a big question:
How do these weight loss drugs work?Â
âWe have new blockbuster drugs, and we donât even know why they reduce body weight,â says Samuel Klein, MD, professor of medicine and nutritional science at Washington University School of Medicine in St. Louis. âIt was by accident that this was discovered.â
Oops, We Created a Weight Loss Drug
Developed to treat diabetes, the GLP-1 drugsâ weight loss effects were a surprise. Now that those effects are confirmed, pharmaceutical companies and researchers are racing to figure out how these drugs work.Â
In the 1960s, scientists discovered the incretin effect â when you eat glucose (sugar), your body makes more insulin than it does if you inject it. Glucose passes through the GI tract and the gut releases hormones that stimulate insulin secretion. Itâs âessentially a feed-forward signal to your pancreas to tell it, 'By the way, you need to be ready because thereâs a bunch of glucose coming,'â said Randy Seeley, MD, director of the Michigan Nutrition Obesity Research Center, funded by the National Institutes of Health.Â
One of these hormones -- or âincretinsâ -- is GLP-1. In experiments, people with type 2 diabetes who were hooked up to GLP-1 saw their blood sugar go down.Â
âThat led to the idea that if we could take this native hormone and make it last longer, weâd have a therapy for type 2 diabetes,â said Seeley. Thanks to a GLP-1-like compound in the saliva of the Gila monster, that idea became reality in the 2000s.Â
Along the way, a surprising side finding came to light: In early trials, diabetes patients on these drugs dropped weight.Â
Both Ozempic and Wegovy -- brand names for semaglutide -- are once-weekly injections (pill forms are on the way), but the latter is a higher dose.Â
âThat dose results in about 40% of patients in the clinical trials achieving a 20% weight loss. Weâve just had nothing like that in terms of efficacy before,â said Seeley, who has worked with some of the drug companies (including Novo Nordisk, the maker of Ozempic and Wegovy, and Eli Lilly, maker of Mounjaro) that market the GLP-1s.Â
By contrast, semaglutideâs once-a-day predecessor liraglutide (Saxenda, also made by Novo Nordisk) can lead to about 10% weight loss.Â
âAnd one of the ironies is, we donât really know why,â Seeley says. âWe donât know why semaglutide is a better molecule for weight loss than liraglutide.âÂ
Initially, scientists believed that the drugs, in addition to telling the pancreas to secrete more insulin, were also signaling the brain that youâre full. âTurns out thatâs not really the way it works,â Seeley says. âGLP-1 made from your gut probably doesnât get into your brain very much. But you make GLP-1 in your brain as well.â
For weight loss, itâs the brainâs GLP-1 system, not the gutâs, that the drugs are thought to hijack. But exactly which parts of the brain they affect and how is unknown. âThatâs something lots of people are working on, including our own lab,â Seeley said. (Another surprise: The drugs may have potential as an anti-addiction treatment.)
The diabetes medication tirzepatide (Mounjaro), expected to be approved for weight loss as early as this year, is also a weekly injection, but it has a unique feature: Itâs starts a response not just for GLP-1 but also for another incretin called GIP. Turns out, two is better than one: Trial participants on tirzepatide lost up to 22.5% of their body weight.Â
More of these hybrid drugs are on the way, Seeley said. In mid-stage clinical trials, the drug retatrutide, which targets three hormones, led to 24% weight loss. âThe idea is the more bullets we can load into the gun, the more we can push the biology into a place where itâs easier to lose weight.â
Shifting From Prevention to Damage Control
Less invasive and more scalable than surgery (only 1% of the eligible population gets bariatric surgery), the drugs offer doctors a safe, effective way to treat many patients with obesity. Thatâs cause for excitement, but concerns remain because they are expensive, costing about $800 to $1,300 per month out of pocket. Many health insurers, including Medicare, do not cover them for weight loss.Â
âYou have this significant advance in obesity treatment, but very few will be able to access it,â said Gary Foster, PhD, adjunct professor of psychology in psychiatry at the University of Pennsylvania and chief scientific officer at WW (formerly Weight Watchers).
There is a push, including a proposed bill, to get Medicare to cover obesity medication. But given the expense of the drugs, the health economics do not support that move, according to an editorial in the New England Journal of Medicine. If Medicare were to cover obesity meds, the budget impact would likely be huge, potentially driving up premiums. If other payers followed suit, the impact could be felt across the U.S. health care system.Â
Other drawbacks include side effects â including nausea, diarrhea, stomach pain, and vomiting â that can be so bad that some patients canât tolerate them.
And critically, the drugs do not deal with the root cause of the problem, said Robert Lustig, MD, an endocrinologist and pediatrician at the University of California, San Francisco, who has suggested that excess insulin is driving obesity. âNo one has the disease that these drugs are treating. No one has GLP-1 deficiency. Theyâre bypassing the problem. Theyâre band-aiding the problem.âÂ
Because the drugs work by mimicking starvation â they appear to curb hunger, so you eat less â people on them lose not just fat but also healthy lean mass, Lustig said.Â
Concerns about pancreatitis did not really bear out in post-marketing reports. (The drugs are still not recommended in people with pancreatitis, or a history of a type of thyroid cancer or a type of tumor called multiple endocrine neoplasia.) But predicting longer-term outcomes can be hard, notes Lustig.
Then there are philosophical questions, Hill said. âIf youâre continuing to not exercise and eat not healthy foods and take a medication, is that success? Have we won when people are at a lower weight but not doing a healthy behavior?â
âWe Canât Treat Our Way Out of Thisâ
The fact is, ending the obesity epidemic is a tall order, even for drugs as impressive as these.Â
âWe canât treat our way out of this,â said Jamy Ard, MD, co-director of Wake Forest Baptist Health Weight Management Center in Winston-Salem, NC. âThe treatments we have now are great, and there will be more coming. But we do need to figure out the prevention side of things.âÂ
Seeley agrees but adds we canât diet-and-exercise our way out either.Â
âThereâs no switch to be flipped,â Seeley says. âIf you told me we shouldnât spend all this money on these drugs, we should spend it on prevention â great! What would we do?âÂ
And prevention efforts wonât help the millions already living with health problems from obesity, Aronne said.Â
âGetting people to stop smoking prevents lung cancer. But stopping smoking doesnât treat lung cancer,â Aronne said. âOnce the physical changes occur in the lung that cause a tumor to grow, itâs too late. You have to think of obesity the same way.âÂ
Seeley points out that âfearmongeringâ around the drugs highlights our lingering bias that obesity is a lifestyle issue that should not be medically treated.Â
âPeople say, âWhen you stop taking it, youâre going to gain the weight back,ââ Seeley said. âThereâs truth to that, but when you stop taking your hypertension medication, your blood pressure goes up. We donât think of that as a [reason] for why you shouldnât take your blood pressure medication. But that gets trumpeted into all these conversations about whether people [with obesity] should be treated at all.â
Like obesity, blood pressure was once thought to be a behavioral problem too, Aronne said. But blood pressure meds prevent heart attacks and strokes. And obesity meds can do the same.Â
One 55-year-old patient on the road to kidney failure lost weight on obesity medications, including semaglutide, Aronne said. Now, 6 years later, his kidney function is back to normal. âNormally, we think of kidney disease as irreversible,â Aronne said.Â
In that respect, these drugs should save money in the long run by virtue of heading off those health care costs, said Seeley, who imagines a future where obesity is not gone but better managed, like high blood pressure is now.Â
In the end, the drugs are another step toward what Aronne and many others have always pushed for: Treating obesity as a disease.Â
How doctors and patients can do everything better -- read part three here. [LINK] | Biology |
How the ancient messengers cAMP and cGMP deliver their messages
Two highly similar molecules with essential but often contrasting signaling roles in most life forms exert their distinct effects through subtle differences in their bindings to their signaling partners, according to a new study led by researchers at Weill Cornell Medicine.
In the study, published March 27 in Nature Structural & Molecular Biology, the researchers used exquisitely sensitive measurement techniques to reveal at the single-molecule level how the signaling molecules cAMP and cGMP bind to an ion channel from the pacemaker channel family, one of the major types of proteins whose activities they regulate.
Ion channels are common features of cell membranes, and control basic cell functions by allowing calcium, sodium, potassium and other charged elements called ions to flow in and out of cells. Many ion channels can bind both cAMP and cGMP while being effectively switched open by only one of them. Precisely how the two molecules exert their differing effects on ion channel activity had been a mystery.
The study details how cAMP/cGMP bind to ion channels and advances the understanding of a fundamental aspect of cell biology. These findings could eventually inspire new treatments for disorders involving ion channel malfunctions.
"We found clear differences in the interaction and binding strength of these two molecules to the ion channels, which we think explains why one can open the channel and the other cannot," said study senior author Dr. Simon Scheuring, a professor of physiology and biophysics in anesthesiology at Weill Cornell Medicine.
Cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) are known as cyclic nucleotides: "cyclic" because their chemical structures contain cyclic or ring motifs, and "nucleotides" because they are part of the same family of molecules as the nucleotide building blocks A and G of DNA. They appear to have evolved as multipurpose switches capable of regulating the activity of a wide range of different protein targets.
Often only one of them, cAMP or cGMP, is the activator, while the other does little or nothing directly to the target but can force it into an inactive state by binding to the same site, thus the competition between the two molecules switches the channels on and off.
The proteins regulated by cAMP/cGMP include a large class of ion channels called cyclic nucleotide-gated (CNG) ion channels. CNG channels have important roles across the nervous system, including in the sensory neurons mediating smell and vision, and in the pacemaker cells that govern heartbeat rhythm.
Dr. Scheuring, who has helped pioneer the use of a sensitive measurement technique called atomic force microscopy (AFM), and Dr. Crina Nimigean, an ion channel expert and a professor of physiology and biophysics in anesthesiology at Weill Cornell Medicine, have already made considerable progress in understanding how cAMP/cGMP regulate CNG channels. In a 2018 paper, for example, they used high speed AFM to show how a bacterial CNG channel, SthK changes conformation when bound by the channel-opener cAMP or the effective channel-closer cGMP.
In the new study they teamed up again and were also joined by a molecular-dynamics modeling expert Dr. Helmut Grubmüller of the Max Planck Institute for Multidisciplinary Sciences in Germany. Their main technique this time was an AFM-related force-sensing method called AFM single molecule force spectroscopy, which is sensitive enough to measure the binding force of just one cAMP or cGMP molecule to its binding site on the ion channel. With that, and help from computational modeling, they quantified how cAMP and cGMP differ in their binding strengths and depth to the same binding site on SthK, via interactions with different clusters of atoms within the binding site.
"Cyclic AMP can access a more strongly bound state; that is, it stays longer in its binding site on the ion channel, compared with cGMP, suggesting that this deep-bound state is the key to channel activation," said study first author Dr. Yangang Pan, a postdoctoral researcher in the Scheuring laboratory.
The SthK channel is just one model for mammalian CNG channels, and the researchers plan future studies with mammalian CNG channels. But they believe that their SthK findings already illuminate the fundamental mechanism of how cAMP and cGMP work as regulators in their many roles throughout biology.
"Binding sites for cAMP/cGMP are found not just on ion channels but also on signaling enzymes, transcription factors, and other proteins," Dr. Nimigean said. "We suspect that in every case, nature has tuned how these proteins recognize cAMP/cGMP, in accordance with these proteins' functions."
More information: Yangang Pan et al, Discrimination between cyclic nucleotides in a cyclic nucleotide-gated ion channel, Nature Structural & Molecular Biology (2023). DOI: 10.1038/s41594-023-00955-3
Journal information: Nature Structural & Molecular Biology
Provided by Weill Cornell Medical College | Biology |
A Yale-led study has discovered a new way to potentially treat aortic aneurysms (AA), a condition where the aorta ruptures, in individuals with Marfan Syndrome (MFS). Recently a study by Martin Schwartz, PhD, Robert W. Berliner Professor of Medicine, and professor of biomedical engineering and of cell biology, published in the journal Arteriosclerosis, Thrombosis and Vascular Biology, suggests that fibronectin amplifies inflammatory responses through its main receptor, integrin α5β1 in MFS.
MFS is a genetic disorder which affects the development of stable connective tissue, including the aorta. MFS is caused by mutations in the FBN1 gene that encode fibrillin-1. This leads to the destabilization of elastic fibers and accumulation of fibronectin (FN) in the extracellular matrix, which can contribute to the development of aortic aneurysms.
First authors Minghao Chen, PhD, and Cristina Cavinato, PhD, demonstrate that the increase in FN, resulting from fibrillin insufficiency, affects smooth muscle cells (SMCs). This occurs by decreasing contractile gene expression and activating inflammatory pathways (via integrin α5-NF-kB signaling), both of which contribute to aneurysm development. The authors used integrin α2 chimeric mice, crossed with Fbn1mgR/mgR (mgR: animal model of Marfan syndrome), to investigate the molecular mechanisms by which FN affects SMCs. They found that the mutation in integrin α5/2 greatly prolonged the survival of Marfan mice and improved the integrity of elastic fibers, mechanical properties, SMC density, and SMC contractile gene expression. The study highlights the NF-kB pathway as a critical regulator of the SMC phenotypic switching in the presence of FN. These findings suggest a potential therapeutic strategy for the treatment of MFS by targeting the adverse signaling pathways involving FN-integrin α5.
Other authors of this study are Jens Hansen, Ravi Iyengar, Keiichiro Tanaka, Pengwei Ren, Abdulrahman Hassab, David S. Li, Eric Youshao, George Tellides, and Jay D. Humphrey. | Biology |
People frequently exposed to racial or ethnic discrimination may be more susceptible to obesity and related health risks in part because of a stress response that changes biological processes and how we process food cues. These are findings from UCLA researchers conducting what is believed to be the first study directly examining effects of discrimination on responses to different types of food as influenced by the brain-gut-microbiome (BGM) system.
The changes appear to increase activation in regions of the brain associated with reward and self-indulgence -- like seeking "feel-good" sensations from "comfort foods" -- while decreasing activity in areas involved in decision making and self-control.
"We examined complex relationships between self-reported discrimination exposure and poor food choices, and we can see these processes lead to increased cravings for unhealthy foods, especially sweet foods, but also manifested as alterations in the bidirectional communication between the brain and the gut microbiome," said Arpana Gupta, PhD, a researcher and co-director of the UCLA Goodman-Luskin Microbiome Center and the UCLA G. Oppenheimer Center for Neurobiology of Stress and Resilience.
"Our results show that a person's brain-gut crosstalk may change in response to ongoing experiences of discrimination -- affecting food choices, cravings, brain function, and contributing to alterations in gut chemistry that have been implicated in stress and inflammation. It appears that in response to stressful discrimination experiences, we seek comfort in food, manifested as increased cravings, and increased desire for highly palatable foods, such as high-calorie foods and, especially, sweet foods. These alterations may ultimately cause people exposed to discrimination to be more vulnerable to obesity and obesity-related disorders," said Gupta, senior author of the paper, which appears in Nature Mental Health.
Previous studies have looked into many factors -- genetics, diet, exercise, and others -- that could contribute to disproportionately high rates of obesity and related disorders occurring in African Americans and others in communities of color. Few studies have addressed the potential role of discrimination in obesity, and this is the first known study providing direct evidence of possible brain-gut interactions linking discrimination to eating behaviors.
The findings are based on results of functional MRI brain scans, sophisticated statistical modeling techniques, and analyses of metabolites of the glutamate pathway in the digestive tract.
Participants included 107 people -- 87 women and 20 men -- of diverse racial and ethnic backgrounds who completed a validated and widely used questionnaire that measures chronic experiences of unfair treatment. Based on their scores, participants' responses were divided into "high discrimination exposure" and "low discrimination exposure" groups.
All participants provided stool samples. They also completed a "food-cue" task while MRI brain scans were acquired to evaluate brain responses to pictures of five different types of food:
Using these measurements, the researchers focused on discrimination-related differences in the various food group categories -- looking at responses to the food cues in key regions of the brain. Results showed:
Through analysis of fecal samples, the researchers looked for changes in 12 glutamate metabolites -- substances resulting from the breakdown of glutamate. As a neurotransmitter, glutamate has been associated with numerous stress responses and aging, and in this study, participants in the greater discrimination group had higher levels of two glutamate metabolites that have been implicated in inflammatory processes, oxidative stress and increased risk for developing obesity.
The authors say considering both the present results and previously published research, greater discrimination exposure may lead to alterations in the bidirectional brain-gut microbiome communication that skews our biology towards unhealthy eating behaviors and cravings for unhealthy foods. This occurs via inflammatory processes in the brain-gut microbiome system involved in dysregulations of glutamatergic signaling and modulation of the frontal-striatal circuits.
Gupta said the revelations may help researchers develop treatments that target the brain or the gut.
"At the brain level, treatments could be developed to modulate the food-related reward system or the hyper-aroused brain circuits associated with stress and discrimination exposure. On the other end of the spectrum, at the gut level, it also means we can target the glutamatergic pathways -- possibly with probiotic supplementation or anti-inflammatory dietary changes -- as a therapeutic approach to treat stress-related experiences such as discrimination," she said.
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Researchers discover new method to inhibit cholera infection
Recent research investigates a novel strategy for inhibiting the spread and infection of Vibrio cholerae, the bacteria responsible for the disease, cholera.
The research article is titled, "A peptide-binding domain shared with an Antarctic bacterium facilitates Vibrio cholerae human cell binding and intestinal colonization" and was recently published by The Proceedings of the National Academy of Sciences.
V. cholerae is found naturally on various surfaces within marine environments. When water or food contaminated with V. cholerae is consumed by humans, it colonizes the gastrointestinal tract and causes cholera.
According to the Centers for Disease Control and Prevention, cholera is an intestinal infection that causes diarrhea, vomiting, circulatory collapse and shock. If left untreated, 25 to 50% of severe cholera cases can be fatal. Cholera is a leading cause of epidemic diarrhea in parts of the world and the World Health Organization (WHO) estimates up to four million people are infected each year.
Karl Klose, director of The South Texas Center for Emerging Infectious Diseases (STCEID) and the Robert J. Kleberg, Jr. and Helen C. Kleberg College of Sciences Endowed Professor, coauthored the research article with Cameron Lloyd, a UTSA doctoral student who graduated in August with a Ph.D. in molecular microbiology and immunology.
Lloyd was the primary author and completed the article as his thesis project under the advisement of Klose, who has been studying the pathogenic mechanisms of V. cholerae for 30 years. Lloyd worked in Klose's laboratory for five years.
He learned how to study V. cholerae, genetically manipulate the bacteria, and measure its ability to spread disease, bind to red blood cells and form biofilms, which are surfaces where communities of bacteria form that are more resistant to antibiotics. Lloyd is currently interviewing for several postdoctoral fellowship positions in laboratories across the nation.
"By taking advantage of the structural similarities of functional domains in two large adhesins [cell-surface components or appendages of bacteria that facilitate adhesion to other cells, usually in the host they are infecting or living in] produced by two different organisms, we were able to characterize an effective inhibitor to intestinal colonization and biofilm formation," said Lloyd.
In collaboration with the laboratories of Peter Davies, Canada research chair in Protein Engineering and professor of biomedical and molecular sciences at Queens University, Canada, and Ilja Voets, professor of chemical engineering and chemistry at Eindhoven University, Netherlands, Lloyd and Klose successfully identified a peptide, a short chain of amino acids that make up proteins, that can inhibit the virulence of V. cholerae.
They discovered that the peptide inhibiters that bind to Marinomonas primoryensis, an Antarctic bacterium that sticks to microalgae in a similar manner to how V. cholerae sticks to human intestines, can also disrupt V. cholerae from adhering to human cells, forming biofilms and colonizing the gastrointestinal tract.
"We demonstrated that these peptide inhibitors could inhibit both biofilm formation as well as intestinal colonization by V. cholerae," said Klose. "It is possible that this could be part of intervention strategies to inhibit these bacteria from causing disease and persisting in the environment."
The Klose Lab is a part of The South Texas Center for Emerging Infectious Diseases (STCEID) and specializes in studying how bacteria cause disease. The lab has worked most extensively with V. cholerae and Francisella tularensis, the bacterium that causes tularemia, or rabbit fever.
STCEID researchers specialize in the study of infectious diseases and form one of the premier centers for this type of research in the nation. The Center connects state-of-the art facilities with the diverse expertise of its faculty to cultivate an environment that answers critical questions relating to emerging and bioweapon-related diseases.
The facilities and faculty at the Center also serve an important role in providing hands-on training to undergraduate and graduate students who intend to pursue careers in science and technology.
"This project and others like it have equipped me with an in-depth knowledge of molecular biology, coding, and high throughput data analysis," said Lloyd.
"Our graduate students that come to UTSA to get Master's and Ph.D. degrees are in the best place to study infectious diseases," added Klose.
More information: Cameron J. Lloyd et al, A peptide-binding domain shared with an Antarctic bacterium facilitates Vibrio cholerae human cell binding and intestinal colonization, Proceedings of the National Academy of Sciences (2023). DOI: 10.1073/pnas.2308238120
Journal information: Proceedings of the National Academy of Sciences
Provided by University of Texas at San Antonio | Biology |
Study finds how some ion channels form structures permitting drug delivery
A member of an important class of ion channel proteins can transiently rearrange itself into a larger structure with dramatically altered properties, according to a study led by researchers at Weill Cornell Medicine. The discovery is a significant advance in cell biology, likely solves a long-standing mystery about an unusual feature of some ion channels and has implications for the development of drugs targeting these proteins and for drug delivery.
Ion channels are ubiquitous in the cell membranes of higher organisms. They conduct small, charged molecules called ions into or out of cells, in order to regulate cell activity. They are necessary for most biological functions, from sensation to cognition to heartbeat. Although about 15 percent of pharmaceuticals work by targeting ion channels, scientists could target them more effectively if they knew more about the dynamics of their complex structures.
In the study, published in Nature, the researchers examined the structural dynamics of an ion channel called TRPV3. They discovered an uncommon but striking structural rearrangement in which TRPV3, normally a "tetramer" made of four identical protein subunits, becomes a five-protein "pentamer." The researchers found strong evidence that this structural rearrangement underlies a hitherto unexplained ion-channel phenomenon called pore dilation.
"These findings open up a broad new avenue of research on the workings of ion channels," said study senior author Dr. Simon Scheuring, a professor of physiology and biophysics in anesthesiology at Weill Cornell Medicine.
The study's first author was Dr. Shifra Lansky, a postdoctoral research associate in the Scheuring lab in the Department of Anesthesiology. The work was performed in collaboration with Dr. Crina Nimigean's lab in the Department of Anesthesiology at Weill Cornell Medicine.
TRPV3 is an ion channel that is involved in the sensing of warm temperatures, skin health, itch, hair growth, and other functions throughout the body. It belongs to the larger family of TRP ion channels, which have numerous biological roles in higher organisms. Drs. Scheuring and Lansky and their colleagues initially set out to map TRPV3's structural dynamics—how its structure changes as it opens and closes its channel—using an advanced tool called high-speed atomic-force microscopy.
To the researchers' surprise, they soon discovered that TRPV3, normally a tetramer, occasionally assembles itself into a pentamer, and can exist in this uncommon state for only about three minutes.
The scientists recognized that this substantial enlargement of the TRPV3 structure might account for the phenomenon of ion channel pore dilation, an oddity first reported in another ion channel in 1999, and in TRPV3 in 2005. Pore dilation is an unusual, transient state in which an ion channel opens to an abnormal extent, admitting much larger ions than usual, and becomes insensitive to its normal activators and inactivators. Whether pore dilation serves an evolved biological function isn't clear, though it can be triggered by prolonged ion channel activation, and the researchers suspect it works as a protective mechanism against excessive exposure to a stimulus.
"If you bite on a strong chili pepper, for example, your mouth will be insensitive and in pain for a few minutes, during which you won't want to take another bite," Dr. Scheuring said. "Maybe that kind of protective alteration of sensitivity is what ion channel pore dilation is for."
Pore dilation is also of interest to drug developers—inhibiting it may be therapeutic in some cases and activating it may provide a way to get large, water-soluble drug molecules into cells that would otherwise be impermeable to them.
Subsequently, the team used electron microscopy to obtain a high-resolution 3D structure of TRPV3 in its pentameric state. They showed that the pore of the TRPV3 pentamer is indeed much larger than the pore of the tetramer, corresponding to increased ion conductance and the ability to transport molecules. These features are associated with the pore dilation phenomenon. They also found that a compound known to make pore dilation more likely destabilizes the TRPV3 tetramer, making it about twice as likely to turn into a pentamer.
Thus, they concluded, pore dilation is related to this transient pentameric state of ion channels that are normally tetramers.
Pore dilation appears to be a quite common property of ion channels, functionally reported in at least seven channels from two different families, and so the discovery is expected to lead to much further research in this area, with the goal of understanding exactly how it occurs and how it can be controlled, perhaps for treating diseases.
"There are genetic diseases linked to mutations in TRPV channels, and we suspect that some of these mutations cause disease by increasing pentamer formation," Dr. Lansky said. "If we can prove that, it would be a big step towards curing these diseases."
Dr. Scheuring also noted that the process in which TRPV3 subunits diffuse through the cell membrane to turn tetramers into pentamers, and back again, represents a previously undiscovered mechanism for how proteins reshape their structures to modulate their functions.
"This is a completely novel way of thinking about protein conformational change," he said.
Journal information: Nature
Provided by Weill Cornell Medical College | Biology |
Image source, Current Biology/Sorensen et al.Image caption, Delta, one of the dolphins, with a sound tag to measure his clicks and whistles during the experimentDolphins struggle to hear each other and cooperate in a world of increasing noise pollution, a new study reveals.They are one of many marine mammals that rely on whistles and echolocation to work together for hunting and reproducing. But noise pollution from human activity like shipping and construction have risen dramatically in recent years. If they are no longer able to cooperate it could have detrimental effects, the researchers said.Media caption, Dolphins Delta and Reese use sound to cooperate during a test"If groups of animals in the wild are less efficient at foraging cooperatively, then this will negatively impact individual health, which ultimately impacts population health," said co-author Stephanie King, associate professor at the University of Bristol. Sound is one of the most important senses for marine animals. Unlike light, which is quickly absorbed by water, it can travel tens if not hundreds of kilometres.As a result, cetaceans - whales, dolphins, porpoises - have developed a complex range of sounds to "talk" to each other. It was already known that they will increase the volume of their calls or the frequency to try and compensate for noise pollution caused by human activity. Pernille Mayer Sørenson, a PhD candidate at Bristol University who led the research team which included the Dolphin Research Centre and St Andrews University, said: "We knew from previous studies that noise pollution impacts animals, but from this study what we do for the first time is look at how noise impacts how animals work together."The study, published in the journal Current Biology, revealed that the efforts of dolphins to compensate for pollution by "shouting" were not enough and they struggled to work together.The study was carried out with two bottlenose dolphins Delta and Reese - who goes by the nickname "Reese's pieces" - in an experimental lagoon with their trainers. They were required to perform a cooperative task - in this case each pressing a button within a certain time of each other.Each dolphin was fitted with a temporary sound-and-movement tag which sits behind their blowhole and measures their behaviour and sounds.The scientists found that as the dolphins were exposed to increasing levels of anthropogenic (human-created) noise they nearly doubled their whistle durations and also loudness to compensate for this interference. Reese and Delta were also more likely to face each other. Previous work has shown that this may be because their hearing is sensitive to direction, meaning that facing each other could help separate the signal of their partner and the polluting noise - a process known as "spatial release".Despite their best efforts though, Delta and Reese were only 62.5% successful when they were exposed to very high noise pollution compared to 85% during the control experiment with ambient background noise.The highest level of noise they were exposed to was 150 decibels (dB). The sound produced by a super tanker cargo vessel as it moves through the ocean, will reach volumes of up to 200 dB according to the Natural History Museum. Image source, Dolphin Research CentreImage caption, Reese's whistles were on average 1.85 times longer in the highest noise exposure trialsMs Sørenson explained why it is a concern if dolphins cannot communicate properly: "If you are exposed to noise and that prevents you from you communicating with your friends when you are foraging together that might lead to missed opportunities and could have an impact on your individual health if that's a certain behaviour that is essential to your survival."And she warned: "If you are exposed to that over longer and longer time it could have bigger consequences at a population level."This work adds to existing research linking noise pollution to negative impacts for marine mammals. Whales have been observed suffering from decompression sickness, behavioural changes and strandings after being exposed to noise pollution from ships, oil and gas surveying and construction. Image source, ReutersImage caption, Whales can become stranded if they become disorientated by noise pollution from ships and other human activitiesThe next step would be to repeat the experiment for dolphins in the wild, but this is a challenge because of the difficulties in creating a controlled scenario with no noise pollution to compare with. But Ms Sørensen suspects that wild dolphins would perform even worse when exposed to noise pollution than their counterparts at the research centre.She said: "These individuals [Delta and Reese] are highly motivated and know this task well - they have done it hundreds of times for previous studies. But if we go out into the wild, if an animal wants to initiate behaviour with someone else, they might not know that its partner wants to cooperate."Around the BBC | Biology |
Google's AI firm DeepMind has used artificial intelligence to identify changes in human DNA that might cause diseases.
The researchers believe they have pinpointed 89% of all the key mutations.
The development is expected to speed up diagnosis and help in the search for better treatments.
A leading independent scientist told BBC News that the work was "a big step forward".
Prof Ewan Birney, deputy director general of the European Molecular Biology Laboratory, said: "It will help clinical researchers prioritise where to look to find areas that could cause disease."
The technique works by checking the order of the components in human DNA strands.
All living organisms are built from DNA. It is made from four blocks of chemicals called adenine (A), cytosine (C), guanine (G) and thymine (T). In humans, when an embryo is developing, the order of these letters are read to produce proteins, which are the building blocks of the the cells and tissues that make up various parts of the body.
But if the letters are in the wrong order - perhaps because of an inherited disorder - the body cells and tissues aren't made properly - and this can lead to disease.
Last year Google DeepMind's AI worked out the shape of nearly all proteins in the human body.
The new system, called AlphaMissense, can tell If the letters in the DNA will produce the correct shape. If not, it is listed as potentially disease-causing.
Currently genetic disease hunters have fairly limited limited knowledge of which areas of human DNA can lead to disease. They have classified 0.1% of letter changes, or mutations, as either benign or disease causing.
Google DeepMind's Pushmeet Kohli said that the new model pushed that percentage up to 89%.
Currently, researchers have to search for potentially disease-causing regions across billions of chemical building blocks that make up DNA. That has now changed, according to Mr Kohli.
''Researchers can now focus their efforts on the new areas, that they were not aware of and we have highlighted as potentially disease-causing,'' he said.
The new tool - published in the journal Science - has been tested by Genomics England, who work with the NHS. According to Dr Ellen Thomas, who is the deputy chief medical officer at Genomics England, the health service will be among the first organisations to benefit from the new development.
"The new tool is really bringing a new perspective to the data. It will help clinical scientists make sense of genetic data so that it is useful for patients and for their clinical teams," she said.
Prof Birney said he expected AI to become a massive part of molecular biology and life sciences.
"I don't know where it's going to end but it's changing nearly everything we do at the moment," he said.
Follow Pallab on X, formally known as Twitter | Biology |
Scientists have created “synthetic” mouse embryos from stem cells without a dad’s sperm or a mom’s egg or womb.The lab-created embryos mirror a natural mouse embryo up to 8 ½ days after fertilization, containing the same structures, including one like a beating heart.In the near term, researchers hope to use these so-called embryoids to better understand early stages of development and study mechanisms behind disease without the need for as many lab animals. The feat could also lay the foundation for creating synthetic human embryos for research in the future.“We are undoubtedly facing a new technological revolution, still very inefficient … but with enormous potential,” said Lluís Montoliu, a research professor at the National Biotechnology Centre in Spain who is not part of the research. “It is reminiscent of such spectacular scientific advances as the birth of Dolly the sheep” and others.A study published Thursday in the journal Nature, by Magdalena Zernicka-Goetz at the California Institute of Technology and her colleagues, was the latest to describe the synthetic mouse embryos. A similar study, by Jacob Hanna at the Weizmann Institute of Science in Israel and his colleagues, was published earlier this month in the journal Cell. Hanna was also a coauthor on the Nature paper.Zernicka-Goetz, an expert in stem cell biology, said one reason to study the early stages of development is to get more insight into why the majority of human pregnancies are lost at an early stage and embryos created for in vitro fertilization fail to implant and develop in up to 70% of cases. Studying natural development is difficult for many reasons, she said, including the fact that very few human embryos are donated for research and scientists face ethical constraints.Building embryo models is an alternative way to study these issues.To create the synthetic embryos, or “embryoids,” described in the Nature paper, scientists combined embryonic stem cells and two other types of stem cells – all from mice. They did this in the lab, using a particular type of dish that allowed the three types of cells to come together. While the embryoids they created weren’t all perfect, Zernicka-Goetz said, the best ones were “indistinguishable” from natural mouse embryos. Besides the heart-like structure, they also develop head-like structures.”This is really the first model that allows you to study brain development in the context of the whole developing mouse embryo,” she said.The roots of this work go back decades, and both Zernicka-Goetz and Hanna said their groups were working on this line of research for many years. Zernicka-Goetz said her group submitted its study to Nature in November.Scientists said next steps include trying to coax the synthetic mouse embryos to develop past 8 ½ days – with the eventual goal of getting them to term, which is 20 days for a mouse.At this point, they “struggle to go past” the 8 1/2-day mark, said Gianluca Amadei, a coauthor on the Nature paper based at the University of Cambridge. “We think that we will be able to get them over the hump, so to speak, so they can continue developing.”The scientists expect that after about 11 days of development the embryo will fail without a placenta, but they hope researchers can someday also find a way to create a synthetic placenta. At this point, they don’t know if they will be able to get the synthetic embryos all the way to term without a mouse womb.Researchers said they don’t see creating human versions of these synthetic embryos soon but do see it happening in time. Hanna called it “the next obvious thing.”Other scientists have already used human stem cells to create a “blastoid, ” a structure mimicking a pre-embryo, that can serve as a research alternative to a real one.Such work is subject to ethical concerns. For decades, a “14-day rule” on growing human embryos in the lab has guided researchers. Last year, the International Society for Stem Cell Research recommended relaxing the rule under limited circumstances.Scientists stress that growing a baby from a synthetic human embryo is neither possible nor under consideration.“Perspective on this report is important since, without it, the headline that a mammalian embryo has been built in vitro can lead to the thought that the same can be done with humans soon,” said developmental biologist Alfonso Martinez Arias of the Universitat Pompeu Fabra in Spain, whose group has developed alternative stem cell based models of animal development.“In the future, similar experiments will be done with human cells and that, at some point, will yield similar results,” he said. “This should encourage considerations of the ethics and societal impact of these experiments before they happen.”___The Associated Press Health and Science Department receives support from the Howard Hughes Medical Institute’s Department of Science Education. The AP is solely responsible for all content.Before You GoWild X-Rays And Medical Photos | Biology |
A model human embryo with a heartbeat and traces of blood has been created by scientists in a move that could offer insights into the first weeks of life.
The synthetic structure was created from human stem cells without the need for eggs, sperm or fertilisation.
It replicates some of the cells and structures that would usually appear in the third and fourth weeks of pregnancy, but was designed to never have the ability to develop into a foetus.
Despite the heartbeat, the structure does not have the tissues that go on to form the placenta and yolk sac in a natural embryo.
'I'd like to emphasise that these are neither embryos nor are we trying to make embryos,' said Dr Jitesh Neupane, from the University of Cambridge's Gurdon Institute.
'They are just models that could be used to look into specific aspects of human development.'
Beating heart cells typically appear at day 23 in a natural embryo, while red blood cells begins to appear during the fourth week.
'When I saw the [heartbeat] for the first time, I was scared, honestly,' Dr Neupane said. But he warned it would be 'dangerous' to compare the structures directly to natural embryos, adding: 'At the later time points, they don't have all the features of embryos.'
The breakthrough was achieved using embryonic stem cells – 'blank' cells taken from a human embryo which can then become any cell in the body, The Guardian reported.
They were coaxed to grow into an embryo-like structure in the laboratory and transferred into a rotating bottle, designed to act as an artificial uterus.
It is hoped the findings – which are yet to be published – could provide greater understanding of the causes of recurrent miscarriage and the impact of genetic disorders.
Professor Robin Lovell-Badge, head of stem cell biology and developmental genetics at the Francis Crick Institute in London, who was not involved in the work, said the synthetic embryos 'could not possibly develop to be implanted to form a child'.
The work follows a separate breakthrough, reported last week, in which scientists created embryos that did not include the beginnings of a brain or a beating heart, but did include cells that would go on to form the placenta and yolk sac.
Sarah Norcross, director of the Progress Educational Trust, a charity that helps people struggling with infertility, said: 'We must remember that these models are not actual human embryos.' | Biology |
Scientists propose 10 measures to prevent women from abandoning their academic careers after motherhood
The challenges of motherhood often lead women to leave academia after their first child. In fact, studies in the United States suggest that about 50% of women scientists in the U.S. leave science after motherhood. To address this problem, a group of Spanish women scientists, who are themselves mothers, propose 10 urgent measures that academic institutions should adapt in order to create a friendlier environment to prevent women from leaving academia after motherhood.
These guidelines cover a range of issues, from support during pregnancy to work-life balance, including career advancement opportunities. They propose measures such as support during pregnancy, childcare and breastfeeding and the school phase, actions aimed at organizing, making research and teaching activities more flexible and equitably distributed, and measures for the career advancement of mothers, thus combating mental health problems, discrimination and harassment.
This work, published in the journal PLOS Computational Biology under the title "Ten simple rules for a mom-friendly academia," highlights the need for greater representation of women in science, including mothers, because equality is a fundamental right and, in addition, there are studies that certify that diverse work environments are more productive and innovative.
According to Esther Sebastián-González, lead researcher from the Department of Ecology at the University of Alicante (UA), the benefit of implementing many of these ideas will not only be for trans mothers and fathers, but also for parents, caregivers of dependents, women, and even the academic community at large. It is imperative that academic institutions take proactive steps to promote gender equality and empower all people, including mothers, in the development of their scientific careers.
Among the measures proposed by this group of women scientists is technical support for pregnant women for field and laboratory work, as well as policies to facilitate flexible working hours and remote working. Another point highlighted in the article is that maternity and paternity leave should be taken into account in selection processes and in eligibility criteria for grants and research positions. They also call for the creation of crèches and breastfeeding centers at work and at scientific meetings, flexibility in working hours and location, and giving priority to parents with children in the selection of teaching hours during school hours.
To support the career advancement of mothers, the authors raise other issues such as extending the eligibility window for fellowships and grants for scientific mothers to at least 18 months per child, waiving the geographical mobility requirement for fellowships and grants for scientific mothers and creating specific grants after long career breaks. They also propose to create, disseminate and enforce anti-harassment and anti-discrimination policies in all research institutions and to reduce women's unpaid and unrecognized work, such as membership of hiring or thesis committees, and equalize this administrative burden to that of men.
More information: Esther Sebastián-González et al, Ten simple rules for a mom-friendly academia, PLOS Computational Biology (2023). DOI: 10.1371/journal.pcbi.1011284
Journal information: PLoS Computational Biology
Provided by Asociacion RUVID | Biology |
Finding ways to integrate electronics into living tissue could be crucial for everything from brain implants to new medical technologies. A new approach has shown that it’s possible to 3D print circuits into living worms.
There has been growing interest in finding ways to more closely integrate technology with the human body, in particular when it comes to interfacing electronics with the nervous system. This will be crucial for future brain-machine interfaces and could also be used to treat a host of neurological conditions.
But for the most part, it’s proven difficult to make these kinds of connections in ways that are non-invasive, long-lasting, and effective. The rigid nature of standard electronics means they don’t mix well with the squishy world of biology, and getting them inside the body in the first place can require risky surgical procedures.
A new approach relies instead on laser-based 3D printing to grow flexible, conductive wires inside the body. In a recent paper in Advanced Materials Technologies, researchers showed they could use the approach to produce star- and square-shaped structures inside the bodies of microscopic worms.
“Hypothetically, it will be possible to print quite deep inside the tissue,” John Hardy at Lancaster University, who led the study, told New Scientist. “So, in principle, with a human or other larger organism, you could print around 10 centimeters in.”
The researchers’ approach involves a high-resolution Nanoscribe 3D printer, which fires out an infrared laser that can cure a variety of light-sensitive materials with very high precision. They also created a bespoke ink that includes the conducting polymer polypyrrole, which previous research had shown could be used to electrically stimulate cells in living animals.
To prove the scheme could achieve the primary goal of interfacing with living cells, the researchers first printed circuits into a polymer scaffold and then placed the scaffold on top of a slice of mouse brain tissue being kept alive in a petri dish. They then passed a current through the flexible electronic circuit and showed that it produced the expected response in the mouse brain cells.
The team then decided to demonstrate the approach could be used to print conductive circuits inside a living creature, something that had so far not been achieved. The researchers decided to use the roundworm C. elegans due to its sensitivity to heat, injury, and drying out, which they said would make for a stringent test of how safe the approach is.
First, the team had to adjust their ink to make sure it wasn’t toxic to the animals. They then had to get it inside the worms by mixing it with the bacterial paste they’re fed on.
Once the animals had ingested the ink, they were placed under the Nanoscribe printer, which was used to create square and star shapes a few micrometers across on the worms’ skin and within their guts. The shapes didn’t come out properly in the moving gut though, the researchers admit, due to the fact it was constantly moving.
The shapes printed inside the worms’ bodies had no functionality. But Ivan Minev from the University of Sheffield told New Scientist the approach could one day make it possible to build electronics intertwined with living tissue, though it would still take considerable work before it was applicable in humans.
The authors also admit that adapting the approach for biomedical applications would require significant further research. But in the long run, they believe their work could enable tailor-made brain-machine interfaces for medical purposes, future neuromodulation implants, and virtual reality systems. It could also make it possible to easily repair bioelectronic implants within the body.
All that’s likely still a long way from being realized, but the approach shows the potential of combining 3D printing with flexible, biocompatible electronics to help interface the worlds of biology and technology.
Image Credit: Kbradnam/Wikimedia Commons | Biology |
Theoretical biologists uncover novel mechanism for flight control in fruit flies
Researchers at the Institute for Theoretical Biology at Humboldt Universität have solved a long-standing mathematical puzzle about the emergence of electrical activity patterns during insect flight. Together with colleagues at the Johannes Gutenberg University in Mainz, they report a novel function for electrical synapses in governing the flight of fruit flies in the current issue of Nature.
To keep their small bodies up in the air, fruit flies have to beat their wings extremely fast. They use a trick that is widespread in the animal kingdom: their nerve cells do not keep pace with the flapping of their wings. In order to control the flight muscles, each nerve cell instead generates an electrical pulse—also called action potential—only about every twentieth wing beat. This action potential, however, is precisely tuned to interact with other nerve cells. In a small circuit consisting of a few nerve cells, special activity patterns are generated: each cell regularly fires pulses, yet not at the same time as the other cells but rather spread out asynchronously at fixed intervals relative to each other.
In the fruit fly, such activity patterns have been known since the 1970s. Until now, their emergence was attributed to a connectivity of the nerve cells via chemical synapses. It was assumed that inhibitory messenger substances between nerve cells are released in response to action potentials, mutually preventing the cells from generating pulses at the same time.
Using mathematical analysis, however, Prof. Susanne Schreiber's team has now been able to show that such pulse-distributed activity can also occur when the nerve cells are not connected chemically, but electrically—that is, without the use of messenger substances. In this case, the cells have to use a special kind of action potential that comes along with a high sensitivity to the inputs from others, especially when a cell has just been active. This type of sensitivity is not typical of "normal" action potentials and, therefore, in the latter case no pulse-distributed activity is to be expected if the cellular coupling is purely electrical.
Experimental evidence for the type of pulse generation predicted by the Berlin researchers was provided by Prof. Carsten Duch's research group in Mainz. The scientists strengthened or weakened certain ionic currents in the cells of the fruit fly in order to change the type of action potentials that were generated. They were able to show that these manipulations influenced the activity patterns in the flight circuit exactly as predicted by the mathematical model. In addition, they proved that the connections among cells are indeed electrical and that knocking down this coupling has the expected effects on the activity patterns and wing beats of the animals.
The finding of the teams in Berlin and Mainz is particularly surprising, as it had so far been assumed that electrical coupling serves to promote the simultaneous activity of nerve cells. The activity patterns arising from electrical synapses reveal new principles of information processing in nervous systems. The same mechanism could be used not only in thousands of other insect species but also in the human brain, where the function of electrical coupling is still far from being understood.
More information: Silvan Hürkey et al, Gap junctions desynchronize a neural circuit to stabilize insect flight, Nature (2023). DOI: 10.1038/s41586-023-06099-0
Journal information: Nature
Provided by Humboldt-Universität zu Berlin | Biology |
Male fruit flies don't usually like each other. Socially, they reject their fellow males and zero in on the females they discern via chemical receptors -- or so scientists thought.
New research from Cornell University biologists suggests the fruit fly's visual system, not just chemical receptors, are deeply involved with their social behaviors. The work sheds light on the possible origin of differences in human social behaviors, such as those seen in people with bipolar disorder and autism.
The paper, "Visual Feedback Neurons Fine-tune Drosophila Male Courtship via GABA-mediated Inhibition," published in Current Biology on Sept. 5.
Many species of animals use vision to regulate their social behaviors, but the underlying mechanisms are largely unknown. In fruit flies, vision is thought to be used explicitly for motion detection and following, not to regulate social behaviors -- but the researchers found that may not be the case.
"In our study, we found that hyperactivating the visual system overran the inhibition generated by chemical signals emitted by the male fly to say to the other male, 'Okay, you know, I'm another male, don't mess with me,'" said senior author Nilay Yapici, assistant professor of neurobiology and behavior. "Surprisingly, increasing the visual gain in the brain somehow overrides the chemosensory inhibition, attracting male flies to other males."
The researchers found that altering the GABARAP/GABAA receptor signaling in visual feedback neurons in the male brain affected the flies' social inhibitions. When GABARAP is knocked down in the visual system, the males unexpectedly exhibit increased courtship toward other males.
The researchers have found that genes similar to those in the human brain control the fruit fly's visual neurons. Decreasing GABA signaling in the human brain has been associated with social withdrawal characteristics in conditions such as autism and schizophrenia.
"Our results offer a promising avenue for investigating how these proteins regulate social behaviors in the mammalian brain and their potential contribution to human psychiatric conditions," said lead author Yuta Mabuchi, Ph.D. '23.
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BOSTON – Oxygen is vital for life, and clinicians can provide supplemental oxygen to patients through face masks and nasal tubes, but there are no methods available for delivering oxygen directly into cells.
This capability would be useful initially as a research tool but could eventually have important medical applications—for example, to enhance therapies that lose effectiveness when oxygen levels are low.
As reported in PNAS, investigators at Massachusetts General Hospital (MGH) recently developed a technology that allows them to engineer cells to make oxygen on demand in response to an added chemical.
The work was led by Vamsi K. Mootha, MD, a Professor of Systems Biology and Medicine in the Department of Molecular Biology at MGH, whose laboratory focuses on mitochondria. These specialized compartments within cells produce energy, and they require oxygen to do so. “We are interested in how mitochondria, cells, and organisms adapt to changes in ambient oxygen,” says Mootha.
Currently, if the scientists want to manipulate cells’ oxygen levels in the lab, they place a petri dish containing cells in an environmentally controlled chamber. While this is useful, they can’t change oxygen levels in select cells at a specific time.
“From this need came the idea for a genetically encoded system that could be deployed in human cells to produce their own oxygen on demand,” says Mootha.
The technology involves simultaneously expressing a transporter and a bacterial enzyme within a cell—together, these proteins promote the uptake of chlorite into the cell and enzymatically convert it into oxygen and chloride.
The researchers call their new genetic technology SNORCL, for SupplemeNtal Oxygen Released from ChLorite. The first generation SNORCL is capable of producing short and modest pulses of oxygen inside of cells in response to added chlorite.
“In the near-term SNORCL is really for the research arena, for evaluating the role of oxygen in signaling, metabolism, and physiology in great detail. But then in the future, technologies based on SNORCL could have a variety of clinical uses,” says Mootha.
For example, tumors often have low oxygen levels that limit the effectiveness of some anti-cancer therapies. SNORCL might be used to improve these therapies’ effectiveness in such environments.
Additional co-authors include Andrew L. Markhard, Jason G. McCoy, and Tsz-Leung To.
This work was supported by the Howard Hughes Medical Institute.
Paper Cited:
Markhard, A. L., McCoy, J. G., To, T. L., & Mootha, V. K. (2022). A genetically encoded system for oxygen generation in living cells. Proceedings of the National Academy of Sciences of the United States of America, 119(43), e2207955119. https://doi.org/10.1073/pnas.2207955119
About the Massachusetts General Hospital
Massachusetts General Hospital, founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The Mass General Research Institute conducts the largest hospital-based research program in the nation, with annual research operations of more than $1 billion and comprises more than 9,500 researchers working across more than 30 institutes, centers and departments. In July 2022, Mass General was named #8 in the U.S. News & World Report list of "America’s Best Hospitals." MGH is a founding member of the Mass General Brigham healthcare system. | Biology |
Introduction
Marie Delattre was studying the sexual reproduction practices of microscopic worms when she noticed something unexpected. Under the microscope, an embryo of the nematode Mesorhabditis belari was dividing as it should, progressing from one cell to two to four. But inside a few cells she saw an inexplicable spray of DNA fragments floating around where they didn’t belong.
“There was DNA everywhere, inside the nuclei and outside the nuclei — big chunks of DNA,” she said. “I thought it was a dead embryo.”
The embryo was not dead, but it was doing something that usually only dead cells do: destroying its genome. “I started to try to trace when these fragments appear, at what stage, and what they look like,” said Delattre, a cell biologist at the École Normale Supérieure in Lyon. “That’s how I figured out that this is not accidental. All the embryos did this.”
What Delattre had stumbled across, and what she and her lab described in a paper published in August in Current Biology, was an instance of programmed DNA elimination (PDE), in which organisms seem to purposefully eliminate portions of their genome. It’s an odd phenomenon that flies in the face of the precept that a genome is a vital, sacrosanct resource to be passed on faithfully to the next generation.
So far, researchers have identified PDE in only about 100 species across all branches of life: Single-celled ciliates with multiple nuclei do PDE; so do tiny worms, as well as the meters-long intestinal parasites of horses, many insects, and even songbirds. But PDE can be so difficult to spot that no one knows how common it really is. “It’s not very well known even among biologists,” Delattre said.
In addition to confirming the existence of another case of PDE, Delattre’s new paper also hints at an explanation for it. PDE points to a long-running fight between cells and DNA sequences that are of no use to their owner, or maybe even weigh it down. Like gardeners, cells must protect their genomes to remain functional and productive. What should a cell do when the weeds come in? The new study suggests that some species, like M. belari, might just pull the weeds out using PDE.
Despite its seeming novelty, PDE was discovered in the early days of molecular biology, long before researchers even knew that DNA is life’s genetic material. In 1887, the German biologist Theodor Boveri was studying the development of Parascaris, a nematode that parasitizes horses, when he witnessed its large genome coalesce, fragment and then reassemble into smaller portions during mitosis. The missing pieces were seemingly trashed without ceremony.
Introduction
During the 20th century, researchers discovered only a handful of other organisms — ciliates, moths, copepods, bandicoots — that did PDE, and it remained a fringe concept. But why any of those species did it remained unclear.
To figure out what was going on, Delattre’s lab looked at the DNA of an adult worm. The researchers compared the genomes of M. belari’s germline cells — the specialized reproductive cells like sperm and eggs — with the genomes of the worm’s somatic (nonreproductive) cells. The somatic genomes were missing long strings of sequences present in germline genomes. Sometime between the embryo’s growth from seven cells to 32, huge chunks of DNA had vanished.
The scientists then watched nematode embryos develop under a microscope. As the cells grew and replicated their genomes, they broke 20 chromosomes down into fragments and then reassembled them into 40 miniature chromosomes. Most of the fragments rejoined in this new, smaller genome — but a substantial fraction were left out.
In total, the nematode deleted a whopping one-third of its genome. The deleted sequences weren’t selected at random. There was a pattern: They were mostly highly repetitive stretches of DNA that didn’t code for genes at all, Delattre found.
Similar stretches of repeating or noncoding sequences pack the genomes of eukaryotic cells. Some perform necessary functions. Satellite DNA, for instance, forms structures such as heterochromatin and centromeres that package DNA, while other repetitive sections regulate gene expression. However, some repeated sequences do not contribute to their host’s survival — and may even interfere with it.
Introduction
That group includes transposons, self-replicating DNA sequences that steal the cell’s machinery to copy themselves by the thousands or millions. This amounts to molecular grand larceny, as well as a waste of the time and energy that the cell must spend to suppress these sequences. Cells routinely curb transposons with epigenetic marks that silence them, or by intercepting and destroying their RNA. But some species, such as M. belari, may remove them entirely through PDE.
That’s what Delattre suspects her nematodes are doing. Jonathan Wells, an evolutionary geneticist at Cornell University who studies transposons and was not involved in the new study, agrees that the DNA parasites are a likely target. For managing transposons, “the more you look, the more systems there are,” he said.
However, transposons and other types of self-replicating DNA are not necessarily villains. By copying themselves repeatedly across the genome, transposons also provide the cell with fresh material that can mutate and evolve into new genes. Host cells freely and liberally take genetic sequences from parasitic DNA and make them part of the normal genome — or, to look at it another way, the parasites ingratiate themselves with their hosts enough to be adopted. “[Repetitive DNA elements] are the soil that all other genes are sitting in,” Wells said. “They are a rich source of novelty.”
Since transposons can be both harmful and helpful, PDE might have uses aside from combating them. Even Delattre is not convinced that transposons are the whole story. Though the repetitive DNA that M. belari deleted was harmful, “why would you get rid of [parasitic DNA] just in somatic cells and not the germline?” she asked.
Besides fighting parasites, PDE may help cells streamline their genomes as they progress through different life stages. Many genes that are critical for an organism’s embryonic development are unnecessary in maturity. If a cell can rid itself of those genes, why wouldn’t it for efficiency’s sake? A larger genome is harder to copy and maintain, and inappropriately expressing developmental genes could cause problems. In somatic cells, which don’t need to pass a full genome along to offspring as germline cells do, removing unessential elements could be a winning evolutionary strategy.
No one knows for sure why PDE happens. Since it is under-studied and contradicts many deeply held genetic concepts (one paper, describing how some songbirds eliminate an entire chromosome, called these deletions “Mendelian nightmares”), almost any hypothesis could hold water.
That’s all the more reason for biologists to widen their search for it, Delattre said: “If it exists in other species we don’t know, we need to look for it.” By better understanding who is using PDE, scientists can get closer to understanding why some organisms would take such drastic and potentially risky measures to manage their genome. “I think it’s a good bet that PDE is more widespread than we know,” Wells said. | Biology |
Most birds that flit through dense, leafy forests have a strategy for maneuvering through tight windows in the vegetation — they bend their wings at the wrist or elbow and barrel through.
But hummingbirds can't bend their wing bones during flight, so how do they transit the gaps between leaves and tangled branches?
A study published today in the Journal of Experimental Biology shows that hummingbirds have evolved their own unique strategies — two of them, in fact. These strategies have not been reported before, likely because hummers maneuver too quickly for the human eye to see.
For slit-like gaps too narrow to accommodate their wingspan, they scooch sideways through the slit, flapping their wings continually so as not to lose height.
For smaller holes — or if the birds are already familiar with what awaits them on the other side — they tuck their wings and coast through, resuming flapping once clear.
"For us, going into the experiments, the tuck and glide would have been the default. How else could they get through?" said Robert Dudley, a professor of integrative biology at the University of California, Berkeley, and senior author of the paper. "This concept of sideways motion with a total mix-up of the wing kinematics is quite amazing — it's a novel and unexpected method of aperture transit. They're changing the amplitude of the wing beats so that they're not dropping vertically when they do the sideways scooch."
Using the slower sideways scooch technique may allow birds to better assess upcoming obstacles and voids, thereby reducing the likelihood of collisions.
"Learning more about how animals negotiate obstacles and other 'building-blocks' of the environment, such as wind gusts or turbulent regions, can improve our overall understanding of animal locomotion in complex environments," noted first author Marc Badger, who obtained his Ph.D from UC Berkeley in 2016. "We still don't know very much about how flight through clutter might be limited by geometric, aerodynamic, sensory, metabolic or structural processes. Even behavioral limitations could arise from longer-term effects, such as wear and tear on the body, as hinted at by the shift in aperture negotiation technique we observed in our study."
Understanding the strategies that birds use to maneuver through a cluttered environment may eventually help engineers design drones that better navigate complex environments, he noted.
"Current remote control quadrotors can outperform most birds in open space across most metrics of performance. So is there any reason to continue learning from nature?" said Badger. "Yes. I think it's in how animals interact with complex environments. If we put a bird's brain inside a quadrotor, would the cyborg bird or a normal bird be better at flying through a dense forest in the wind? There may be many sensory and physical advantages to flapping wings in turbulent or cluttered environments."
Obstacle course
To discover how hummingbirds — in this case, four local Anna’s hummingbirds (Calypte anna) — slip through tiny openings, despite being unable to fold their wings, Badger and Dudley teamed up with UC Berkeley students Kathryn McClain, Ashley Smiley and Jessica Ye.
"We set up a two-sided flight arena and wondered how to train birds to fly through a 16-square- centimeter gap in the partition separating the two sides," Badger said, noting that the hummingbirds have a wingspan of about 12 centimeters (4 3/4 inches). "Then, Kathryn had the amazing idea to use alternating rewards."
That is, the team placed flower-shaped feeders containing a sip of sugar solution on both sides of the partition, but only remotely refilled the feeders after the bird had visited the opposite feeder. This encouraged the birds to continually flit between the two feeders through the aperture.
The researchers then varied the shape of the aperture, from oval to circular, ranging in height, width and diameter, from 12 cm to 6 cm, and filmed the birds’ maneuvers with high-speed cameras. Badger wrote a computer program to track the position of each bird’s bill and wing tips as it approached and passed through the aperture.
They discovered that as the birds approached the aperture, they often hovered briefly to assess it before travelling through sideways, reaching forward with one wing while sweeping the second wing back, fluttering their wings to support their weight as they passed through the aperture. They then swiveled their wings forward to continue on their way.
"The thing is, they have to still maintain weight support, which is derived from both wings, and then control the horizontal thrust, which is pushing it forward. And they're doing this with the right and left wing doing very peculiar things," Dudley said. "Once again, this is just one more example of how, when pushed in some experimental situation, we can elicit control features that we don't see in just a standard hovering hummingbird."
Alternatively, the birds swept their wings back and pinned them to their bodies, shooting through — beak first, like a bullet — before sweeping the wings forward and resuming flapping once safely through.
"They seem to do the faster method, the ballistic buzz-through, when they get more acquainted with the system," Dudley said.
Only when approaching the smallest apertures, which were half a wingspan wide, would the birds automatically resort to the tuck and glide, even though they were unfamiliar with the setup.
The team pointed out that only about 8% of the birds clipped their wings as they passed through the partition, although one experienced a major collision. Even then, the bird recovered quickly before successfully reattempting the maneuver and going on its way.
"The ability to pick among several obstacle negotiation strategies can allow animals to reliably squeeze through tight gaps and recover from mistakes," Badger noted.
Dudley hopes to conduct further experiments, perhaps with a sequence of different apertures, to determine how birds navigate multiple obstacles.
The work was funded primarily by a CiBER-IGERT grant from the National Science Foundation (DGE-0903711).
RELATED INFORMATION
- Sideways maneuvers enable narrow aperture negotiation by free-flying hummingbirds (J. of Exp. Biology)
- Robert Dudley's website
- Marc Badger's website
- Do hummingbirds drink alcohol? More often than you think. (June 2023) | Biology |
Home News Spaceflight NASA's LunaH-Map cubesat is designed to measure the distribution and abundance of hydrogen in the moon's south polar region.
(Image credit: NASA/Arizona State University) A tiny NASA moon probe failed to perform a crucial maneuver as planned on Monday (Nov. 21), but the cubesat might still be able to salvage its water-hunting mission.The LunaH-Map spacecraft is one of 10 cubesats that launched as ride-along payloads last Wednesday (Nov. 16) on NASA's Artemis 1 mission. LunaH-Map was designed to map the distribution and abundance of hydrogen — and, by extension, water ice — near the moon's south pole. Such data is of great interest to NASA's Artemis program, which aims to build a crewed research outpost in this region.Related: Amazing views of NASA's Artemis 1 moon rocket debut (photos)
Live updates: NASA's Artemis 1 moon missionThe cubesat was supposed to perform an engine firing during its flyby of the moon on Monday but failed to do so, likely because of a stuck valve in its propulsion system, NASA officials said.But all is not necessarily lost. LunaH-Map's other systems appear to be functioning normally, and heating the valve might free it, bringing the propulsion system online as well. "If the propulsion system is able to achieve thrust within the next few months, the mission may still recover some or all of LunaH-Map's original science mission," NASA officials said in an update on Tuesday (opens in new tab) (Nov. 22). "On the spacecraft's current path, alternate trajectories are available to achieve lunar orbit — including orbits that could enable low-altitude measurements of the lunar surface."And LunaH-Map could still find work farther afield if it takes even longer to fix the current glitch, NASA officials explained in the update: "Trajectory solutions outside of the Earth-moon system may exist to fly close to certain asteroids and characterize their hydrogen content."LunaH-Map, which is led by researchers at Arizona State University, isn't the only Artemis 1 cubesat to suffer problems after being deployed by the mission's Space Launch System rocket. For example, Japan's OMOTENASHI probe experienced communications issues and failed to drop a tiny lander on the moon as a result.NASA's Near Earth Asteroid (NEA) Scout probe has apparently been silent since the Nov. 16 launch, as has the citizen scientist cubesat Team Miles. And the LunIR spacecraft may be experiencing some trouble as well.Artemis 1, the first mission of the Artemis program, is sending an uncrewed Orion capsule on a nearly 26-day journey to lunar orbit and back. Orion is scheduled to slip into a distant retrograde orbit around Earth's natural satellite on Friday (Nov. 25). The capsule will spend about a week there and then head back toward Earth, arriving here in an ocean splashdown on Dec. 11.If all goes according to plan, Artemis 2 will launch astronauts around the moon in 2024 and Artemis 3 will put boots down near the lunar south pole a year or so later.Mike Wall is the author of "Out There (opens in new tab)" (Grand Central Publishing, 2018; illustrated by Karl Tate), a book about the search for alien life. Follow him on Twitter @michaeldwall (opens in new tab). Follow us on Twitter @Spacedotcom (opens in new tab) or Facebook (opens in new tab). Join our Space Forums to keep talking space on the latest missions, night sky and more! And if you have a news tip, correction or comment, let us know at: [email protected].
Michael Wall is a Senior Space Writer with Space.com (opens in new tab) and joined the team in 2010. He primarily covers exoplanets, spaceflight and military space, but has been known to dabble in the space art beat. His book about the search for alien life, "Out There," was published on Nov. 13, 2018. Before becoming a science writer, Michael worked as a herpetologist and wildlife biologist. He has a Ph.D. in evolutionary biology from the University of Sydney, Australia, a bachelor's degree from the University of Arizona, and a graduate certificate in science writing from the University of California, Santa Cruz. To find out what his latest project is, you can follow Michael on Twitter. | Biology |
Genetically modified bacteria may eat up ocean plastic wasteThis genetically engineered microorganism has the ability to break down a type of plastic known as polyethylene terephthalate (PET).Mrigakshi Dixit| Sep 15, 2023 10:58 AM ESTCreated: Sep 15, 2023 10:58 AM ESTinnovationPlastic water bottles lying on ocean bed.Eoneren/iStock Get a daily digest of the latest news in tech, science, and technology, delivered right to your mailbox. Subscribe now.By subscribing, you agree to our Terms of Use and Policies You may unsubscribe at any time.Various bacterial species have demonstrated an extraordinary ability to degrade plastics, which are synthetic polymers known for their long-lasting and non-biodegradable characteristics.Research in this area continues to advance to create viable and sustainable solutions to combat the growing menace of plastic waste in terrestrial and marine environments. Now, researchers from North Carolina State University have put to use the remarkable biological traits of two bacterial species to enable efficient plastic breakdown in saltwater.This genetically engineered microorganism can break down a type of plastic known as polyethylene terephthalate (PET), which contributes significantly to microplastic pollution in the global oceans. PET is widely used to manufacture many items, including water bottles and clothing. See Also Related Forest fungi can eat and dissolve plastics, much like they do with bark Cold-loving microbes could eat away our plastic crisis Newly discovered Arctic microbes may make recycling plastics carbon-neutral “This is exciting because we need to address plastic pollution in marine environments. One option is to pull the plastic out of the water and put it in a landfill, but that poses challenges of its own. It would be better if we could break these plastics down into products that can be re-used. For that to work, you need an inexpensive way to break the plastic down. Our work here is a big step in that direction,” said Nathan Crook, corresponding author of a paper on the work, in an official release. The creation of genetically engineered bacteriaThe research team conducted experiments involving two bacterial species: Vibrio natriegens and Ideonella sakaiensis.Vibrio natriegens primarily inhabits saltwater ecosystems and is notable for its rapid reproduction rate. On the other hand, Ideonella sakaiensis possesses enzymes that give it the power to break down as well as ingest PET quickly, distinct from its. As a result, the researchers isolated the genetic sequence from the latter (Ideonella sakaiensis) and integrated it into a plasmid. Plasmids are genetic sequences that may replicate independently within a cell even when it is distinct from the cell's original chromosome.“In other words, you can sneak a plasmid into a foreign cell, and that cell will carry out the instructions in the plasmid’s DNA. And that’s exactly what the researchers did here,” noted the release. The scientists then carefully incorporated the plasmid containing Ideonella sakaiensis genes into Vibrio natriegens bacterium in the lab. The resultant, V. natriegens was able to produce the required enzymes on its cell surface. The researchers demonstrated that V. natriegens could degrade PET in a room-temperature-based saltwater setting. “From a practical standpoint, this is also the first genetically engineered organism that we know capable of breaking down PET microplastics in saltwater. That’s important because it is not economically feasible to remove plastics from the ocean and rinse high concentration salts off before beginning any processes related to breaking the plastic down,” said Tianyu Li, the first author of this new study. Three main challenges to addressThe researchers emphasize that while this is a significant milestone that has created the essential groundwork, three important challenges need to be addressed before the modified bacteria can operate effectively on a large scale.Crook concluded: “First, we’d like to incorporate the DNA from I. sakaiensis directly into the genome of V. natriegens, which would make the production of plastic-degrading enzymes a more stable feature of the modified organisms. Second, we need to further modify V. natriegens so that it is capable of feeding on the byproducts it produces when it breaks down the PET. Lastly, we need to modify the V. natriegens to produce a desirable end product from the PET – such as a molecule that is a useful feedstock for the chemical industry.”The results were reported in the AIChE Journal. Study abstract:Poly(ethylene terephthalate) (PET) is a highly recyclable plastic that has been extensively used and manufactured. Like other plastics, PET resists natural degradation, thus accumulating in the environment. Several recycling strategies have been applied to PET, but these tend to result in downcycled products that eventually end up in landfills. This accumulation of landfilled PET waste contributes to the formation of microplastics, which pose a serious threat to marine life and ecosystems, and potentially to human health. To address this issue, our project leveraged synthetic biology to develop a whole-cell biocatalyst capable of depolymerizing PET in seawater environments by using the fast-growing, nonpathogenic, moderate halophile Vibrio natriegens. By leveraging a two-enzyme system—comprising a chimera of IsPETase and IsMHETase from Ideonella sakaiensis—displayed on V. natriegens, we constructed whole-cell catalysts that depolymerize PET and convert it into its monomers in salt-containing media and at a temperature of 30°C. HomeInnovationAdd Interesting Engineering to your Google News feed.Add Interesting Engineering to your Google News feed.SHOW COMMENT (1) For You Does hydrogen have a future as a clean energy source?Stop crowding earth’s orbital environment: ESA reportRechargeable batteries made from wasteWhy only icebreakers can break ice & other ships can’tMaybe you can hear sounds in space after allGermany signs Artemis Accords, eyes peaceful space futureCan AI accurately identify patients with respiratory symptoms?Universe slows cosmic growth defying the theory of relativityTrue-zero emissions cement gets ASTM approvalMagnetic fields reveal lost undersea worlds Job Board | Biology |
It’s no secret that alternative protein companies and others leveraging fermentation technology have an issue scaling to commercial production. Founders say that this is perhaps the number one challenge to taking their products from expensive to cost parity with traditional meat.
Meet Pow.bio, a company founded by Ouwei Wang and Shannon Hall (no relation to the author) in 2019, that aims to help synthetic biology companies manufacture their products at cost parity amid a market of biomade products estimated to reach $4 trillion by 2040.
“Biology is the technology of today,” Hall told TechCrunch. “We see that in lots of consumer-facing goods, and lots of biomedicines and in Impossible Foods products. More importantly, it's behind our aspirations for how we're going to deal with some of the biggest challenges in the world. For example, climate change impacts, population growth impacts and our aspirations to live and travel in space. All of that is predicated on having biology technology working.”
While companies like No Meat Factory, Planetary and Prolific Machines raised capital to build production facilities, Hall said the solution to the scaling problem won’t come from building large-scale bioreactors, even if the funding comes from the government.
“The real true story here is that most of the biology design stuff just is too damn expensive to take to the market,” Hall added. “Building bigger bioreactors doesn't make that better, and as a result, what you see made are things you either need very tiny amounts of, like the heme protein in the Impossible Burger, or things that are crazy expensive, like lactoferrin, or human collagen, which is also nice to have alternatives.”
She explained that prototyping, a necessary step in synthetic biology production, is where the time and cost factor come into play. For example, involving a six-month wait and $50,000 investment each time.
Pow.bio intends to bring down biomanufacturing costs by unlocking the potential of synthetic biology via a “broader palette of wins,” that involves the reimagining of fermentation facility operations, Hall said.
And that’s what Pow.bio is doing: Building more efficient bioreactor capacity through its continuous fermentation technology. Anchoring the technology is artificial intelligence-controlled software called SOFe that is designed to accelerate process optimization and drive autonomous operation.
Simply put, Pow.bio’s hardware and software combination has the capability to allow for a steady pace of inputs and outputs that is 5x faster for a fraction of traditional capital expenses, Hall said.
“Let us be your rapid prototyping partner,” she added. “You can get stuff in two or three months, at the most, and you'll be able to turn quickly.”
Pow.bio is still in the early stages; however, it is already working with multiple clients and bringing in revenue. The company has seen “at least 50% year over year growth in demand,” Hall said.
It is also now buoyed by $9.5 million in Series A capital. Re:Food and Thia Ventures led the round and were joined by Hitachi Ventures, Possible Ventures, XFactor, iSelect, Climate Capital, Vectors, Better Ventures and Cantos. The new investment gives Pow.bio around $13 million in total funding.
Much of that new funding will be deployed into a demonstration facility in Alameda, California. Once it opens in the summer of 2024, it will be able to transition from gram-scale experimentation to the production of hundreds of kilograms of finished products.
“It will demonstrate our system at scales above where we're at today, which will enable more partners — we think 20 to 50 partners — to drive product through there, as well as be the blueprint for taking that to multiple locations,” Hall said. “With this proof, we can copy/paste it anywhere. That's what we think is needed.” | Biology |
Feral Mink Brains Suggest That the Effects of Domestication Can Be Reversed
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In a highly unexpected defiance of evolutionary biology, feral populations of the American mink have been shown to reverse key changes to their brain size that occur during domestication. The study reaffirms the amazingly plastic nature of the animal brain, even in the face of many generations of selective breeding.
The research was published in Royal Society Open Science.
Domesticated brain decreases
Domesticated animals are selectively bred for traits that can produce rapid changes to their bodies. Chickens are bulked into hulking meatballs and domesticated sheep become wrapped in excessive wool coats that require regular shearing. One trait that is seen across domesticated animals, despite not being outwardly selected for, is a reduction in brain size.
This so-called domestication effect was thought to be an irreversible process; previous analysis of feral animals – such as pigs found on the Galapagos Islands – had shown that, even after many generations, smaller brain size was retained. The overarching theory was that “once animals lose parts of their body, such as certain brain regions, over the course of evolution, they are gone and cannot simply be regained,” says Dina Dechmann, senior author on the paper, and a group leader at the Max Planck Institute.
Regaining the brain
Now, a well-crafted study involving mink suggests that, at least in this species, lost brain mass can be restored within 50 generations of leaving captivity. “Our results show that loss of brain size is not permanent in domesticated animals,” says Ann-Kathrin Pohle, first author of the paper and a Master’s student at the Max Planck Institute of Animal Behavior. “This finding deepens our understanding of how domestication has changed the brains of animals, and how these changes might be affecting animals when they return to the wild.”
One of the most challenging aspects of the study was its design. To prove that feral populations differed from captive populations and that the cause of that difference wasn’t due to feral animals breeding with wild ones, the team had to identify a sample of animals where feral and wild animals were isolated.
Luckily, the American mink has this exact distribution. Native to North America, mink have been domesticated and are farmed in Europe for their fur. The animals that have escaped and formed feral populations there are separated from any wild mink by roughly 3,000 miles of ocean. With access to these separate groups—wild mink from North America, domesticated mink from European fur farms, and feral mink from Europe—the team was perfectly equipped to scrutinize the changes in brain size.
To measure differences in brain size without the need for living animals, the scientists adopted a clever strategy, using skull size as an indirect measure for brain size. Using skull collections from Cornell University and European fur farms, alongside a collection of feral mink skulls courtesy of Andrzej Zalewski from the Polish Mammal Research Institute, the team had all the pieces they needed to put the puzzle together. “Usually, the difficulty with skull studies is finding big enough collections to work with,” says Dechmann. “We were incredibly fortunate to work with multiple organizations to obtain the population samples we needed.”
The skull measurements suggested that the relative brain size of the domesticated mink had dramatically dropped by 25%. In contrast to what the team expected, the feral minks’ brains had regrown to almost the same size as wild mink.
Dehnel’s phenomenon
This unlikely finding, says Dechmann, could be explained by a rare aspect of mink biology. The American mink, along with shrews, moles and weasels, belong to a group of small mammals capable of seasonally altering their brain sizes—a process known as Dehnel’s phenomenon. “While other domesticated animals seem to lose brain size permanently, it’s possible that mink can regain their ancestral brain sizes because they have flexible brain size built into their system,” she says.
This cranial flexibility could offer significant advantages to rewilded mink. “If you escape from captivity back to nature, you would want a fully capable brain to navigate the challenges of living in the wild. Animals with flexible brains, like the mink, could restore their brains even if they had shrunk it during an earlier time,” says Dechmann. The team hopes to get their hands on actual brains in a future study, which would enable them to see firsthand how changes in these elastic structures affect how mink brains function.
Reference: Pohle AK, Zalewski A, Muturi M, et al. Domestication effect of reduced brain size is reverted when mink become feral. R. Soc. Open Sci. 2023;10(7):230463. doi:10.1098/rsos.230463. | Biology |
How to assemble a complete jaw
A USC-led team of scientists has made a drool-worthy discovery about how tendons and salivary glands develop in the jaw. Their results are published in a new study in Developmental Cell.
In order for our jaws to function, they require not only a precisely patterned skeleton, but also tendons that connect the jaw skeleton to muscles and salivary glands that lubricate the mouth. Remarkably, the skeleton, tendons, and glands all derive from the same population of stem cells, which arise from a cell population known as neural crest. How these neural crest-derived cells know to make the right type of cell in the right location has remained a mystery.
To begin answering this question, first author Hung-Jhen (Olivia) Chen from the lab of corresponding author Gage Crump, professor and vice-chair of stem cell biology and regenerative medicine at the Keck School of Medicine of USC, and colleagues examined all the genes that were active in the developing face of zebrafish. They then honed in on one particular gene, Nr5a2, that was active in a region of the face that makes tendons and glands, but not skeleton.
To understand the role of Nr5a2, the scientists created zebrafish lacking this gene. These mutant zebrafish generated excess cartilage and were missing tendons in their jaws.
The scientists also developed mice lacking this gene specifically in their neural crest cells. These mice not only had skeletal and tendon defects in their jaws, but also failed to develop salivary glands. Similar defects were also seen in the middle ear, reflecting a dramatic evolutionary transition in which part of the fish jaw became the mammalian middle ear.
To clarify how this was happening, the scientists examined the structure of the genome in zebrafish lacking Nr5a2. They found that Nr5a2 was essential for opening up regions of the genome that enable neural crest cells to maintain their stem cell features, while at the same time priming these cells to form tendons and salivary glands later in jaw development.
"Discovery of a very specific role of Nr5a2 in jaw patterning was unexpected, as this gene had previously been shown to be essential for maintaining embryonic stem cells," said Crump. "Our work shows how a key stem cell factor can be used in a different way later in development to control how diverse cell types are made."
More information: Hung-Jhen Chen et al, Nuclear receptor Nr5a2 promotes diverse connective tissue fates in the jaw, Developmental Cell (2023). DOI: 10.1016/j.devcel.2023.02.011
Journal information: Developmental Cell
Provided by Keck School of Medicine of USC | Biology |
Summary The intestinal barrier, which primarily consists of a mucus layer, an epithelial barrier, and a gut vascular barrier, has a crucial role in health and disease by facilitating nutrient absorption and preventing the entry of pathogens. The intestinal barrier is in close contact with gut microbiota on its luminal side and with enteric neurons and glial cells on its tissue side. Mounting evidence now suggests that the intestinal barrier is compromised not only in digestive disorders, but also in disorders of the central nervous system (CNS), such as Parkinson's disease, autism spectrum disorder, depression, multiple sclerosis, and Alzheimer's disease. After providing an overview of the structure and functions of the intestinal barrier, we review existing preclinical and clinical studies supporting the notion that intestinal barrier dysfunction is present in neurological, neurodevelopmental, and psychiatric disorders. On the basis of this evidence, we discuss the mechanisms that possibly link gut barrier dysfunction and CNS disorders and the potential impact that evaluating enteric barriers in brain disorders could have on clinical practice, in terms of novel diagnostic and therapeutic strategies, in the near future. To read this article in full you will need to make a paymentReferences1.Kirchgessner AL Gershon MD Identification of vagal efferent fibers and putative target neurons in the enteric nervous system of the rat.J Comp Neurol. 1989; 285: 38-532.Browning KN Travagli RA Central nervous system control of gastrointestinal motility and secretion and modulation of gastrointestinal functions.Compr Physiol. 2014; 4: 1339-13683.Bruce-Keller AJ Salbaum JM Berthoud HR Harnessing gut microbes for mental health: getting from here to there.Biol Psychiatry. 2018; 83: 214-2234.Mayer EA Nance K Chen S The gut-brain axis.Annu Rev Med. 2022; 73: 439-4535.Bercik P Collins SM Verdu EF Microbes and the gut-brain axis.Neurogastroenterol Motil. 2012; 24: 405-4136.Miller WL The hypothalamic-pituitary-adrenal axis: a brief history.Horm Res Paediatr. 2018; 89: 212-2237.Rothhammer V Mascanfroni ID Bunse L et al.Type I interferons and microbial metabolites of tryptophan modulate astrocyte activity and central nervous system inflammation via the aryl hydrocarbon receptor.Nat Med. 2016; 22: 586-5978.Wang X Liu GJ Gao Q Li N Wang RT C-type lectin-like receptor 2 and zonulin are associated with mild cognitive impairment and Alzheimer's disease.Acta Neurol Scand. 2020; 141: 250-2559.Stevens BR Goel R Seungbum K et al.Increased human intestinal barrier permeability plasma biomarkers zonulin and FABP2 correlated with plasma LPS and altered gut microbiome in anxiety or depression.Gut. 2018; 67: 1555-155710.Esnafoglu E Cırrık S Ayyıldız SN et al.Increased serum zonulin levels as an intestinal permeability marker in autistic subjects.J Pediatr. 2017; 188: 240-24411.Camara-Lemarroy CR Silva C Greenfield J Liu WQ Metz LM Yong VW Biomarkers of intestinal barrier function in multiple sclerosis are associated with disease activity.Mult Scler. 2020; 26: 1340-135012.Forsyth CB Shannon KM Kordower JH et al.Increased intestinal permeability correlates with sigmoid mucosa alpha-synuclein staining and endotoxin exposure markers in early Parkinson's disease.PLoS One. 2011; 6e2803213.Brescia P Rescigno M The gut vascular barrier: a new player in the gut-liver-brain axis.Trends Mol Med. 2021; 27: 844-85514.Chelakkot C Ghim J Ryu SH Mechanisms regulating intestinal barrier integrity and its pathological implications.Exp Mol Med. 2018; 50: 1-915.Vindigni SM Zisman TL Suskind DL Damman CJ The intestinal microbiome, barrier function, and immune system in inflammatory bowel disease: a tripartite pathophysiological circuit with implications for new therapeutic directions.Therap Adv Gastroenterol. 2016; 9: 606-62516.Chong PP Chin VK Looi CY Wong WF Madhavan P Yong VC The microbiome and irritable bowel syndrome—a review on the pathophysiology, current research and future therapy.Front Microbiol. 2019; 10113617.Aho VTE Houser MC Pereira PAB et al.Relationships of gut microbiota, short-chain fatty acids, inflammation, and the gut barrier in Parkinson's disease.Mol Neurodegener. 2021; 16: 618.Cox AJ Zhang P Bowden DW et al.Increased intestinal permeability as a risk factor for type 2 diabetes.Diabetes Metab. 2017; 43: 163-16619.D'Antongiovanni V Pellegrini C Fornai M et al.Intestinal epithelial barrier and neuromuscular compartment in health and disease.World J Gastroenterol. 2020; 26: 1564-157920.Breugelmans T Oosterlinck B Arras W et al.The role of mucins in gastrointestinal barrier function during health and disease.Lancet Gastroenterol Hepatol. 2022; 7: 455-47121.Shan M Gentile M Yeiser JR et al.Mucus enhances gut homeostasis and oral tolerance by delivering immunoregulatory signals.Science. 2013; 342: 447-45322.Bansil R Turner BS The biology of mucus: composition, synthesis and organization.Adv Drug Deliv Rev. 2018; 124: 3-1523.Willemsen LE Koetsier MA van Deventer SJ van Tol EA Short chain fatty acids stimulate epithelial mucin 2 expression through differential effects on prostaglandin E(1) and E(2) production by intestinal myofibroblasts.Gut. 2003; 52: 1442-144724.Grondin JA Kwon YH Far PM Haq S Khan WI Mucins in intestinal mucosal defense and inflammation: learning from clinical and experimental studies.Front Immunol. 2020; 11205425.Kong S Zhang YH Zhang W Regulation of intestinal epithelial cells properties and functions by amino acids.BioMed Res Int. 2018; 2018281915426.Bevins CL Salzman NH Paneth cells, antimicrobial peptides and maintenance of intestinal homeostasis.Nat Rev Microbiol. 2011; 9: 356-36827.Clevers HC Bevins CL Paneth cells: maestros of the small intestinal crypts.Annu Rev Physiol. 2013; 75: 289-31128.Odenwald MA Turner JR The intestinal epithelial barrier: a therapeutic target?.Nat Rev Gastroenterol Hepatol. 2017; 14: 9-2129.Cheng X Voss U Ekblad E Tuft cells: distribution and connections with nerves and endocrine cells in mouse intestine.Exp Cell Res. 2018; 369: 105-11130.Rios D Wood MB Li J Chassaing B Gewirtz AT Williams IR Antigen sampling by intestinal M cells is the principal pathway initiating mucosal IgA production to commensal enteric bacteria.Mucosal Immunol. 2016; 9: 907-91631.Turner JR Intestinal mucosal barrier function in health and disease.Nat Rev Immunol. 2009; 9: 799-80932.Fasano A Intestinal permeability and its regulation by zonulin: diagnostic and therapeutic implications.Clin Gastroenterol Hepatol. 2012; 10: 1096-110033.Fasano A Not T Wang W et al.Zonulin, a newly discovered modulator of intestinal permeability, and its expression in coeliac disease.Lancet. 2000; 355: 1518-151934.Sturgeon C Fasano A Zonulin, a regulator of epithelial and endothelial barrier functions, and its involvement in chronic inflammatory diseases.Tissue Barriers. 2016; 4e125138435.Lu Z Ding L Lu Q Chen YH Claudins in intestines: distribution and functional significance in health and diseases.Tissue Barriers. 2013; 1e2497836.Anderson JM Van Itallie CM Physiology and function of the tight junction.Cold Spring Harb Perspect Biol. 2009; 1a00258437.Günzel D Yu AS Claudins and the modulation of tight junction permeability.Physiol Rev. 2013; 93: 525-56938.Lechuga S Ivanov AI Disruption of the epithelial barrier during intestinal inflammation: quest for new molecules and mechanisms.Biochim Biophys Acta Mol Cell Res. 2017; 1864: 1183-119439.Hartsock A Nelson WJ Adherens and tight junctions: structure, function and connections to the actin cytoskeleton.Biochim Biophys Acta. 2008; 1778: 660-66940.Abraham C Abreu MT Turner JR Pattern recognition receptor signaling and cytokine networks in microbial defenses and regulation of intestinal barriers: implications for inflammatory bowel disease.Gastroenterology. 2022; 162 (): 160241.Guo S Nighot M Al-Sadi R Alhmoud T Nighot P Ma TY Lipopolysaccharide regulation of intestinal tight junction permeability is mediated by TLR4 signal transduction pathway activation of FAK and MyD88.J Immunol. 2015; 195: 4999-501042.Sharma R Young C Neu J Molecular modulation of intestinal epithelial barrier: contribution of microbiota.J Biomed Biotechnol. 2010; 201030587943.Peng L Li ZR Green RS Holzman IR Lin J Butyrate enhances the intestinal barrier by facilitating tight junction assembly via activation of AMP-activated protein kinase in Caco-2 cell monolayers.J Nutr. 2009; 139: 1619-162544.Zheng L Kelly CJ Battista KD et al.Microbial-derived butyrate promotes epithelial barrier function through IL-10 receptor-dependent repression of claudin-2.J Immunol. 2017; 199: 2976-298445.Kelly CJ Zheng L Campbell EL et al.Crosstalk between microbiota-derived short-chain fatty acids and intestinal epithelial HIF augments tissue barrier function.Cell Host Microbe. 2015; 17: 662-67146.Kim CH Control of lymphocyte functions by gut microbiota-derived short-chain fatty acids.Cell Mol Immunol. 2021; 18: 1161-117147.Yang W Yu T Huang X et al.Intestinal microbiota-derived short-chain fatty acids regulation of immune cell IL-22 production and gut immunity.Nat Commun. 2020; 11445748.Bischoff SC Barbara G Buurman W et al.Intestinal permeability—a new target for disease prevention and therapy.BMC Gastroenterol. 2014; 14: 18949.Pellegrini C D'Antongiovanni V Ippolito C et al.From the intestinal mucosal barrier to the enteric neuromuscular compartment: an integrated overview on the morphological changes in Parkinson's disease.Eur J Histochem. 2021; 65327850.Vergnolle N Cirillo C Neurons and glia in the enteric nervous system and epithelial barrier function.Physiology (Bethesda). 2018; 33: 269-28051.Spadoni I Zagato E Bertocchi A et al.A gut-vascular barrier controls the systemic dissemination of bacteria.Science. 2015; 350: 830-83452.Benvenuti L D'Antongiovanni V Pellegrini C et al.Enteric glia at the crossroads between intestinal immune system and epithelial barrier: implications for Parkinson disease.Int J Mol Sci. 2020; 21E919953.Reinhardt C Bergentall M Greiner TU et al.Tissue factor and PAR1 promote microbiota-induced intestinal vascular remodelling.Nature. 2012; 483: 627-63154.Stappenbeck TS Hooper LV Gordon JI Developmental regulation of intestinal angiogenesis by indigenous microbes via Paneth cells.Proc Natl Acad Sci USA. 2002; 99: 15451-1545555.Schirbel A Kessler S Rieder F et al.Pro-angiogenic activity of TLRs and NLRs: a novel link between gut microbiota and intestinal angiogenesis.Gastroenterology. 2013; 144 (): 61356.Pellegrini C Antonioli L Colucci R Blandizzi C Fornai M Interplay among gut microbiota, intestinal mucosal barrier and enteric neuro-immune system: a common path to neurodegenerative diseases?.Acta Neuropathol. 2018; 136: 345-36157.Fung TC Olson CA Hsiao EY Interactions between the microbiota, immune and nervous systems in health and disease.Nat Neurosci. 2017; 20: 145-15558.Cani PD Everard A Duparc T Gut microbiota, enteroendocrine functions and metabolism.Curr Opin Pharmacol. 2013; 13: 935-94059.Layunta E Buey B Mesonero JE Latorre E Crosstalk between intestinal serotonergic system and pattern recognition receptors on the microbiota-gut-brain axis.Front Endocrinol (Lausanne). 2021; 1274825460.Clairembault T Leclair-Visonneau L Coron E et al.Structural alterations of the intestinal epithelial barrier in Parkinson's disease.Acta Neuropathol Commun. 2015; 3: 1261.Schwiertz A Spiegel J Dillmann U et al.Fecal markers of intestinal inflammation and intestinal permeability are elevated in Parkinson's disease.Parkinsonism Relat Disord. 2018; 50: 104-10762.Perez-Pardo P Dodiya HB Engen PA et al.Role of TLR4 in the gut-brain axis in Parkinson's disease: a translational study from men to mice.Gut. 2019; 68: 829-84363.Buscarinu MC Romano S Mechelli R et al.Intestinal permeability in relapsing-remitting multiple sclerosis.Neurotherapeutics. 2018; 15: 68-7464.Saresella M Marventano I Barone M et al.Alterations in circulating fatty acid are associated with gut microbiota dysbiosis and inflammation in multiple sclerosis.Front Immunol. 2020; 11139065.Asbjornsdottir B Snorradottir H Andresdottir E et al.Zonulin-dependent intestinal permeability in children diagnosed with mental disorders: a systematic review and meta-analysis.Nutrients. 2020; 12E198266.Fiorentino M Sapone A Senger S et al.Blood-brain barrier and intestinal epithelial barrier alterations in autism spectrum disorders.Mol Autism. 2016; 7: 4967.Wang X Niu Y Yue CX Fu S Wang RT Increased ileal bile acid binding protein and galectin-9 are associated with mild cognitive impairment and Alzheimer's disease.J Psychiatr Res. 2019; 119: 102-10668.Duan M Liu F Fu H Lu S Wang T Preoperative microbiomes and intestinal barrier function can differentiate prodromal Alzheimer's disease from normal neurocognition in elderly patients scheduled to undergo orthopedic surgery.Front Cell Infect Microbiol. 2021; 1159284269.Rundek T Roy S Hornig M et al.Gut permeability and cognitive decline: a pilot investigation in the northern Manhattan study.Brain Behav Immun Health. 2021; 1210021470.Stadlbauer V Engertsberger L Komarova I et al.Dysbiosis, gut barrier dysfunction and inflammation in dementia: a pilot study.BMC Geriatr. 2020; 20: 24871.Engen PA Dodiya HB Naqib A et al.The potential role of gut-derived inflammation in multiple system atrophy.J Parkinsons Dis. 2017; 7: 331-34672.Maes M Sirivichayakul S Kanchanatawan B Vodjani A Upregulation of the intestinal paracellular pathway with breakdown of tight and adherens junctions in deficit schizophrenia.Mol Neurobiol. 2019; 56: 7056-707373.Wu JH Guo Z Kumar S Lapuerta P Incidence of serious upper and lower gastrointestinal events in older adults with and without Alzheimer's disease.J Am Geriatr Soc. 2011; 59: 2053-206174.Warnecke T Schäfer KH Claus I Del Tredici K Jost WH Gastrointestinal involvement in Parkinson's disease: pathophysiology, diagnosis, and management.NPJ Parkinsons Dis. 2022; 8: 3175.Levinthal DJ Rahman A Nusrat S O'Leary M Heyman R Bielefeldt K Adding to the burden: gastrointestinal symptoms and syndromes in multiple sclerosis.Mult Scler Int. 2013; 201331920176.Mishima T Fujioka S Kawazoe M Inoue K Arima H Tsuboi Y Constipation symptoms in multiple system atrophy using Rome criteria and their impact on personalized medicine.J Pers Med. 2022; 12: 83877.Parra-Cantu C Zaldivar-Ruenes A Martinez-Vazquez M Martinez HR Prevalence of gastrointestinal symptoms, severity of dysphagia, and their correlation with severity of amyotrophic lateral sclerosis in a Mexican cohort.Neurodegener Dis. 2021; 21: 42-4778.Leader G Abberton C Cunningham S et al.Gastrointestinal symptoms in autism spectrum disorder: a systematic review.Nutrients. 2022; 14147179.Huang J Cai Y Su Y et al.Gastrointestinal symptoms during depressive episodes in 3256 patients with major depressive disorders: findings from the NSSD.J Affect Disord. 2021; 286: 27-3280.Chapelet G Leclair-Visonneau L Clairembault T Neunlist M Derkinderen P Can the gut be the missing piece in uncovering PD pathogenesis?.Parkinsonism Relat Disord. 2019; 59: 26-3181.Hasegawa S Goto S Tsuji H et al.Intestinal dysbiosis and lowered serum lipopolysaccharide-binding protein in Parkinson's disease.PLoS One. 2015; 10e014216482.Devos D Lebouvier T Lardeux B et al.Colonic inflammation in Parkinson's disease.Neurobiol Dis. 2013; 50: 42-4883.Houser MC Chang J Factor SA et al.Stool immune profiles evince gastrointestinal inflammation in Parkinson's disease.Mov Disord. 2018; 33: 793-80484.Cossais F Schaeffer E Heinzel S et al.Expression profiling of rectal biopsies suggests altered enteric neuropathological traits in Parkinson's Disease patients.J Parkinsons Dis. 2021; 11: 171-17685.Hui KY Fernandez-Hernandez H Hu J et al.Functional variants in the LRRK2 gene confer shared effects on risk for Crohn's disease and Parkinson's disease.Sci Transl Med. 2018; 10eaai779586.Pellizoni FP Leite AZ Rodrigues NC et al.Detection of dysbiosis and increased intestinal permeability in Brazilian patients with relapsing-remitting multiple sclerosis.Int J Environ Res Public Health. 2021; 18462187.Prosperi M Guiducci L Peroni DG et al.Inflammatory biomarkers are correlated with some forms of regressive autism spectrum disorder.Brain Sci. 2019; 9: E36688.Italiani P Puxeddu I Napoletano S et al.Circulating levels of IL-1 family cytokines and receptors in Alzheimer's disease: new markers of disease progression?.J Neuroinflammation. 2018; 15: 34289.Osimo EF Pillinger T Rodriguez IM Khandaker GM Pariante CM Howes OD Inflammatory markers in depression: a meta-analysis of mean differences and variability in 5,166 patients and 5,083 controls.Brain Behav Immun. 2020; 87: 901-90990.Theoharides TC Asadi S Patel AB Focal brain inflammation and autism.J Neuroinflammation. 2013; 10: 4691.Enache D Pariante CM Mondelli V Markers of central inflammation in major depressive disorder: a systematic review and meta-analysis of studies examining cerebrospinal fluid, positron emission tomography and post-mortem brain tissue.Brain Behav Immun. 2019; 81: 24-4092.Pellegrini C Antonioli L Calderone V Colucci R Fornai M Blandizzi C Microbiota-gut-brain axis in health and disease: is NLRP3 inflammasome at the crossroads of microbiota-gut-brain communications?.Prog Neurobiol. 2020; 19110180693.Fasano A All disease begins in the (leaky) gut: role of zonulin-mediated gut permeability in the pathogenesis of some chronic inflammatory diseases.F1000 Res. 2020; 9: 994.Feng X-Y Yang J Zhang X Zhu J Gastrointestinal non-motor dysfunction in Parkinson's disease model rats with 6-hydroxydopamine.Physiol Res. 2019; 68: 295-30395.Pellegrini C Ippolito C Segnani C et al.Pathological remodelling of colonic wall following dopaminergic nigrostriatal neurodegeneration.Neurobiol Dis. 2020; 13910482196.Zhang YG Wu S Yi J et al.Target intestinal microbiota to alleviate disease progression in amyotrophic lateral sclerosis.Clin Ther. 2017; 39: 322-33697.Lai F Jiang R Xie W et al.Intestinal pathology and gut microbiota alterations in a methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease.Neurochem Res. 2018; 43: 1986-199998.Yang X Yu D Xue L Li H Du J Probiotics modulate the microbiota-gut-brain axis and improve memory deficits in aged SAMP8 mice.Acta Pharm Sin B. 2020; 10: 475-48799.Wu ML Yang XQ Xue L Duan W Du JR Age-related cognitive decline is associated with microbiota-gut-brain axis disorders and neuroinflammation in mice.Behav Brain Res. 2021; 402113125100.Bhattarai Y Si J Pu M et al.Role of gut microbiota in regulating gastrointestinal dysfunction and motor symptoms in a mouse model of Parkinson's disease.Gut Microbes. 2021; 131866974101.Kim MS Kim Y Choi H et al.Transfer of a healthy microbiota reduces amyloid and tau pathology in an Alzheimer's disease animal model.Gut. 2020; 69: 283-294102.Pellegrini C D'Antongiovanni V Miraglia F et al.Enteric α-synuclein impairs intestinal epithelial barrier through caspase-1-inflammasome signaling in Parkinson's disease before brain pathology.NPJ Parkinsons Dis. 2022; 8: 9103.Kelly LP Carvey PM Keshavarzian A et al.Progression of intestinal permeability changes and alpha-synuclein expression in a mouse model of Parkinson's disease.Mov Disord. 2014; 29: 999-1009104.Guo S Al-Sadi R Said HM Ma TY Lipopolysaccharide causes an increase in intestinal tight junction permeability in vitro and in vivo by inducing enterocyte membrane expression and localization of TLR-4 and CD14.Am J Pathol. 2013; 182: 375-387105.Dodiya HB Forsyth CB Voigt RM et al.Chronic stress-induced gut dysfunction exacerbates Parkinson's disease phenotype and pathology in a rotenone-induced mouse model of Parkinson's disease.Neurobiol Dis. 2020; 135104352106.Wu S Yi J Zhang YG Zhou J Sun J Leaky intestine and impaired microbiome in an amyotrophic lateral sclerosis mouse model.Physiol Rep. 2015; 3e12356107.Secher T Kassem S Benamar M et al.Oral administration of the probiotic strain Escherichia coli Nissle 1917 reduces susceptibility to neuroinflammation and repairs experimental autoimmune encephalomyelitis-induced intestinal barrier dysfunction.Front Immunol. 2017; 81096108.Gutierrez B Gallardo I Ruiz L et al.Oleanolic acid ameliorates intestinal alterations associated with EAE.J Neuroinflammation. 2020; 17: 363109.Marczynski M Rickert CA Semerdzhiev SA et al.α-Synuclein penetrates mucin hydrogels despite its mucoadhesive properties.Biomacromolecules. 2019; 20: 4332-4344110.Fang X Yue M Wei J et al.Evaluation of the anti-aging effects of a probiotic combination isolated from centenarians in a SAMP8 mouse model.Front Immunol. 2021; 12792746111.Chen LH Wang MF Chang CC et al.Lacticaseibacillus paracasei PS23 effectively modulates gut microbiota composition and improves gastrointestinal function in aged SAMP8 mice.Nutrients. 2021; 131116112.Ou Z Deng L Lu Z et al.Protective effects of Akkermansia muciniphila on cognitive deficits and amyloid pathology in a mouse model of Alzheimer's disease.Nutr Diabetes. 2020; 10: 12113.Han D Li Z Liu T et al.Prebiotics regulation of intestinal microbiota attenuates cognitive dysfunction induced by surgery stimulation in APP/PS1 mice.Aging Dis. 2020; 11: 1029-1045114.Shi Y Qiao CM Zhou Y et al.Protective effects of prucalopride in MPTP-induced Parkinson's disease mice: neurochemistry, motor function and gut barrier.Biochem Biophys Res Commun. 2021; 556: 16-22115.Leblhuber F Steiner K Schuetz B Fuchs D Gostner JM Probiotic supplementation in patients with Alzheimer's dementia—an explorative intervention study.Curr Alzheimer Res. 2018; 15: 1106-1113116.Becker A Pierre Schmartz G Gröger L et al.Effects of resistant starch on symptoms, fecal markers and gut microbiota in Parkinson's disease—the RESISTA-PD trial.Genomics Proteomics Bioinformatics. 2021; ()117.Shah PA Park CJ Shaughnessy MP Cowles RA Serotonin as a mitogen in the gastrointestinal tract: revisiting a familiar molecule in a new role.Cell Mol Gastroenterol Hepatol. 2021; 12: 1093-1104118.Kim S Kwon SH Kam TI et al.Transneuronal propagation of pathologic α-synuclein from the gut to the brain models Parkinson's disease.Neuron. 2019; 103 (): 627119.Lemprière S Exosomal α-synuclein as a biomarker for Parkinson disease.Nat Rev Neurol. 2020; 16: 242-243120.Tarutani A Arai T Murayama S Hisanaga SI Hasegawa M Potent prion-like behaviors of pathogenic α-synuclein and evaluation of inactivation methods.Acta Neuropathol Commun. 2018; 6: 29121.Arotcarena ML Dovero S Prigent A et al.Bidirectional gut-to-brain and brain-to-gut propagation of synucleinopathy in non-human primates.Brain. 2020; 143: 1462-1475122.Tajik N Frech M Schulz O et al.Targeting zonulin and intestinal epithelial barrier function to prevent onset of arthritis.Nat Commun. 2020; 111995123.Zhao J Zhao R Cheng L Yang J Zhu L Peroxisome proliferator-activated receptor gamma activation promotes intestinal barrier function by improving mucus and tight junctions in a mouse colitis model.Dig Liver Dis. 2018; 50: 1195-1204124.Alhamoruni A Wright KL Larvin M O'Sullivan SE Cannabinoids mediate opposing effects on inflammation-induced intestinal permeability.Br J Pharmacol. 2012; 165: 2598-2610Article InfoPublication HistoryPublished: November 02, 2022IdentificationDOI: https://doi.org/10.1016/S2468-1253(22)00241-2Copyright© 2022 Elsevier Ltd. 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Warmer, wetter winters bring risks to river insects
Research by Cardiff University has shown that the warmer, wetter winters in the U.K. caused by climate change are likely to impact the stability of insect populations in streams.
The research, spanning four decades, has demonstrated that stream insects are affected by warmer, wetter winters caused by fluctuating climate over the Atlantic Ocean. The consequences are felt by insect populations even in the smallest Welsh river sources.
The paper, "Climatic effects on the synchrony and stability of temperate headwater invertebrates over four decades," has been published in Global Change Biology.
"U.K. winters are becoming warmer and wetter on average, and we wanted to understand how this might impact our rivers. Streams and rivers are profoundly affected by climate through changes in global air temperatures and precipitation which affect flow patterns and water temperature.
"Over the years, we've noticed increasingly that changes in our rivers also track global climatic patterns over the Atlantic and these provide important clues about climate change," said Professor Steve Ormerod, the Water Research Institute at Cardiff University.
The research is based on samples from the Llyn Brianne Stream Observatory in Central Wales, which is one of the longest-running catchment projects anywhere in the world. The headwaters that form the Llyn Brianne Stream Observatory were first sampled in 1981, allowing scientists to investigate changes to streams and rivers for over forty years.
By tracking changes in the water quality, flow patterns, temperature and river species since the 1980s, the researchers have been able to track how climate changes are impacting Welsh waters. But their work also highlights how climatic fluctuations in other areas—including the Atlantic Ocean—impacts U.K. river quality and wildlife.
"The North Atlantic Oscillation is a large area of atmospheric pressure over the North Atlantic region. Depending on air pressure at sea, the North Atlantic Oscillation brings either cold, dry winters to north west Europe or warm, wet winters—increasing temperatures in upland Wales on average by up to 3°C and rainfall by up to 40%.
"These changes are very similar to the likely scale of climate change, so they provide valuable insight into the effects of global warming. But the more surprising finding was how much these changes affected stream insects over the years of the study.
"Warm, wet winters led to bigger changes in insect populations that were synchronized across the 10 streams we investigated. These effects meant that the species composition was less similar and more unstable between warmer years—which are becoming more frequent as the climate changes," said Dr. Stefano Larsen, of the Fondazione Edmund Mach in Italy.
"It's remarkable that variations among some of the smallest animals in some of the smallest streams in upland Wales are linked to climatic conditions generated thousands of kilometers away over the Atlantic Ocean. Our long-term study shows those effects clearly while warning us of what could become significant climate change patterns.
"But this work also reveals some positive actions to reduce climate change effects, for example, by protecting and restoring biodiversity, and by managing upland landscapes for example to reduce flood impacts," Professor Ormerod added.
More information: Stefano Larsen et al, Climatic effects on the synchrony and stability of temperate headwater invertebrates over four decades, Global Change Biology (2023). DOI: 10.1111/gcb.17017
Journal information: Global Change Biology
Provided by Cardiff University | Biology |
Fat is a normal and necessary part of the body. Fat cells store and release energy, as well as play significant roles in hormonal regulation and immunity.
In recent decades, a concerning rise in metabolic illnesses -- such as cardiovascular disease, high blood pressure and diabetes -- has focused scientific attention on the biology and chemistry of fat, resulting in a wealth of information about how fat cells work.
But fat cells and their metabolic activities are only part of the story.
Fat-filled lipid droplets, tiny spheres of fat many times smaller than fat cells, are a growing subject of scientific interest. Found inside many different cell types, these lipid particles have long been little understood. Studies have begun to illuminate these droplets' participation in metabolic functions and cellular protection, but we still know next to nothing about the physical nature of fat.
Now, researchers at the University of Pennsylvania School of Engineering and Applied Science have looked beyond biochemistry to publish groundbreaking work on the physics of these droplets, revealing them to be a potential threat to a cell's nucleus. In the August issue of the Journal of Cell Biology, they are the first to discover fat-filled lipid droplets' surprising capability to indent and puncture the nucleus, the organelle which contains and regulates a cell's DNA.
The stakes of their findings are high: a ruptured nucleus can lead to elevated DNA damage that is characteristic of many diseases, including cancer.
The study was led by Dennis E. Discher, Robert D. Bent Professor in the Department of Chemical and Biomolecular Engineering, Irena Ivanovska, Ph.D. Research Associate in Penn's Molecular and Cell Biophysics Lab, and Michael Tobin, Ph.D. Candidate in the Department of Bioengineering.
"Intuitively, people think of fat as soft," says Discher. "And on a cellular level it is. But at this small size of droplet -- measuring just a few microns rather than the hundreds of microns of a mature fat cell -- it stops being soft. Its shape has a much higher curvature, bending other objects very sharply. This changes its physics in the cell. It can deform. It can damage. It can rupture."
"Imagine," adds Ivanovska, "trying to pop a balloon with your fist. Impossible. You can deform the balloon, but you won't puncture it. Now imagine trying to pop it with a pen. That's the difference between a fat cell and a cell with small fat droplets in the body. It's a fundamental physical difference, not a metabolic one."
The team's research reframes scientific inquiry into fat, underlining that fat's role in the body is much more than just a number on the scales.
"This isn't fat canonically conceived," says Tobin. "This is about how fat works at scales smaller than a cell and poses physical risks to cellular components, even at the level of DNA."
The team's work builds on a decade of foundational research, including leading contributions by Ivanovska, into the behaviors of nuclear proteins that give the nucleus its protective structural qualities. These proteins are dynamic, shifting levels to respond to their mechanical environments and provide what the nucleus needs to maintain its integrity.
"There's a constant process of repair to DNA damage that goes on in cells," says Ivanovska. "For this to happen, the nucleus needs to have enough DNA repair proteins. If a nucleus is ruptured, these proteins scatter and cannot repair damage in a timely manner. This causes DNA damage accumulation and can potentially result in a cancer cell."
A cell lives in a dynamic physical and mechanical environment where things can and do go wrong. But it also has an army of molecular helpers always working to maintain and repair it.
"The problem is," says Discher, "when a nucleus is compromised -- by toxins, overexposure to UV rays, or these fat-filled lipid droplets. Then there is a strong potential for DNA damage and that comes with consequences for health."
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Materials provided by University of Pennsylvania School of Engineering and Applied Science. Original written by Devorah Fischler. Note: Content may be edited for style and length.
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Scientists in Russia discovered seven perfectly intact sea otters in the belly of a beached orca, according to a new study. The doomed killer whale was found far from its normal hunting grounds, raising the question of what it was doing there.
The female orca (Orcinus orca) was found in 2020 on the coastline of one of the Commander Islands, which lie offshore the Russian Far East in the Bering Sea. Scientists performed a necropsy on the animal and discovered not only the seven dead sea otters (Enhydra lutris), which collectively weighed 258 pounds (117 kilograms), but also 256 cephalopod beak parts.
One sea otter was lodged between the oral cavity and the esophagus, which may have led to the whale's demise, the researchers wrote in the study, which was published Sept. 28 in the journal Aquatic Mammals.
Several things about the killer whale have puzzled the researchers.
"It is very unusual because orcas don't normally eat sea otters," study co-author Olga Filatova, a cetacean researcher at Moscow State University, told Live Science in an email.
Instead, they hunt seals, sea lions, dolphins and even other whales. And whatever prey species they hunt, "they normally don't swallow prey whole — they usually tear it apart and eat only the best (most fatty) parts," Filatova said.
Gulping down whole sea otters was likely challenging for the doomed orca, as adult sea otters can reach up to 5 feet (1.5 meters) long. The researchers think the orca may have taken this extraordinary step because it was starving.
The researchers also analyzed the orca's DNA and determined that this individual was part of a population, known as "Bigg's killer whales," that have a vast home range that stretches from the Aleutian Islands and the Gulf of Alaska, to the coastline of California.
This is the first time any member of this orca population has ever been found in the Western Pacific, leading the study authors to hypothesize that the orca learned this hunting strategy elsewhere. Feeding strategies are usually passed on from mothers to calves, the study authors noted.
While the stranded orca raises some questions, it may help answer others. For some time, sea otter populations between the Aleutian Islands and the Gulf of Alaska have dwindled.
While some scientists suspected orcas were behind the area's decreasing sea otter population, this is the first direct evidence of an orca originally from that region preying on sea otters. The finding raises the possibility that orca predation may be behind the drop in sea otters.
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Elise studied marine biology at the University of Portsmouth in the U.K. She has worked as a freelance journalist focusing on the aquatic realm. Elise is working with Live Science through Future Academy, a program to train future journalists on best practices in the field. | Biology |
A cold-specialized icefish species underwent major genetic changes as it migrated to temperate waters, new study finds
Many animals have evolved to tolerate extreme environments, including being able to survive crushing pressures of ocean trenches, unforgiving heat of deserts, and limited oxygen high in the mountains. These animals are often highly specialized to live in these specific environments, limiting them from moving to new locations.
Yet, there are rare examples of species that once lived in harsh environments but have since colonized more temperate settings. Angel Rivera-Colón, a former graduate student now postdoc in the lab of Julian Catchen (CIS/GNDP), an associate professor in the department of Evolution, Ecology, and Behavior at the University of Illinois Urbana-Champaign, explores the genetic mechanisms underlying this anomaly in Antarctic Notothenioid fish.
Antarctic notothenioids, or cryonotothenioids, have evolved to live in freezing waters around Antarctica, where most fish would otherwise freeze solid if exposed to such cold temperatures. However, cryonotothenioid fish are able to survive in these waters due to antifreeze glycoproteins they produce in their cells. The AGFPs bind to any ice crystals that form, preventing them from growing and the cells from freezing.
Antarctic icefishes, a family within cryonotothenioids, are even more specialized to live in the icy waters. Icefishes also are the only vertebrate that has adapted to live without hemoglobin in their blood cells, causing their cells and tissues to be translucent/white in color. Hemoglobin is a protein in blood cells that helps increase oxygen uptake and results in the red coloration of cells. Normally animals need hemoglobin to get enough oxygen, but in the cold, oxygen-rich waters around Antarctica, icefishes have developed morphological changes, such as bigger hearts for pumping blood, that they no longer need hemoglobin to get enough oxygen.
Despite this extreme specialization, one species of icefish called Champsocephalus esox, or the pike icefish, has escaped Antarctica and now lives in warmer, less oxygenated, South American waters. "The movement of this species to warmer waters posed an interesting evolutionary mystery that I wanted to try to solve," Rivera-Colón said. "If you're specialized to only live in very cold environments, how do you survive and adapt to this new warmer environment?"
To understand how the genome of the fish changed as it migrated into warmer waters, Rivera-Colón compared the genetics of the pike icefish to that of an Antarctic species of icefish, C. gunnari. The team took tissue samples collected by collaborators and fishermen from southern Chile, South Georgia, and the Sandwich Islands to sequence the genomes.
"This is the first time we've looked at a genome of a notothenioid species that escaped Antarctica into this new temperate environment. A big part of that is because the pike icefish is very rare and elusive, so the help of these fishermen as well as collaborators for gathering samples was indispensable," Rivera-Colón said. The researchers used continuous long read sequencing to generate a chromosome-level genome for each fish species.
After comparing the genomes, they found that while the genome was highly conserved between the species, there was divergence in areas of the pike icefish genome associated with the physiology that would need to change as the fish moved to warmer waters. Surprisingly, the pike icefish genome still contained multiple copies of the gene that codes for AGFPs, but the genes were full of mutations that may render it non-functional.
"Most of the genes had stop codons inserted in," Catchen explained. "Assuming everything works as we'd expect, we wouldn't see them transcribed into AGFPs. But the genes are still there and presumably could still active. We're not sure." The researchers say that while mutations in this gene in cold water cryonotothenioids could spell death if the gene no longer works, in warmer waters the selection on this gene in pike icefish would've loosened, as the fish would no longer need to prevent themselves from freezing.
Researchers also found the pike icefish genome displayed chromosomal inversions—when part of the chromosome becomes flipped in orientation. "We know that inversions and other chromosomal changes can be very important for mediating adaptive processes as well as creating barriers between species," explained Rivera-Colón. "So finding them here suggests that they could be important for adaptation to the warmer environment in South America." Rivera-Colón further explained that inversions could make it more difficult for the two species to mix, speeding up speciation between the sister species, despite only splitting less than 2 million years ago.
In addition to evolving to live in warmer waters, the pike icefish would've also needed to adapt to a different light environment. The sea around the Antarctic is dark much of the year, and the surface ice blocks much of the light. But in temperate waters, pike icefish experience a more normal day-night cycle. The team is currently examining gene expression in related fish to see how their physiology and circadian rhythms have adapted to these new light cycles.
The researchers also plan to look at the genomes and mitochondria of another pair of related species, Trematomus borchgrevinki and Notothenia angustata. Similar to this study, T. borchgrevinki lives in the cold Antarctic waters, while N. angustata has secondarily transitioned to live in warm waters on the coast of New Zealand. The current study, as well as this planned study on the other species pair, will help researchers better understand how species highly specialized to live in certain environments can escape and adapt to new environments.
"I think one of the really interesting aspects of this study is that it challenges how we tell stories about 'why evolution acted the way it did,'" Catchen described. "We use the classic story of the icefish to explain loss of hemoglobin due to the cold, oxygenated waters it specializes in, but then you have this species that escaped back to normal temperatures and is managing fine. Selection pushed an organism to the extreme in this direction, and then the environment shifted, and now it's being pushed in a different direction."
Rivera-Colón added "Our study just goes to show that this specialization for extreme cold is not an evolutionary dead end, and it helps explain how these transitions happen in nature."
The study, titled "Genomics of secondarily temperate adaptation in the only non-Antarctic icefish," is published in Molecular Biology & Evolution.
More information: Angel G Rivera-Colón et al, Genomics of Secondarily Temperate Adaptation in the Only Non-Antarctic Icefish, Molecular Biology and Evolution (2023). DOI: 10.1093/molbev/msad029
Journal information: Molecular Biology and Evolution
Provided by University of Illinois at Urbana-Champaign | Biology |
Can lions coexist with cattle in Africa?
Protecting lions and the interests of cattle producers in Kenya is a difficult balancing act. In a recent Frontiers in Ecology and Evolution article, Dr. Laurence G Frank, a researcher at the Museum of Vertebrate Zoology at the University of California, Berkeley, and the Mpala Research Centre in Laikipia, Kenya, explored how protecting livestock can help protect endangered lions.
As part of our "Frontiers Scientist" series, Frank, who also is the director of "Living With Lions", a conservation research group working in nonprotected areas of Kenya to save the remaining wild lions and other predators outside National Parks, caught up with Frontiers to tell us about his career and research.
What inspired you to become a researcher?
All children love animals and some who never grow up become zoologists. At the age of 10 I was introduced to field biology at a local community museum, where we were taught basic ecology and animal behavior, collecting and specimen preparation technique, and formal field note format. My weekends were spent pestering local reptiles and trapping small mammals in the Bay Area hills; many of my juvenile specimens are in the California Academy of Sciences research collection.
A field course on east African mammals at the age of 18 hooked me on Africa and I returned to Kenya a few years later to study pesticides in raptors. After an MSc in ecology at the University of Aberdeen, I did my Ph.D. at Berkeley, studying the social behavior of spotted hyenas in Kenya's Masai Mara National Reserve. With Prof. Stephen Glickman, I helped create the Berkeley Hyena Project—a large research colony in the hills overlooking San Francisco Bay—to study the unique biology of female masculinization in this species.
Can you tell us about the research you're currently working on?
After 20 years of hyena research, in 1997 I turned to the conservation biology of lions, creating three projects in different parts of Kenya with two basic remits: helping traditional pastoralists (herding peoples) and modern ranchers better protect their cattle from lion predation, and understanding how lions adapt their behavior to avoid being killed by people angered at losing livestock to predators.
Those were carried out by Ph.D. and MSc students from Kenyan, American, and British universities, as well as dozens of Maasai warriors and colleagues from a variety of universities. I am partially retired now but am still active in Laikipia.
In your opinion, why is your research important?
Lions are one of the most iconic of animals but, like all African wildlife, are rapidly disappearing under the pressures of a burgeoning human population. National parks are critical to conservation, but most are too small and too far apart to protect wide-ranging animals like elephants and lions, which move beyond the boundaries of parks, create problems for humans, and are then killed in retaliation. If these species are to persist, viable breeding populations must be maintained in the human-dominated landscapes between parks, requiring coexistence, however uneasy, between people and problematic wildlife.
For large carnivores like lions, tigers, hyenas, and wolves, this requires managing both livestock and predators to minimize predation on livestock and subsequent retaliatory killing. It also means managing humans' ancient antipathy towards these animals, which are threats to livelihoods and occasionally to human lives.
Of course, it also means maintaining healthy populations of wild prey such as zebra, giraffes, buffalo, and smaller grazers, without which lions would have only livestock to prey upon. Conserving lions and other large carnivores necessarily means conserving their habitat and all the wildlife it supports.
Are there any common misconceptions about this area of research?
There are two major misconceptions among the western public: Firstly, that parks are all we need in order to protect lions and other African wildlife, and secondly that the primary threats are disease, climate change, and trophy hunting. Disease may affect individuals but only in rare exceptions threaten entire local populations, let alone entire species.
The climate crisis threatens much of life on Earth, but other human impacts are much more immediate. Trophy hunting removes individuals—primarily older males—but is a minor factor compared to pervasive killing by local people to protect livestock. The widespread use of cheap and lethal agricultural pesticides has devastated lion and hyena populations in much of Africa.
Because lions return to a kill to feed again the following night, an aggrieved cattle owner need only sprinkle a dollar's worth of pesticide on the carcass and a whole pride is dead in the morning. Scavengers drawn to a carcass also die: vultures were ubiquitous until very recently but have nearly disappeared from much of Africa in this century due to poisoning targeted at lions and hyenas.
How would you address them?
Large carnivores are difficult neighbors if one's livelihood depends on livestock production. African pastoralists perceive little benefit from tolerating lions or expending time, effort, and money to protect their cattle if they can solve the problem permanently with a handful of poison.
As most remaining lion range is also occupied by people and their domestic animals, to promote coexistence conservationists must help pastoralists reduce cattle losses while also ensuring that wildlife improves rather than harms their economic and emotional well-being. Tourism is central to the latter but few tourist dollars reach the family whose favorite cow was eaten by lions last night. Moreover, much of lion range consists of hot, scrubby bushlands, unattractive for tourism.
What are some of the areas of research you'd like to see tackled in the years ahead?
Making lions and other wildlife worth tolerating is one of the great challenges to preserving wildlife in the developing world and will require much greater western investment than is spent today. Finding ways to promote tolerance of wildlife where impoverished people have more urgent immediate concerns will be key in stemming the wave of extinction sweeping the world today.
How has open science benefited the reach and impact of your research?
Our "Living with Lions" program in the Amboseli region of Kenya produced the highly successful Lion Guardians project, which employs uneducated Maasai warriors, most of them former lion killers, as citizen scientists, helping their communities avoid livestock losses to predators and working alongside professional biologists in collecting data on lion numbers and ecology.
Covering a vast region on foot, the Guardians turned around a rapidly dwindling lion population and produced invaluable data on persecuted lions which are nocturnal, secretive, and very hard to study with standard wildlife research methods. In Laikipia, most ranchers have invested heavily in new methods to protect their cattle from predators, building 'lion-proof' nighttime bomas (corrals) of moveable steel fencing rather than local thorn bush, and today very few lions are killed after taking livestock.
Innovations such as the Lion Guardians project and the lion-proof mobile bomas invented by a Laikipia rancher are too important to hide in academic publications, which are expensive and often inaccessible to the public and practicing conservationists. The current extinction crisis is progressing with terrifying speed.
All advances in finding effective measures to protect dwindling species must be made readily available to everyone working to protect life on Earth. Frontiers is at the forefront in the movement to put progress in science and conservation ahead of profits.
More information: Laurence G. Frank, Twenty years of lion conservation in a commercial rangeland, Frontiers in Ecology and Evolution (2023). DOI: 10.3389/fevo.2023.1141195
Journal information: Frontiers in Ecology and Evolution
Provided by Frontiers | Biology |
Scientists discover key to a potential natural cancer treatment's potency
Slumbering among thousands of bacterial strains in a collection of natural specimens at The Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology, several fragile vials held something unexpected, and possibly very useful.
Writing in the journal Nature Chemical Biology, a team led by chemist Ben Shen, Ph.D., described discovery of two new enzymes, ones with uniquely useful properties that could help in the fight against human diseases including cancer. The discovery, published last week, offers potentially easier ways to study and manufacture complex natural chemicals, including those that could become medicines.
The contribution of bacterial chemicals to the history of drug discovery is remarkable, said Shen, who directs the Natural Products Discovery Center at the institute, one of the world's largest microbial natural product collections.
"Few people realize that nearly half of the FDA-approved antibiotics and anticancer drugs on the market are natural products or are inspired by them," Shen said. "Nature is the best chemist to make these complex natural products. We are applying modern genomic technologies and computational tools to understand their fascinating chemistry and enzymology, and this is leading to progress at unprecedented speed. These enzymes are the latest exciting example."
The enzymes the team discovered have a descriptive—if unwieldy—name. They are called "cofactorless oxygenases." This means the bacterial enzymes pull oxygen from the air and incorporate it into new compounds, without requiring the typical metals or other cofactors to initiate the necessary chemical reaction.
This new way of synthesizing defensive substances would confer a survival advantage, enabling the organism to fend off infections or invaders. And because enzymes are to chemists what drill bits or saw blades are to a carpenter, they offer scientists new ways to create useful things, said the paper's first authors, postdoctoral researchers Chun Gui, Ph.D., and Edward Kalkreuter, Ph.D.
Most immediately, the discovery of the enzymes, TnmJ and TnmK2, solves a lingering mystery of how a potential antibiotic and anticancer compound the Shen lab had first discovered in 2016, tiancimycin A, achieved such potency, Gui and Kalkreuter said.
The enzymes enable the bacteria to produce compounds for targeting and breaking up DNA, Gui said. This would be immensely useful in fighting off a virus or other germ—or killing cancer.
Tiancimycin A is being developed as part of a cancer-targeting antibody therapy. These types of combined antibody-drug therapeutics represent a rapidly growing new approach to fighting cancer. But a critical step to using tiancimycin A as an antibody's payload is making enough to study it at a larger scale. That proved challenging.
"Even after we identified genes responsible for encoding tiancimycin A, several of the steps required to synthesize it could not be predicted," Gui said. "The two enzymes described in the current study are highly unusual."
Tiancimycin A was first found in a soil-dwelling bacteria, a type of Streptomyces from the strain collection at the Natural Products Discovery Center. To make its powerful chemical weapon, the organism had to solve a problem. It somehow had to break three highly stable carbon-carbon bonds and replace them with more reactive carbon-oxygen bonds. For a long time, the scientists couldn't understand how the bacteria managed that feat.
Cracking the mystery involved finding other tiancimycin A-like natural product-producing bacteria among the institute's Natural Products Discovery Center collection of 125,000 bacterial strains, and analyzing their genomes to search for the evolutionary hints.
The historic collection had long been housed in a pharmaceutical company's basement, collected over decades following the discovery of penicillin in the scientific community's hopeful rush to find the next great antibiotic. The collection did generate several historically important drugs through the years, including the tuberculosis antibiotic streptomycin and the organ transplant drug sirolimus. But the majority of the collection's freeze-dried bacterial strains had rested in their glass vials, unexplored.
In 2018, Shen won a competition for the collection, so that it could be fully investigated in an academic setting, where it would be open to science. His team is now developing ways to study the strains, read their genomes and deposit the information into a searchable database for the scientific community to access.
Modern genome sequencing and bioinformatics techniques are proving that there may be as many as 30 interesting gene clusters in each strain of bacteria they study, and many of them code for natural products never before documented by scientists, said Shen, who is a member of the UF Health Cancer Center.
The discovery of the new cofactorless enzymes is but the latest example of the chemical riches that lie within The Wertheim UF Scripps Institute's collection, Shen said. Their discovery has sparked new excitement about further investigating the reasons the unique chemistry evolved, and the ways it may prove useful.
"This publication underscores how many surprises nature still has for us," Shen said, "It can teach us much about fundamental chemistry and biology and provide us with the tools and inspiration we need to translate laboratory findings into medicines that impact society and address many problems faced by humanity."
In addition to Shen, Gui and Kalkreuter, the authors of the study, "Cofactorless oxygenases guide anthraquinone-fused enediyne biosynthesis," include Yu-Chen Liu, Ph.D.; Gengnan Li, Ph.D.; Andrew D. Steele, Ph.D.; Dong Yang, Ph.D. of The Wertheim UF Scripps Institute, and Changsoo Chang, Ph.D., of Argonne National Laboratory.
More information: Chun Gui et al, Cofactorless oxygenases guide anthraquinone-fused enediyne biosynthesis, Nature Chemical Biology (2023). DOI: 10.1038/s41589-023-01476-2
Journal information: Nature Chemical Biology
Provided by University of Florida | Biology |
A molecular machine's secret weapon exposed
RNAs are having a moment. The foundation of COVID-19 vaccines, they've made their way from biochemistry textbooks into popular magazines and everyday discussions. Entire companies have been launched that are dedicated to RNA research. These tiny molecules are traditionally known for helping cells make proteins, but they can do much more. They come in many shapes and sizes, from short and simple hairpin loops to long and seemingly tangled arrangements. RNAs can help activate or deactivate genes, change the shape of chromosomes, and even destroy other RNA molecules.
It takes a lot to keep RNAs in check. Our cells have molecular "machines" that eliminate RNAs at the right time and place. Most come equipped with a "motor" to generate the energy needed to untangle RNA molecules. But one machine in particular, named Dis3L2, is an exception. The enzyme can unwind and destroy RNA molecules on its own. This action has puzzled scientists for years. Now, Cold Spring Harbor Laboratory (CSHL) biochemists have pieced together what's happening.
It turns out Dis3L2 changes shape to unsheathe an RNA-splitting wedge.
Using state-of-the-art molecular imaging technology, CSHL Professor and HHMI Investigator Leemor Joshua-Tor and her team captured Dis3L2 at work. They fed the molecular machine hairpin snippets of RNA and imaged it getting "eaten" at various stages. After the machine had chewed up the tip of the RNA, it swung open a big arm of its body to peel apart the hairpin and finish the job.
"It's dramatic," Joshua-Tor says. "We know things change conformation. They buckle. But opening something out like that and exposing a region in this way—we didn't quite see something like this before."
Joshua-Tor's team then began tinkering with the Dis3L2 machine, searching for the gears and parts enabling it to unwind and destroy RNA. The researchers narrowed it down to a protruding wedge left unsheathed after the machine shifted shapes. If the researchers removed the wedge, Dis3L2 could no longer untangle the RNA hairpin, putting the machine out of commission.
The findings reveal a surprising new way that RNA-controlling machines in our cells execute their tasks. Rather than solid structures, these molecular workhorses need to be considered malleable and versatile. This new outlook may help scientists develop better treatments for diseases and disorders caused by RNA gone haywire. "We have to start thinking about these things as much more dynamic entities," Joshua-Tor says, "and take that into account when we are designing therapeutics."
The findings are published in the journal Nature Structural & Molecular Biology.
More information: Leemor Joshua-Tor, A shape-shifting nuclease unravels structured RNA, Nature Structural & Molecular Biology (2023). DOI: 10.1038/s41594-023-00923-x. www.nature.com/articles/s41594-023-00923-x | Biology |
September 12, 2022 Analysis reveals how restoring relatively narrow forest buffers could substantially improve regional water quality and carbon storage in Costa Rica and elsewhere. Such changes could have outsized benefits for vulnerable populations that rely on rivers for their water supply. Stanford Woods Institute for the Environment A new Stanford University-led study in Costa Rica reveals that restoring relatively narrow strips of riverfront forests could substantially improve regional water quality and carbon storage. The analysis, available online and set to be published in the October issue of Ecosystem Services, shows that such buffers tend to be most beneficial in steep, erosion-prone, and intensively fertilized landscapes – a finding that could inform similar efforts in other countries. Costa Rican naturalist and Stanford research collaborator Dunia Villalobos examines a river in Las Cruces, Costa Rica. (Image credit: Rebecca Chaplin-Kramer) “Forests around rivers are key places to target for restoration because they provide huge benefits with very little impediment to productive land,” said study lead author Kelley Langhans, a PhD student in biology at Stanford University affiliated with the Natural Capital Project. “A small investment could have a really big impact on the health of people and ecosystems.”
Unleashing potential
Vegetated areas adjacent to rivers and streams absorb harmful pollutants in runoff, keeping them out of waterways. Creating effective policies to safeguard these riparian buffers and prioritizing where to implement them is a challenge in part because of a lack of data quantifying the impact of restoring such areas. The researchers, in partnership with officials from Costa Rica’s Ministry of Environment and Energy, Central Bank, and PRIAS Laboratory, analyzed one such policy – Costa Rica’s Forest Law 7575. Passed in 1996 and unevenly enforced since then, the law mandates protection of forested riverfront strips 10 meters (about 33 feet) to 50 meters (about 164 feet) wide.
Using InVEST, the Natural Capital Project’s free, open-source software, the team compared a scenario in which the law was fully enforced with a business-as-usual scenario. They modeled the effects of reforesting 10-meter-wide strips, thereby underestimating the effects of the law’s provisions. Still, their models showed such a change would boost retention of phosphorus by nearly 86%, retention of nitrogen by more than 81%, and retention of sediment by about 4%. The expanded forest cover – an increase of about 2% nationwide – would also increase carbon sequestration by 1.4%.
This reforestation would be most impactful in areas below steep slopes with erosion-prone land uses (such as pastures), high levels of fertilizer application (such as widely cultivated oil palm trees), and low levels of nutrient retention (such as urban areas). Such changes could have huge impacts on areas of Costa Rica where large numbers of people are directly dependent on rivers for drinking water.
“When quantifying the benefits of ecosystem restoration, it’s crucial to consider how it affects people, especially the most vulnerable populations,” said Langhans. “That is why in this research we explicitly mapped out how increases in water quality would reach those who rely on rivers the most.”
Even regions with water treatment infrastructure could benefit because such infrastructure is particularly vulnerable to hurricanes and earthquakes in Costa Rica. As recently as 2020, a tropical storm combined with a hurricane knocked out water service to 120,000 Costa Ricans for several days, forcing people to temporarily rely on other water sources, including streams. Typical water treatment methods also do not remove nitrates, which are especially susceptible to leaching into groundwater due to their high solubility. This is a particular concern in Costa Rica, which uses nitrogen-based fertilizers at one of the highest rates in the world.
Most of the land that would need to be reforested to create these buffers is farmland and pasture for cattle. Past research has shown that Costa Rican farmers value trees on their land and are generally supportive of reforestation, but feel that the upfront costs of transitioning to forest, and – on more productive lands – the opportunity costs of forgoing agricultural production, are too high. Improved financial incentives – such as expanding Costa Rica’s Payments for Ecosystem Services program – and community-based efforts could help, according to the researchers.
The study comes at a key time for Costa Rica, which is implementing a National Decarbonization Plan aimed at increasing forest cover to 60%.
“Our study provides a model for using realistic, policy-based scenarios to pinpoint areas where forest restoration could have the largest impact in terms of improving people’s health and meeting national adaptation and emissions goals,” study co-author Rafael Monge Vargas, director of Costa Rica’s National Geoenvironmental Information Center in the Ministry of Environment and Energy. Stanford co-authors of the study also include Rafael Schmitt, a research engineer at the Natural Capital Project; Rebecca Chaplin-Kramer, a lead scientist at the Natural Capital Project and co-founder of SPRING; Rodolfo Dirzo, a professor of biology, Bing Professor of Environmental Science in the Stanford School of Humanities and Sciences, and a senior fellow at the Stanford Woods Institute for the Environment.; Jesse Goldstein and Stacie Wolny, GIS analysts at the Stanford Natural Capital Project and Stanford Woods Institute for the Environment; Taylor Powell, a graduate student; and Gretchen Daily, co-founder and faculty director of the Stanford Natural Capital Project, Bing Professor of Environmental Science, and a senior fellow at the Stanford Woods Institute for the Environment; and Christopher Anderson of Salo Sciences and Jeffrey Smith of Princeton University, who were Stanford PhD students at the time of the research. Other coauthors include Christian Vargas Bolaños and Cornelia Miller Granados of the National Center for High Technology in Costa Rica, Fermin Vargas Cabezas of the Costa Rican Institute of Electricity; Theodora Horangic of Yale University; Irene Alvarado Quesada of the Central Bank of Costa Rica; and Alvaro Umaña Quesada of Costa Rica’s Tropical Agricultural Research and Teaching Center.
This research was funded by the National Science Foundation, the Winslow Foundation, the LuEsther T. Mertz Charitable Trust, the Gordon and Betty Moore Foundation, and the NASA A.50 GEO Work Programme. The GEO-Amazon Earth Observation Cloud Credits Programme provided technical support. | Biology |
Half-Synthetic Yeast Engineered for the First Time
Scientists engineer a strain of yeast that has an over half synthetic genome.
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The Synthetic Yeast Genome Project 2.0 (Sc2.0) is a global consortium working to synthesize the entire yeast genome. In a collection of papers, the project declares a major milestone: it has created a yeast strain comprising over 50% synthetic DNA.
Generating synthetic genomes
Synthetic genomes are created by designing and assembling DNA sequences that are then inserted into an organism’s cells, effectively allowing researchers to “customize” the organism with certain characteristics. It’s an area of research within synthetic biology that utilizes recent advances in molecular biology, genetic engineering and gene synthesis.
“Writing a genome is in many ways a test of how well you understand its function and its evolved natural ‘design’," says Dr. Jef Boeke, a synthetic biologist at New York University (NYU) Langone Health and the leader of Sc2.0.
The first efforts to generate synthetic genomes largely focused on viruses or bacteria. In 2010, scientists from the J. Craig Venter Institute synthesized the first synthetic bacterial genome, Mycoplasma mycoides JCVI-syn1.0.
Boeke and colleagues have been working hard on Sc2.0 for at least 18 years, as synthesizing a yeast genome is more technologically challenging than a bacterial genome. “It’s substantially bigger. It’s more repetitive than bacterial genomes, and it’s made up of many individual chromosomes, whereas most bacteria have only one,” Boeke explains.
It’s a challenge that is worthwhile in Boeke’s mind, considering that humans are more closely related to yeast than bacteria, making yeast a better model for understanding how human cells work.
Yeast’s designer genome
The half-synthetic yeast has a “designer” genome that is based on Saccharomyces cerevisiae (S. cerevisiae), commonly referred to as baker’s or brewer’s yeast. Boeke and colleagues wanted to create a strain that could help them understand how the model organism functions and how it could be improved. It was therefore important that the synthetic yeast was highly modified.
Non-coding and repetitive elements of DNA were removed and a diversity generator, called Synthetic Chromosome Recombination and Modification by LoxP-mediated Evolution, or the “SCRaMbLE” system, was added.
Boeke and colleagues also created a new chromosome, which does not exist in nature. Genes encoding transfer RNA (tRNA) are often associated with regulatory elements that can lead to stability issues when integrated into a synthetic chromosome. The researchers decided to remove these genes and created a tRNA “neochromosome”.
“The tRNA neochromosome is not modeled on an existing natural chromosome but was literally designed piece by piece, on a computer, and the pieces came from at least 5 different species of microorganisms,” says Boeke. “The fact that it can function, by producing tRNAs like a natural genome does, is pretty amazing. It is also designed to avoid ‘head-on collisions’ between RNA polymerase and DNA polymerase which can lead to DNA breaks and other challenges for the cell.”
Strain generated that is over 50% synthetic
S. cerevisiae’s genome is organized into 16 chromosomes, with each team in the consortium responsible for producing one synthetic chromosome at a time. “Sc2.0 started small and grew to be a project involving researchers in 4 continents and 9 countries,” says Boeke. The teams independently assembled each chromosome to produce 16 strains, each of which comprised 15 native chromosomes and one synthetic chromosome. The next challenge was finding a way to pull all of the synthetic chromosomes together.
The researchers developed a new method called chromosome substitution to bring the synthetic chromosomes together in a single strain. “We combined two methods to do this: transfer of the synthetic chromosome to a recipient strain by doing a special kind of genetic cross. In this cross, a single chromosome moves from one nucleus to the other – a process called ‘chromoduction’,” explains Boeke.
“This leads to a cell with one extra synthetic chromosome. At this point, the resident natural chromosome corresponding to it can be destabilized by forcing RNA polymerase to traverse its centromere, a process that greatly destabilizes it. Et voila! A cell with a synthetic chromosome swapped in place of a native chromosome.” By integrating seven of the synthetic chromosomes, Sc2.0 has succeeded in generating a strain that is over 50% synthetic.
The synthetic yeast strain was found to possess genetic defects, or “bugs”, such as genetic interactions between genes located on the synthetic chromosomes. Such issues had been anticipated, so Boeke and colleagues were prepared to map the bugs and find a fix. “The defects can result from RNA not folding up as it should,” says Boeke. “Once mapped, bugs can be easily corrected by removing the changed bases and restoring the native sequence. This has already been done for every bug.”
A major milestone
The collection of papers marks a milestone in genomics and synthetic biology, but the real fun will begin once the rest of the synthetic chromosomes are integrated. “That’s when we’re really going to be able to start shuffling that deck and producing yeast that can do things that we’ve never seen before,” says Boeke. Synthetic genomes designed for the production of medicines or biofuels might well become a reality in the near future – the foundations are being laid, after all.
Boeke is often asked, “which genome is next"? His team at NYU Langone Health is currently working on “The Dark Matter Project”, which seeks to understand what new information lies in the non-protein-coding portion of the mammalian genome.
Dr. Jef Boeke was speaking to Molly Campbell, Senior Science Writer for Technology Networks.
References:
Zhao Y, Coelho C, Hughes A, et al. Debugging and consolidating multiple synthetic chromosomes reveals combinatorial genetic interactions. Cell. 2023. doi: 10.1016/j.cell.2023.09.025
Schindler D, Walker R, Jiang S, et al. Design, construction, and functional characterization of a tRNA neochromosome in yeast. Cell. 2023. doi: 10.1016/j.cell.2023.10.015
Shen Y, Gao F, Wang Y, et al. Dissecting aneuploidy phenotypes by constructing Sc2.0 chromosome VII and SCRaMbLEing synthetic disomic yeast. Cell Genomics. 2023. doi: 10.1016/j.xgen.2023.100364
McCulloch L, Sambasivam V, Hughes A, et al. Consequences of a telomerase-related fitness defect and chromosome substitution technology in yeast synIX strains. Cell Genomics. 2023. doi: 10.1016/j.xgen.2023.100419 | Biology |
Sign up for CNN’s Wonder Theory science newsletter. Explore the universe with news on fascinating discoveries, scientific advancements and more. London CNN — The world’s oldest mammal has been identified using fossil dental records – predating the previously confirmed earliest mammal by about 20 million years – in a new discovery hailed as “very significant” by researchers. Brasilodon quadrangularis was a small shrew-like creature, around 20 centimeters (8 inches) long, that walked the earth 225 million years ago at the same time as some of the oldest dinosaurs and sheds light on the evolution of modern mammals, according to a team of Brazilian and British scientists. The discovery was made by researchers from the Natural History Museum in London, King’s College London and the Federal University of Rio Grande do Sul in Porto Alegre. Scientists relied on clues provided by fossils of hard tissues such as bones and teeth. This is because mammalian glands, which produce milk, have not been preserved in any fossils found to date. Until now, the Morganucodon had been considered the first mammal, with isolated teeth showing that it dated back around 205 million years. The Morganucodon had a small gerbil-like body and a long face similar to those of shrews or civets. The dental records in the study published Tuesday in the Journal of Anatomy date Brasilodon quadrangularis to 225 million years ago – 25 million years after the Permian-Triassic mass extinction event – the third and biggest mass extinction, when more than 90% of species in the ocean disappeared and 70% of land animals died out. Martha Richter, a scientific associate at the museum and senior author on the paper, told CNN that the Brasilodon quadrangularis was previously believed to be an “advanced reptile,” but examination of its teeth show “definitively” that it was a mammal. “If you think about reptiles, they have many, many different replacement teeth throughout their lives but we mammals only have two. Firstly, the milk teeth and then the second dentition which replaces the original set. This is what defines mammals,” Richter said. Brasilodon is the oldest extinct vertebrate with two successive sets of teeth – baby teeth and one permanent set – also known as a diphyodonty, the news release said. The first set starts developing during the embryonic stage and the second set develops after birth. Richter and her colleagues examined three lower jaws of the species, which lived in the region covered today by the southern-most section of Brazil. Under the microscope they discovered “the type of replacement teeth that are only present in mammals,” she said. Richter added: “This was a very, very small mammal that was probably a burrowing animal living in the shadows of the oldest dinosaurs that we know from that period.” She said the team had been working on the project for more than five years and described their discovery as “very significant.” In the news release, Richter said the findings contributed “to our understanding of the ecological landscape of this period and the evolution of modern mammals.” Moya Meredith Smith, contributing author and professor of evolutionary dentoskeletal biology at King’s College London, said in the release: “Our paper raises the level of debate about what defines a mammal and shows that it was a much earlier time of origin in the fossil record than previously known.” | Biology |
Microbes can ‘mine’ metals from toxic waste — while fighting climate change: study
Tiny organisms could help solve the massive pollution caused by mining.
Growing microbes on toxic mine waste could help companies capture pollutants while meeting rising demand for critical minerals, a new study has found.
The paper published on Thursday in PLoS Biology, delves deeper into the practice known as bioleaching, or the use of living organisms to pull minerals from rock, soil and waste. (The process is also sometimes called “biomining.”)
The researchers from Canada’s University of Waterloo found that cyanobacteria — a kind of bacteria that gets energy from light, like plants — helped bind trace metals in mine waste into more easily retrievable minerals.
As an added bonus, these techniques could help cut a sizable minority of carbon emissions from mining, the researchers wrote.
By doing so, they could help increase efficiency and reduce ecological damage from surging production of the wide array of minerals expected to be essential in the move to electrify transportation and the grid, the study said.
That push for electrification has long rested on a difficult paradox: achieving the large-scale climate benefits of getting off of fossil fuels requires a huge uptick in mining — one of the most polluting sectors worldwide.
Mining is heavily polluting because it requires crushing up rock to reveal ores within. These then must be pulled from the debris, often using dangerous heavy metals, in particular mercury.
Mercury is dangerous for the same reason it’s effective: It binds very effectively to metals, creating blobs of ore and mercury that can then easily be refined down into pure metal.
That stickiness, however, also means that it binds into animal tissues, reaching greater and more toxic concentrations as you move up the food chain.
Sulfur and arsenic are two other toxic materials associated with metal production. Like mercury, they are easily swept into groundwater from the dumps of mining waste known as “tailings,” according to the Environmental Protection Agency.
Those tailings contain trace amounts of valuable ores as well as toxic materials, but extracting the one while permanently removing the other is sufficiently expensive and difficult that companies largely don’t do it, and past a certain point, regulators largely don’t make them.
Many research teams around the world are proposing using bioleaching techniques to help change that. For example, in 2020 a German team used a variety of bacteria to pull cobalt, copper and other useful metals from sulfur-containing tailings at a large copper mine.
“We can take tailings that were produced in the past and recover more resources from those waste materials,” Jenine McCutcheon, an environmental sciences assistant professor at the University of Waterloo, said in a statement.
In doing so, she added, companies can “also reduce the risk of residual metals entering into local waterways or groundwater.”
This also helps pull carbon out of the atmosphere. As the cyanobacteria grow, they speed up the process by which the pulverized rock “weathers” — pulling carbon dioxide from the atmosphere to be stored as stable carbonate minerals.
The test projects run by the researchers managed to pull down enough carbon dioxide from the atmosphere to offset about a third of the emissions generated during mining.
That makes the technology “a potential game-changer in the fight against climate change,” McCutcheon said.
That could mean that legacy mine sites get a second life, as their once-worthless tailings become cost-effective sources of new materials.
For new mines, she said, the possibilities are even greater.
Integrating bioleaching processes with cyanobacteria at the start of production could “result in mines that are carbon neutral from the get-go rather than thinking about carbon storage as an add-on at the end,” she said.
Copyright 2023 Nexstar Media Inc. All rights reserved. This material may not be published, broadcast, rewritten, or redistributed. | Biology |
For the first time, researchers have harnessed the body’s own chemistry to “grow” electrodes inside the tissues of living fish, blurring the boundary between biology and machines.
The technique uses the body’s sugars to turn an injected gel into a flexible electrode without damaging tissues, experiments show. Zebrafish with these electrodes grown in their brains, hearts and tail fins showed no signs of ill effects, and ones tested in leeches successfully stimulated a nerve, researchers report in the Feb. 24 Science.
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Someday, these electrodes could be useful for applications ranging from studying how biological systems work to improving human-machine interfaces. They also could be used in “bioelectronic medicine,” such as brain stimulation therapies for depression, Parkinson’s disease and other conditions (SN: 2/10/19).
Soft electronics aim to bridge the gap between soft, curvy biology and electronic hardware. But these electronics typically still must carry certain parts that can be prone to cracks and other issues, and inserting these devices inevitably causes damage to tissues.
“All the devices we have made, even though we have made them flexible, to make them more soft, when we introduce them, there will still be a scar. It’s like sticking a knife into the organ,” says Magnus Berggren, a materials scientist at Linköping University in Sweden. That scarring and inflammation can degrade electrode performance over time.
Previous efforts to grow soft electronics inside tissues have drawbacks. One approach uses electrical or chemical signals to power the transformation from chemical soup to conducting electrodes, but these zaps also cause damage. A 2020 study got around this problem by genetically modifying cells in worms to produce an engineered enzyme that does the job, but the new method achieves its results without genetic alterations.
Berggren and colleagues’ electrodes instead exploit a natural energy source already present in the body: sugars. The gel cocktail contains molecules called oxidases that react with the sugars — glucose or lactate — to produce hydrogen peroxide. That then activates another ingredient in the cocktail, an enzyme called hydrogen peroxidase, which is the catalyst needed to transform the gel into a conducting electrode.
“The approach leverages elegant chemistry to overcome many of the technical challenges,” says biomedical engineer Christopher Bettinger of Carnegie Mellon University in Pittsburgh, who was not involved in the study.
To test the technique, the researchers injected the cocktail into the brains, hearts and tail fins of transparent zebrafish. The gel turns blue when it becomes conductive, giving a visual readout of its success.
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“The beautiful thing is you can see it: The zebrafishes’ tail changes color, and we know that blue indicates a conducting polymer,” says materials scientist Xenofon Strakosas, also of Linköping University. “The first time I saw it, I thought ‘Wow, it’s really working!’”
The fish appeared to suffer no ill effects, and the researchers saw no evidence of tissue damage. In partially dissected leeches, the team showed that delivering a current to a nerve via a soft electrode could induce muscle contractions. Ultimately, devices like this could be paired with various wireless technologies in development.
Long-term implant performance remains to be determined, however. “The demonstrations are impressive,” Bettinger says. “What remains to be seen is the stability of the electrode.” Over time, substances in the body could react with the electrode materials, degrading it or even producing toxic substances.
The team still needs to refine how precisely the electrodes can stimulate nerves, says chemical engineer Zhenan Bao of Stanford University, who was not involved in the work. She and colleagues developed the way to “grow” electrical components using genetic modifications. Ensuring stimulation is concentrated where it’s needed for a treatment, while preventing the leakage of current to unwanted regions will be important, she says.
In the new study, the relative abundance of different sugars in different tissues determines exactly where electrodes form. But in the future, a component of the main ingredient could be swapped out for elements that attach to specific bits of biology to make targeting much more precise, Berggren says. “We’re conducting experiments right now where we’re trying to bind these materials directly on individual cells.” Notes Strakosas: “There are some applications where precision is really important; that’s where we have to invest effort.” | Biology |
We all discard a huge amount of plastic and other human-made materials into the environment, and these are often picked up by birds. New research has shown that 176 bird species around the world are now known to include a wide range of anthropogenic materials in their nests. All over the world, birds are using our left-over or discarded materials. Seabirds in Australia incorporate fishing nets into their nests, ospreys in North America include baler twine, birds living in cities in South America add cigarette butts, and common blackbirds in Europe pick up plastic bags to add to their nests.
This material found in birds' nests can be beneficial say researchers. For example, cigarette butts retain nicotine and other compounds that repel ectoparasites that attach themselves to nestling bird's skin and suck blood from them. Meanwhile, there are suggestions that harder human-made materials may help to provide structural support for birds' nests, while plastic films could help provide insulation and keep offspring warm. Despite such potential benefits, it is important to remember that such anthropogenic material can also be harmful to birds.
This research was published in a special issue of the Philosophical Transactions of the Royal Society B on "The evolutionary ecology of nests: a cross-taxon approach." The special issue was jointly organised by Mark Mainwaring, a Lecturer in Global Change Biology in the School of Natural Sciences at Bangor University.
Mark Mainwaring said, "The special issue highlights that the nests of a wide range of taxa -- from birds to mammals to fish to reptiles -- allow them to adapt to human-induced pressures. Those pressures range from the inclusion of anthropogenic materials into their nests through to providing parents and offspring with a place to protect themselves from increasingly hot temperatures in a changing climate."
Anthropogenic materials sometimes harm birds. Parents and offspring sometimes become fatally entangled in baler twine. Meanwhile, offspring sometimes ingest anthropogenic material after mistaking it for natural prey items. Finally, the inclusion of colourful anthropogenic materials into nests attracts predators to those nests who then prey upon the eggs or nestlings. This means that we need to reduce the amount of plastic and other anthropogenic material that we discard.
The lead author of the study, Zuzanna Jagiełło who is based at the Poznań University of Life Sciences in Poland, added, "A wide variety of bird species included anthropogenic materials into their nests. This is worrying because it is becoming increasingly apparent that such materials can harm nestlings and even adult birds."
The second author of the study, Jim Reynolds, a researcher in the Centre for Ornithology at the University of Birmingham in the UK, remarked,
"In a rapidly urbanizing world which we share with many different animal taxa, it is not surprising that birds use our discarded materials in their nests. Although much needs to be understood about how plastics, for example, impact birds, it is exciting that birds, through their high mobility and breeding biology, may prove to be potent biomonitors of environmental anthropogenic material pollution."
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PRESS RELEASES A plant common to Japan, Causonis japonica, is the first to show a newly discovered trait. Its flowers can change color depending on the stage of its maturation cycle, and then change back to its original color. Although many flowers have been shown to change color depending on their maturation phase, Causonis japonica is the only known example of bidirectional color change. The pigments involved in the colors are related to nutrient-rich colorful vegetables, so understanding the flowers’ color-changing tricks could have downstream applications in improving nutrient yields in certain food crops. We all like flowers, and one of the most appealing things about flowers is presumably the wide array of shapes, sizes and, of course, colors they come in. But did you know that some flowers can change their colors? Although it’s not all flowers, this trait has been observed in hundreds of different species for at least a number of decades. It’s thought that color-changing flowers do so because it signals to pollinating insects that the flower is ready to supply nectar or pollen which rewards them. This is considered to be an “honest” signal. But the reverse can also be seen; some plants show a “dishonest” signal, with some of their flowers displaying their default color whilst others display their signal color. That behavior is thought to increase the overall visibility of the plant from a distance to would-be pollinators. But whatever the strategy of the plant in question, all examples of color-changing flowers found have been unidirectional: Once the color has changed, it does not change back. So, imagine the surprise University of Tokyo Professor Hirokazu Tsukaya must have felt when he saw a flower of the plant Causonis japonica change color, and then, change again, and again. Causonis japonica. A magnified image clearly showing the alternating orange and pink colors of the flower petals. ©2022 H. Tsukaya CC-BY “Even though I’ve studied this plant in detail, having discovered there were at least two varieties back in 2000, the bidirectional color-changing flowers were a completely unexpected finding,” said Tsukaya. “My colleague Professor Nobumitsu Kawakubo from Gifu University is an expert in time-lapse, long-period video recordings of pollinating flowers. He and his student originally tried to explore the pollinating behaviors between the different kinds of Causonis japonica and expected to see the familiar change from its default orange color to bright pink. But they couldn’t believe it when they reviewed the time-lapse video and saw that it not only changed back to orange again, but that this change oscillated between the two states. They informed me on this finding; this compelled us to find out why. So we started a collaboration.” Thanks to the carefully captured time-lapse videos from the field and detailed observations in the laboratory, Tsukaya managed to connect what physiological changes took place in the flowers concurrent with their changes in colors. “The initial orange state is coincident with the male stage of the flower’s maturation, when it is secreting nectar,” said Tsukaya. “When the stamen — male part — becomes old and detaches, the flowers turn pink. Mere hours later, the pistil — female part — begins to mature, secretes nectar, and the flower turns orange again. Once that stage is over, the flower fades to pink. The main chemical responsible for the color changing is orange-yellow carotenoid; its cycle of accumulation and degradation is also the fastest known to date. That fact was another surprise to us.” Time-lapse images. The unique bidirectional color-changing petals were only observed now because in nature, the plant is a chaotic bundle of buds, leaves and flowers that grows quite rapidly. So, it was not really possible to track individual flowers over time. But thanks to carefully controlled time-lapse video recording, now individual flowers can be tracked and hence lead to observations such as this one. © 2022 H. Tsukaya CC-BY You probably noticed the chemical name carotenoid sounds a little like the word carrot. This is not a coincidence, as the same chemical is what gives typical carrots their orange hue. It’s a good source of vitamin A, and given the color-changing flowers show the most rapid accumulation of carotenoids ever seen, it’s no surprise the researchers think their discovery might have some future application in developing carotenoid-containing vegetables that mature faster or contain higher yields of beneficial vitamins. “Our next steps will be to find out what is governing the behaviors we have observed,” said Tsukaya. “One big question we have is, at what level are the stages of the cycles regulated? Is it caused by proteins caught in a feedback cycle, or does something occur on a genetic level? We will continue to explore this and hope to find an explanation soon. It’s strange to think that several hundred years ago, agriculturalists in Japan hated Causonis japonica because of its vigorous nature. But a novelist, Kyoka Izumi, wrote about them so favorably, I wonder if it helped maintain some interest in preserving them. Whatever the reason, I’m glad they are around now to share their secrets with us. I wonder what we’ll discover next.” Papers Furukawa Y, Tsukaya H, and Kawakubo N, "Oscillating flower colour changes of Causonis japonica (Thunb.) Raf. (Vitaceae) linked to sexual phase changes," Scientific Reports: December 1, 2022, doi:10.1038/s41598-022-24252-z.
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While the German government is planning to relax legislation on the use of cannabis, researchers from the Friedrich Schiller University Jena, together with colleagues from Italy, Austria and the USA, have identified the mode of action underlying anti-inflammatory effects demonstrated by cannabinoids. A few days ago, the federal government took the controversial decision to make the acquisition and possession of small amounts of cannabis exempt from punishment. Provided the German parliament approves the draft bill, the “Cannabis Act” will come into force next year. While some consider this move to be long overdue, others continue to warn strongly against the health risks of cannabis use.
The Jena researchers and their colleagues are now taking a different look at cannabis – at the traditional medicinal plant – with a study published in the journal “Cell Chemical Biology”. The team from the Institute of Pharmacy investigated how certain ingredients from the cannabis plant counteract inflammation. It was already known from previous studies that cannabis is not only an analgesic and an antispasmodic, but also has an anti-inflammatory effect. “However, the reason for the anti-inflammatory effect was largely unclear until now,” says Dr Paul Mike Jordan, who led the study together with Prof. Oliver Werz.
The researchers studied how different cannabinoids, including the psychoactive THC (tetrahydrocannabinol) and CBD (cannabidiol), which is already found in freely available products today, act on human immune cells. “We found that all eight cannabinoids we studied had anti-inflammatory effects,” says Lukas Peltner, doctoral student and first author of the study. “All the compounds we studied were found to inhibit the formation of pro-inflammatory messenger substances in cells while enhancing the formation of inflammation-resolving substances.”
CBD induces a switch in immune cells
CBD in particular proved to be highly effective and the team investigated it in more detail with regard to its mode of action. The researchers were able to determine that CBD activates the 15-lipoxygenase-1 enzyme, which triggers the production of inflammation-resolving messenger substances that subsequently cause the inflammation to subside. “CBD thus induces a switch in the affected cells, so to speak, which steers the inflammatory process from the promoting to the inhibiting side,” explains Dr Jordan. The researchers were also able to confirm these results, which were obtained in cell cultures, in animal experiments on mice.
In the long term, the insights gained could lead to new therapeutic strategies for treating inflammatory diseases, the researchers conclude. The focus should be on CBD, which was the most effective cannabinoid in the study. Previously approved preparations with cannabinoids contain CBD, “but also the psychoactive THC, which can be associated with a variety of side effects”, notes Dr Jordan. Therapeutics containing only CBD would reduce this problem.
The research work has been carried out within the Collaborative Research Centres „ChemBioSys“External link and „PolyTarget“ de of the University of Jena and has been funded by the German Research Foundation.
Dr Paul Mike Jordan (l.) investigates the actions of cannabinoids in humans with Lukas K. Peltner (r.). | Biology |
Habitat split may impact disease risk in amphibians and other vertebrates
Habitat split is a common event in the environment that occurs when different classes of natural habitats, such as forests and water, are disconnected. As a consequence, the movement of organisms between these environments is disrupted, which can be particularly harmful to species with both an aquatic and terrestrial life stage, like amphibians.
Human disturbances, such as logging of forests and agricultural expansion, are leading causes of this environmental fragmentation and have important implications for the spread of diseases in wildlife communities.
According to new research led by Penn State Associate Professor of Biology Gui Becker, published in January 2023 in Biological Reviews, habitat split has a significant impact on amphibian disease immunity, likely due to changes in the composition of the microbes living on the amphibians, disruptions to normal immune system development, and increased stress. With this knowledge, Becker's team aims to discover new ways to help reduce disease risk.
"We propose several mechanisms by which habitat split could impact different branches of wildlife's immune systems," Becker said, "but also propose that targeted habitat-restoration strategies aiming to connect multiple classes of natural habitats (e.g., terrestrial–freshwater, terrestrial–marine, marine–freshwater) could enhance vertebrate immune system responses."
The Biological Reviews article comes on the heels of recent research published by Becker, Penn State postdoctoral scholar Daniel Medina, and a group of international collaborators in the December 2022 issue of Animal Microbiome.
In that paper, Becker and colleagues compared the microbes that live on the skin—skin microbiomes—of 43 threatened and 90 non-threatened amphibian species, and discovered that amphibian species threatened by extinction have fewer species of microbes living on their skin. Previous work by Becker, found that resident microbes on skin are an important component of the frog innate immune system and can impact disease outcomes. Therefore, the authors conclude that the amphibians threatened by extinction may have weaker disease defenses, due to their lower skin microbiome diversity. Overall, these results suggest that amphibian skin microbiomes could be an important factor in species conservation.
Together, these articles highlight potential avenues for protecting global diversity, but further research is needed to develop successful microbial management strategies from scales ranging from individual hosts to ecosystems, the researchers said.
"We have been radio-tracking amphibians across landscapes with varying levels of habitat split, manipulating their microbiomes, looking at immune gene expression, quantifying stress hormone levels," Becker explained, "and I think these field studies will help us dive into the mechanisms of how landscape configuration impacts host resistance to pathogens."
Understanding factors that contribute to population resilience is particularly critical as animals in the wild are faced with increasing climate, pathogen, and anthropogenic stressors, such as pollution and habitat split, said the researchers.
"Conserving and managing microbial diversity across wildlife habitats are important to environmental and ecosystem sustainability efforts as the climate changes in significant ways," said Seth Bordenstein, director of the Penn State Microbiome Center. "Becker's team is shining a bright light on the crucial need to holistically understand how human- and climate-induced habit changes will have major ripple effects on microbial and animal diversity and health. This work is one of the major types of interdisciplinary research that many of the Center investigators are engaged in."
More information: C. Guilherme Becker et al, Habitat split as a driver of disease in amphibians, Biological Reviews (2023). DOI: 10.1111/brv.12927
Sasha E. Greenspan et al, Low microbiome diversity in threatened amphibians from two biodiversity hotspots, Animal Microbiome (2022). DOI: 10.1186/s42523-022-00220-w
Journal information: Biological Reviews
Provided by Pennsylvania State University | Biology |
Jessica Suarez
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A Chittenango ovate amber snail moves about its new waterfall habitat after being released into the wild.
Jessica Suarez
A Chittenango ovate amber snail moves about its new waterfall habitat after being released into the wild.
Jessica Suarez
Hiking is tricky when you're carrying a federally threatened species. Ally Whitbread carefully hopped over logs and dodged prickers while toting a cooler full of tiny, rare snails.
"I feel like I've got like 500 babies to take care of — just a very crazy mother hen," she said.
The Chittenango ovate amber snails and eggs inside are facing extinction — only dozens are estimated to remain at one waterfall in Upstate New York — but Whitbread is part of a team transporting a captive-bred population to a new, remote home for a shot at survival. Such a recovery process can take years to decades, and success is uncertain, but scientists are racing to better understand our planet's biodiversity before species are wiped out.
Jessica Suarez
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John Wiley (left) and Cody Gilbertson work together to find Chittenango ovate amber snails hidden amongst leaves in their terrarium before releasing them into the wild.
Jessica Suarez
John Wiley (left) and Cody Gilbertson work together to find Chittenango ovate amber snails hidden amongst leaves in their terrarium before releasing them into the wild.
Jessica Suarez
The team of snail researchers spent years growing a population in a lab at the College of Environmental Science and Forestry, a state school in Syracuse, N.Y. The hike to a hidden waterfall is a chance to examine what makes them thrive in the wild, or what doesn't.
These efforts to sustain and study rare species can unlock their hidden benefits to humans, said University of Colorado Boulder ecology professor Laura Dee. She said some plants and animals may possess unique traits that can provide what she calls option value.
"The idea that we might want to have a species down the line because of uncertainty of what the future is going to bring, and what role that species might play," Dee said.
Jessica Suarez
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Ally Whitbread carefully places Chittenango ovate amber snails into their new waterfall habitat.
Jessica Suarez
Like the once-rare Madagascar rosy periwinkle—a compound from the plant is now used in leukemia treatments. While not every species will cure cancer, Dee said more study is needed because we don't fully know what happens if we lose them.
"Theory and other papers have shown that actually the loss of rare species can be particularly destabilizing, because they might have these really unique and important feeding relationships or links," she said.
Even just observing species in their habitats can prove helpful. University of Utah biology professor Jack Longino is cataloging the planet's ants. He said understanding how the insects communicate could help programmers with robotics.
Jessica Suarez
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Cody Gilbertson holds up a tagged Chittenango ovate amber snail that's ready for release.
Jessica Suarez
Jessica Suarez
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Cody Gilbertson lifts Chittenango ovate amber snails eggs out of their terrarium with a spoon to place them into their new waterfall habitat.
Jessica Suarez
"To create things, to make new technologies, we're sort of imitating nature all the time," Longino said.
The Chittenango ovate amber snail doesn't have any known unique traits critical to humans, and it's been a lengthy journey just to attempt to save them. The half-hour hike to the new habitat is the latest step in a process that's lasted more than five years—from site surveys and land negotiations to just keeping the sensitive species alive in the lab.
Jessica Suarez
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Two tagged Chittenango ovate amber snails glide around the lid of their terrarium before their release.
Jessica Suarez
Senior research support specialist Cody Gilbertson said the drive to save them can go deeper than just science.
"There's no way that I'm not going to be emotionally attached to these guys—they're so cute," Gilbertson said.
The critter is no bigger than a fingertip and peers up at its caregivers from the black tips of its translucent tentacles.
"You know their big eyes are staring back at you like — there's no way that you're not going to kind of fall in love," Gilbertson said.
Dropping them off at their new waterfall home wasn't even the end — it'll be another 5 years before the team knows whether the snails can survive there. They'll take the hike twice a month to track their progress. | Biology |
Nature's great survivors: Flowering plants survived the mass extinction that killed the dinosaurs
A new study published in Biology Letters by researchers from the University of Bath (UK) and Universidad Nacional Autónoma de México (Mexico) shows that flowering plants escaped relatively unscathed from the mass extinction that killed the dinosaurs 66 million years ago. While they suffered some species loss, the devastating event helped flowering plants become the dominant type of plant they are today.
There have been several mass extinctions in the Earth's history, the most famous caused by an asteroid hit 66 million years ago, which steered the course of life on Earth profoundly. The Cretaceous-Paleogene (K-Pg) extinction event eradicated at least 75% of all species on Earth, including the dinosaurs, but until now it has been unclear what kind of impact it had on flowering plants.
Plants do not have skeletons or exoskeletons like most animals, meaning fossils are relatively rare compared to animals, making it very difficult to understand the timeline of evolution from fossil evidence alone.
Dr. Jamie Thompson of the Milner Centre for Evolution and Dr. Santiago Ramírez-Barahona of Universidad Nacional Autónoma de México analyzed evolutionary "trees" constructed from mutations in the DNA sequences of up to 73,000 living species of flowering plants (angiosperms).
Using complex statistical methods, they fitted "birth-death" models to estimate the rates of extinction throughout geological time.
While the fossil record shows that many species did disappear, the lineages to which they belong, such as families and orders, survived enough to flourish and then dominate—out of around 400,000 plant species living today, approximately 300,000 of these are flowering plants.
Molecular clock evidence suggests that the vast majority of angiosperm families around today existed before the K-Pg event: Species including the ancestors of orchids, magnolia and mint all shared Earth with the dinosaurs.
Dr. Thompson said, "After most of Earth's species became extinct at K-Pg, angiosperms took the advantage, similar to the way in which mammals took over after the dinosaurs, and now pretty much all life on Earth depends on flowering plants ecologically."
So what made them tough enough to survive despite being immobile and relying on the sun for energy?
Dr. Ramírez-Barahona said, "Flowering plants have a remarkable ability to adapt: They use a variety of seed-dispersal and pollination mechanisms, some have duplicated their entire genomes and others have evolved new ways to photosynthesize. This 'flower power' is what makes them nature's true survivors."
More information: No phylogenetic evidence for angiosperm mass extinction at the Cretaceous–Paleogene (K-Pg) boundary, Biology Letters (2023). DOI: 10.1098/rsbl.2023.0314. royalsocietypublishing.org/doi … .1098/rsbl.2023.0314
Journal information: Biology Letters
Provided by University of Bath | Biology |
Identifying new genes may elevate efficiency of photosynthesis in crops, could boost yields
Awash in a rowed sea of its brethren, a corn leaf relegated to the lowest rung of its stem spends much of a June afternoon doused in shade cast by the higher-ups.
Then a gust begins pushing, pulling and twisting the waxy wings in concert, cracking a window to the fireball roiling 93 million miles away. It's a prime, precious opportunity for photosynthesis to transform the sunlight into food. Unfortunately, the photosynthetic equivalent of a surge protector—one evolved to help plants mitigate damage driven by sudden spikes of high-intensity light—is slow to reset after so much time in the shade. The gust dissipates, the moment gone before the leaf and its cellular kitchen can take advantage.
A summer's worth of those minute but missed opportunities to harvest light can cost cornfields, and those who farm them, a sizable portion of the potential harvests they yield in the fall. By recently identifying and measuring the influence of new genes that regulate the surge protector, the University of Nebraska–Lincoln's Kasia Glowacka and colleagues could help increase those yields by upward of 20%.
Which isn't to downplay the importance of the safeguard, which goes by the name of non-photochemical quenching, or NPQ, and can transform light to heat whenever a plant absorbs more of the former than it can put toward photosynthesis. A failure to cut the biochemical circuit, after all, can lead to a toxic buildup of ultra-reactive oxygen that damages DNA and can even kill a cell. But the safety measure has a downside: The slower it is to relax and resume letting the absorbed light fuel photosynthesis, the more of that energy-granting light it wastes.
"When you think from the perspective of a chloroplast in a plant cell, life is really difficult," said Glowacka, assistant professor of biochemistry at Nebraska. "Every few seconds, the environment is changing."
In 2016, Glowacka contributed to a study showing that cranking up the activity of three particular genes allowed tobacco plants to switch NPQ on and off at a much faster pace, granting it both better protection and more efficient photosynthesis. That tobacco, in turn, produced leaves roughly 20% larger, with simulations suggesting that even greater gains might be possible. Follow-up research found that the same technique could generate similar benefits in soybean—not just for leaves, but the beans, too.
But tobacco and soybean employ a different form of photosynthesis than corn, sorghum, sugarcane and several other crops better suited to hot and dry conditions—crops whose yields must increase to help feed the 10 billion people expected to populate the globe by 2050. Glowacka wondered whether the genes that coded for NPQ activity in one might play that same role in the other. Even if they did, Glowacka and Nebraska's James Schnable figured there must be other genes aiding a process as complex as NPQ.
They were right. Their discovery began with toiling in the fields during the summers of 2020 and 2021, when the team planted more than 700 genetically different lines of corn at the Havelock Research Farm in northeast Lincoln. Glowacka's plan: look for differences in NPQ performance among the lines, then try to tease out which genes were ultimately responsible for those differences. Still, the existing methods for measuring NPQ, Glowacka knew, were expensive and time-consuming. More than that, they struggled to flatten out daily disparities in each line's exposure to light, potentially spoiling the validity of any findings.
Rather than settle, Glowacka developed her own method. The team used a modified hole-punch to extract tiny samples from the leaves of every line in the field. Back in the lab, the researchers gave the tissue samples nearly a day to adapt to the dark, eventually measuring their fluorescence—a proxy for photosynthesis and NPQ—before and after exposing them to flashes of light. Instead of measuring one sample every 20 minutes, the team was able to handle 96 samples over that same span.
The researchers found that the speed and magnitude of NPQ responses varied widely among the lines, a fact that helped ease the search for any new genes potentially driving that variation in corn. A comparison of the lines' genetic code, cross-referenced against the differences in NPQ performance, eventually revealed six promising gene candidates. Several of those candidates were already familiar to the team. Others were not—including one called PSI3, which introduced more of that variation than any other candidate.
After identifying counterparts of those six genes in Arabidopsis, a flowering plant commonly used to study plant biology, the team proceeded to order mutants: Arabidopsis seeds each lacking one of the six genes. In all six of the mutants, the surge protector was generally sluggish to respond under the lights but also slower to relax when the lights were turned out. The NPQ peaks were typically lower, too, and the troughs higher, suggesting that the plants both buffered less against surges and squandered more of the light available for photosynthesis.
The identification of those genes, combined with the amount of natural NPQ variation across lines of corn, could open the way to breeding plants far better at capitalizing on yield-boosting sunlight, the researchers said. In the best case, Schnable said, those efforts might come to bear fruit in as little as a half-dozen years.
If they do, the results could prove a boon for crop breeders now investigating every and all possibilities to preclude global food shortages in the coming decades.
"We can gain 22% of that yield from the crops, potentially, if we were to speed up the NPQ," Glowacka said.
Given that the researchers kicked off the study early in 2020, their attempts to help stem an impending global crisis meant dealing with a contemporary one. Two of the team's members, Seema Sahay and Marcin Grzybowski, had only recently arrived in the United States—recently enough that neither had yet gotten a driver's license. Prior to COVID-19, the two would have hitched rides out to the Havelock Research Farm.
University protocols designed to slow the spread of the virus, though, temporarily put that option on hold. Undeterred, Sahay and Grzybowski regularly resorted to biking roughly seven miles out to the research farm—a 30-plus-minute trek amid the heat and humidity of a Nebraska summer.
"Seema and Marcin," Glowacka said, "are the real heroes of this experiment."
The study is published in the journal New Phytologist.
More information: Seema Sahay et al, Genetic control of photoprotection and photosystem II operating efficiency in plants, New Phytologist (2023). DOI: 10.1111/nph.18980
Journal information: New Phytologist
Provided by University of Nebraska-Lincoln | Biology |
Deep ocean currents around Antarctica that are vital to marine life have slowed by 30% since the 1990s and could soon grind to a complete halt, a new study finds.
These currents, known as Antarctic bottom waters, are powered by dense, cold water from the Antarctic continental shelf that sinks to depths below 10,000 feet (3,000 meters). The water then spreads north into the Pacific and eastern Indian oceans, fueling a network of currents called the global meridional overturning circulation and supplying 40% of the world's deep ocean with fresh nutrients and oxygen.
But warming global temperatures are unlocking large volumes of less-dense fresh water from the Antarctic ice shelves, slowing this circulation down.
"If the oceans had lungs, this would be one of them," Matthew England, a professor of ocean and climate dynamics at the University of New South Wales in Sydney, Australia who contributed to the research, said in a statement. Researchers in the U.K. and Australia collaborated in a study published in March in the journal Nature that predicted a 40% reduction in the strength of Antarctic bottom waters by 2050.
He also warned that the currents could eventually stop altogether. "We are talking about the possible long-term extinction of an iconic water mass," England said.
In a new study published Thursday (May 25) in the journal Nature Climate Change, England and his colleagues say they have confirmed these predictions with real life observations in the Australian Antarctic Basin, which spans the polar waters between Australia and Antarctica.
The researchers examined changes in the amount of bottom water entering the basin between 1994 and 2017 and recorded a 30% reduction in velocity, which suggests that these deep ocean, or abyssal, currents, are beginning to stagnate.
Dwindling circulation around Antarctica could slow down the global network of abyssal currents and trap nutrients and oxygen in the ocean depths, with knock-on effects for marine life and productivity.
"The thing about the oceans is that all of the marine life that we have at the surface, when it dies off, it sinks to the bottom of the ocean, so there's a lot of nutrient-rich water in the ocean abyss," England said in a video produced by the Australian Academy of Science. "If we slow down the overturning circulation that brings that very bottom water back up to the surface, we cut off a way that nutrients get back to the surface to regenerate marine life."
Roughly 276 trillion tons (250 trillion metric tons) of cold, salty, oxygen-rich water sinks around Antarctica each year, according to the new study. In a warming climate, fresh meltwater reduces the density of this sinking mass, meaning that more of it stays in the upper layers of the ocean. "These regions supply the abyssal waters of the entire Pacific and the eastern Indian basins, so the changes quantified here are likely to impact a large fraction of the global abyssal ocean," the researchers wrote.
The scientists warned that fresh water entering Antarctic waters will likely continue and accelerate in the coming decades, meaning that these vital currents could soon collapse. "Such profound changes to the ocean's overturning of heat, freshwater, oxygen, carbon and nutrients will have a significant impact on the oceans for centuries to come," England said.
The new findings reinforce the dramatic estimates researchers made earlier this year, said Ariaan Purich, a researcher at Monash University's School of Earth, Atmosphere and Environment in Australia who was not involved in the research.
"This new study is significant because alongside a recent landmark modeling study, it provides further support including observational evidence that the melting Antarctic ice sheet and shelves will impact the global ocean overturning circulation, with important impacts to the ocean uptake of heat and carbon," Purich told Australia's Science Media Exchange.
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Sascha is a U.K.-based trainee staff writer at Live Science. She holds a bachelor’s degree in biology from the University of Southampton in England and a master’s degree in science communication from Imperial College London. Her work has appeared in The Guardian and the health website Zoe. Besides writing, she enjoys playing tennis, bread-making and browsing second-hand shops for hidden gems. | Biology |
Allergy study on 'wild' mice challenges the hygiene hypothesis
The notion that some level of microbial exposure might reduce our risk of developing allergies has arisen over the last few decades and has been termed the hygiene hypothesis. Now, an article published in Science Immunology by researchers from Karolinska Institutet challenges this hypothesis by showing that mice with high infectious exposures from birth have the same, if not an even greater ability to develop allergic immune responses than 'clean' laboratory mice.
How microbes may prevent allergy has been a topic of great interest in recent times. Studies have suggested that certain infections might reduce the production of inflammatory antibodies to allergens and alter the behaviour of T cells involved in allergies. It has also been suggested that good bacteria in our intestines may be able to switch off inflammation in other parts of our body.
Robust allergic responses
Researchers have now compared the allergic immune response in ‘dirty’ wildling mice to those of typical clean laboratory mice. They found very little evidence that the antibody response was altered or that the function of T cells changed in a meaningful way. Nor did anti-inflammatory responses evoked by good gut bacteria appear to be capable of switching off the allergic immune response. On the contrary, wildling mice developed robust signs of pathological inflammation and allergic responses when exposed to allergens.
"This was a little unexpected but suggests that it’s not as simple as saying, ‘dirty lifestyles will stop allergies while clean lifestyles may set them off’. There are probably very specific contexts where this is true, but it is perhaps not a general rule”, says Jonathan Coquet, co-author of the study and Associate Professor at the Department of Microbiology, Tumor and Cell Biology at Karolinska Institutet in Sweden.
More like the human immune system
The wildling mice are genetically identical to clean laboratory mice but are housed under seminatural conditions and have rich microbial exposures from birth.
"The immune systems of wildling mice better represent the human immune system and so we hope that they can bring us closer to the truth of how microbes act upon the body," says Jonathan Coquet.
The findings contribute to our general understanding of how allergies may arise and may also have clinical implications. In clinical trial settings, researchers and clinicians have recently made attempts to treat patients suffering from inflammatory diseases with experimental infections. For example, infecting people with worms or performing faecal transplantations has been proposed as a tool to combat inflammatory diseases. Newborns delivered through C-section, have had maternal fecal transplantation and bacterial supplementation with the aim of promoting good bacteria in the baby’s gut and the child’s future health.
Can provide important insights
“This field of research can provide important insights into how infections and microbes can be used to facilitate health, but it is still in its infancy. Our study is a reminder that general and broad exposures to microbes may not have the clear beneficial effects that we wish them to have”, says Susanne Nylén, co-author of the study and Associate Professor at the Department of Microbiology, Tumor and Cell Biology at Karolinska Institutet.
The work was led by Junjie Ma and Egon Urgard, researchers in Jonathan Coquet's group, and done in close collaboration with Professor Stephan Rosshart at University Medical Center Freiburg in Germany and Susanne Nylén (MTC). Several other research groups at Karolinska Institutet and elsewhere also contributed to this work, including the teams of Assistant professors Itziar Martinez Gonzalez and Juan Du (both at the Department of Microbiology, Tumor and Cell Biology).
The study was financed by several bodies, including the Swedish Research Council, the Swedish Cancer Foundation, KI intramural funds, and the Wenner Gren Foundation.
Publication
"Laboratory mice with a wild microbiota generate strong allergic immune responses”, Junjie Ma, Egon Urgard, Solveig Runge, Cajsa H. Classon, Laura Mathä, Julian M. Stark, Liqin Cheng, Javiera Alvarez, Silvia von Zedtwitz, Austeja Baleviciute, Sergio Martinez Hoyer, Muzhen Li, Anne Marleen Gernand, Lisa Osbelt, Agata Anna Bielecka, Till R. Lesker, Huey-Jy Huang, Susanne Vrtala, Louis Boon, Rudi Beyaert, Mikael Adner, Itziar Martinez Gonzalez, Till Strowig, Juan Du, Susanne Nylén, Stephan P. Rosshart, Jonathan M. Coquet, Science Immunology, online 29 September 2023, doi: 10.1126/sciimmunol.adf7702. | Biology |
Comprehensive analysis of single plant cells provides new insights into natural product biosynthesis
Plants are impressive in their diversity, but especially in the variety of metabolites they produce. Many plant natural products are highly complex molecules, such as the alkaloids vincristine and vinblastine, which are produced by the Madagascar periwinkle Catharanthus roseus. These two substances are already indispensable in cancer therapy.
Researchers are very interested in finding out which individual biosynthetic steps are required to form the complex molecules. "Currently, these compounds are still obtained in very small quantities from the plant's leaf extract. We can learn from the plant how this compound is produced and use this knowledge to develop production systems that are more cost-effective, scalable and sustainable," said first author Chenxin Li of the University of Georgia's Center for Applied Genetic Technologies, describing the research goal. The study is published in the journal Nature Chemical Biology.
Assigning genetic and metabolic information to individual cells of plant organs
The scientists know that gene activity is not the same in all cells of a plant and that the chemistry can differ drastically from cell to cell. Therefore, the goal of the current study was to use a new set of methods collectively termed single-cell omics to investigate specialized and rare cell types that play a central role in the biosynthesis of plant natural products, and whose signals are often obscured by more abundant cell types in plant organs.
"With single-cell omics, we have a method that allows researchers to assign genetic and metabolic information to individual cells. The term omics refers to the fact that an entire collection of genes or metabolites is quantified and analyzed," says Lorenzo Caputi, head of the Alkaloid Biosynthesis Project Group in the Department of Natural Product Biosynthesis in Jena and one of the lead authors.
Biosynthetic pathway of vinblastine is organized in three distinct cell types
As the analyses showed, the entire biosynthetic pathway for the alkaloid vinblastine is organized in three stages and three discrete cell types. "The first stage is expressed exclusively in specialized cells associated with vascular bundles in the leaf, called IPAP. The second stage of the biosynthetic pathway is expressed only in cells of the epidermis, the layer of cells that cover the leaves, and the last known steps of the biosynthetic pathway are expressed exclusively in idioblasts, a rare cell type of the leaf," says Chenxin Li.
The researchers measured the concentrations of several intermediates in the metabolic pathway for vinblastine in single cells and were surprised. "Two important precursors of vinblastine, catharanthine and vindoline, occur in the idioblast cells at millimolar concentrations, about three orders of magnitude higher than vinblastine itself. The concentration of the two precursors in these cells was much higher than we expected and even exceeded their concentrations in whole organ extracts. However, this observation makes sense in that catharanthine and vindoline were found only in the rare idioblast cells. The abundant other cells in the leaf dilute the high concentration when whole leaves are crushed," says Sarah O'Connor, head of the Department of Natural Product Biosynthesis.
The research team is confident that the organization of biosynthetic pathways for medicinally relevant alkaloids in Catharanthus roseus is not an isolated phenomenon. "We are just beginning to understand how and why such a cell type-specific organization exists. In addition, analysis of genes expressed simultaneously in a particular cell type has helped us identify new players in this metabolic pathway. The same technique can be used to study the biosynthesis of many other natural products.
"Finally, the exact sites of accumulation of plant compounds, such as the epidermis, the vascular system, or latex duct, can help us hypothesize the ecological roles of natural products. For example, depending on the pattern of accumulation, the compounds may be more effective against biting insects than they are against sap-sucking insects," says Robin Buell, Professor at Georgia University.
A better understanding of the biosynthetic pathways of the anti-cancer drugs vincristine and vinblastine may also help to produce or harvest these compounds more effectively in the long term. The use of methods described is also promising for the study of many other interesting and medically important natural products from the plant kingdom. The approach described here will help to narrow down these rare and specialized cells and uncover the gene activities and chemistry that are exclusive to them.
More information: Lorenzo Caputi, Single-cell multi-omics in the medicinal plant Catharanthus roseus, Nature Chemical Biology (2023). DOI: 10.1038/s41589-023-01327-0. www.nature.com/articles/s41589-023-01327-0
Journal information: Nature Chemical Biology
Provided by Max Planck Society | Biology |
Whether you opt for repellant, long sleeves or citronella coils, the dreaded drone of a mosquito always seems to find its way back to you.Now researchers say they have found the mechanism behind the insect’s ability to home in on humans.Humans give off a fragrant cocktail of body odour, heat and carbon dioxide, which varies from person to person and mosquitoes use to locate their next meal. While most animals have a specific set of neurons that detect each type of odour, mosquitoes can pick up on smells via several different pathways, suggests the study, which is published in the science journal Cell.“We found that there’s a real difference in the way mosquitoes encode the odours that they encounter compared to what we’ve learned from other animals,” said Meg Younger, an assistant professor of biology at Boston University and one of the lead authors of the study.Researchers at the Rockefeller University, in New York, were baffled when mosquitoes were somehow still able to find people to bite after having an entire family of human odour-sensing proteins removed from their genome.The team then examined odour receptors in the antennae of mosquitoes, which bind to chemicals floating around in the environment and signal to the brain via neurons.“We assumed that mosquitoes would follow the central dogma of olfaction, which is that only one type of receptor is expressed in each neuron,” said Younger. “Instead, what we’ve seen is that different receptors can respond to different odours in the same neuron.”This means losing one or more receptors does not affect the ability of mosquitoes to pick up on human smells. This backup system could have evolved as a survival mechanism, the researchers say.“The mosquito Aedes aegypti is specialised to bite humans, and it is believed that they evolved to do that because humans are always close to fresh water and mosquitoes lay their eggs in fresh water. We are basically the perfect meal, so the drive to find humans is extremely strong,” said Younger.Ultimately, the researchers say, understanding how the mosquito brain processes human odour could be used to intervene in biting behaviour and reduce the spread of mosquito-borne diseases, such as malaria, dengue and yellow fever.“One major strategy for controlling mosquitoes is to attract them to traps to remove them from the biting population. If we could use this knowledge to understand how human odour is represented in the mosquito antennae and brain, we could develop blends that are more attractive to mosquitoes than we are. We could also develop repellants that target those receptors and neurons that detect human odour,” said Younger.Dr Olena Riabinina, from the Insect Neuro Lab at Durham University, who was not involved in the research, said: “We already knew that mosquitoes are hard-wired to bite humans, but this research tells us that their olfactory system is different and more complex than we thought. Interventions based on this new information could be very promising.”Dr Marta Andres Miguel, from University College London, who was also not involved, said: “This is a remarkable discovery not only from a fundamental biology perspective, but also from a disease-control perspective, as it opens new paths for the development of novel tools to control mosquitoes, either to attract them to traps, or to repel them and avoid human biting.” | Biology |
When the Hunga Tonga-Hunga Ha'apai volcano in Tonga erupted in 2022, it generated the most intense lightning ever recorded, a new study finds.
Located off the coast of the Kingdom of Tonga in the South Pacific, the submarine volcano produced one of the most violent eruptions in history, with more explosive force than 100 simultaneous Hiroshima bombs, according to NASA. The volcano spewed magma that immediately vaporized the seawater, sending a mushroom cloud of ash, gas and more than 50 million tons (45 million metric tons) of water vapor into the sky.
According to the new study, published Tuesday (June 20) in the journal Geophysical Research Letters, these conditions produced electrically charged collisions between ash, supercooled water and hailstones in the plume and triggered "a supercharged thunderstorm, the likes of which we've never seen," study lead author Alexa Van Eaton, a volcanologist at the U.S. Geological Survey (USGS), said in a statement. The storm generated more than 192,000 lightning flashes — composed of nearly 500,000 electrical pulses — and peaked at 2,615 flashes per minute. Some of the lightning reached altitudes of up to 19 miles (30 kilometers) above sea level, the highest lightning flashes ever measured, the researchers said.
"With this eruption, we discovered that volcanic plumes can create the conditions for lightning far beyond the realm of meteorological thunderstorms we've previously observed," Van Eaton said. "It turns out, volcanic eruptions can create more extreme lightning than any other kind of storm on Earth." That includes lightning from supercell storms and tropical cyclones, according to the study.
For their analysis, the scientists compiled data from four sources, including the satellite-based Geostationary Lightning Mapper, a NASA tool that tracks lightning from space. When the volcanic plume mushroomed outward after reaching its maximum height, in a pattern known as a gravity wave, some of the lightning followed suit, rippling out around the volcano in concentric rings that expanded and contracted, the study found.
"It wasn't just the lightning intensity that drew us in," Van Eaton said. "The scale of these lightning rings blew our minds. We've never seen anything like that before; there's nothing comparable in meteorological storms. Single lightning rings have been observed, but not multiples, and they're tiny by comparison."
The data also revealed that the plumes created by the Hunga Tonga-Hunga Ha'apai eruption grew for at least 11 hours — much longer than original projections of only an hour or two, the researchers said. This method of tracking lightning intensity alongside eruptive activity could enable scientists to better monitor the duration of volcanic eruptions and thus warn people about eruption-related risks.
"These findings demonstrate a new tool we have to monitor volcanoes at the speed of light and help the USGS's role to inform ash hazard advisories to aircraft," Van Eaton said.
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Kiley Price is a Live Science staff writer based in New York City. Her work has appeared in National Geographic, Slate, Mongabay and more. She holds a bachelor's degree from Wake Forest University, where she studied biology and journalism, and is pursuing a master's degree at New York University's Science, Health and Environmental Reporting Program. | Biology |
Single primer enrichment technology: A new genomic resource to investigate the diversity of lettuce germplasm
For the first time, the single primer enrichment technology (SPET)—a novel high-throughput genotyping method—was used in lettuce to study the genetic diversity of a collection of 160 Lactuca accessions originating from 10 countries in Europe, America and Asia, and to identify genomic regions that underpin important agronomic traits.
In recent years, technologies to investigate the genomic diversity of crops have made extraordinary progress and novel methodologies such as single primer enrichment technology (SPET) offer promising and cost-effective opportunities. SPET has so far been used in several crop plants, such as in maize, poplar, oil palm, tomato, eggplant and peach, showing its power for genotyping germplasm collections and crossing populations.
SPET was used in lettuce (Lactuca sativa L.) for the first time by a consortium of European researchers in the context of the European Evaluation Network (EVA) of the European Cooperative Programme for Plant Genetic Resources (ECPGR), with the aim to study its genetic diversity and identify genomic regions that underpin important agronomic traits.
Lettuce is a commercially important crop, widely appreciated by consumers for its fiber content and low calories. It is also a good source of vitamin C, iron, folate and different health-beneficial nutrients.
"Given the lack of cost-effective options for genotyping in lettuce, the EVA Network decided to design a SPET panel for this crop, together with IGATech, and applied it to a collection of 155 accessions of Lactuca sativa and 5 of the closely related wild species Lactuca serriola," said Pasquale Tripodi, lead author of the study and Senior Researcher at CREA, Italy.
The EVA initiative was established in 2019 by ECPGR to improve knowledge of crop genetic diversity and exploit it to breed more resilient crops that can meet the major problems facing agriculture.
"The EVA Lettuce network is one of currently five crop-specific public–private partnerships, bringing together breeding companies, genebanks and research institutes to jointly generate phenotypic and genotypic evaluation data for numerous accessions and landraces available in European genebanks," explained Sandra Goritschnig, coordinator of the EVA initiative and co-author of the study.
The plant materials in the study were selected in the frame of the EVA Lettuce Network and originated from the germplasm collections of four European genebanks: the Institute for Plant Genetic Resources "K.Malkov" (Bulgaria), the Centre for Genetic Resources, the Netherlands, the Unité de Génétique et Amélioration des Fruits et Légumes, Plant Biology and Breeding, INRAe (France), and the Nordic Genetic Resource Center (NordGen) (Sweden).
The studied genotypes encompassed cultivars, breeding materials, and landraces originating from ten different countries in Europe, America and Asia, included different horticultural types, such as Butterhead, Iceberg, Romaine, Batavia, Crisp, and were phenotyped in multilocation field trials across three countries.
Why SPET?
Compared to other genotyping methods, SPET combines the advantages of arrays and high-throughput sequencing, and has a high capacity to detect new single-nucleotide polymorphisms (SNPs), which are variations in the genetic sequence that determine the diversity among individuals in a species.
"Having a large number of SNPs increases our ability to understand the genetic diversity of a collection and investigate the function that some genomic regions play. In our case, we designed a SPET assay for 40,000 SNPs and succeeded in covering up to 96% of gene-rich regions, compared to previous studies in lettuce using different genotyping techniques, which covered only up to 27.6%. This demonstrates how effective SPET is," said Tripodi.
Also, using a fixed probes panel guarantees the reproducibility of the assay across different laboratories, unlike other sequencing methods. It also fosters the establishment of larger scientific communities that can leverage interoperable markers.
The analysis generated over 80,000 high-quality SNPs that allowed the researchers to group the accessions by type and geographic origin, and to identify gene associations for seed color, leaf color, leaf anthocyanin content and bolting time.
"We are very excited about this new application of SPET in lettuce, which confirmed previous findings, refined our knowledge of the genomic position of some agronomic traits and demonstrated the power of SPET to investigate the genetic diversity of germplasm collections, thus allowing a better characterization of lettuce collections. The SPET panel will be a cost-effective tool for both breeders and researchers in lettuce," concluded Goritschnig.
The findings are published in the journal Frontiers in Plant Science.
More information: Pasquale Tripodi et al, Development and application of Single Primer Enrichment Technology (SPET) SNP assay for population genomics analysis and candidate gene discovery in lettuce, Frontiers in Plant Science (2023). DOI: 10.3389/fpls.2023.1252777
Journal information: Frontiers in Plant Science
Provided by The Alliance of Bioversity International and the International Center for Tropical Agriculture | Biology |
New research finds that reducing antibiotic usage in animal feed is not enough to combat antibiotic resistance
A new study led by the University of Oxford has found that natural evolution of antibiotic resistance genes has maintained resistance in bacteria despite a reduction in the use of antibiotics. The findings demonstrate the importance of understanding the regulatory evolution of resistance genes to strategically combat AMR.
The study, "Regulatory fine-tuning of mcr-1 increases bacterial fitness and stabilizes antibiotic resistance in agricultural settings," has been published in the Journal of the International Society for Microbial Ecology.
Antimicrobial resistance (AMR) is a serious and growing threat to global health, with 1.2 million people dying each year due to drug-resistant infections. The overuse and misuse of antibiotics is a major driver of AMR, and there is an urgent need to protect the efficacy of 'last-line' antibiotics to treat multidrug-resistant infections.
"Our study shows how evolution can rapidly stabilize resistance genes in pathogen populations, reducing the impact of restricting antibiotic consumption. Limiting consumption is one of most widely advocated strategies to combat AMR, and the main lesson of our work moving forward is that we need new, innovative strategies to actively eliminate AMR bacteria," says Professor Craig MacLean, Department of Biology, University of Oxford
In 2017, the Chinese government banned the use of last-line antibiotic colistin as a growth promotor in animal feed in response to the rapid spread of antibiotic-resistant bacteria Escherichia coli (E.coli) carrying mobile colistin resistance (MCR) genes. Bacteria carrying MCR genes are resistant to treatment with colistin and cause hard to treat drug-resistant infections in humans and animals.
The ban led to a 90% reduction in colistin consumption, and scientists expected to see a corresponding drop in rates of AMR. This is because the MCR gene is associated with fitness costs, such as reduced competitive ability and virulence. However, large-scale surveillance studies across China following the ban found that the decline in the mcr-1 gene was slower than anticipated.
Researchers at the University of Oxford led by Maclean explored this discrepancy by focusing on the regulatory region of DNA that controls the expression of the mcr-1 gene. They found that this region shows high levels of variation, and that certain variants were able to offset the fitness costs of the mcr-1 gene. By 'fine tuning' mcr-1 expression to a lower level, these variants enabled the bacteria to achieve high growth rates while simultaneously increasing colistin resistance.
The researchers then analyzed DNA sequence data from E.coli carrying mcr-1 from before and after the colistin ban. This revealed that the regulatory mutations that increased fitness in the lab had remained stable in E.coli populations from farms, and had hardly declined in response to the ban.
Lead researcher MacLean said, "Our results provide strong evidence that the evolution of the mcr-1 gene has helped to stabilize colistin resistance in agricultural settings, even though colistin use in agriculture has declined by 90%. This finding is of major importance for all future interventions targeting the reduction of antibiotic usage, demonstrating the need to consider the evolution and transmission of resistance genes to introduce viable strategies to reduce resistance."
Professor Tim Walsh, director of biology at the Ineos Oxford Institute and co-author on the paper, said, "Colistin resistance across many strains of E.coli and in diverse environments from pig farms to hospital wards should act as our warning of the dangers of antibiotic overuse and misuse. Simply put, it is not enough to reduce antibiotic consumption in order to effectively combat antibiotic resistance. We need urgent and innovative approaches to combat antibiotic resistance, and new strategies to protect our last-resort antibiotics for when we need them most."
More information: Lois Ogunlana et al, Regulatory fine-tuning of mcr-1 increases bacterial fitness and stabilises antibiotic resistance in agricultural settings, The ISME Journal (2023). DOI: 10.1038/s41396-023-01509-7
Journal information: ISME Journal
Provided by University of Oxford | Biology |
For the first time, scientists have created baby mice from two males.
This raises the distant possibility of using the same technique for people – although experts caution that very few mouse embryos developed into live mouse pups and no one knows whether it would work for humans.
Still, “It’s a very clever strategy,” said Diana Laird, a stem cell and reproductive expert at the University of California, San Francisco, who was not involved in the research. “It’s an important step in both stem cell and reproductive biology.”
Scientists described their work in a study published Wednesday in the journal Nature.
First, they took skin cells from the tails of male mice and transformed them into “induced pluripotent stem cells,” which can develop into many different types of cells or tissues.
Then, through a process that involved growing them and treating them with a drug, they converted male mouse stem cells into female cells and produced functional egg cells.
Finally, they fertilized those eggs and implanted the embryos into female mice. About 1% of the embryos – 7 out of 630 – grew into live mouse pups.
The pups appeared to grow normally and were able to become parents themselves in the usual way, research leader Katsuhiko Hayashi of Kyushu University and Osaka University in Japan told fellow scientists at the Third International Summit on Human Genome Editing last week.
In a commentary published alongside the Nature study, Laird and her colleague, Jonathan Bayerl, said the work “opens up new avenues in reproductive biology and fertility research” for animals and people.
Down the road, for example, it might be possible to reproduce endangered mammals from a single male.
“And it might even provide a template for enabling more people,” such as male same-sex couples, “to have biological children, while circumventing the ethical and legal issues of donor eggs,” they wrote.
But they raised several cautions. The most notable one? The technique is extremely inefficient.
They said it’s unclear why only a tiny fraction of the embryos placed into surrogate mice survived; the reasons could be technical or biological.
They also stressed that it’s still too early to know if the protocol would work in human stem cells at all.
Laird also said scientists need to be mindful of the mutations and errors that may be introduced in a culture dish before using stem cells to make eggs.
The research is the latest to test new ways to create mouse embryos in the lab. Last summer, scientists in California and Israel created “synthetic” mouse embryos from stem cells without a dad’s sperm or a mom’s egg or womb.
Those embryos mirrored natural mouse embryos up to 8 ½ days after fertilization, containing the same structures, including one like a beating heart.
Scientists said the feat could eventually lay the foundation for creating synthetic human embryos for research in the future. | Biology |
Tropical butterflies' wings could help them withstand climate change, study suggests
Tropical butterflies with bigger, longer and narrower wings are better able to stay cool when temperatures get too hot.
In fact, tropical species' ability to keep cool at higher air temperatures mean they are more able to thermoregulate and keep a balanced body temperature compared to their evolutionary cousins in milder climates.
Scientists say that the strategies of butterflies from Central America to stay cool mean they could actually be better equipped to deal with global warming than previously thought.
The team behind the latest study argue that conservation researchers should be careful not to assume creatures in hotter parts of the world will suffer most under rising temperatures—rather, some butterflies in temperate regions, such as Western and central Europe, could be at greater risk.
Equipped with hand-held nets, ecologists took the temperature of more than 6,800 butterflies in Panama, Austria, the Czech Republic and the U.K. using a tiny thermometer-like probe. They compared the butterfly's temperature to that of the surrounding air or the vegetation it was perched on.
They found that tropical butterflies were able to maintain a lower body temperature at higher air temperatures than butterflies from milder climates. The results are published in the journal Global Change Biology.
Researchers from the University of Cambridge and the Czech Academy of Sciences spent nine months, over the course of two trips, in the tropical lowland forests of Central Panama, working with collaborators at the Smithsonian Tropical Research Institute. Working for nine hours a day they assessed 54 species of butterflies and surrounding temperatures. They compared these measurements with those of butterflies from alpine meadows in Austria, pastures in the Czech Republic and chalk grasslands in the U.K.
Researchers discovered that butterflies from different climates used specialized strategies to warm up or cool down. But physical factors—particularly wing size and shape—were key to keeping body temperature at an optimal level for butterflies across both climates studied.
Senior author Dr. Andrew Bladon from the Department of Zoology, University of Cambridge, said, "We were surprised to see that it was physical differences like wing size and shape that drove a butterfly species' ability to keep their temperature constant in both regions, rather than an inherent difference between species adapted to tropical and temperate climates. We expected to find that tropical species would be more sensitive to temperature changes, but this may not be the case."
The team say that when it comes to butterflies' ability to buffer against changing temperatures—and ultimately survive—bigger appears to be better. For tropical butterflies, bigger wings mean they are more mobile and can fly quicker to cooler areas. And for butterflies who live in mild climates, bigger wings allow them to warm up faster when basking in the sun, giving them the energy boost they need to fly.
"Our results have highlighted how unique these species are—they're using different strategies to cool down or warm up," said co-lead author Esme Ashe-Jepson, University of Cambridge. "What's exciting is that these results suggest that physiological measures could be used to make predictions about how species might respond to climate change."
"We showed that changes in size and wing shape are important for coping with temperature change," said co-lead Benita Laird-Hopkins, University of South Bohemia. "For example, small butterflies, regardless of where they are from, are likely to be more impacted by climate change than big butterflies."
While the current study suggests a note of optimism in terms of the ability of some butterfly species to live in hot temperatures, what is not known is how butterflies may cope with dramatic shifts in temperature like heatwaves, or what effect a warming climate will have on other life stages, such as caterpillars and eggs.
Bladon says more research is needed to understand how other insect groups, as well as butterflies, respond to temperature change. "The dual threats of climate and habitat change threaten to push many insects to their physiological limits. Understanding how and where this happens is crucial for designing conservation mitigation strategies, but we also need to act fast to protect and restore diverse habitats."
More information: Benita C. Laird‐Hopkins et al, Thermoregulatory ability and mechanism do not differ consistently between neotropical and temperate butterflies, Global Change Biology (2023). DOI: 10.1111/gcb.16797
Journal information: Global Change Biology
Provided by University of Cambridge | Biology |
The availability of foods based on plant proteins to substitute for meat has increased dramatically as more people choose a plant-based diet. At the same time, there are many challenges regarding the nutritional value of these products. A study from Chalmers University of Technology in Sweden now shows that many of the meat substitutes sold in Sweden claim a high content of iron – but in a form that cannot be absorbed by the body. A diet largely made up of plant-based foods such as root vegetables, pulses, fruit and vegetables generally has a low climate impact and is also associated with health benefits such as a reduced risk of age-related diabetes and cardiovascular disease, as has been shown in several large studies. But there have been far fewer studies of how people’s health is affected by eating products based on what are known as textured* plant proteins. In the new study from Chalmers, a research team in the Division of Food and Nutrition Science analysed 44 different meat substitutes sold in Sweden. The products are mainly manufactured from soy and pea protein, but also include the fermented soy product tempeh and mycoproteins, that is, proteins from fungi. ‘Among these products, we saw a wide variation in nutritional content and how sustainable they can be from a health perspective. In general, the estimated absorption of iron and zinc from the products was extremely low. This is because these meat substitutes contained high levels of phytates, antinutrients that inhibit the absorption of minerals in the body,’ says Cecilia Mayer Labba, the study’s lead author, who recently defended her thesis on the nutritional limitations of switching from animal protein to plant-based protein. The body misses out on necessary minerals Phytates are found naturally in beans and cereals – they accumulate when proteins are extracted for use in meat substitutes. In the gastrointestinal tract, where mineral absorption takes place, phytates form insoluble compounds with essential dietary minerals, especially non-heme iron (iron found in plant foods) and zinc, which means that they cannot be absorbed in the intestine. ‘Both iron and zinc also accumulate in protein extraction. This is why high levels are listed among the product’s ingredients, but the minerals are bound to phytates and cannot be absorbed and used by the body,’ says Cecilia Mayer Labba. Iron deficiency among women is a widespread, global problem. In Europe, 10 to 32 per cent of women of childbearing age are affected** and almost one in three teenage girls at secondary school in Sweden***. Women are also the group in society most likely to have switched to a plant-based diet and to eat the least amount of red meat, which is the main source of iron that can be easily absorbed in the digestive tract. ‘It is clear that when it comes to minerals in meat substitutes, the amount that is available for absorption by the body is a very important consideration. You cannot just look at the list of ingredients. Some of the products we studied are fortified with iron but it is still inhibited by phytates. We believe that making nutrition claims on only those nutrients that can be absorbed by the body could create incentives for the industry to improve those products,’ says Ann-Sofie Sandberg, Professor of Food and Nutrition Science at Chalmers and co-author of the study. The food industry needs new methods Tempeh, made from fermented soybeans, differed from the other meat substitutes in the amount of iron available for absorption by the body. This was expected, as the fermentation of tempeh uses microorganisms that break down phytates. Mycoproteins stood out for their high zinc content, without containing any known absorption inhibitors. However, according to the researchers, it is still unclear how well our intestines can break down the cell walls of mycoprotein and how this in turn affects the absorption of nutrients. ‘Plant-based food is important for the transition to sustainable food production, and there is huge development potential for plant-based meat substitutes. The industry needs to think about the nutritional value of these products and to utilise and optimise known process techniques such as fermentation, but also develop new methods to increase the absorption of various important nutrients,’ says Cecilia Mayer Labba. Production of plant proteins Most existing plant-based protein products on the market are based on protein extracted from a cultivated plant, such as soybeans, and separated from the plant’s other components. The protein is then subjected to high pressure and temperature, which restructures the proteins, known as *texturization, so that a product can be achieved that is meatier and chewier in combination with other ingredients. Chalmers’ study shows that the nutritional value of meat substitutes available today is often deficient depending on the choice of raw material (often imported soy) and processing conditions (content of anti-nutrients), and on additives (fat quality and salt). A meal containing 150 grams of meat substitutes contributes up to 60 per cent of the maximum recommended daily intake of salt, which according to the Nordic Nutrition Recommendations is 6 grams. * The protein is restructured by high pressure and temperature. ** Milman, Taylor, Merkel and Brannon: Iron status in pregnant women and women of reproductive age in Europe. Am J Clin Nutr 2017; 106 (Suppl): 1655S-62S. *** Riksmaten Adolescents Survey 2016-2017, Swedish National Food Agency (Livsmedelsverket) report series no. 23, 2018. Swedish National Food Agency (Livsmedelsverket) 2018. Read the full article in Nutrients: Nutritional Composition and Estimated Iron and Zinc Bioavailability of Meat Substitutes Available on the Swedish Market The authors of the study are Cecilia Mayer Labba, Hannah Steinhausen, Linnéa Almius, Knud Erik Bach Knudsen and Ann-Sofie Sandberg. The researchers are active at Chalmers University of Technology and Aarhus University. The study was funded by the Bertebos Foundation, the Swedish Research Council Formas and the region of Västra Götaland. For more information, contact: Dr Cecilia Mayer Labba, The Department of Biology and Biological Engineering, Chalmers University of Technology, [email protected] Professor Ann-Sofie Sandberg, The Department of Biology and Biological Engineering, Chalmers University of Technology, [email protected] +46 (0)31 772 38 26 Captions: Dr Cecilia Mayer Labba, The Department of Biology and Biological Engineering, Chalmers University of Technology. Credit: Martina Butorac/Chalmers Professor Ann-Sofie Sandberg, The Department of Biology and Biological Engineering, Chalmers University of Technology. Credit: Chalmers Photo of vegetarian meat. Credit: Unsplash Karin Wik
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[email protected] ________________ Chalmers University of Technology in Gothenburg, Sweden, conducts research and education in technology and natural sciences at a high international level. The university has 3100 employees and 10,000 students, and offers education in engineering, science, shipping and architecture. With scientific excellence as a basis, Chalmers promotes knowledge and technical solutions for a sustainable world. Through global commitment and entrepreneurship, we foster an innovative spirit, in close collaboration with wider society.The EU’s biggest research initiative – the Graphene Flagship – is coordinated by Chalmers. We are also leading the development of a Swedish quantum computer. Chalmers was founded in 1829 and has the same motto today as it did then: Avancez – forward. --- Images provided in Chalmers University of Technology press releases are, unless specified otherwise, free for download and publication as long as credit is given to the University and the individual creator. Cropping and rescaling of the images is permitted when required for adaptation to the publication’s format, but modifications that would influence the message and content of the original are not. The material is primarily intended for journalistic and informative use, to assist in communication and coverage of Chalmers’ research and education. Commercial usage, for example the marketing of goods and services, is not permitted. We kindly request credit to be given in the following format where possible: Image/Graphic/Illustration: Chalmers University of Technology | Name Surname | Biology |
LONDON -- American toymaker Mattel, the parent company of the iconic Barbie dolls, has honored British STEM trailblazer Dr. Maggie Aderin-Pocock MBE with a unique Barbie in her likeness.
Aderin-Pocock -- space scientist and science educator -- is well known for hosting the BBC show "The Sky at Night" as well as children's television show "Stargazing."
Dressed in a starry dress and adorned with a telescope accessory, her doll aims to recognize her achievements and work with the James Webb Space Telescope, as well as inspire young girls to follow their passion in science.
It is one of the seven unique custom dolls created by Mattel to celebrate women in STEM and introduce girls to inspiring stories that "show them they can be anything."
"Barbie is dedicated to showcasing women who are role models from all backgrounds, professions and nationalities so that girls around the world can see themselves in careers that might not always seem accessible," said Lisa McKnight, executive vice president and global head of Barbie & Dolls.
"STEM is a field where women are severely underrepresented, and our hope is that honoring these seven leaders in science and technology will encourage girls to follow their passion in this field. This International Women's Day, we're proud to continue our work in closing the Dream Gap and reminding girls of heir limitless potential."
The child of immigrants, Aderin-Pocock was diagnosed with dyslexia at the age of 8 and grew up hating school.
"Because of my dyslexia, my reading and writing weren't good at all," said Aderin-Pocock. "Because science was an interest and a passion, I started reading about the subject. I was reading about it in school and I was reading about it at home. Suddenly my marks kept going up and up and up and I was at the top of the class."
Aderin-Pocock hopes her doll can remind girls to follow careers in STEM.
"I hope my doll will remind girls that when you reach for the stars, anything is possible," she said.
Aderin-Pocock has been honored alongside other trailblazers in STEM, such as Katya Echazarreta, the first Mexican woman in space; Susan Wojciki, long-time Google executive; and German marine biology professor Antje Boetius. | Biology |
Humans’ ancestors survived asteroid impact that killed the dinosaurs
Press release issued: 27 June 2023
A Cretaceous origin for placental mammals, the group that includes humans, dogs and bats, has been revealed by in-depth analysis of the fossil record, showing they co-existed with dinosaurs for a short time before the dinosaurs went extinct.
The catastrophic destruction triggered by the asteroid hitting the Earth resulted in the death of all non-avian dinosaurs in an event termed the Cretaceous-Paleogene (K-Pg) mass extinction. Debate has long raged among researchers over whether placental mammals were present alongside the dinosaurs before the mass extinction, or whether they only evolved after the dinosaurs were done away with. Fossils of placental mammals are only found in rocks younger than 66 million years old, which is when the asteroid hit Earth, suggesting that the group evolved after the mass extinction. However, molecular data has long suggested an older age for placental mammals.
In a new paper published in the journal Current Biology, a team of palaeobiologists from the University of Bristol and the University of Fribourg used statistical analysis of the fossil record to determine that placental mammals originated before the mass extinction, meaning they co-existed with dinosaurs for a short time. However, it was only after the asteroid impact that modern lineages of placental mammals began to evolve, suggesting that they were better able to diversify once the dinosaurs were gone.
The researchers collected extensive fossil data from placental mammal groups extending all the way back to the mass extinction 66 million years ago.
Lead author Emily Carlisle of Bristol’s School of Earth Sciences said: “We pulled together thousands of fossils of placental mammals and were able to see the patterns of origination and extinction of the different groups. Based on this, we could estimate when placental mammals evolved.”
Co-author Daniele Silvestro (University of Fribourg) explained: “The model we used estimates origination ages based on when lineages first appear in the fossil record and the pattern of species diversity through time for the lineage. It can also estimate extinction ages based on last appearances when the group is extinct.”
Co-author Professor Phil Donoghue, also from Bristol, added: “By examining both origins and extinctions, we can more clearly see the impact of events such as the K-Pg mass extinction or the Paleocene-Eocene Thermal Maximum (PETM).”
Primates, the group that includes the human lineage, as well as Lagomorpha (rabbits and hares) and Carnivora (dogs and cats) were shown to have evolved just before the K-Pg mass extinction, which means our ancestors were mingling with dinosaurs. After they survived the asteroid impact, placental mammals rapidly diversified, perhaps spurred on by the loss of competition from the dinosaurs.
Paper:
‘A timescale for placental mammal diversification based on Bayesian modelling of the fossil record’ by Emily Carlisle, Phil Donoghue et al in Current Biology. | Biology |
Viruses are intricate collections of molecules that can infect all types of life forms, from plants and animals to microorganisms like bacteria. The origins of viruses in the evolutionary history of life are still a mystery to scientists. We don't even know whether we can even consider them 'alive.' Because viruses cannot survive on their own and need living cells to multiply, many think of them as non-living entities. One thing is for sure though: they challenge our concept of what 'alive' even means. In this article, postdoctoral researcher in Microbiology and Bioinformatics, Hugh Harris shares his thoughts on the subject. Enjoy!By Hugh Harris - Postdoctoral researcher in Microbiology and Bioinformatics, University College Cork Viruses are an inescapable part of life, especially in a global viral pandemic. Yet ask a roomful of scientists if viruses are alive and you’ll get a very mixed response.The truth is, we don’t fully understand viruses, and we’re still trying to understand life. Some properties of living things are absent from viruses, such as cellular structure, metabolism (the chemical reactions that take place in cells) and homeostasis (keeping a stable internal environment).This sets viruses apart from life as we currently define it. But there are also properties that viruses share with life. They evolve, for instance, and by infecting a host cell they multiply using the same cellular machinery.Many viruses can cut the DNA of infected cells and intertwine their own genetic material so that they are copied along with the DNA of their host whenever the cell divides. This process is called lysogeny and it can be contrasted with the more destructive lytic strategy of viruses where they multiply in great numbers within a cell, only to burst the cell open and spread out to infect other cells.There is an undeniable genetic and physiological connection between viruses and the organisms they infect. The discovery of giant viruses further blurs the distinction. These viruses can have as many genes as bacteria, some of which code for functions previously thought to be unique to cellular organisms.Does this new information lead to confusion or clarity? Can we ever answer the elusive question of whether viruses are alive, instead of just a non-living part of the living world? If we approach this puzzle correctly, we may find that we are focusing on the wrong question. Is “life” a box-like category that we can place things in as we discover them, or is it something far more mysterious?A cosmological thought experimentLet us distance ourselves from the details and indulge in a thought experiment. There are hundreds of billions of stars spread out across the universe, clustered into galaxies, many guiding the orbits of planets around them. Some planets, in turn, are acting as gravitational centres for orbiting moons. We know this much.Now, imagine that lifeforms are scattered across these moons and planets, uncommon in any one galaxy perhaps, but numerous over the vast expanse of the universe. A team of intergalactic scientists has been working diligently for centuries, characterising the different forms of life and their unique properties and, more importantly, what they share. They might all use a certain type of molecule, for instance, or share a definitive process like Darwinian evolution.Why would a shared characteristic of life be so important? Because it suggests that life is not a chance happening but an emergent property of the universe. The team of alien scientists might conclude that life is less of an accident and more of a universal principle. This all feels reassuring but is not necessarily true. Carol Cleland, professor of philosophy and author of several books on the nature and origin of life, speculates that life might not be a “natural kind”. This means that life is defined by people instead of by nature.It is like grouping bats with birds due to their shared ability to fly, instead of with mammals. This categorisation gives flight a priority over evolutionary history, even though it is evolution that reflects the most natural relationships among lifeforms on our planet.Cleland ultimately doubts that life is just a manmade concept. She might well be right. This is what makes the alternative so intriguing. What if there is life on a distant planet so unimaginably unlike our own that we would not recognise it if we found it? Could we even call it “life”?Back down on EarthWe are not so advanced as our hypothetical intergalactic explorers. We have yet to find life on another planet, despite our missions to Mars and recent speculation about Saturn’s icy moon, Enceladus, and Jupiter’s Europa.These moons are thought to have active hydrothermal vents that spew out geothermally heated water, much like those at the bottom of Earth’s oceans. One hypothesis on the origin of life on our planet is that it began close to these energetic, chemically rich fissures in the ocean floor.Our scientists have a sample size of one. All life on Earth arose from a common ancestor in the deep geological past. This was long before we had oxygen, or even continents. We do not know what this ancestor looked like in any detail, but it is hypothesised to be a primitive cell containing the basic machinery for copying genetic material and expressing proteins.Did viruses predate this common ancestor? Or did they somehow originate from early evolving lifeforms? Events so ancient are always tortured with uncertainty, but speculation involves numerous intriguing scenarios, all of which may be false.The tree of life, a model of the evolutionary history of life on Earth, might find viruses among its branches after all. The caveat is to keep an open mind. Models themselves evolve with our increased understanding of reality. And who knows what the future of biology will reveal?Are viruses alive? Perhaps this isn’t the question we should be asking. Viruses are evolving entities that are intimately related to cellular life. But we do not understand life.Whenever we get too confident with our opinions and our definitions, we should wonder at that hypothetical planet holding lifelike entities in a remote galaxy, the existence of which could change everything we know.Someday, we may be lucky enough to find it.Sources and further reading: The ConversationViruses: Structure, Function, and UsesScientific American: Are viruses alive? The Origins of VirusesFeatured Articles:Will AI rescue us from a world without working antibiotics?Taking a bath every day reduces the risk of a heart disease related deathAstronomers discovered a planet where it actually rains iron from the skyFeel like time is flying? Here’s how to slow it downA weird thing happened to men about 7,000 years ago If you enjoy our selection of content please consider following Universal-Sci on social media | Biology |
The average human brain shrinks by approximately 5% per decade after the age of 40. This can have a major impact on memory and focus.What's more, brain disorders are on the rise. In 2020, 54 million people worldwide had Alzheimer's disease or other dementias, and that number is expected to grow. But serious mental decline doesn't have to be an inevitable part of aging. In fact, certain lifestyle factors have a greater impact than your genes do on whether you'll develop memory-related diseases.As a neuroscience researcher, here are seven hard rules I live by to keep my brain sharp and fight off dementia.1. Keep blood pressure and cholesterol levels in checkYour heart beats roughly 115,000 times a day, and with every beat, it sends about 20% of the oxygen in your body to your brain.High blood pressure can weaken your heart muscle, and is one of the leading causes of strokes. Ideally, your blood pressure should be no higher than 120/80.Cholesterol is critical to your brain and nervous system health, too. The American Heart Association recommends getting your cholesterol levels measured every four to six years.2. Manage sugar levelsBlood sugar is the primary fuel of the brain. Not enough of it, and you have no energy; too much, and you can destroy blood vessels and tissue, leading to premature aging and cardiovascular disease.Keep in mind that sugar isn't enemy, excess sugar is. It's easy for grams of sugar to add up, even if you think you're being careful — and usually, sugar will sneak in through packaged foods. Where is the sugar hidden? Look for these in the ingredients list:DextroseFructoseGalactoseGlucoseLactoseMaltoseSucroseAnd be wary of any product that includes syrup, such as agave nectar syrup or high-fructose corn syrup.3. Get quality sleepStudies show that people with untreated sleep apnea raise their risk of memory loss by an average of 10 years before the general population.For most people, a healthy brain needs somewhere between seven and nine hours of sleep a night. My tips for memory-boosting, immune-enhancing sleep:Keep a consistent bedtime and wake-up schedule. Turn off devices one hour before bedtime.Do something relaxing before bedtime, like listening to soft music or doing mindful breathing exercises.Go outside and get in natural sunlight as soon as you can after waking up.4. Eat a nutritious dietOne way I keep things simple is to have most, if not all, of these items in my grocery cart:Fatty fish like salmonAvocadosNutsBlueberriesCruciferous veggies like arugula, broccoli, Brussels sprouts and collard greensWhen food shopping, I ask myself three questions to help determine whether something is good for my brain:1. Will it spoil? In many cases, perishable is a good thing. The additives and preservatives that keep food from spoiling wreak havoc on your gut bacteria.2. Are there tons of ingredients in that packaged food? And for that matter, can you pronounce the ingredients? Or does it look like the makings of a chemical experiment? Also avoid anything where sugar is one of the first few ingredients.3. Do you see a rainbow on your plate? The chemicals that give fruits and vegetables their vibrant colors help boost brain health. 5. Don't smoke (and avoid secondhand and thirdhand smoke)Smokers have a 30% higher risk of developing dementia than non-smokers. They also put those around them at risk: Secondhand smoke contains 7,000 chemicals — and at least 70 of them can cause cancer. Then there's thirdhand smoke, which is not actually smoke. It's the residue of cigarette smoke that creates the telltale smell on clothing or in a room. That residue alone can emit chemicals that are toxic to the brain.6. Make social connectionsIn a recent study, people over the age of 55 who regularly participated in dinner parties or other social events had a lower risk of losing their memory. But it wasn't because of what they ate, it was the effect of the repeated social connection.To lessen isolation and loneliness, you can also boost brain chemicals like serotonin and endorphins by performing small acts of kindness:Wish others well or check in with somebody.Give a compliment without expecting anything in return.Make a phone call to somebody you don't usually reach out to.7. Continuously learn new skillsMaintaining a strong memory is not all about brain games like Sudoku, Wordle and crossword puzzles. Learning skills and acquiring information are much more effective ways to make new connections in the brain. The more connections you make, the more likely you are to retain and even enhance your memory.When you think about learning something new, approach it the way you would with fitness training. You want to work out different muscles on different days. The same goes for the brain. Over the course of this week, try cross-training your brain by mixing mental activities (learning a new language or reading a book) and physical learning activities (playing tennis or soccer) .Marc Milstein, PhD, is a brain health expert and author of "The Age-Proof Brain: New Strategies to Improve Memory, Protect Immunity, and Fight Off Dementia." He earned both his PhD in Biological Chemistry and his Bachelor of Science in Molecular, Cellular, and Developmental Biology from UCLA, and has conducted research on genetics, cancer biology and neuroscience. Follow him on Twitter and Instagram.Don't miss:A Harvard nutritionist shares the 6 best brain foods: 'Most people aren't eating enough of' theseThis is the 'worst food ingredient for your immune system,' says immunologistA Harvard nutritionist shares the No. 1 vitamin that keeps her brain 'young and healthy'—and foods she eats 'every day'Want to earn more and work less? Register for the free CNBC Make It: Your Money virtual event on Dec. 13 at 12 p.m. ET to learn from money masters like Kevin O'Leary how you can increase your earning power. | Biology |
Fossil find in California shakes up the natural history of cycad plants
Cycads, a group of gymnosperms which can resemble miniature palm trees (like the popular sago palm houseplant) were long thought to be "living fossils," a group that had evolved minimally since the time of the dinosaurs. Now, a well-preserved 80-million-year-old pollen cone discovered in California has rewritten scientific understanding of the plants.
The findings are detailed in a paper by two University of Kansas paleobotanists just published in the journal New Phytologist.
"Cycads aren't well-known but make up a significant part of plant diversity, accounting for around 25% of all gymnosperms," said lead author Andres Elgorriaga, postdoctoral researcher with the KU Department of Ecology & Evolutionary Biology and KU Biodiversity Institute and Natural History Museum.
"Cycads are plants that have thick stems and short stature, with thick, palm-like leaves on top. They produce cones like pine cones and are related to other seed-bearing plants that also don't produce flowers, like Ginkgo and the monkey puzzle tree. But they're also highly endangered, with the highest level of endangerment among all plant groups. Trafficking of cycads also is a significant issue."
Despite their importance, a lack of fossil evidence and confusion over the years about how to classify some fossil specimens has led to a murky scientific grasp of the plants' evolutionary history. One prominent idea was that cycads today are nearly identical to their prehistoric ancestors.
"The prevailing school of thought is that cycads did not change much in deep time," said co-author Brian Atkinson, assistant professor of ecology & evolutionary biology and curator of paleobotany at the KU Biodiversity Institute and Natural History Museum.
"But the fossil record of cycads is poorly understood, and many things that have been called cycads have turned out not to be cycads at all. Here, we have a three-dimensionally preserved cone clearly assignable to cycads because it has internal anatomy and pollen grains typical of this group. However, the external morphology of this pollen cone is different from living cycads today. This finding suggests cycads aren't really 'living fossils' and they probably have a more dynamic evolutionary history than previously thought."
According to the KU researchers, their analysis of an 80-million-year-old permineralized pollen cone found in the Campanian Holz Shale formation located in Silverado Canyon, California, tells a more accurate cycad natural history—one where the plants diversified during the Cretaceous.
"With this type of discovery, we realize during this time there were cycads that were really different than the ones today in their size, in their number of pollen sacs, in a lot of things," Elgorriaga said. "Maybe we haven't found that many cycad fossils as well—or maybe we're finding them but we're just not recognizing them because they were so different from how they are today. They aren't 'living fossils.' They were different in the past."
To perform their analysis, Elgorriaga and Atkinson studied the specimen's cone's architecture, anatomical details and vasculature organization using serial sectioning, scanning electron microscopy and 3D reconstruction. They also performed a series of evolutionary analyses to place the fossil within the cycad family tree.
Relying partly on the shapes of the cone's scales, pollen and pollen sacs, they assigned the ancient plant to Skyttegaardia, a recently described genus based on isolated cone scales found in Denmark and dated to the Early Cretaceous (about 125 million years ago). Further, they erase some initial doubt about the new genus' placement in the cycad group.
"The 3D reconstruction was striking because it only had two pollen sacs per cone scale, and the form of this cone scale reminded us of a fossil described from Scandinavia called Skyttegaardia," Atkinson said. "There were many similarities, but the original in Scandinavia was only described in 2021 based on isolated cone scales. They cautiously explored the idea that the fossil belonged to cycad but were uncomfortable with firmly concluding this primarily because it only had two pollen sacs per cone scale—while cycads today have 20 to 700. Most cycad pollen cones are quite large, while this fossil was only half a centimeter in length."
The investigators said their description of the primordial plant shows how paleobotany can tell us more about how nature works through deep time.
"This shows us that the information we collect from the fossil record greatly impacts our understanding of evolutionary patterns," Atkinson said. "Time, just like fossils, can reveal insights that aren't apparent from studying only living plants or organisms. This case study is an excellent example of how fossils can contribute to our understanding of evolution over extended periods."
More information: Andres Elgorriaga et al, Cretaceous pollen cone with three‐dimensional preservation sheds light on the morphological evolution of cycads in deep time, New Phytologist (2023). DOI: 10.1111/nph.18852
Journal information: New Phytologist
Provided by University of Kansas | Biology |
Researchers at North Carolina State University used a CRISPR gene-editing system to breed poplar trees with reduced levels of lignin, the major barrier to sustainable production of wood fibers, while improving their wood properties. The findings -- published in the journal Science -- hold promise to make fiber production for everything from paper to diapers greener, cheaper and more efficient.
Led by NC State CRISPR pioneer Rodolphe Barrangou and tree geneticist Jack Wang, a team of researchers used predictive modeling to set goals of lowering lignin levels, increasing the carbohydrate to lignin (C/L) ratio, and increasing the ratio of two important lignin building blocks -- syringyl to guaiacyl (S/G) -- in poplar trees. These combined chemical characteristics represent a fiber production sweet spot, Barrangou and Wang say.
"We're using CRISPR to build a more sustainable forest," said Barrangou, the Todd R. Klaenhammer Distinguished Professor of Food, Bioprocessing and Nutrition Sciences at NC State and co-corresponding author of the paper. "CRISPR systems provide the flexibility to edit more than just single genes or gene families, allowing for greater improvement to wood properties."
The machine-learning model predicted and then sorted through almost 70,000 different gene-editing strategies targeting 21 important genes associated with lignin production -- some changing multiple genes at a time -- to arrive at 347 strategies; more than 99% of those strategies targeted at least three genes.
From there, the researchers selected the seven best strategies that modeling suggested would lead to trees that would attain the chemical sweet spot -- 35% less lignin than wild, or unmodified, trees; C/L ratios that were more than 200% higher than wild trees; S/G ratios that were also more than 200% higher than wild trees; and tree growth rates that were similar to wild trees.
From these seven strategies, the researchers used CRISPR gene editing to produce 174 lines of poplar trees. After six months in an NC State greenhouse, an examination of those trees showed reduced lignin content of up to 50% in some varieties, as well as a 228% increase in the C-L ratio in others.
Interestingly, the researchers say, more significant lignin reductions were shown in trees with four to six gene edits, although trees with three gene edits showed lignin reduction of up to 32%. Single-gene edits failed to reduce lignin content much at all, showing that using CRISPR to make multigene changes could confer advantages in fiber production.
The study also included sophisticated pulp production mill models that suggest reduced lignin content in trees could increase pulp yield and reduce so-called black liquor, the major byproduct of pulping, which could help mills produce up to 40% more sustainable fibers.
Finally, the efficiencies found in fiber production could reduce greenhouse gases associated with pulp production by up to 20% if reduced lignin and increased C/L and S/G ratios are achieved in trees at industrial scale.
Forest trees represent the largest biogenic carbon sink on earth and are paramount in efforts to curb climate change. They are pillars of our ecosystems and the bioeconomy. In North Carolina, forestry contributes over $35 billion to the local economy and supports approximately 140,000 jobs.
"Multiplex genome editing provides a remarkable opportunity to improve forest resilience, productivity, and utilization at a time when our natural resources are increasingly challenged by climate change and the need to produce more sustainable biomaterials using less land," said Wang, assistant professor and director of the Forest Biotechnology Group at NC State and co-corresponding author of the paper.
Next steps include continued greenhouse tests to see how the gene-edited trees perform compared to wild trees. Later, the team hopes to use field trials to gauge whether the gene-edited trees can handle the stresses provided by life outdoors, outside the controlled greenhouse environment.
The researchers stressed the importance of multidisciplinary collaboration that enabled this study, encompassing three NC State colleges, multiple departments, the N.C. Plant Sciences Initiative, NC State's Molecular Education, Technology and Research Innovation Center (METRIC), and partner universities.
"An interdisciplinary approach to tree breeding that combines genetics, computational biology, CRISPR tools, and bio-economics has profoundly expanded our knowledge of tree growth, development, and forest applications," said Daniel Sulis, a postdoctoral scholar at NC State and the first author of the paper. "This powerful approach has transformed our ability to unravel the complexity of tree genetics and deduce integrated solutions that could improve ecologically and economically important wood traits while reducing the carbon footprint of fiber production."
Building on the long-standing legacy of innovations in the fields of plant sciences and forestry at NC State, Barrangou and Wang created a startup company called TreeCo to advance the use of CRISPR technologies in forest trees. This collaborative effort led by NC State faculty members aims to combine tree genetic insights with the power of genome editing to breed a healthier and more sustainable future.
Researchers from several NC State departments co-authored the paper, along with researchers from the University of Illinois at Urbana-Champaign, Beihua University and Northeast Forestry University. Funding was provided by National Institute of Food and Agriculture of the U.S. Department of Agriculture -- Agriculture and Food Research Initiative grant 2018-67021-27716; the National Science Foundation Small Business Technology Transfer Program grant 2044721; Cooperative State Research Service of the U.S. Department of Agriculture grant NCZ04214; North Carolina Specialty Crop Block Grants 19-019-4018, 19-092-4012, and 20-070-4013; an NC State University Chancellor's Innovation Fund grant 190549MA; and an NC State University Goodnight Early Career Innovator Award.
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A new study found a moderately higher risk of autism spectrum disorder in children born to pregnant people exposed to tap water with higher levels of lithium, but experts caution that this association does not show a direct link between the two.
About 1 in 36 children in the US is diagnosed with autism spectrum disorder (ASD) each year, according to data from the US Centers for Disease Control and Prevention.
Scientists still don’t know the exact cause of autism, a developmental disorder. Genetics may be a factor, but some have been looking at potential environmental causes, too.
Cases may be on the rise, but that is also unclear. One study published this year on cases in the New York-New Jersey area found that autism diagnosis rates tripled among certain age groups between 2000 and 2016. A 2021 report found similar increases in cases, but the CDC says the increased number of cases is most likely linked to more doctors screening for the condition.
Lithium is a rare earth element that can be found naturally in some food and ground water. It’s used in batteries, grease and air conditioners, as well as in the treatment of bipolar disorder and some blood disorders. Its levels in US drinking water are not regulated, according to the US Geological Survey.
A new study, published Monday in the journal JAMA Pediatrics, found a small association between lithium and autism diagnosis in Denmark, where the researchers say the level of lithium in drinking water is similar to that in American water systems.
The researchers checked a database of people with psychiatric disorders for children born between 2000 and 2013 to find information on 8,842 cases of ASD and 43,864 participants who did not have ASD. They then measured the concentration of lithium in 151 public waterworks that served more than half of the Danish population and mapped out where pregnant people lived in relation.
As lithium levels in water increased, there was a modest increased risk of an ASD diagnosis. Specifically, compared with people at the lowest exposure level, those who had the second and third highest exposure during pregnancy had a 24% to 26% higher risk of ASD diagnosed in children. The group with the highest exposure had a 46% higher risk than those at the lowest level of exposure.
The researchers could not tell how much water the pregnant people drank, but they picked Denmark in part because residents there consume some of the lowest amounts of bottled water in Europe.
Experts say it’s important to note that the research can’t show that lithium exposure leads directly to an autism diagnosis.
Further study is required, said study co-author Dr. Beate Ritz, a professor of neurology in the David Geffen School of Medicine at UCLA, and a professor of epidemiology and environmental health at the UCLA Fielding School of Public Health.
“Any drinking water contaminants that may affect the developing human brain deserve intense scrutiny,” Ritz said in a news release. She added that the research would need to be replicated in other countries to look for a similar connection.
The implications of the findings are complex as far as public health policy is concerned, according to an editorial published alongside the study. Lithium levels in water, at concentrations that the study associated with a potential ASD risk, have also been linked with health benefits such as lower rates of hospitalization for psychiatric disorders and suicide.
“If all these of associations are valid, the wisdom of Solomon will be required to develop guidelines for lithium in drinking water that are maximally protective of the entire population,” wrote Dr. David C. Bellinger, a professor of neurology and psychology at Harvard Medical School. “Until the basic biology of ASD is better understood, it will be difficult to distinguish causal from spurious associations.”
Dr. Max Wiznitzer, director of the Rainbow Autism Center at University Hospitals Rainbow Babies and Children’s Hospital in Cleveland, points to other research on the effects of lithium on pregnant people who take it for mental health disorders. Those studies – which look at people exposed to much higher levels than are found in drinking water – do not show a connection with autism spectrum disorder.
“It’s an interesting association, but causation is definitely not proven,” said Wiznitzer, who was not involved in the new research. “We have to see if there’s a viable and biologically plausible mechanism by which a small amount of lithium in the water supply can somehow do this, yet pharmacologic dosing of lithium in women with bipolar disorder has not been reported to be causing increased risk of ASD.”
Other studies have also suggested connections between ASD and environmental exposures to things like pesticides, air pollution and phthalates. But none of them points to any of these factors as a direct cause of the disorder.
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A link between environmental exposure and ASD is hard to prove, Wiznitzer said. With research showing that increased exposure to air pollution raises the risk of giving birth to a child with ASD, for example, he often wonders whether pollution is the determining factor or if it’s just the populations who live in more polluted areas.
“There’s a lot of speculation about about environmental factors, but how many of them are truly causally associated?” Wiznitzer said. “We are bombarded with a variety of environmental stressors in our everyday lives. We have to figure out how to basically safely navigate them, and this is probably not one that’s high on our list.” | Biology |
When you haven't eaten in a while, your body has ways of reminding you that it needs fuel. Often, the stomach nudges you toward your next meal by making loud gurgling noises. But why, exactly, do our stomachs growl?
"Stomach growling is due to peristalsis," Tiffany Weir, professor of food science and human nutrition at Colorado State University, told Live Science.
Peristalsis is a series of wavelike muscular contractions that propel gas, food and liquids along the hollow tube of the digestive tract. The human digestive tract, which includes the mouth, esophagus, stomach, intestines and rectum, is essentially a long, muscular pipe. To get food from one end to the other, the muscles built into the lining of this tube contract in a sequence, one set of muscles after another, which pushes digestive contents along.
Stomach growling, or borborygmi, is the sound caused by these muscle contractions, and they don't just happen when you are hungry.
"Your stomach can growl when it's hungry or when it's full because we have hormones that regulate our appetite and trigger peristalsis," Weir said. Immediately after a meal, there is a lot of peristalsis going on. There are an average of three waves per minute in the stomach and 12 along the small intestine. As food is pushed through the digestive tract, it is mixed and churned for easier digestion, and the mixing of solids and liquids during digestion is not a silent process.
Related: Will eating pet food kill you?
This peristaltic action often goes unnoticed because the contents of the stomach and intestines muffle any sound the digestive tract may make. But an empty digestive tract is much noisier, which may explain why stomach growling is noticeable when someone is hungry, making it commonly associated with hunger..
According to the National Institutes of Health, when the stomach has been empty for a few hours, it begins to secrete a hormone called ghrelin. When this hormone reaches the brain, it triggers feelings of hunger and stimulates peristalsis in the digestive tract.
The reason the stomach and intestines might contract in the absence of food may be to clear out any excess liquid, solid or microbial debris that may be lingering in the stomach or intestines, Mark A. W. Andrews, a professor of physiology and associate director of the Independent Study program at the Lake Erie College of Osteopathic Medicine in Pennsylvania, said in an article for Scientific American.
This peristalsis is much slower than when the digestive tract is full, as it only occurs about once every 20 minutes. However, because there is more air than solid material in the tract, loud rumblings can often be heard when the digestive tract is empty.
Sometimes, stomach growling and gurgling is caused by digestive problems. Incomplete digestion of certain foods, like plant material, such as beans, and dairy products, can produce excess gas that amplifies the sounds of peristalsis. Digestive illnesses like gastroenteritis can cause diarrhea, which involves increased peristaltic action in an attempt to clear the intestines, which can also be quite noisy.
Illnesses aside, stomach rumbling is a common and harmless side effect of the way the human digestive system operates.
This article is for informational purposes only, and is not meant to offer medical advice.
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Cameron Duke is a contributing writer for Live Science who mainly covers life sciences. He also writes for New Scientist as well as MinuteEarth and Discovery's Curiosity Daily Podcast. He holds a master's degree in animal behavior from Western Carolina University and is an adjunct instructor at the University of Northern Colorado, teaching biology. | Biology |
A host of genetic variants associated with dyslexia have been identified by researchers, shedding light on the hereditary aspect of the disorder.It is estimated that about 10% of the UK population, about 6.3 million people, are dyslexic. Previous research has suggested it has a heritable component, with studies suggesting genetics account for somewhere between 40% and 80% of the average differences between those with dyslexia and general population.However, pinpointing specific genetic variants that may play a role has proved challenging. Now researchers say they have identified about 170 genes and 42 specific genetic variants significantly associated with dyslexia in the largest such study to date.While 15 of these variants have previously been linked to cognitive ability and educational attainment, the remaining 27 are newly identified – meaning they have not previously been linked to traits associated with dyslexia.“At the moment, there are no direct implications for people with dyslexia, although it helps them understand that the condition has very complex causes,” said lead researcher Dr Michelle Luciano of the University of Edinburgh.But Luciano said the results do offer insights into the biology underlying dyslexia. “We can follow up the significant genes to see what their function is and how it might relate to the cognitive processes involved in reading and spelling,” she said.Writing in the journal Nature Genetics, Luciano and colleagues report how they analysed the genomes of 51,800 adults with a self-reported diagnosis of dyslexia, as well as those of 1,087,070 adults who said they did not have such a diagnosis. All of the participants are involved in research with the personal genetics company 23andMe.The team add that several of the newly identified variants were subsequently found to be significantly associated with dyslexia in data analysed by the team that was collected in other genomic studies of people of European ancestry, as well as in data from people of Chinese ancestry.The team found some genetic variants previously thought to be associated with dyslexia were not flagged up in the latest work.“Our study was much more powerful than these previous ones, so the results are more reliable,” said Luciano.Using results from other studies the team found genetic correlations between dyslexia and a number of other traits. These included having ADHD, having equal use of right and left hands and greater reporting of pain.Luciano added there were some surprises, including a lack of genetic overlap between dyslexia and brain imaging measures. That, she said, was unexpected given various brain regions and networks have been linked to reading skill. “This suggests that the relationship is influenced by the environment,” she said.A representative from the British Dyslexia Association welcomed the research. “There is much to understand about the complexity of dyslexia and neurodiversity, we always welcome and encourage new research which may help give us a better understanding and help our community,” they said. | Biology |
Small and precise: These are the ideal characteristics for CRISPR systems, the Nobel-prize winning technology used to edit nucleic acids like RNA and DNA.
Rice University scientists have described in detail the three-dimensional structure of one of the smallest known CRISPR-Cas13 systems used to shred or modify RNA and employed their findings to further engineer the tool to improve its precision. According to a study published in Nature Communications, the molecule works differently than other proteins in the same family.
"There are different types of CRISPR systems, and the one our research was focused on for this study is called CRISPR-Cas13bt3," said Yang Gao, an assistant professor of biosciences and Cancer Prevention and Research Institute of Texas Scholar who helped lead the study. "The unique thing about it is that it is very small. Usually, these types of molecules contain roughly 1200 amino acids, while this one only has about 700, so that's already an advantage."
A diminutive size is a plus as it allows for better access and delivery to target-editing sites, Yang Gao said.
Unlike CRISPR systems associated with the Cas9 protein -- which generally targets DNA -- Cas13-associated systems target RNA, the intermediary "instruction manual" that translates the genetic information encoded in DNA into a blueprint for assembling proteins.
Researchers hope these RNA-targeting systems can be used to fight viruses, which generally encode their genetic information using RNA rather than DNA.
"My lab is a structural biology lab," Yang Gao said. "What we are trying to understand is how this system works. So part of our goal here was to be able to see it in three-dimensional space and create a model that would help us explain its mechanism."
The researchers used a cryo-electron microscope to map the structure of the CRISPR system, placing the molecule on a thin layer of ice and shooting a beam of electrons through it to generate data that was then processed into a detailed, three-dimensional model. The results took them by surprise.
"We found this system deploys a mechanism that's different from that of other proteins in the Cas13 family," Yang Gao said. "Other proteins in this family have two domains that are initially separated and, after the system is activated, they come together -- kind of like the arms of a scissor -- and perform a cut.
"This system is totally different: The scissor is already there, but it needs to hook onto the RNA strand at the right target site. To do this, it uses a binding element on these two unique loops that connect the different parts of the protein together."
Xiangyu Deng, a postdoctoral research associate in the Yang Gao lab, said it was "really challenging to determine the structure of the protein and RNA complex."
"We had to do a lot of troubleshooting to make the protein and RNA complex more stable, so we could map it," Deng said.
Once the team figured out how the system works, researchers in the lab of chemical and biomolecular engineer Xue Sherry Gao stepped in to tweak the system in order to increase its precision by testing its activity and specificity in living cells.
"We found that in cell cultures these systems were able to hone in on a target much easier," said Sherry Gao, the Ted N. Law Assistant Professor of Chemical and Biomolecular Engineering. "What is really remarkable about this work is that the detailed structural biology insights enabled a rational determination of the engineering efforts needed to improve the tool's specificity while still maintaining high on-target RNA editing activity."
Emmanuel Osikpa, a research assistant in the Xue Gao lab, performed cellular assays that confirmed the engineered Cas13bt3 targeted a designated RNA motif with high fidelity.
"I was able to show that this engineered Cas13bt3 performed better than the original system," Osikpa said. "Xiangyu's comprehensive study of the structure highlights the advantage that a targeted, structurally guided approach has over large and costly random mutagenesis screening."
The research was supported by the Welch Foundation (C-2033-20200401, C-1952), the Cancer Prevention and Research Institute of Texas (RR190046), the National Science Foundation (2031242) and the Rice startup fund.
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NASA and the China National Space Agency (CNSA) plan to mount the first crewed missions to Mars in the next decade. These will commence with a crew launching in 2033, with follow-up missions launching every 26 months to coincide with Mars and Earth being at the closest point in their orbits. These missions will culminate with the creation of outposts that future astronauts will use, possibly leading to permanent habitats. In recent decades, NASA has conducted design studies and competitions (like the 3D-Printed Habitat Challenge) to investigate possible designs and construction methods. For instance, in the Mars Design Reference Architecture 5.0, NASA describes a “commuter” architecture based on a “centrally located, monolithic habitat” of lightweight inflatable habitats. However, a new proposal envisions the creation of a base using organisms that extract metals from sand and rock (a process known as biomineralization). Rather than hauling construction materials or prefabricated modules aboard a spaceship, astronauts bound for Mars could bring synthetic bacteria cultures that would allow them to grow their habitats from the Red Planet itself. The concept, known as “Biomineralization-Enabled Self-Growing Building Blocks for Habitat Outfitting on Mars,” was proposed by Dr. Congrui Grace Jin – an assistant professor of Civil and Environmental Engineering at the University of Nebraska-Lincoln. Her proposal was one of several selected by the NASA Innovative Advanced Concepts (NIAC) for Phase I development, which includes a grant of $12,500. This program makes annual solicitations for advanced, innovative, and technically feasible concepts that assist NASA missions and further the agency’s space exploration objectives. Since the 1990s, several architectures have been drafted for crewed missions to Mars, all of which have emphasized the need for keeping launch mass low. Suggestions for how this could be accomplished include inflatable modules. But as Dr. Jin emphasized in her proposal, the physical structures used to outfit the inflatable modules cannot be carried by a crewed spacecraft and generally require a second vehicle to launch them. This is a logistical challenge for missions and drastically increases launch costs.
Another possibility is to use local resources to reduce the amount of supplies that must be transported – a process known as In-Situ Resource Utilization (ISRU). Examples range from the Mars Direct proposal drafted in 1991 by Dr. Robert Zubrin and colleagues from NASA’s Ames Research Center to NASA’s Journey to Mars program launched in 2010. For missions to Mars, this would include using local regolith to create building materials and water ice for astronaut consumption, irrigation, and to create propellant and oxygen gas. However, this mission architecture requires equipment (like robotic 3D printers) to be transported to Mars. In addition, many designs for ISRU-3D printed habitats still require inflatable modules, which provide scaffolding for 3D-printed structures. For her proposal, Dr. Jin suggests that rather than shipping prefabricated elements or machinery to Mars, habitats could be realized through in-situ construction using cyanobacteria and fungi as building agents. Universe Today recently interviewed Dr. Jin via Zoom, who explained the road that led to her NAIC proposal: “In the past few years, I was working on self-healing concrete. So when concrete generates cracks, we use bacteria or fungi to induce the biominerals to heal the cracks. And then we think about other possibilities, like self-growing materials. So one would have soil particles or aggregates, we want to use fungi or bacteria to make them into a cohesive body.” “This will be very important if there is no human labor, especially on Mars. They can do this automatically. We propose that instead of shipping materials from Earth to Mars, we can directly use in-situ materials. Fro sample, the soil, the atmosphere, and the water on Mars, then we can just bring some bacteria or fungal spores and they will build the bricks for us.” Artists’ impression of robots assembling the Sprout concept using lego-like bricks. Credit: Mars City Design/Giuseppe Calabrese
The key to this is “biomineralization,” a process where bacteria and spores can assemble minerals like calcium carbonate (CaCO3), otherwise known as limestone. Scientists have known that there is limestone and other carbonates on Mars, as demonstrated by the Pheonix Mars Lander that found traces of CaCO3 at its landing site in 2008. This was backed up by subsequent sample analysis conducted by the Spirit and Opportunity rovers and mineral mapping conducted by missions like NASA’s Mars Reconnaissance Orbiter (MRO).
According to Dr. Jin’s proposal, future missions could be equipped with “synthetic biology toolkits” to create synthetic lichen systems (diazotrophic cyanobacteria and filamentous fungi). These will turn CaO3 into abundant biopolymers that can be combined with Martian regolith to “grow” building materials. “They will work as a catalyst to promote the calcium carbonate formation, and those calcium carbonate crystals will work as a glue to bind those soil particles together,” said Dr. Jin. “You need to put the sand particles into the mould you want, then the bacteria and the fungi will grow them into the shape of the mould.”
In this proposed autonomous system, the cyanobacteria and filamentous fungi perform different (but complementary functions. As per the NAIC proposal, the cyanobacteria are responsible for 1) capturing carbon dioxide and converting it to carbonate ions and 2) providing oxygen and organic compounds to support the filamentous fungi. The fungi, meanwhile, are responsible for 1) binding calcium ions onto fungal cell walls and serving as nucleation sites for calcium carbonate deposition and 2) assisting the survival and growth of cyanobacteria by providing them additional carbon dioxide and reducing their oxidative stress. In addition, the cyanobacteria and fungi secrete “extracellular polymeric substances” that enhance adhesion between regolith particles and biopolymers and cohesion among precipitated particles. Dr. Jin also detailed the process for creating these synthetic bacteria and fungi, which ensures that they work symbiotically and not competitively:
“We need to find those strains that can get along with each other. It’s called mutualistic co-culturing. Basically, some of them can enhance the living of the partner. We need filamentous fungi because of their filamentous structure. They can promote larger amounts of calcium carbonate crystals. But we also need the cyanobacteria can do photosynthesis – they can capture the CO2 and generate organic carbon for the fungi.” Self-healing of a bio-encapsulated concrete specimen during a period of 3 weeks. Credit: Jakhrani et al. (2019)
To get this process started, there is still equipment that will need to be brought to Mars. Due to the low-pressure atmosphere, radiation, and temperature extremes, Dr. Jin says that future missions will need to bring a photobioreactor. This bioreactor is where the cultures of bacteria and lichens will grow and where the assembly process will occur. Ultimately, the proposal envisions bioreactors producing bricks that are removed to build surface structures. As for the rate of production, Dr. Jin contends that more research is needed:
“It really depends on the nutrients, the temperature, and the pressure. So we are still studying this process. We want to optimize the factors that influence the process so that we can do this much faster,” she said. However, another benefit is how these building materials will also be self-healing. “If you don’t kill the bacteria or fungi, they can always generate those limestone crystals. So later, when the structure generates cracks, they can heal them automatically. So this material is self-growing and self-repairing. So they have a lot of features that we don’t have with materials on Earth.”
While biomineralization is something researchers have been investigating for years, this proposal represents a first for two reasons. For starters, it is the first project to consider filamentous fungi as a biomineral producer instead of bacteria. Dr. Jin has conducted extensive research on biomineralization in recent years, and her results have demonstrated that filamentous fungi possess distinctive advantages over bacteria. Foremost among them is their extraordinary capacity to produce large amounts of minerals in a short space of time. Second, this project is the first to employ self-growing technology by creating a synthetic lichen system and using symbiotic interactions between photoautotrophic cyanobacteria and heterotrophic filamentous fungi. Photoautotrophs are noted for using sunlight to turn inorganic carbon into organic materials (in this case, organic carbon). None of the self-growing practices investigated so far have been fully-autonomous since they were generally restricted to a single species or strain of heterotrophs dependent on a constant external supply of organic carbon. Illustration of a photobioreactor that could grow food and building materials on Mars. Credit: Joris Wegner/ZARM/Universität Bremen
This technology has applications beyond space exploration as well. Aside from building habitats on Mars and other bodies beyond Earth, the technology also has the potential to revolutionize construction here on Earth. In regions that have been affected by war, natural disasters, and climate change, this autonomous, self-growing technology has the potential of “healing” damaged structures and building new infrastructure in a way that has a negative carbon footprint. Since the process relies on CO2 captured from the atmosphere, it is consistent with global climate restoration efforts. This technology is yet another example of how Earth organisms and biological processes inspire sustainable and regenerative space systems. These same technologies, which could allow humanity to live sustainably in space, could also help us combat and reverse climate change here at home. Much like the process that powers this proposed bioreactor technology, the relationship is symbiotic. Further Reading: NASA
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Comparing the genetics and relocation patterns of habitat “haves” and “have-nots” among two populations of threatened rattlesnakes has produced a new way to use scientific landscape data to guide conservation planning that would give the “have-nots” a better chance of surviving.The study suggests that a collection of six relatively closely situated but isolated populations of Eastern massasauga rattlesnakes in northeast Ohio could grow their numbers if strategic alterations were made to stretches of land between their home ranges. The findings contributed to the successful application for federal funding of property purchases to make some of these proposed landscape changes happen.Reconnecting these populations could not only help restore Eastern massasaugas to unthreatened status, but establish a thriving habitat for other prey and predator species facing threats to their survival – satisfying two big-picture conservation concerns, researchers say.“We aren’t just protecting massasaugas – we’re protecting everything else that’s there,” said H. Lisle Gibbs, professor of evolution, ecology and organismal biology at The Ohio State University and senior author of the study. “Even though we are focused on this species, protection of the habitat has all these collateral benefits.” The research was published recently in the journal Ecological Applications. Eastern massasauga rattlesnakes live in isolated spaces in midwestern and eastern North America and were listed as threatened under the Endangered Species Act in 2016 because of loss and fragmentation of their wetland habitat.This study involves two known groups of Eastern massasaugas in Ohio: The Killdeer Plains Wildlife Area in north central Ohio, home to one of the most genetically diverse and largest populations in the country, numbering in the thousands, and six small, separate populations of Eastern massasaugas clustered near each other in Ashtabula County.Study co-author Gregory Lipps, a field biologist at Ohio State, has studied the northeast Ohio groups for years. Federal officials once told him the populations are too small in number to be viable – but the genetics portion of this study showed that the populations had once been connected and deserve a second chance to rebuild. “So now we are working on trying to reconnect them, to get them back to a viable population large enough to sustain itself even when disturbances happen that cause populations to fluctuate,” Lipps said.First author Scott Martin, who completed this work as a PhD student in Gibbs’ lab, had previously sequenced genomes of 86 snakes from the six fragmented sites in northeast Ohio. For a genetic comparison in this new study, the team captured and collected blood samples from 109 snakes living together in the Killdeer Plains site. The genetic analysis, combined with where snakes were located at the time of capture, showed that the snakes living in fragmented sites in northeast Ohio were very distantly related, having stopped mingling at least three generations ago. “Once we knew that they didn’t seem to be moving around, the real question is why aren’t they moving? It’s not that big of a distance – so we focused on finding out what was stopping them from being connected,” Martin said.Previous research had indicated how far a male Eastern massasauga snake could safely travel to find a mate and establish a family in a new location. GPS and genetic data from the Killdeer Plains and northeast Ohio population samples showed how much movement was common among related snakes in a successful group, and how uncommon relocation was among snakes living in fragmented habitats. Martin came up with the idea to combine all the data to see what was different about the landscapes in the two regions – and what could be interfering with snake relocation in the Ashtabula County groups. “It seemed to be about specific features of the habitat,” Martin said. “If the snakes in northeast Ohio were moving as far as we would expect them to based on how the Killdeer snakes move and data on the species’ range, they should be able to move between these little sites. And yet when we look at the genetics and use pedigrees to see if there is any breeding between the sites, there’s just not.” Using landscape maps, the researchers created models from the data that detailed the “resistance value” of various landscape features that would either help or hinder the northeast Ohio snakes’ movement to find mates. Wooded areas, cropland, and roads and housing developments – also called impervious surfaces – were found to be the main obstacles to snake relocation. Wet prairies are the ideal habitat for Eastern massasaugas. “You can imagine two snakes in the same habitat that are probably likely very genetically similar because they can move easily. And then in this other region you have two snakes near each other, but on either side of a four-lane highway, and they will be genetically different because snakes don’t move across that highway, and over time they’ve diverged,” Martin said. “That means a highway would have a high resistance value and an open field would have a very low resistance value.” These findings, and Lipps’ longtime work with northeast Ohio landowners and numerous conservation agencies, helped Ohio and Michigan collaborate on applying for and receiving a $2.3 million grant from the U.S. Fish and Wildlife Service to acquire land to benefit Eastern massasaugas in both states.“To me, this is a clear example of where Ohio State basic research has produced practical results that have then been directly used to help conserve wildlife in Ohio – in other words, achieving one of the goals of a land-grant institution, which is to provide useful, practical knowledge of value to the citizens of the state,” Gibbs said.This research was supported by the State Wildlife Grants Program, administered jointly by the U.S. Fish and Wildlife Service and the Ohio Division of Wildlife, the Ohio Biodiversity Conservation Partnership and the National Science Foundation.William Peterman, School of Environment and Natural Resources at Ohio State, was also a co-author on this study. | Biology |
A map of the 3,016 neurons that make up a baby fruit fly's brain is the first of its kind, according to a new study.
Researchers say the map of the insect's brain is the largest ever completed and shows every neuron - or messenger cell - in the organ and how they are wired together.
Experts say it could bring them closer to understanding the mechanism of thought and behaviour and has been described as a "big step forward".
The project was led by Professor Marta Zlatic and Professor Albert Cardona, of the Medical Research Council Laboratory of Molecular Biology, which is based at the University of Cambridge.
"The way the brain circuit is structured influences the computations the brain can do," said Professor Zlatic. "But, up until this point, we've not seen the structure of any brain except of the roundworm C. elegans, the tadpole of a low chordate, and the larva of a marine annelid, all of which have several hundred neurons.
"This means neuroscience has been mostly operating without circuit maps.
"Without knowing the structure of a brain, we're guessing on the way computations are implemented.
"But now, we can start gaining a mechanistic understanding of how the brain works."
The work took researchers 12 years to complete, with the imaging alone taking about a day per neuron.
The research, which has been published in the Science journal, was a joint project with experts at the University of Cambridge and Johns Hopkins University in the US, combining to complete the largest ever described brain connectome - a detailed map of neural connections in the brain.
In order to build an image of the fruit fly's neural connections, the researchers had to scan thousands of slices of the larva's brain before painstakingly reconstructing them to complete the map.
Then they could begin to meticulously annotate the connections between neurons on to the reconstructed image.
"This is a big step forward in addressing key questions about how the brain works," said Jo Latimer, head of neurosciences and mental health at the Medical Research Council.
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Current technology is not advanced enough to map the connectome for more complex animals such as large mammals, but this breakthrough could start to change that.
As well as mapping the 3,016 neurons, researchers mapped an incredible 548,000 synapses - the points of contact between neurons where information is passed between them. | Biology |
The incessant drumming of a woodpecker on a hollow tree can be an annoying distraction for anyone who has to listen to it. To other woodpeckers, however, it’s as distinct and as telling as any bird song.A new study, published last week in the journal PLOS Biology, found that both a woodpecker’s drumming and a songbird’s singing are governed by similar specialized structures in the birds’ brains, structures that are not found in other nonsinging birds. And both behaviors serve the same purposes of marking out territory and attracting mates, the researchers said.The findings are especially intriguing because the singing of songbirds has important parallels to human speech, and so the drumming of woodpeckers could now, too, give new scientific insights into how humans talk.“Woodpeckers use drumming as songbirds use song,” said evolutionary biologist Matthew Fuxjager, an associate professor of ecology, evolution and organismal biology at Brown University in Providence, Rhode Island, and senior author of the new research. “The structures are similar in size and shape, and are similar in terms of where we find them in the brain.”The research combines two approaches to the study of woodpeckers: work by Fuxjager into their ecology, and work by his collaborator, Erich Jarvis, a professor of neurogenetics at Rockefeller University in New York, into the genetic mechanisms at play.The researchers found that drumming by woodpeckers and singing by songbirds are governed by very similar structures in the forebrains of the animals, made of cells that strongly express the protein parvalbumin.“When you study songbirds, hummingbirds and parrots, you find areas that control vocal learning express parvalbumin more than other parts of the brain,” Fuxjager said.He noted that structures of cells that strongly express parvalbumin are also seen in human brains, but they aren’t seen in birds that don’t communicate with vocalizations.It was a surprise, therefore, when the research led by Fuxjager and Jarvis found such structures in the woodpecker brains but not in birds that don’t sing, such as emus, penguins and ducks (quacks don’t count).Fuxjager suggested in the study that both the singing and the drumming originated in specialized brain structures for refined motor control in the ancestors of modern birds.Although they might sound quite different, both behaviors are remarkably similar. Both involve complex muscle coordination, and both are used to mark out territory to competitors, which can hear the drumming or singing from afar.Both drumming and singing are also used as courtship signals when a male hopes to attract a mate. Future studies will look for other similarities, such as if the patterns of woodpecker drumming are learned at an early age, like the singing of songbirds, he said.Fuxjager noted that there are more than 200 species of woodpecker around the world and that they inhabit every continent, except Australia.Each species of woodpecker drums in short bursts with a specific rhythm and at a specific speed, depending on what they want to communicate and to whom.If a woodpecker doesn’t get its drumming pattern right, that will be noticed by other woodpeckers of that species, which use it to assess whether an individual is a worthy competitor. If they get it wrong, however, then other woodpeckers won’t be able to recognize it or understand it.Drumming also has certain advantages over singing, since it has other uses: It’s used to reveal edible insects in wood and to make cavities in tree trunks for nesting.But the drumming to find insects or make nests is much slower than the repetitive — and loud — drumming that woodpeckers use to mark out territory and attract mates, Fuxjager said.Scientists study the singing of songbirds — and possibly now the drumming of woodpeckers — because it has parallels to human speech.Both are learned when young, for example, but have a genetic component. Both require complex muscle coordination and both are controlled by specialized regions of the brain.Jon Sakata, an associate professor of biology at McGill University in Montréal who specializes in the neurophysiological and behavioral mechanisms of songbird communications, noted the similarities between the forebrain structures that seem to control drumming in woodpeckers, described in the new study, and singing in songbirds. Sakata wasn’t involved in the latest study.In both cases, structures of brain cells — neurons — that contain parvalbumin seem to be important for performing complex motor movements and for learning to produce such movements, Sakata said in an email.“Because parvalbumin neurons are also implicated in speech production and learning, this is a wonderful example of how similar brain mechanisms can be co-opted for different behaviors across species,” he said.Tom MetcalfeTom Metcalfe writes about science and space for NBC News. | Biology |
A strange class of brain cell has two features that seem to contradict each other, leading scientists to question whether it really exists. But now, a new study of mouse and human brains not only supports these paradoxical cells' existence but also hints that they could help explain the neurological underpinnings of conditions like autism and schizophrenia.
Published in July in the journal Molecular Psychiatry, the study found that two chemical markers, which were once thought to mark neurons with opposite roles, are sometimes found in the same neuron. Neurons with both of these markers, researchers found, frequently activate, or "express" genes related to the production of cellular energy using oxygen.
In postmortem brain tissue from donors with either autism or schizophrenia, neurons with these markers had altered gene expression related to this process, compared with tissue from people without the conditions.
This finding potentially jibes with research linking schizophrenia and autism to genetic changes that contribute to oxidative stress, or the buildup of reactive byproducts of energy production in cells. The research could be a step toward better understanding these complex neurological conditions.
Related: How do brain cells send messages?
In the study, researchers specifically documented the existence of a special class of inhibitory neurons, or neurons that suppress electrical activity in the brain. The cells carry two chemical markers: a protein called parvalbumin (PV) and a smaller molecule called cholecystokinin (CCK).
Neurons with PV are fast-spiking, meaning they generate short-lived signals repeatedly and more quickly than almost any other type of neuron in the brain. Neurons with CCK typically fire at a slower, more typical speed. Previous research, such as a 2021 article in the journal Neuron, suggested that these neurons are usually active at opposite times, with PV neurons often firing before and even inhibiting those with CCK.
"It's kind of like you have this dichotomy," said Steven Grieco, lead author of the study and a project scientist in the Department of Anatomy and Neurobiology at the University of California, Irvine. "Our finding … blurs that dichotomy a little bit."
To confirm these seemingly unlikely cells' existence, the researchers used several methods in mice, including molecular staining and RNA sequencing, which takes stock of which genes are actively being used to make proteins. After establishing that some cells had both markers, they did the RNA sequencing to determine what the cells' function might be. They also examined the cells in postmortem brain tissue from people with neuropsychiatric conditions and those without.
Out of the inhibitory neurons with PV in the mouse hippocampus, a brain region involved in memory, 40% to 56% also had CCK, the team found. Such cells also appeared in other parts of the mouse brain, including the neocortex, a key region for "higher" cognitive functions, like perception.
Cells with both PV and CCK more heavily activate genes related to oxidative phosphorylation, a process by which cells use oxygen and enzymes to create adenosine triphosphate (ATP), the body's main source of cellular energy. This suggests that the cells require a lot of energy to run.
However, these genes' expression seemed altered in the tissue from people with autism and schizophrenia, pointing to a potential role for the neurons in the conditions. The findings could also support the potential link between these conditions and oxidative stress, and may align with previous research linking the conditions to dysfunction in the brain's inhibitory neurons and a resulting overload of electrical activity.
The researchers aren't the first to find these cells, said Simon Pieraut, an assistant professor of biology at the University of Nevada, Reno who was not involved in the work. But they are likely the first to focus on the cells in this way, he said.
Pieraut told Live Science that his lab and others had previously found cells with both PV and CCK, but he was unsure if the findings might be the result of a technical quirk or error. He said that, to show that this isn't the case, it was particularly valuable that the researchers used multiple methods to support the existence of these cells.
The findings don't necessarily establish a link between these neurons and conditions like schizophrenia, but they provide justification for further research into if and how the cells might be related to the disorders, Pieraut said. Such research could potentially be used to develop future treatments.
"If we want to find treatment in the future, knowing exactly what pathway needs to be targeted … will be very helpful," he said.
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Rebecca Sohn is a freelance science writer. She writes about a variety of science, health and environmental topics, and is particularly interested in how science impacts people's lives. She has been an intern at CalMatters and STAT, as well as a science fellow at Mashable. Rebecca, a native of the Boston area, studied English literature and minored in music at Skidmore College in Upstate New York and later studied science journalism at New York University. | Biology |
AI predicts enzyme function better than leading tools
A new artificial intelligence tool can predict the functions of enzymes based on their amino acid sequences, even when the enzymes are unstudied or poorly understood. The researchers said the AI tool, dubbed CLEAN, outperforms the leading state-of-the-art tools in accuracy, reliability and sensitivity. Better understanding of enzymes and their functions would be a boon for research in genomics, chemistry, industrial materials, medicine, pharmaceuticals and more.
"Just like ChatGPT uses data from written language to create predictive text, we are leveraging the language of proteins to predict their activity," said study leader Huimin Zhao, a University of Illinois Urbana-Champaign professor of chemical and biomolecular engineering. "Almost every researcher, when working with a new protein sequence, wants to know right away what the protein does. In addition, when making chemicals for any application—biology, medicine, industry—this tool will help researchers quickly identify the proper enzymes needed for the synthesis of chemicals and materials."
The researchers will publish their findings in the journal Science and make CLEAN accessible online March 31.
With advances in genomics, many enzymes have been identified and sequenced, but scientists have little or no information about what those enzymes do, said Zhao, a member of the Carl R. Woese Institute for Genomic Biology at Illinois.
Other computational tools try to predict enzyme functions. Typically, they attempt to assign an enzyme commission number—an ID code that indicates what kind of reaction an enzyme catalyzes—by comparing a queried sequence with a catalog of known enzymes and finding similar sequences. However, these tools don't work as well with less-studied or uncharacterized enzymes, or with enzymes that perform multiple jobs, Zhao said.
"We are not the first one to use AI tools to predict enzyme commission numbers, but we are the first one to use this new deep-learning algorithm called contrastive learning to predict enzyme function. We find that this algorithm works much better than the AI tools that are used by others," Zhao said. "We cannot guarantee everyone's product will be correctly predicted, but we can get higher accuracy than the other two or other three methods."
The researchers verified their tool experimentally with both computational and in vitro experiments. They found that not only could the tool predict the function of previously uncharacterized enzymes, it also corrected enzymes mislabeled by the leading software and correctly identified enzymes with two or more functions.
Zhao's group is making CLEAN accessible online for other researchers seeking to characterize an enzyme or determine whether an enzyme could catalyze a desired reaction.
"We hope that this tool will be used widely by the broad research community," Zhao said. "With the web interface, researchers can just enter the sequence in a search box, like a search engine, and see the results."
Zhao said the group plans to expand the AI behind CLEAN to characterize other proteins, such as binding proteins. The team also hopes to further develop the machine-learning algorithms so that a user could search for a desired reaction and the AI would point to a proper enzyme for the job.
"There are a lot of uncharacterized binding proteins, such as receptors and transcription factors. We also want to predict their functions as well," Zhao said. "We want to predict the functions of all proteins so that we can know all the proteins a cell has and better study or engineer the whole cell for biotechnology or biomedical applications."
Zhao also is a U. of I. professor of bioengineering, of chemistry, and of biomedical and translational sciences in the Carle Illinois College of Medicine.
The paper is titled "Enzyme function prediction using contrastive learning."
Journal information: Science
Provided by University of Illinois at Urbana-Champaign | Biology |
Brazil’s golden monkeys swing from near extinction to thousands
After the number of golden lion tamarins fell to 200 in the 1970s, conservationists successfully brought the species back up to nearly 5,000. Anti-poaching, disease control, and reconnecting forest cover are all thought to be behind the rebound.
There are now more golden lion tamarins bounding between branches in the Brazilian rainforest than at any time since efforts to save the species started in the 1970s, a new survey reveals.
Once on the brink of extinction, with only about 200 animals in the wild, the population has rebounded to around 4,800, according to a study released Tuesday by the Brazilian science and conservation nonprofit Golden Lion Tamarin Association.
“We are celebrating, but always keeping one eye on other threats, because life’s not easy,” said the nonprofit’s president, Luís Paulo Ferraz.
Golden lion tamarins are small monkeys with long tails and copper-colored fur that live in family groups led by a mated pair. Usually, they give birth annually to twins, which all family members help to raise by bringing them food and carrying them on their backs.
The monkeys, which live only in Brazil’s Atlantic Forest, are still considered endangered.
The population survey was conducted over roughly a year. Researchers went to specific locations and checked whether monkeys responded to recordings of the tamarins’ long call, which basically means “I’m here. Are you there?” said James Dietz, a biologist and vice president of the U.S.-based nonprofit Save the Golden Lion Tamarin.
The new population figures are notable because the species had experienced a sharp decline from a yellow fever outbreak. In 2019, there were 2,500 monkeys, down from 3,700 in a 2014 survey.
Scientists intervened by vaccinating more than 370 monkeys against yellow fever, using shots adapted from a formula for humans – a fairly novel approach for conservation.
Scientists “cannot pinpoint a single exact cause for the recovery,” but believe several factors may be at play, said Carlos R. Ruiz-Miranda, a State University of Northern Rio de Janeiro biologist who advised on the population study.
Firstly, the yellow fever outbreak has subsided, perhaps due to a combination of the virus’ natural cycle and the vaccination campaign.
The animals may also be benefiting from an increase in forest habitat, said Mr. Dietz, who is also a research associate at the Smithsonian Institution’s Conservation Biology Institute. Between 2014 and 2022, the amount of connected forest habitat increased 16%, mostly through forests regrown on converted cattle pasture, he said.
Currently, about three dozen farmers and ranchers in the Atlantic Forest region participate in such reforestation programs.
“It makes me so happy to see the tamarins playing free on my farm. They don’t only live in protected areas,” said Ayrton Violento, a farmer and entrepreneur in the small city of Silva Jardim. His family’s Fazenda dos Cordeiros has planted native fruit trees and also manages a tree nursery for native Atlantic Forest seedlings to plant on other farms.
“Recently, every year I see more tamarin families, more frequently,” he said.
Mr. Ferraz, of the nonprofit Golden Lion Tamarin Association, said that despite the good news, he was still concerned about a renewed risk of trafficking for the illegal pet trade. The problem was rampant in the 1960s but had almost disappeared in recent decades due to enforcement.
In July, the anti-poaching nonprofit Freeland Brazil reported that Suriname’s forest service had seized seven golden lion tamarins and 29 endangered Lear’s macaws believed to have been trafficked from Brazil for sale in Europe.
“We have seen the resilience of the species, but also know they are still vulnerable,” said Mr. Ferraz.
This story was reported by The Associated Press. | Biology |
The Wnt signaling pathway: The foundation of cell growth, development, and potential therapeutics
The Wnt signaling pathway, a system present in living organisms, plays a pivotal role in cell growth, differentiation, and migration. It has a long history dating back to 1982, when the first Wnt gene, essential for cellular growth, was discovered. The pathway is initiated by Wnt ligands, a set of 19 glycoproteins that transmit signals through specific receptors and proteins, leading to modifications in gene expression.
In a review published in the journal Genes & Diseases, researchers from The University of Chicago Medical Center have not only delved into the history of Wnt signaling, but also examined the different types of Wnt signaling, highlighting the components of each and their interplay with other cellular functions.
The review emphasizes the interactions and overlaps between Wnt signaling and other cellular pathways, showcasing the intricate web of communication within our cells. Wnt signaling serves as a bridge connecting numerous cellular functions, making it integral to overall health. Its mismanagement can result in a multitude of diseases, from cancer to developmental anomalies, underlining the importance of its precise regulation.
The pathway is so central that deviations can even lead to embryonic fatality. Wnt's widespread involvement in our body's processes makes it an attractive target for therapeutics. Potential treatments focusing on Wnt signaling can address ailments ranging from cancer to heart disease. However, as with any powerful tool, the utilization of these treatments carries inherent risks. Unintended consequences, such as tumor formation or accidental suppression of essential cellular functions, are possible.
While our understanding of Wnt signaling has grown leaps and bounds over the past four decades, mysteries remain. The exact mechanisms by which the 19 Wnt ligands interact with their receptors are not entirely understood. The complete spectrum of pathways influenced by Wnt signaling is yet to be fully mapped. Furthermore, while the components of the Wnt signaling pathway are being deciphered, their full range of functions might still be hidden.
The ultimate goal is to harness the power of the Wnt signaling pathway for therapeutic use, but this requires a deeper understanding and utmost caution. Current treatments, both activators and inhibitors, come with potential risks. Further research aims to ensure the safety of these therapies and expand our understanding, with the hope of capitalizing on the potential benefits of regulating Wnt signaling.
The Wnt signaling pathway, while complex, is undeniably central to many processes in living organisms. The past 40 years have offered a plethora of insights, yet the pathway remains a treasure trove of potential knowledge. As researchers continue to unveil its secrets, there's hope that these findings will catalyze advances in biology, medicine, and overall human well-being.
More information: Kevin Qin et al, Canonical and noncanonical Wnt signaling: Multilayered mediators, signaling mechanisms and major signaling crosstalk, Genes & Diseases (2023). DOI: 10.1016/j.gendis.2023.01.030
Provided by KeAi Communications Co. | Biology |
Scientists have successfully recorded brain activity from freely moving octopuses, a feat made possible by implanting electrodes and a data logger directly into the creatures.
The study, published online in Current Biology on February 23, is a critical step forward in figuring out how octopus' brains control their behavior, and could provide clues to the common principles needed for intelligence and cognition to occur.
"If we want to understand how the brain works, octopuses are the perfect animal to study as a comparison to mammals. They have a large brain, an amazingly unique body, and advanced cognitive abilities that have developed completely differently from those of vertebrates," said Dr. Tamar Gutnick, first author and former postdoctoral researcher in the Physics and Biology Unit at the Okinawa Institute of Science and Technology (OIST).
But measuring the brainwaves of octopuses has proven a real technical challenge. Unlike vertebrates, octopuses are soft bodied, so they have no skull to anchor the recording equipment onto, to prevent it being removed.
"Octopuses have eight powerful and ultra-flexible arms, which can reach absolutely anywhere on their body," said Dr. Gutnick. "If we tried to attach wires to them, they would immediately rip if off, so we needed a way of getting the equipment completely out of their reach, by placing it under their skin."
The researchers settled on small and lightweight data loggers as the solution, which were originally designed to track the brain activity of birds during flight. The team adapted the devices to make them waterproof, but still small enough to easily fit inside the octopuses. The batteries, which needed to work in a low-air environment, allowed up to 12 hours of continuous recording.
The researchers chose Octopus cyanea, more commonly known as the day octopus, as their model animal, due to its larger size. They anesthetized three octopuses and implanted a logger into a cavity in the muscle wall of the mantle. The scientists then implanted the electrodes into an area of the octopus' brain called the vertical lobe and median superior frontal lobe, which is the most accessible area. This brain region is also believed to be important for visual learning and memory, which are brain processes that Dr. Gutnick is particularly interested in understanding.
Once the surgery was complete, the octopuses were returned to their home tank and monitored by video. After five minutes, the octopuses had recovered and spent the following 12 hours sleeping, eating and moving around their tank, as their brain activity was recorded. The logger and electrodes were then removed from the octopuses, and the data was synchronized to the video.
The researchers identified several distinct patterns of brain activity, some of which were similar in size and shape to those seen in mammals, whilst others were very long lasting, slow oscillations that have not been described before.
The researchers were not yet able to link these brain activity patterns to specific behaviors from the videos. However, this is not completely surprising, Dr. Gutnick explained, as they didn't require the animals to do specific learning tasks.
"This is an area that's associated with learning and memory, so in order to explore this circuit, we really need to do repetitive, memory tasks with the octopuses. That's something we're hoping to do very soon!"
The researchers also believe that this method of recording brain activity from freely moving octopuses can be used in other octopus species and could help solve questions in many other areas of octopus cognition, including how they learn, socialize and control the movement of their body and arms.
"This is a really pivotal study, but it's just the first step," said Prof. Michael Kuba, who led the project at the OIST Physics and Biology Unit and now continues at the University of Naples Federico II. "Octopus are so clever, but right now, we know so little about how their brains work. This technique means we now have the ability to peer into their brain while they are doing specific tasks. That's really exciting and powerful."
The study involved an international collaboration between researchers in Japan, Italy, Germany, Ukraine, and Switzerland.
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Materials provided by Okinawa Institute of Science and Technology (OIST) Graduate University. Original written by Dani Ellenby. Note: Content may be edited for style and length.
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The benefit of redundancy in biological systems
When viewed from an engineer's perspective, biology is often messy and imperfect. For example, redundancy is a common feature of biological systems, with the job of one biological component overlapping with that of another.
A study, recently published in the journal eLife, investigates whether some types of biological redundancy can—despite the apparent inefficiency—actually be beneficial.
Translation: A biological process with a high degree of redundancy
Translation is an energetically costly process by which cells convert genetic information into proteins. The decoding process is performed by ribosomes and transfer RNAs (tRNAs). These important biological molecules are themselves encoded in the cell's genetic information, often by several (and sometimes hundreds) of identical gene copies.
For example, the commonly used laboratory bacterial strain Escherichia coli K-12 MG1655 contains seven copies of the ribosomal RNA (rRNA) genes and up to six copies of each tRNA gene. This apparent redundancy is, at first, unexpected; why pay the cost of maintaining numerous identical gene copies?
One hypothesis is that more gene copies may allow more or faster production of ribosomes and tRNAs, leading to faster growth and division in supportive conditions. To test this hypothesis, Deepa Agashe's group at the National Centre for Biological Sciences (India) teamed up with the Microbial Evolutionary Dynamics group at the Max Planck Institute for Evolutionary Biology (led by Jenna Gallie).
Levels of translational redundancy in E. coli can be manipulated in the laboratory
Various redundant rRNA and/or tRNA gene copies were removed from the E. coli K-12 MG1655 genome. The result was a panel of derived strains, each with a lower degree of translational redundancy than in the original strain. Biological assays were used to demonstrate that the gene deletion events lead to either a reduction in mature tRNA expression (via YAMAT-seq) and/or the slowing of translation (via β-galactosidase reporter assays).
These results show that (i) the genetic redundancy of E. coli translational components can be decreased, and (ii) the genetic reductions are reflected in the mature translational machinery.
More gene copies are beneficial under increased translational demand
The growth profiles of all strains were measured across different environments, in which nutrient availability ranged from poor to rich. Generally speaking, the lower-redundancy strains grew faster than the original strain when nutrients were scarce, but slower than the original strain when nutrients were freely available. These results are consistent with the initial hypothesis: genetic redundancy comes at a cost when translation is slow, and this cost is alleviated under conditions that support faster translation and growth.
This study has demonstrated that carrying multiple rRNA/tRNA gene copies can be beneficial under conditions that support increasingly faster translation and growth. More broadly, the results highlight that (apparent) redundancy can play a beneficial role in complex biological systems, particularly under changing environmental conditions.
More information: Parth K Raval et al, The layered costs and benefits of translational redundancy, eLife (2023). DOI: 10.7554/eLife.81005
Journal information: eLife
Provided by Max Planck Society | Biology |
Cubs Can Be Viewed on the New Live Cheetah Webcam Oct. 06, 2022 Video Carnivore keepers at the Smithsonian’s National Zoo and Conservation Biology Institute (NZCBI) in Front Royal, Virginia, welcomed a litter of two cheetah cubs. First-time mother, 4-year-old female Amani, birthed the cubs Oct. 3 around 9:17 p.m. and 11:05 p.m. ET. This is also the first litter sired by 7-year-old father Asante. As the first offspring of both parents, the cubs are genetically valuable. They appear to be strong, active, vocalizing and nursing well. Animal care staff are closely monitoring Amani and her cubs’ behaviors via the Cheetah Cub Cam on the Zoo’s website. Virtual visitors can also observe Amani and her cubs on this temporary platform until the cubs leave the dens. Keepers will leave Amani to bond with and care for her cubs without interference, so it may be some time before they can determine the cubs’ sexes. They will perform a health check on the cubs when Amani is comfortable leaving them for an extended period. “Seeing Amani successfully care for this litter—her first—with confidence is very rewarding,” said Adrienne Crosier, cheetah biologist at NZCBI and head of the Association of Zoos & Aquariums’ Cheetah Species Survival Plan (SSP). “Being able to watch our cheetah family grow, play and explore their surroundings is incredibly special. We hope this experience brings Cheetah Cub Cam viewers joy and helps them feel a deeper connection to this vulnerable species.” NZCBI is part of the Cheetah Breeding Center Coalition—a group of 10 cheetah breeding centers across the United States that aim to create and maintain a sustainable North American cheetah population under human care. These cubs are a significant addition to the Cheetah SSP, as each individual contributes to this program. The SSP scientists determine which animals to breed by considering their genetic makeup, health and temperament, among other factors. Amani and Asante were paired and bred naturally July 2 and 3. Keepers trained Amani to voluntarily participate in ultrasounds, and veterinarians confirmed her pregnancy Aug 8. Since 2007, 17 litters of cheetah cubs have been born at NZCBI’s Front Royal campus. Significant scientific studies by NZCBI researchers have demonstrated that maintaining breeding males in group coalitions (as they would live in the wilds of Africa) promotes reproductive performance, specifically improving sperm quality. Other ongoing research focuses on gamete (sperm and egg) biology, health and disease, the influence of age on reproduction, as well as understanding the hormonal complexities of the species. Such data is used by conservationists to modify reproductive strategies for this vulnerable felid, including ensuring that prime-breeding-age cheetahs are maintained in spacious breeding centers, such as at NZCBI, to promote optimal reproduction and cub production. Cheetahs live in small, isolated populations mostly in sub-Saharan Africa. Many of their strongholds are in eastern and southern African parks. Due to human conflict and poaching, habitat and prey-base loss, there are only an estimated 7,000 to 7,500 cheetahs left in the wild. The International Union for Conservation of Nature considers cheetahs vulnerable to extinction. About the Smithsonian’s National Zoo and Conservation Biology Institute The Smithsonian’s National Zoo and Conservation Biology Institute (NZCBI) leads the Smithsonian’s global effort to save species, better understand ecosystems and train future generations of conservationists. Its two campuses are home to more than 2,000 animals, including some of the world’s most critically endangered species. Always free of charge, the Zoo’s 163-acre park in the heart of Washington, D.C., features 1,800 animals representing 360 species and is a popular destination for children and families. At the Conservation Biology Institute’s 3,200-acre campus in Virginia, breeding and veterinary research on 200 animals representing 20 species provide critical data for the management of animals in human care and valuable insights for conservation of wild populations. NZCBI’s 305 staff and scientists work in Washington, D.C., Virginia and with partners at field sites across the United States and in more than 30 countries to save wildlife, collaborate with communities and conserve native habitats. NZCBI is a long-standing accredited member of the Association of Zoos & Aquariums. # # # | Biology |
The extinction of critically endangered elephants could amplify global warming, scientists have warned.As if the prospect of Earth's largest land mammal disappearing forever wasn't bad enough, losing them would have a potentially devastating impact on the planet's second-biggest rainforest.
The Congo Basin, which spans several countries in central and western Africa, has seen its elephant population plummet over the past decade - down 60% to an estimated 40,000, according to the Wildlife Conservation Society.Poaching is a major cause of their decline, with thousands killed every year for their ivory tusks.Researchers say that if the animals were to completely vanish, the Congo's rainforest - second to Brazil's Amazon - would lose up to 9% of its ability to capture atmospheric carbon.
"If we lose forest elephants, we will be doing a global disservice to climate change mitigation," said Stephen Blake, assistant professor of biology at Saint Louis University."The importance of forest elephants for climate mitigation must be taken seriously by policymakers to generate the support needed for elephant conservation."The role of forest elephants in our global environment is too important to ignore."Read more:African elephants 'at risk of extinction' Please use Chrome browser for a more accessible video player 'We kill elephants because we love them' The crucial role of elephantsProfessor Blake is senior author of a new paper in Proceedings of the National Academy of Sciences.His team's research describes how crucial elephants are to Africa's rainforests, maintaining their valuable status as a carbon sink, when they absorb more carbon dioxide than they emit.Elephants favour low carbon density trees when it comes to feeding, as they are more nutritious, promoting the growth of higher carbon density trees.The elephants' feeding habits "thins" the forest, which reduces competition among the trees and provides more light, space, and soil nutrients to the high carbon trees.When elephants do feed from high carbon trees, it's the often large fruit that grows from them - the seeds from which pass through the animals' gut undamaged.These are released in the elephants' dung, primed to germinate and grow into some of the forest's largest trees.Read more:'Very difficult' to protect Congo Basin Image: The Congo Basin is home to the world's second-largest rainforest 'Save the elephants - help save the planet'Professor Blake hailed them as "the gardeners of the forest" - and said the research was yet more reason to provide them with better protection.He added: "As a global society, we can continue to hunt these highly social and intelligent animals and watch them become extinct, or we can find ways to stop this illegal activity."Save the elephants and help save the planet, it really is that simple."The WWF estimates there are just 415,000 elephants left across Africa, and 40,000-50,000 in the wild in Asia. | Biology |
Melanie Rutkowski, PhD, of the UVA School of Medicine and the UVA Cancer Center, studies how gut health affects breast cancer and its spread. An unhealthy gut triggers changes in normal breast tissue that helps breast cancer spread to other parts of the body, new research from UVA Cancer Center reveals. The gut microbiome – the collection of microbes that naturally live inside us – can be disrupted by poor diet, long-term antibiotic use, obesity or other factors. When this happens, the ailing microbiome reprograms important immune cells in healthy breast tissue, called mast cells, to facilitate cancer’s spread, UVA Health’s new discovery shows. The finding could help scientists develop ways to keep breast cancer from metastasizing (spreading to other parts of the body). When it does, it is often deadly: Only 29% of women with metastatic breast cancer survive five years; for men with metastatic breast cancer, that figure is just 22%. The discovery could also let doctors predict which patients are at greatest risk of cancer recurrence after treatment, the UVA scientists say. “We show gut commensal dysbiosis, an unhealthy and inflammatory gut microbiome, systemically changes the mammary tissues of mice that do not have cancer. The tissue changes enhance infiltration of mast cells that, in the presence of a tumor, facilitate breast tumor metastasis,” said researcher Melanie R. Rutkowski, PhD, of UVA Cancer Center and the University of Virginia School of Medicine. “Mast cells recruited into the tissue environment during dysbiosis restructure the tissue architecture in such a way that tumor cells metastasize to other organs.” The Microbiome and Breast Cancer Rutkowski has been a pioneer in unveiling the surprising relationship between gut health and breast cancer. Her latest work reveals complex interactions between our gut microbes and mast cells in the breast. Mast cells are blood cells which help regulate the body’s immune response to disease and allergens. Rutkowski’s new work suggests that the gut microbiome can systemically influence mast cell behavior and function in the presence of tumors. Rutkowski and her team found that an unhealthy microbiome caused the mast cells to accumulate in the breast. These changes continued after tumor formation in a mouse model of hormone receptor-positive breast cancer, making the breast tissue a prime launching ground for the cancer’s incursions into other parts of the body. Further, the scientists found that the mast cells increased the amount of collagen in the mice’s breast tissue and spurred earlier cancer spread. Blocking the process that led to mast-cell accumulation prevented both, significantly reducing tumor spread to the lungs. Based on their lab results, the researchers examined tissue samples taken from human patients with hormone receptor-positive breast cancer. They found these patients, like the mice, had increased numbers of mast cells and increased deposits of collagen. The numbers of mast cells correlated with the amount of collagen and, notably, the patients’ risk for a recurrence of breast cancer. “Mast cells have had a controversial role in breast cancer, with some studies identifying a positive correlation with outcome while others have identified negative associations,” said Rutkowski, of UVA’s Department of Microbiology, Immunology and Cancer Biology. “Our investigation suggests that to better define the relationship between mast cells and risk for breast tumor metastasis, we should consider the mast cell functional attributes, tissue collagen density and mast cell location with respect to the tumor.” Ultimately, she says, doctors may be able to target the gut-mast cell relationship in patients with breast cancer to help prevent the cancer from recurring and spreading. They also may be able to use the discovery to identify patients at risk for recurrence, allowing them to tailor the treatment strategy for the prevention of metastatic disease. “Personalized medicine in oncology is a promising approach to facilitate better outcomes for patients,” said researcher Tzu-Yu Feng, PhD, the first author of a new scientific paper outlining the findings. “Our research on the gut-mast cell axis has identified possible intervention points that could be targeted for a customized approach to therapy. The ultimate goal would be to improve survival for patients diagnosed with breast cancer.” Rutkowski’s cutting-edge research is part of UVA Cancer Center’s urgent mission to better understand and better treat cancer. UVA is one of only 52 cancer centers in the country to be designated as a Comprehensive Cancer Center by the National Cancer Institute (NCI). The designation recognizes elite cancer centers with the most outstanding cancer research and treatment programs in the nation. UVA Cancer Center is the only Comprehensive Cancer Center in Virginia. Findings Published Rutkowski and her collaborators have published their findings in the scientific journal Cancer Immunology Research. The research team consisted of Tzu-Yu Feng, Francesca N. Azar, Sally A. Dreger, Claire Buchta Rosean, Mitchell T. McGinty, Audrey M. Putelo, Sree H. Kolli, Maureen A. Carey, Stephanie Greenfield, Wesley J. Fowler, Stephen D. Robinson and Melanie Rutkowski. The work was supported by Susan G. Komen, grant CCR17483602; the National Institutes of Health’s National Cancer Institute, grant R01CA253285; and the American Cancer Society, grant IRG 81-001-26. Additional support came from UVA Cancer Center, the BBSRC Institute Strategic Programme Gut Microbes and Health, and Cancer Research UK. To keep up with the latest medical research news from UVA, subscribe to the Making of Medicine blog. | Biology |
Nose-picking primates are helping scientists to understand the evolution and possible functional role of the behaviour in humans.For the first time researchers have recorded the aye-aye - a long-fingered lemur - inserting its longest finger up its nostrils and then licking its finger clean.
So far 12 other primate species, including humans, have been documented picking their nose and eating the mucus.The scientists said their findings, published in the Journal of Zoology, could shed some light on how this behaviour has evolved and whether it has a functional role.The lead author Anne-Claire Fabre, a scientific associate at the Natural History Museum in London, said: "There is very little evidence about why we, and other animals, pick our nose.
"Nearly all the papers that you can find were written as jokes. Of the serious studies, there are a few in the field of psychology, but for biology there's hardly anything."One study shows that picking your nose can spread bacteria such as staphylococcus, while another shows that people who eat their own snot have fewer dental cavities."The aye-aye, the world's biggest nocturnal primate, belongs to a category of species known as strepsirrhine primates and is native to Madagascar.It has rodent-like teeth and a specialised long, thin middle finger. The aye-aye's fingers are used to locate food inside wood by tapping on it and then extracting small grubs. The researchers also noticed the lemur uses its longest finger to pick its nose.Ms Fabre said: "It was impossible not to notice this aye-aye picking its nose."This was not just a one-off behaviour but something that it was fully engaged in, inserting its extremely long finger a surprisingly long way down its nose and then sampling whatever it dug up by licking its finger clean!" Image: Scientists believe the aye aye's finger might be able to reach right to the back of its throat The researchers used a CT scan to look inside the skull and hand of an aye-aye specimen at the museum and found that the finger could go all the way into the throat.Read more science news:Fungal infections 'increased significantly' during COVID pandemicIn pictures: Partial solar eclipse as it happenedPrevious scientific research has suggested there may be health benefits to eating snot, but the researchers believe that in this case there is a chance that the animal ingesting its own mucus may simply be down to its texture, crunchiness and saltiness.Roberto Portela Miguez, a senior curator at the Natural History Museum and a co-author of the paper, said: "It is great to see how museum specimens and digital methods can help us elucidate behaviours that are generally quite difficult to observe in their natural habitat."We hope that future studies will build on this work and help us understand why we and our closest relatives insist on picking our noses." | Biology |
A new cancer drug has been found to “annihilate” solid tumours in the lab, researchers in the US have announced.
The chemotherapy was tested on 70 different cancer cells, along with some healthy human cells as a control. It was effective against all the cancer cells, including those derived from breast, prostate, brain, ovarian, cervical, skin and lung cancers, says a report in Cell Chemical Biology, but it did not harm the healthy ones.
The drug is codenamed AOH1996 after Anna Olivia Healey, who died from neuroblastoma aged nine in 1996. Dr Linda Malkas, who led the team at the City of Hope centre in Los Angeles, had met Anna’s father just before she died, and promised to look for new treatments in her memory.
She was true to her word. The culmination of years of research, AOH1996 works by targeting cells with faulty DNA, and disrupting the process of division and repair. "Our cancer-killing pill is like a snowstorm that closes a key airline hub, shutting down all flights in and out only in planes carrying cancer cells," says Malkas.
Malkas must now establish whether the drug is safe and effective when used on human patients.
A phase one trial currently under way involves eight people who have exhausted existing treatment options taking two pills of AOH1996 a day to determine if it is safe. If this trial goes well, larger ones will follow. | Biology |
WASHINGTON -- U.S. health officials on Friday approved a closely watched Alzheimer's drug that modestly slows the brain-robbing disease, albeit with potential safety risks that patients and their doctors will have to carefully weigh.The drug, Leqembi, is the first that's been convincingly shown to slow the decline in memory and thinking that defines Alzheimer's by targeting the disease's underlying biology. The Food and Drug Administration approved it for patients with Alzheimer's, specifically those with mild or early-stage disease.Leqembi, from Japan's Eisai and its U.S. partner Biogen, is a rare success in a field accustomed to failed experimental treatments for the incurable condition. The delay in cognitive decline brought about by the drug likely amounts to just several months, but some experts say it could still meaningfully improve people's lives."This drug is not a cure. It doesn't stop people from getting worse, but it does measurably slow the progression of the disease," said Dr. Joy Snider, a neurologist at Washington University in St. Louis. "That might mean someone could have an extra six months to a year of being able to drive."Snider stressed that the medicine, pronounced "leh-KEM-bee," comes with downsides, including the need for twice-a-month infusions and possible side effects like brain swelling.The FDA approval came via its accelerated pathway, which allows drugs to launch based on early results, before they're confirmed to benefit patients. The agency's use of that shortcut approach has come under increasing scrutiny from government watchdogs and congressional investigators.Last week, a congressional report found that FDA's approval of a similar Alzheimer's drug called Aduhelm - also from Biogen and Eisai - was "rife with irregularities," including a number of meetings with drug company staffers that went undocumented.Scrutiny of the new drug, known chemically as lecanemab, will likely mean most patients won't start receiving it for months, as insurers decide whether and how to cover it.The drug will cost about $26,500 for a typical year's worth of treatment. Eisai said the price reflects the drug's benefit in terms of improved quality of life, reduced burdens for caregivers and other factors. The company pegged its value at over $37,000 per year, but said it priced it lower to reduce costs for patients and insurers. An independent group that assesses drug value recently said the drug would have to be priced below $20,600 per year to be cost-effective.Some 6 million people in the U.S. and many more worldwide have Alzheimer's, which gradually attacks areas of the brain needed for memory, reasoning, communication and daily tasks.The FDA's approval was based on one mid-stage study in 800 people with early signs of Alzheimer's who were still able to live independently or with minimal assistance.Since then, Eisai has published the results of a larger 1,800-patient study that the FDA will review to confirm the drug's benefit, paving the way for full approval later this year.The larger study tracked patients' results on an 18-point scale that measures memory, judgment and other cognitive abilities. Doctors compile the rating from interviews with the patient and a close contact. After 18 months, patients receiving Leqembi declined more slowly - a difference of less than half a point on the scale - than patients who received a dummy infusion. The delay amounted to just over five months.There is little consensus on whether that difference translates into real benefits for patients, such as greater independence."Most patients won't notice the difference," said Dr. Matthew Schrag, a neurology researcher at Vanderbilt University. "This is really quite a small effect and probably below the threshold of what we'd call clinically significant."Schrag and some other researchers believe a meaningful improvement would require at least a difference of one full point on the 18-point scale.Leqembi works by clearing a sticky brain protein called amyloid that's one hallmark of Alzheimer's. But it's not clear exactly what causes the disease. A string of other amyloid-targeting drugs have failed and many researchers now think combination treatments will be needed.Aduhelm, the similar drug, was marred by controversy over its effectiveness.The FDA approved that drug in 2021 against the advice of the agency's own outside experts. Doctors hesitated to prescribe the drug and insurers restricted coverage.The FDA did not consult the same expert panel before approving Leqembi.While there's "less drama," surrounding the new drug, Schrag said many of the same concerns apply."Is this slight, measurable benefit worth the hefty price tag and the side effects patients may experience?" he asked. "I have pretty serious doubts."About 13% of patients in Eisai's study had swelling of the brain and 17% had small brain bleeds, side effects seen with earlier amyloid-targeting medications. In most cases those problems didn't cause symptoms, which can include dizziness and vision problems.Also, several Leqembi users died while taking the drug, including two who were on blood-thinning medications. Eisai has said the deaths can't be attributed to the drug. The FDA label warns doctors to use caution if they prescribe Leqembi to patients on blood thinners.Insurers are likely to only cover the drug for people like those in the company study - patients with mild symptoms and confirmation of amyloid buildup. That typically requires expensive brain scans. A separate type of scan will be needed to periodically monitor for brain swelling and bleeding.A key question in the drug's rollout will be the coverage decision by Medicare, the federal health plan that covers 60 million seniors and other Americans. The agency severely restricted coverage of Aduhelm, essentially wiping out its U.S. market and prompting Biogen to abandon marketing plans for the drug.Eisai executives said they have already spent months discussing their drug's data with Medicare officials. Coverage isn't expected until after the FDA confirms the drug's benefit, likely later this year."Once we have a Medicare decision, then we can truly launch the drug across the country," said Eisai's U.S. CEO, Ivan Cheung.Betsy Groves, 73, of Cambridge, Massachusetts, was diagnosed with Alzheimer's in 2021. A former lecturer at Harvard's school of education, she noticed she was having trouble remembering some student names and answering questions.Her initial diagnosis, based on a cognitive examination, was later confirmed by a positive test for amyloid.Groves says she is "more than willing" to try Leqembi, despite potential side effects and the need for infusions."For me, the minute that drug comes on the market - and I get my doctor's approval - I'm going to take it," Groves said.Copyright © 2023 by The Associated Press. All Rights Reserved. | Biology |
A new analysis shows that infectious bacteria exposed to the antibiotic albicidin rapidly develop up to a 1,000-fold increase in resistance via a gene amplification mechanism. Mareike Saathoff of Freie Universität Berlin, Germany, and colleagues present these findings August 10 in the open access journal PLOS Biology.
Bacterial resistance to antibiotics is a growing problem associated with millions of deaths around the world every year. Understanding how bacteria evolve resistance is key to developing more effective antibiotics and strategies for using them.
In recent years, albicidin has emerged as a promising antibiotic capable of killing a wide range of bacterial species by disrupting their DNA replication. Researchers are working to develop new albicidin-based medications; yet, despite its promise, some bacteria are able to develop resistance to albicidin.
To further investigate albicidin resistance mechanisms, Saathoff and colleagues conducted a suite of experiments employing a broad set of tools, including RNA sequencing, protein analysis, X-ray crystallography, and molecular modeling. They found that two bacteria often associated with human infection -- Salmonella typhimurium and Escherichia coli -- develop resistance to albicidin when exposed to increasingly higher concentrations of the compound. Their analysis narrowed down the source of this resistance to an increase in the number of copies of a gene known as STM3175 (YgiV) in the bacterial cells, which is amplified in each new generation of cells as they multiply. STM3175 encodes a protein that interacts with albicidin in such a way that protects the bacteria from it.
Further experiments showed that the same albicidin-resistance mechanism is widespread among both pathogenic and harmless bacteria, including the microbes Vibrio vulnificus, which can infect wounds, and Pseudomonas aeruginosa, which can cause pneumonia and other infections. These findings could help inform the ongoing development of albicidin-based antibiotic strategies.
The authors add, "Our study reveals a gene duplication and amplification-based mechanism of a transcriptional regulator in Gram-negative bacteria, that mediates resistance to the peptide antibiotic albicidin."
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Noel Celis/AFP via Getty Images
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Security guards stand in front of the Huanan Seafood Wholesale Market in Wuhan, China, on Jan. 11, 2020, after the market had been closed following an outbreak of COVID-19 there. Two studies document samples of SARS-CoV-2 from stalls where live animals were sold.
Noel Celis/AFP via Getty Images
Security guards stand in front of the Huanan Seafood Wholesale Market in Wuhan, China, on Jan. 11, 2020, after the market had been closed following an outbreak of COVID-19 there. Two studies document samples of SARS-CoV-2 from stalls where live animals were sold.
Noel Celis/AFP via Getty Images
Since the SARS-CoV-2 pandemic began three years ago, its origin has been a topic of much scientific — and political — debate. Two main theories exist: The virus spilled over from an animal into people, most likely in a market in Wuhan, China, or the virus came from the Wuhan Institute of Virology and spread due to some type of laboratory accident.
The Wall Street Journal added to that debate this week when they reported that the U.S. Department of Energy has shifted its stance on the origin of COVID. It now concludes, with "low confidence," that the pandemic most likely arose from a laboratory leak in Wuhan, China.
The agency based their conclusion on classified evidence that isn't available to the public. According to the federal government, "low confidence" means "the information used in the analysis is scant, questionable, fragmented, or that solid analytical conclusions cannot be inferred from the information."
And at this point, the U.S. intelligence community still has no consensus about the origin of SARS-CoV-2. Four of the eight intelligence agencies lean toward a natural origin for the virus, with "low confidence," while two of them – the DOE and the Federal Bureau of Information – support a lab origin, with the latter having "moderate confidence" about their conclusion.
Noel Celis/AFP via Getty Images
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Staff members of the Wuhan Hygiene Emergency Response Team investigate the shuttered Huanan Seafood Wholesale Market on Jan. 11, 2020, after it was linked to cases of COVID-19.
Noel Celis/AFP via Getty Images
Staff members of the Wuhan Hygiene Emergency Response Team investigate the shuttered Huanan Seafood Wholesale Market on Jan. 11, 2020, after it was linked to cases of COVID-19.
Noel Celis/AFP via Getty Images
But at the end of the day, the origin of the pandemic is also a scientific question. Virologists, who study pandemic origins, are much less divided than the U.S. intelligence community. They say there is "very convincing" data and "overwhelming evidence" pointing to an animal origin.
In particular, scientists published two extensive, peer-reviewed papers in Science in July 2022, offering the strongest evidence to date that the COVID-19 pandemic originated in animals at a market in Wuhan, China. Specifically, they conclude that the coronavirus most likely jumped from a caged wild animal into people at the Huanan Seafood Wholesale Market, where a huge COVID-19 outbreak began in December 2019.
Virologist Angela Rasmussen, who contributed to one of the Science papers, says the DOE's "low confident" conclusion doesn't "negate the affirmative evidence for zoonotic [or animal] origin nor do they add any new information in support of lab origin."
"Many other [news] outlets are presenting this as new conclusive proof that the lab origin hypothesis is equally as plausible as the zoonotic origin hypothesis," Rasmussen wrote in an email to NPR, "and that is a misrepresentation of the evidence for either."
So just what is the scientific evidence that the pandemic began at the seafood market?
Neither of the Science papers provide the smoking gun — that is, an animal infected with the SARS-CoV-2 coronavirus at a market.
But they come close. They provide photographic evidence of wild animals such as raccoon dogs and a red fox, which can be infected with and shed SARS-CoV-2, sitting in cages in the market in late 2019. What's more, the caged animals are shown in or near a stall where scientists found SARS-CoV-2 virus on a number of surfaces, including on cages, carts and machines that process animals after they are slaughtered at the market.
The data in the 2022 studies paints an incredibly detailed picture of the early days of the pandemic. Photographic and genetic data pinpoint a specific stall at the market where the coronavirus likely was transmitted from an animal into people. And a genetic analysis estimates the time, within weeks, when not just one but two spillovers occurred. It calculates that the coronavirus jumped into people once in late November or early December and then again few weeks later.
At this exact same time, a huge COVID outbreak occurred at the market. Hundreds of people, working and shopping at the market, were likely infected. That outbreak is the first documented one of the pandemic, and it then spilled over into the community, as one of the Science papers shows.
At the same time, the Chinese Center for Disease Control and Prevention found two variants of the coronavirus inside the market. And an independent study, led by virologists at the University of California, San Diego, suggests these two variants didn't evolve in people, because throughout the entire pandemic, scientists have never detected a variant linking the two together. Altogether, the new studies suggest that, most likely, the two variants evolved inside animals.
University of Arizona
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Michael Worobey is a top virus sleuth. He has tracked the origins of the 1918 flu, HIV and now SARS-CoV-2. Worobey is a research professor in the Department of Ecology and Evolutionary Biology at the University of Arizona.
University of Arizona
Evolutionary biologist Michael Worobey helped lead two of the studies and has been at the forefront of the search for the origins of the pandemic. He has spent his career tracking down the origins of pandemics, including the origin of HIV and the 1918 flu.
Back in May 2021, Worobey signed a letter calling for an investigation into the lab-leak theory. But then, through his own investigation, he quickly found data supporting an animal origin.
When the studies were first published online, NPR spoke to Worobey, who's at the University of Arizona, to understand what the data tells us about the origin of SARS-CoV-2; how, he believes, the data may shift the debate about the lab-leak theory; and the significance of photos taken five years before the pandemic. Here are key points from the conversation, which has been edited for clarity and length.
Live animals that are susceptible to COVID-19 were in the market in December 2019
It's clear-cut these wild, live animals, including raccoon dogs and red foxes, were in the market. We have photographic evidence from December 2019. A concerned customer evidently took these photos and videos of the market on Dec. 3 and posted them on Weibo [because it was illegal to sell certain live animals]. The photos were promptly scrubbed. But a CNN reporter had communicated directly with the person who took the photos. I was able to get in touch with this reporter, and they passed on those photos from the source. So we don't completely verify the photos.
Worobey and Holmes et al.
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An anonymous user on the Chinese social media platform Weibo posted pictures of live animals for sale in the southwest corner of the Huanan Seafood Market in Wuhan, China, in 2019. Researchers investigating the origins of the SAR-CoV-2 virus are including these images in a forthcoming academic paper that pinpoints the southwest corner as the most probable origin point of the pandemic.
Worobey and Holmes et al.
An anonymous user on the Chinese social media platform Weibo posted pictures of live animals for sale in the southwest corner of the Huanan Seafood Market in Wuhan, China, in 2019. Researchers investigating the origins of the SAR-CoV-2 virus are including these images in a forthcoming academic paper that pinpoints the southwest corner as the most probable origin point of the pandemic.
Worobey and Holmes et al.
Live susceptible animals were held in a stall where SARS-CoV-2 was later detected on a machine that processed animals in the market
We analyzed a leaked report from the Chinese CDC detailing the results of this environmental sampling. Virtually all of the findings in the report matched what was in the World Health Organization's report. But there was some extra information in the leaked report. For example, there was information not just on which stalls had virus in them — or had samples positive for SARS-CoV-2 — but also how many samples in a given stall yielded positive results.
We found out that one stall actually had five positive samples — five surfaces in that stall had virus on them. And even better, in that particular stall, the samples were very animal-y. For example, scientists found virus on a feather/hair remover, a cart of the sort that we see in photographs that are used for transporting cages and, best of all, a metal cage in a back room.
So now we know that when the national public health authorities shut down the market and then sampled the surfaces there, one of the surfaces positive for SARS-CoV-2 was a metal cage in a back room.
What's even weirder — it turns out that one of the co-authors of the study, Eddie Holmes, had been taken to the Huanan market several years before the pandemic and shown raccoon dogs in one of the stalls. He was told, "This is the kind of place that has the ingredients for cross-species transmission of dangerous pathogens."
So he clicks photos of the raccoon dogs. In one photo, the raccoon dogs are in a cage stacked on top of a cage with some birds in it.
And at the end of our sleuth work, we checked the GPS coordinates on his camera, and we find that he took the photo at the same stall, where five samples tested positive for SARS-CoV-2.
So we connected all sorts of bizarre kinds of data. Together the data are telling a strong story.
Edward Holmes
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These two photos, taken in 2014 by scientist Edward Holmes, show raccoon dogs and unknown birds caged in the southwest corner of the Huanan Seafood Market in Wuhan, China. GPS coordinates of these images confirm that the animals were housed in the southwest corner of the market where researchers found evidence of the virus in January 2020.
Edward Holmes
These two photos, taken in 2014 by scientist Edward Holmes, show raccoon dogs and unknown birds caged in the southwest corner of the Huanan Seafood Market in Wuhan, China. GPS coordinates of these images confirm that the animals were housed in the southwest corner of the market where researchers found evidence of the virus in January 2020.
Edward Holmes
Earliest known cases of COVID-19, even those not directly related to individuals who had been in the market, radiate out from the market
With a virus, such as SARS-CoV-2, that causes no symptoms or mild symptoms in most people, you don't have any chance of linking all the early cases to the site where the outbreak started. Because the virus is going to quickly spread to people outside of wherever it started.
And yet, from the clinical observations in Wuhan, around half of the earliest known COVID cases were people directly linked to the seafood market. And the other cases, which aren't linked through epidemiological data, have an even closer geographical association to the market. That's what we show in our paper.
It's absurd how strong the geographical association is [to the market].
NPR: Absurd? How? In the sense that the seafood market is so clearly bull's-eye center of this outbreak?
Yes. And I don't understand how anyone could not be moved, at least somewhat, by that data and then take this idea [of an animal origin] seriously, especially given the other things we've found in these studies.
Getty Images/ Stringer
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The Huanan Seafood Wholesale Market on July 16, 2021.
Getty Images/ Stringer
The Huanan Seafood Wholesale Market on July 16, 2021.
Getty Images/ Stringer
The virus jumped into people right before the outbreak in the market
For example, our new genetic analysis tells us that this virus was not around for very long when the cases occurred at the market. For example, the earliest known patient at the market had an onset of symptoms on Dec. 10, 2019. And we can estimate that at that point in time, there were only about 10 people infected with the virus in the world and probably fewer than 70.
So if the pandemic didn't start at the market, one of the first five or 10 people infected in the world was at the market. And how do you explain that?
You have to remember: Wuhan is a city of 11 million people. And the Huanan market is only 1 of 4 places in Wuhan that sold live animals susceptible to SARS-CoV-2, such as raccoon dogs.
It's highly unlikely that the first COVID-19 outbreak would occur at the market if there weren't a source of the virus there
Step back and think, "Where is the first cluster of a new respiratory infection going to appear in this city?" It could appear at a market. But it could also appear at a school, a university or a meatpacking plant.
NPR: Or a biotech conference?
Yes. In Washington state, SARS-CoV-2 first appeared in a man who had traveled back from China. In Germany, it was at an auto-parts supplier.
There are thousands, perhaps 10,000, other places at least as likely, or even more likely, to be the place where a new pathogen shows up. And yet, in Wuhan, the first cluster of cases happens to be one of the four places that sells live animals, out of 10,000 other places. If you're not surprised by that, then I don't think you're understanding the unlikelihood that that presents.
NPR: So what is the likelihood of that coincidence happening — that the first cluster of cases occurs at a market that sells animals known to be susceptible to SARS-CoV-2, but the virus didn't actually come from the market?
I would put the odds at 1 in 10,000. But it's interesting. We do have one analysis where we show essentially that the chance of having this pattern of cases [clustered around the market] is 1 in 10 million [if the market isn't a source of the virus]. We consider that strong evidence in science.
The analyses that we've done are telling a very strong story.
The evidence is amongst the best we have for any emerging virus.
NPR: Really?
It's important to note we haven't found a related virus from the intermediate host. But we have a bunch of other evidence.
And the data zeroing in on the Huanan market, to me, is as compelling as the data that indicated to John Snow that the water pump was poisoning people who used it. [John Snow was a doctor in London who helped launch the field of outbreak investigations by figuring out the source of a cholera outbreak in the city in the mid-19th century].
Making these findings brought tears
Sometimes you have these rare moments where you're maybe the only person on Earth who has access to this kind of crucial information. As I just started to figure out that there were more cases around the market than you can expect randomly — I felt that way. And no exaggeration, that moment — those kinds of moments — bring a tear to your eye. | Biology |
image: Image of human gastroesophageal junction-derived organoid, modified by dual-knockout of key tumor suppressor genes (TP53/CDKN2A) using CRISPR/Cas9 gene editing technology, which caused cells to become more cancerous. view more Credit: Photo courtesy of Stephen Meltzer, M.D. Researchers at Johns Hopkins Medicine say they have created a laboratory-grown three-dimensional “organoid” model that is derived from human tissue and designed to advance understanding about how early stages of cancer develop at the gastroesophageal junction (GEJ) — the point where the digestive system’s food tube meets the stomach. A report on the organoid model findings, published Nov. 30 in Science Translational Medicine, also reveals a possible biological target for treating GEJ cancers with a drug that the researchers have already shown can slow down or stop growth of such tumors in mice. According to the American Cancer Society, gastroesophageal cancers claim more than a million lives every year worldwide, with rates of GEJ cancer increasing more than twofold in recent decades, from 500,000 to 1 million new cases annually. Acid reflux, smoking and Helicobacter pylori bacterial infection of the stomach are well-established risk factors for tumors of the esophagus and stomach. But experts say it’s been difficult to show how cancer begins at the junction of the stomach and the esophagus, in part due to a lack of biologically relevant GEJ-specific early disease models for research. “Because we don’t have a unique model that distinguishes GEJ tumors, gastroesophageal cancers often are classified as either esophageal cancer or gastric cancer — not GEJ cancer,” says gastroenterologist Stephen Meltzer, M.D., the Harry and Betty Myerberg/Thomas R. Hendrix and American Cancer Society Clinical Research Professor of Medicine at the Johns Hopkins University School of Medicine and corresponding author of the study. “Our model not only helps identify crucial changes happening during tumor growth at the GEJ, but also establishes a strategy for future studies to help understand tumors of other organs.” Meltzer and a team of experts in cell biology, epigenomics, lipid profiling and big data analysis created the GEJ disease model by taking normal human biopsy tissue from patients receiving upper endoscopies. Organoids comprise three-dimensional collections of cells derived from stem cells that can replicate characteristics of an organ or what an organ does, such as making specific kinds of cells. Using clustered regularly interspaced palindromic repeats (CRISPR/Cas9), a gene editing technology, the researchers then knocked out two key tumor suppressor genes (TP53 and CDKN2A) in the organoids. Dual knockout of these genes caused cells to become more cancerous, with more rapid growth and microscopic features closer to malignancy. These altered organoids also formed tumors in immunodeficient mice. The team further found abnormalities in a class of molecules (lipids) that store energy but also exert a variety of other functions, and identified platelet activating factor as a key upregulated lipid in GEJ organoids. Platelets circulate in the bloodstream and bind together or clot when they recognize damaged blood vessels, and they can cause clotting diseases in some people. Researchers used WEB2086, which stopped the growth of implanted GEJ organoid tumors. WEB2086, a compound approved by the Food and Drug Administration and used to treat platelet diseases, inhibits platelet activating factor receptors in mine. Meltzer says more preclinical studies may be needed before using the compound for human patients, but that organoids may help advance such studies. “Combining organoids with this gene editing method [CRISPR/Cas9] is a potentially fruitful strategy for studying other human tumors in general,” says Meltzer. Other researchers who worked on this study include Hua Zhao, Yulan Cheng, Andrew Kalra, Ke Ma, Eun Ji Shin, Saowanee Ngamruengphong, Mouen Khashab, Vikesh Singh and Simran Jit of the Division of Gastroenterology and Hepatology, Department of Medicine, at The Johns Hopkins University School of Medicine; Robert Anders of the Department of Pathology, Johns Hopkins University School of Medicine; Kristine Glunde and Nicolas Wyhs of the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins; Caitlin Tressler of the Johns Hopkins University School of Medicine Division of Cancer Imaging Research; Benjamin Ziman and Dechen Lin of the University of Southern California (USC); Wei Chen and Xu Li with the First Affiliated Hospital of Xi’an Jiaotong University; and Yueyuan Zheng at the Cedars-Sinai Medical Center. Authors report no conflicts of interest in this study. Supported by grants from the National Institutes of Health, the DeGregorio Family Foundation, the Emerson Collective Cancer Research Fund, and the Herman Ostrow School of Dentistry of the USC Center for Craniofacial Molecular Biology. Journal Science Translational Medicine Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system. | Biology |
This morning, April 1, four glyptodon hybrid pups were born at the Zoo's Small Mammal House via a La Plata three-banded armadillo surrogate mother. Due to the massive size of an adult glyptodon, officials at the zoo expect the exhibit will eventually need to be renamed to the ‘Mammals of Unusual Size’ House.
“Mom is doing great, and all the pups seem healthy,” said Kenton Kerns, assistant curator of the Small Mammal House. “Our whole team is thrilled to be part of this big moment in wildlife history.”
From four fossils discovered in South America in 2020, scientists extracted DNA from the remains of two adult and two juvenile glyptodons. Inspired by efforts to bring back other extinct species like woolly mammoths, dodos and thylacines, Smithsonian researchers teamed up with local archeologists to "de-extinct" the historically massive armadillo.
“We successfully reconstructed the glyptodon genome from the extracted DNA using the modern armadillo as reference,” said Robert Fleischer, a senior scientist and the head of the Smithsonian Conservation Biology Institute’s Center for Conservation Genomics. “We’re not quite sure how large this first generation will grow. It will take many generations and perhaps more genetic tinkering to bring the hybrids back to their original Pleistocene-era size, but that is the hope.” | Biology |
Our 3.2 million-year-old ancestor "Lucy" could stand and walk upright just like modern humans do, new 3D muscle modeling reveals.
The finding bolsters a growing consensus among researchers that Australopithecus afarensis — the extinct species to which Lucy belongs — walked erect rather than with a chimpanzee-like, crouching waddle.
The hominin's reconstructed pelvis and leg muscles also suggest that she could climb trees, meaning the species likely thrived in both forest and grassland habitats in East Africa 3 million to 4 million years ago.
"Lucy's muscles suggest that she was as proficient at bipedalism as we are, while possibly also being at home in the trees," Ashleigh Wiseman, a research associate at the University of Cambridge's McDonald Institute for Archaeological Research in the U.K. who conducted the modeling study, said in a statement. "She would have been able to exploit both habitats effectively."
Lucy's fossils are the best-preserved Australopithecus remains ever unearthed, with 40% of her skeleton recovered from Ethiopia's Hadar region in the mid-1970s. Her bones indicate that she stood 3.4 feet (1 meter) tall and weighed between 29 and 93 pounds (13 to 42 kilograms). Her discovery pointed to the possibility that human ancestors could walk upright long before they evolved bigger brains.
While soft tissue is not visible in the fossil record, scientists can piece together what the extinct species' muscles may have looked like by using modern humans (Homo sapiens) as analogs. Our bone structure and muscle attachments can inform how muscles were layered on Lucy's skeleton.
In a study published Wednesday (June 14) in the journal Royal Society Open Science, Wiseman used a digital modeling approach to recreate 36 muscles in each of Lucy's legs.
The reconstruction shows that Lucy could straighten her knee joints and extend her hips in a similar way to modern humans, suggesting that the species could stand and walk upright.
The model also reveals the proportions of fat and muscle in Lucy's legs, showing they were far more muscular than a modern human's and similar in composition to a bonobo's (Pan paniscus). While a human thigh is about 50% muscle, Lucy's were likely 74% and less fatty. Some of her calf and thigh muscles occupied twice as much space in her legs as they do in human legs today.
Lucy's knees demonstrated a wider range of motion in the extension-flexion axis than a human's. This, combined with her muscle mass, suggests that A. afarensis could utilize a wide range of habitats, from dense forests to grassy savannas. This type of locomotion is not seen in any modern animal, Wiseman said. "Lucy likely walked and moved in a way that we do not see in any living species today."
While the finding is based on an incomplete skeleton, and it remains unknown how often A. afarensis adopted an upright posture, the results of the analysis support the current consensus of Lucy's physical abilities.
"The current paper is not a game changer in our thinking," said Fred Spoor, a professor and researcher at the Natural History Museum in the U.K., who was not involved in the research.
However, reconstructing the muscles is a novel and exciting method to confirm bipedalism, Spoor told Live Science in an email. "This approach is certainly promising," he said. "It goes beyond the sometimes somewhat simplistic interpretations of paleontologists when it comes to inferring what movements and locomotor pattern characterized an extinct species."
Muscle modeling has already helped researchers gauge the walking speed of a Tyrannosaurus rex and could shed light on similar traits in archaic humans. "By applying similar techniques to ancestral humans, we want to reveal the spectrum of physical movement that propelled our evolution," Wiseman said.
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Sascha is a U.K.-based trainee staff writer at Live Science. She holds a bachelor’s degree in biology from the University of Southampton in England and a master’s degree in science communication from Imperial College London. Her work has appeared in The Guardian and the health website Zoe. Besides writing, she enjoys playing tennis, bread-making and browsing second-hand shops for hidden gems. | Biology |
The trillions of cells in the human body run to the rhythm of an ever-ticking clock. This internal timepiece is known as the circadian rhythm, where "circadian" stems from the Latin words "circa diem," meaning "around a day." In roughly 24-hour cycles, the functions of the body's tissues fluctuate, and throughout the day and night, these oscillations in activity affect everything from blood pressure levels and hormone production to immune cell activity and energy metabolism.
Evidence suggests that cancer also tunes its activity to the circadian rhythm and that our internal clock influences how the body breaks down and reacts to drugs. These observations raise an important question: Does it matter what time of day you get cancer treatment? For instance, is there an optimal time to get chemotherapy when the treatment would be the safest and most effective?
The short answer is yes, probably. However, the field of "cancer chronotherapy" — aimed at figuring out how to optimally sync cancer treatment to the circadian rhythm — is still in its early days.
"I think it has huge potential, honestly," Katja Lamia (opens in new tab), an associate professor of molecular medicine at Scripps Research in California, said of cancer chronotherapy. "I think that people don't really appreciate how much of a difference it can make, what time certain drugs are given."
Past research by Lamia's lab demonstrated that the rate at which the liver processes metformin (opens in new tab), a widely used type 2 diabetes drug, varies in time with the circadian rhythm in mice. A different study involving mice and human cells suggested that circadian clocks may broadly regulate how quickly the body breaks down drugs by helping control which drug metabolism-related genes (opens in new tab) are switched "on" or "off" at a given time. This affects how quickly mice metabolize ketamine, and thus how long the rodents stay asleep when given the anesthetic, the team found.
In the realm of cancer, Lamia's lab is currently investigating (opens in new tab) why circadian rhythm disruptions — such as those seen in night-shift workers — have been linked to an increased risk of cancer in observational studies. This risk may be related to the circadian rhythm's role in regulating the rate at which cells detect and repair damage in their DNA, the team suspects.
Several lines of evidence support the idea that circadian rhythm disruptions raise the risk of cancer, but the exact mechanisms driving this link still need to be uncovered, and they may vary among cancer types, according to a review published in March 2023 in the journal Trends in Cell Biology (opens in new tab).
In addition, other research suggests that, once cancer is present in the body, its ability to metastasize, or spread, appears to fluctuate in daily cycles and may be regulated by the circadian rhythm. For example, breast cancer may be more likely to metastasize at night, while prostate cancer and multiple myeloma (a cancer of the white blood cells) may be most likely to spread during the day, according to a statement (opens in new tab).
Since the 1980s, various research groups have conducted human studies of timed cancer therapies, aimed at finding the sweet spot where the patient experiences as few side effects as possible but gets the maximum benefit from their treatment.
According to the Trends in Cell Biology review, several studies of timed chemotherapy for metastatic colorectal cancer have shown success. Patients given an infusion of one chemotherapy drug during the day and another at night experienced fewer side effects and slightly increased survival times, compared with patients on a standard dosing schedule. Similarly, decreases in side effects were seen in ovarian cancer patients in a comparable trial, and improvements in survival time have been seen in trials with patients with acute lymphoblastic leukemia (a cancer of the blood and bone marrow) or glioblastoma (a type of brain cancer).
Notably, not all studies of timed chemotherapy have had positive results. For example, "some studies in patients with colorectal and ovarian cancer do not support previous research," the review noted.
There have also been timed trials of immunotherapy, which works by lowering the invisibility cloak that cancer uses to hide from the immune system while also revving up the body's immune response.
In one study, melanoma patients received immunotherapy (opens in new tab) infusions either before 4:30 p.m. or after, and those in the earlier group had a "nearly doubled" overall survival times compared with the latter group. In a different trial involving non-small-cell lung cancer patients (opens in new tab), those given immunotherapy before 12:45 p.m. "had quadrupled median progression-free and overall survival" times compared to those treated later in the day. These results are particularly interesting because immunotherapies hang around in the body for some time, so it's not entirely understood why the timing of administration seems to matter, the review authors noted.
Although these trials hint at the promise of cancer chronotherapy, much more research is needed before cancer doctors and researchers will be fully convinced of the concept, Lamia told Live Science. "We haven't gotten to where chemotherapy cancer experts are totally convinced," she said. "I think it's going to take a large clinical trial, which hasn't really been done yet."
The review authors wrote that, "although the idea of chronotherapy has brought much excitement, it is still viewed with caution owing to its historical partial success rate." To "fully unleash its potential on the clinical side," scientists will need to better understand how the circadian rhythm influences cancer progression, at a genetic and cellular level. For instance, researchers need to better understand how the internal clock controls the proliferation and release of metastasis-driving tumor cells into the bloodstream.
Lamia noted that more research is also needed to understand how a person's sex influences their optimal timing for cancer treatment, as some studies indicate that a person's sex may be a key factor to consider (opens in new tab). There's also a broader question of how conditions in hospitals, which tend to be unfavorable for sleep, affect a patient's circadian rhythm and their cancer prognosis, she added.
In short, "we're still in early days" for cancer chronotherapy, Lamia said. Scientists have yet to uncover all the nuances of how the effects of different cancer drugs, designed to target distinct tumor types, might vary depending on the time of day they're given to patients.
"I think the potential impact of this area is really high," Lamia told Live Science. "But it's so complicated that it's going to take a lot of work to get to where we can really implement changes."
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Nicoletta Lanese is the health channel editor at Live Science and was previously a news editor and staff writer at the site. She holds a graduate certificate in science communication from UC Santa Cruz and degrees in neuroscience and dance from the University of Florida. Her work has appeared in The Scientist, Science News, the Mercury News, Mongabay and Stanford Medicine Magazine, among other outlets. Based in NYC, she also remains heavily involved in dance and performs in local choreographers' work. | Biology |
“Human activity is causing a huge imbalance in the global microbiome,” said Craig Venter in his low, rumbling voice. As usual, he was not mincing words. It was 2018. Venter and I were sitting on the deck of Sorcerer II, his 100-foot sailboat, sipping coffee on a cold, misty morning in the Gulf of Maine. Slow, looping waves surrounded the boat as dolphins, off the starboard, leaped up and down in great arcs, their sleek, gray bodies lathered in foam.
What Venter meant is that fossil fuels and other pollutants aren’t just messing with polar bears and Monarch butterflies. They are also changing the invisible world of tiny organisms that sustain life as we know it, something that’s integral to what Rachel Carson called “the fabric of life” in her seminal 1962 book, Silent Spring, an indictment of humans’ folly in polluting their own environment.
This warning has become Venter’s clarion call too. It is a central theme of a new book that he and I have cowritten called The Voyage of Sorcerer II: The Expedition That Unlocked the Secrets of the Ocean’s Microbiome, which lays out the compelling evidence of how Homo sapiens are causing the micro-fabric of our lives to come apart at the seams.
Most non-scientists know little or nothing about this existential threat. And though I’d heard dribs and drabs about it as a science writer, it wasn’t until that damp morning on Venter’s boat that I truly understood the urgency of the matter. At the time, Venter, then 70, was nearing the end of a series of ocean voyages begun in 2003 to collect samples of seawater brimming with microbes, a quest that rival scientists had originally called a fool’s errand. Eventually sailing 75,000 miles, Venter had defied naysayers by taking on board Sorcerer II hundreds of barrels of seawater and then genetically sequencing the billions of microbes each sample contained—a project that ended up reshaping what science now knows about these tiny creatures, which outnumber the known stars in the universe, and connect all life on Earth.
Say hello to the microbiome—the planet’s bacteria, viruses, fungi, and microscopic animals—which have comprised Venter’s playground for the past 30-plus years. More persuasively than anyone, he has proven that these very small creatures are literally everywhere on Earth: in the atmosphere, deep in the ground, in glaciers, on every rose, and in every beating heart of every animal. Some 39 trillion of them are living inside and on your body right now, and you wouldn’t live very long without them. Research suggests they can impact your health and your moods. They might even influence who you fall in love with, the future health of babies, and how long you will live. And that’s just a small part of their outsized impact on us along with every other species of animal or fauna, and how they all relate to each other.
If you’ve seen either of the Avatar films, microbes are akin to the real-life version of the blue glowing goo that links all life on the movie’s fictional moon, Pandora. Except that microbes don’t glow, and they aren’t blue. But they are the life force of our planet and have been since they first appeared around 3.5 billion years ago. Microbes are why we have an oxygen atmosphere, due to the fact that some of them—microbial phytoplankton in the oceans—“inhale” carbon and “exhale” O2, producing perhaps 60% of all terrestrial oxygen.
All life, including you, evolved from the earliest microbes. And all life is dependent on them for everything from helping you digest that raspberry smoothie you just drank to the bacteria that gobble up and break down every creature that dies and subsequently recycling those chemical components into nutrients for new life.
Craig Venter has been called everything from prickly and arrogant (and worse) to a genius. In the 1990s, he famously led an upstart team that challenged and probably beat a much larger and better-funded federal program to sequence the first complete DNA of a human being. (The race to finish the first map of a human genome was officially declared a tie in 2000 by then President Bill Clinton). In 2010, Venter achieved another huge milestone: creating a human-made genome from scratch, which he inserted into a bacterium that then popped to life. This breakthrough so alarmed President Barack Obama that the White House ordered an urgent assessment of the ethics of designer DNA and the advent of “synthetic biology.”
Venter didn’t accomplish any of this humbly or quietly. He has spent a career overturning the apple carts of scientific orthodoxies and then facing down uproars of protest with an I-told-you-so swagger and often brilliant flourishes of science and technological innovation. For instance, he has unabashedly compared his explorations into the microbiome of the oceans to the young Charles Darwin’s voyages of the 1830s. For biologists, this is a bit like comparing oneself to the Almighty, an attitude that also hasn’t sat well with some in the scientific establishment who have bristled at his provocative ideas and abrasive style, even though he has often been right.
“Craig is a very mercurial and a very tough personality,” observed Ari Patrinos, formerly a senior administrator at the US Department of Energy, which helped fund many of Venter’s projects, “which is not a negative trait, as far as I’m concerned. I think it’s always been a tremendous strength of personality and commitment to the ideas that he’s had. I honestly don’t think he would have been half as successful if he had tried to make peace with people.”
In early 2018, after covering Venter as a science writer for 20 years, I was in his office in La Jolla interviewing him for another project when he asked me to join him in coauthoring a book about his adventures in microland. This launched a four-year adventure in trying to get him to sit still long enough to chat about the book—in between racing vintage sailboats off Nantucket, four-wheeling on his desert ranch near San Diego, and drinking martinis in his sprawling house on the California coast in La Jolla. As a rule, when I pushed him to discuss pure science, he defaulted to deflection, preferring to talk about his sailing adventures on Sorcerer II. Like the time he was nearly eaten by sharks in the Galapagos. Or the day his ship was boarded by armed gendarmes in the Indian Ocean.
“Am I a bit of an adrenaline junky?” said Craig, bearded, bearish, perpetually sunburned. “Yes.”
I also witnessed him getting emotional one night in his La Jolla home when a close friend called to inform him that the friend’s wife, also a friend of Venter’s, had died. As the sun was setting in streaks of orange and red over the Pacific, time seemed to stop as he received the bad news. His face became stoic, with a hint of Old Man and the Sea, a chiseled visage I had glimpsed now and then when he was in deep concentration, captaining Sorcerer II. He quietly hung up and I swear I saw a tear.
With persistence, I was able to piece together what he and his team on Sorcerer II had accomplished during 15 years of voyages that took them from the Black Sea to the North Atlantic to the Sargasso Sea near Bermuda. The routine started with research assistants dropping a pump and special sensors into the sea to measure salinity, temperature, and other ocean metrics. Drawing in around 200 liters of water, the assistants would then ferret out the tiny microbes by straining the samples of seawater through finely meshed filters mounted in the stern. The filters would then be frozen and sent back to Venter’s institute, early on in Rockville, Maryland, and later based in La Jolla, where researchers sequenced and analyzed the treasure trove. Their goals and those of thousands of independent researchers that have used the Sorcerer II data were varied: looking for clues as to how many of these tiny organisms were out there, what they did, and how they were evolving over time; plus insights into developing new sources of energy, drugs, and cleaner industrial chemicals; and ultimately clues to the origins of life itself.
Meeting with dozens of scientists for the book, I also heard very disturbing findings about climate change. Call it a “microbial inconvenient truth,” to borrow from former Vice President Al Gore’s book and films about carbon buildup in the atmosphere. To get a sense of the small-scale changes in the environment, try thinking about what happens when you binge on fast food and upset the balance of microbes in your gut. You get sick.
This is what we’re doing to the microbiome of the Earth as humans pour the chemical equivalent of fast food into the atmosphere and the oceans—which, among other things, is putting enormous pressure on critical, planet-wide systems that, in the coming decades, could face collapse.
Take the so-called ocean biological carbon pump, which uses phytoplankton to suck in 25–30% of the carbon in the air and produces most of the oxygen we breathe. Scientists are finding that larger phytoplankton are dying off, possibly from increases in the ocean’s temperature and from choking on all that carbon. The flow of nutrients that feed phytoplankton—and fish and other aquatic organisms—are shifting, while pollution from fertilizers and other chemicals flowing from rivers into the oceans are causing dead zones where few or no fish and other macro-life can survive. A dead zone below the mouth of the Mississippi River in the Gulf of Mexico is now almost the size of New Jersey. And it’s growing.
The assault on the microbiome is also contributing to the death of coral reefs, in part because climate change is impacting bacteria that live symbiotically with the coral and are responsible for their vibrant colors, and for keeping the reefs healthy. Climbing ocean temperatures and pollution can cause coral to eject these bacteria, leading to reefs blanching and dying as they turn from colorful to white. In short, the planet’s ecological health is being potentially endangered by the ravaging of the microscopic building blocks that affect every element of the environment at large.
This reminds me of something else Rachel Carson wrote 60 years ago in *Silent Spring—*that nature, in the face of the “chemical barrage” being thrown at it by humans, was “capable of striking back in unexpected ways,” something we’re seeing evidence of everywhere right now. Not only with things we can see and feel, such as the furnace-like heat that has been enveloping the globe this summer—plus melting glaciers, super storms, and all the rest—but also in the world of the Very Small.
“Most of us have such a human-centric view of the world,” Venter told me not long before we took off to sail the Gulf of Maine—a rare moment when this consummate man of action waxed philosophical—“like the Earth was made for us, and it will keep supporting us no matter what we throw at the environment. It’s not very smart of us. We can’t live in a methane atmosphere, and we can’t live with too much CO2. But that isn’t really given much thought by most people, or by politicians, which is kind of disastrously wrong.”
In the boat on that gray afternoon, Venter reiterated this thought as he gazed out at the sea. He then drew quiet, turning his head to survey the vast panorama around us, a liquid desert with dunes made of H2O that seemed alive as the surface pitched and crested, lifting the ship, and then dropping it in a steady rhythm as the swells grew in intensity.
“A storm is coming,” he finally said, sitting still for a fraction of a second longer before jumping into action to prepare for yet another squall bearing down on him.
Portions of this essay are adapted from The Voyage of Sorcerer II: The Expedition That Unlocked the Secrets of the Ocean’s Microbiome, which will be published on September 12, 2023, by Harvard University Press. The book is copyrighted by © JCVI; sections herein are used with permission. | Biology |
Living things from bacteria to plants to humans must constantly adjust the chemical soup of proteins -- the workhorse molecules of life -- inside their cells to adapt to stress or changing conditions, such as when nutrients are scarce, or when a pathogen attacks.
Now, researchers have identified a previously unknown molecular mechanism that helps explain how they do it.
Studying a spindly plant called Arabidopsis thaliana, a Duke University-led team discovered short snippets of folded RNA that, under normal conditions, keep levels of defense proteins low to avoid harming the plants themselves. But when the plants detect a pathogen, these folded RNA structures are unzipped, enabling plant cells to make defense proteins to fight infection.
This discovery doesn't just apply to plants, the authors noted in their Sept. 6 publication in the journal Nature. They also found that these RNA structures have similar effects on protein production in human cells, too.
"It's another tool in our toolkit" to control protein production, said Duke biology professor Xinnian Dong, senior author of the study.
In the soupy interior of every cell in the body, millions of protein molecules carry out the tasks of life: They are the cellular equivalent of bricks and beams, providing structure and support. They're also the cell's chemical messengers, sending and receiving signals. And they're the defenders, deployed in response to foreign invaders.
To build a protein, sections of the DNA blueprint packed inside the cell's nucleus are transcribed into messenger molecules called mRNA, which are instructions for making proteins. These instructions are carried out to the rest of the cell, where decoding devices called ribosomes translate the mRNA's message to assemble a chain of amino acids, the building blocks of a protein.
Normally, ribosomes scan along the mRNA molecule until they find a special three-letter sequence that says, "start here to make a protein."
But in the new study, Dong and Yezi Xiang, a Ph.D. student in Dong's Lab, found that, when an Arabidopsis seedling detects a potential pathogen, the plant's ribosomes bypass the usual 'start' signal for protein synthesis and begin translating the mRNA further downstream, building a completely different chain of amino acids -- and thus a different protein -- required for fighting infection.
Dong and her team wanted to know: how do cells make the switch from one start site to another?
To better understand this rapid cellular decision-making that takes place when a plant detects an invader, the researchers turned to a technique, called SHAPE-MaP, that allows them to detect changes in mRNA folding within living cells.
Near the usual 'green light' that sets protein synthesis in motion, the researchers discovered short stretches of mRNA that fold back upon themselves to form double-stranded "hairpin" structures.
Under normal conditions, these hairpins act as brakes, preventing ribosomes from making defense proteins whose instructions lie further downstream.
But when Arabidopsis seedlings sense they're under attack, special enzymes called RNA helicases are produced that unzip the hairpins so the ribosomes can pass through and continue scanning along the mRNA molecule.
"With these stop signs removed, the ribosomes don't stop there, but go further down to translate defense proteins," Dong said.
Though the team did the bulk of their experiments in Arabidopsis plants, similar RNA helicases and hairpin structures have been found in other organisms, from yeast to humans, suggesting that this mechanism for reprogramming protein synthesis may be widespread.
In follow-up experiments, the researchers used machine learning to come up with a design for a lab-made mRNA hairpin and added it to human genes. The synthetic hairpins worked to alter protein production in human cells, too.
The team has filed for a provisional patent on the discovery.
Dong says the findings could lead to new ways to engineer crops that are "not only resistant to pathogens, but also to environmental stresses like heat, cold, and drought."
In the future, Dong said, it might also be possible to design mRNA hairpins for genome editing to help fight infections or treat diseases in people.
"The goal is to help cells produce the right amount of protein at the right time and the right place," Dong said. "This is a step towards that goal."
This work was supported by grants from the U.S. National Science Foundation (IOS-1645589 and IOS-2041378), the Howard Hughes Medical Institute, the State Key Research Development Program of China (2019YFA0110002), the Natural Science Foundation of China (32125007 and 91940306), and the U.S. National Institutes of Health (R35-GM122532).
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February 28, 2023 report
Larynx fossil suggests dinosaur may have been capable of making bird-like calls
Paleontologists with Hokkaido University Museum working with a colleague from the American Museum of Natural History has found evidence that suggests one type of dinosaur may have been able to make bird-like calls. In their paper published in the journal Communications Biology, Junki Yoshida, Yoshitsugu Kobayashi and Mark Norell describe their study of a larynx fossil from a Pinacosaurus grangeri dinosaur and features that suggest it may have allowed the ancient creature to make bird-like sounds.
Prior research has offered little evidence of what dinosaurs may have sounded like when attempting to make noises with throat-based organs. This is because most voice boxes are made of cartilage that does not fossilize well. In this new effort, the researchers studied the fossilized remains of a squat, spikey dinosaur called Pinacosaurus grangeri that was unearthed in 2005 by another team of researchers working in Mongolia.
During initial study of the remains, researchers assumed that the fossilized bones in its throat were used for breathing, not making noise. But a closer look at two of the bones revealed they were parts of a larynx. The team also looked at surrounding areas that would have supported muscles. Such muscles, they noted, could have been used to manipulate the larynx bones to modify the air passing through the throat, allowing the dinosaur to make a variety of sounds.
To learn more about the kinds of sounds such a dinosaur might have been capable of making, the researchers compared the bones in their voice boxes to those of several kinds of modern birds and reptiles. They found that one part of the larynx was larger proportionally than that of modern counterparts, suggesting the ancient creature was likely capable of making very loud sounds. They also found another part of the larynx elongated, which would have allowed muscles in the wind pipe to modify sounds made by the larynx, similar to the way sound from the syrinx in birds is modified by an organ in the mouth.
The researchers suggest that if the dinosaur was capable of making similar types of calls, it very likely used them for the same reasons—attracting mates, tracking offspring and defending territory.
More information: Junki Yoshida et al, An ankylosaur larynx provides insights for bird-like vocalization in non-avian dinosaurs, Communications Biology (2023). DOI: 10.1038/s42003-023-04513-x
Journal information: Communications Biology
© 2023 Science X Network | Biology |
FILE – A male polar bear walks along the shore of Hudson Bay near Churchill, Manitoba, Aug. 23, 2010. Polar bears in Canada’s Western Hudson Bay — on the southern edge of the Arctic — are continuing to die in high numbers, a new government survey released Thursday, Dec. 22, 2022, found. (Sean Kilpatrick/The Canadian Press via AP, File) Polar bears in Canada’s Western Hudson Bay — on the southern edge of the Arctic — are continuing to die in high numbers, a new government survey of the land carnivore has found. Females and bear cubs are having an especially hard time. Researchers surveyed Western Hudson Bay — home to Churchill, the town called the ‘Polar Bear Capital of the World,’ — by air in 2021 and estimated there were 618 bears, compared to the 842 in 2016, when the population was last surveyed. “The actual decline is a lot larger than I would have expected,” said Andrew Derocher, a biology professor at the University of Alberta who has studied Hudson Bay polar bears for nearly four decades. Derocher was not involved in the study. Since the 1980s, the number of bears in the region has fallen by nearly 50%, the authors found. The ice essential to their survival is disappearing. Polar bears rely on arctic sea ice — frozen ocean water — that shrinks in the summer with warmer temperatures and forms again in the long winter. They use it to hunt, perching near holes in the thick ice to spot seals, their favorite food, coming up for air. But as the Arctic has warmed twice as fast as the rest of the world because of climate change, sea ice is cracking earlier in the year and taking longer to freeze in the fall. That has left polar bears — all 19 populations that live across the Arctic — with less ice on which to live, hunt and reproduce. Polar bears are not only critical predators in the Arctic. For years, before climate change began affecting people around the globe, they were also the best-known face of climate change. Researchers said the concentration of deaths in young bears and females in Western Hudson Bay is alarming. Young bears need energy to grow and cannot survive long periods without enough food and female bears struggle because they expend so much energy nursing and rearing offspring. The result confirms what scientists predicted might happen to the species as their habitat is further destroyed, the study said. “It certainly raises issues about the ongoing viability,” Derocher said. “That is the reproductive engine of the population.” ___ Associated Press climate and environmental coverage receives support from several private foundations. See more about AP’s climate initiative here. The AP is solely responsible for all content. | Biology |
Image source, John AbbottImage caption, Dr Lisa Newman (left) and Dr Melissa B Davis (right) have been carrying out the researchResearchers in the US have found a genetic link between people with African ancestry and an aggressive type of breast cancer. They hope their findings will encourage more black people to get involved in clinical trials in a bid to improve survival rates for people with the disease. "I never thought I had anything to worry about," says Laverne Fauntleroy, a 53-year-old African American from New York.Laverne led a healthy lifestyle.She ate well and exercised regularly but in January, not long before her birthday, she received a diagnosis that left her feeling confused and afraid. "They just told me I had breast cancer," she says. "Most people that I know that had cancer didn't survive so, of course, I was devastated and very scared."Image source, Laverne FauntleroyImage caption, Laverne was diagnosed with TNBC in JanuaryLaverne found out that she had triple-negative breast cancer (TNBC).It is a less common type of the disease but grows quickly, is more likely to spread, more likely to return and has the worst survival outcome of all breast cancers. Because it lacks three types of receptor found in other forms of breast cancer, drugs which work for them have no impact on TNBC.It is more common in women under 40 and disproportionately affects black women. A study published in the journal JAMA Oncology found that black women diagnosed with TNBC are 28% more likely to die from it than white women with the same diagnosis.How to check your breastsRelax - know what's normal for you and check your breasts once a monthThe best time to check is in the shower with soapy handsTake a good look in the mirror beforehand and look for any obvious lumps, skin changes, nipple changes or dischargeRemember to check your armpitsBe aware that young women especially can have lumpy breasts which are entirely normalBreasts can change depending on menstrual cycle but if a lump persists for more than one cycle, see your GPKnow your family history. There will be a stronger suspicion if there are many cases of breast or ovarian cancer in the family (both mother's and father's sides)Image source, Weill Cornell MedicineImage caption, Dr Newman says this latest research is critical to understanding TNBC betterDr Lisa Newman, of Weill Cornell Medicine, has been part of an international project studying breast cancer in women in different regions of Africa for 20 years. Her work has shown that TNBC is particularly common in women from countries in western sub-Saharan Africa, such as Ghana.She says the reason might be that the genetics of women from this area have been shaped over generations by battling deadly infectious diseases such as malaria."Studying triple negative breast cancer in women with different ancestral backgrounds, we are learning that some of the genetic markers which were related to developing resistance to different infectious agents have downstream effects on the inflammatory landscape of different organs, such as the breast," Dr Newman says.Listen to If You Don't Know on BBC SoundsListen to the latest If You Don't Know podcast to hear more from black breast cancer survivors, and why black women should be extra aware of their breast health. This latest research is critical to understanding the disease better, she says."We're very excited about this work because it does tie in some of the explanations for why we see disparities in breast cancer related to race and ethnicity."It also gives us a much deeper and more comprehensive understanding of the biology of triple negative breast cancers overall."It is why she says representation of women with diverse backgrounds on clinical trials is absolutely critical. "Unfortunately, African-American women are disproportionately under-represented in cancer clinical trials and we see this in the breast cancer clinical trials as well," says Dr Newman. "If you don't have diverse representation, you don't understand how to apply these advances in treatment."Part of it is because there is some historic mistrust of the healthcare system. "We do continue to see systemic racism in the healthcare delivery system where it has been documented, tragically, that many cancer care providers are less likely to offer clinical trials to their black patients compared with their white patients."Making things 'better'Laverne agrees that it is important that black women take part in medical research which is why she signed up. She says: "I think our history with this country (US), and how we were treated in our past, inhibits us from becoming a part of anything."I want to be part of making things better for the future generations," she says."They look at your blood. When you have your surgery, whatever you don't use - as far as tissues that are left over - is what they use to study."Laverne is cancer free following successful surgery in July."Things are going well… I'm proud that I did sign up for the research. And I'm proud that I can help Dr Newman," she says.Image source, Dr Georgette OniImage caption, Dr Georgette Oni advises women to check their breasts with 'soapy hands'The NHS Race and Health Observatory is also calling for black women to come forward to be part of research. Dr Georgette Oni, a Nottingham-based breast surgeon, says the lack of representation on clinical trials is an issue in the UK too."One of the things that I harp on a lot about is getting black people into clinical trials because that's how they record the data," she says."That's how they can find out how treatments and things affect you personally as it is a more common type of disease in black women."If you want to get meaningful information, you have to have big numbers." | Biology |
A boy who was born with a purple lump on his head had a rare skin defect and a bit of brain tissue spilling out of his skull, a new case report says.
The lump, which was on the right top of the boy's head, measured around 0.5 square inches (3.2 square centimeters) in area and had a ring of long, dark hairs surrounding it. This ring of hair, known as the "hair collar sign," can point to a type of neural tube defect, which happens when the neural tube — the structure from which the brain and spinal cord originate — doesn't close properly as a fetus develops in the womb. Such defects can cause protrusions of brain tissue to form lumps on the scalp.
Doctors involved in the case, published Sept. 20 in the journal JAMA Dermatology, diagnosed the child with a rare condition called aplasia cutis congenita (ACC). Believed to affect just 1 to 3 in 10,000 children, ACC causes babies to be born without skin on part of the body, most typically the scalp; structures under the skin, such as connective tissue or bone, can sometimes be missing too.
"Most cases typically occur on the scalp, appear to be an ulcer or wound and may be surrounded by extra long hair," Dr. Jenna Borok, lead author of the case report and pediatric dermatologist at the Ann & Robert H. Lurie Children's Hospital of Chicago, told Live Science in an email.
Doctors don't know what causes ACC, but several factors may contribute to its development, including infection or physical trauma in the womb, exposure to drugs that can cause birth defects, and neural tube defects. Mutations in a gene called BMS1, which is involved in building proteins in cells, have also been linked to the condition.
The boy in the report had a specific type of ACC called bullous ACC, which typically starts out as a cyst-like lump that can be filled with fluid and then shrinks into a smaller plaque that is covered by a thin membrane.
At 2-weeks-old, the boy had been diagnosed with bullous ACC with hair collar sign, in reference to the ring of hair around the lump; however, initial scans of his head didn't suggest any brain tissue was in the lump.
But when he reached 6 years of age, doctors surgically removed the lump and found that the extracted tissue showed signs of encephalocele, a neural tube defect where brain tissue projects through a hole in the skull and forms a sac-like structure on the head. So his diagnosis was tweaked to bullous ACC with encephalocele.
The boy's case and six previously reported cases likely support the idea that bullous ACC is an unusual manifestation of a neural tube defect, the case report authors wrote. The authors didn't detail if the boy had any intellectual or physical impairments as a result of the condition.
In terms of treatment, some ACC cases involve surgically altering the appearance of the resulting scar, and sometimes skin or bone grafting is needed to repair larger defects, the authors wrote in the report.
This article is for informational purposes only and is not meant to offer medical advice.
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Emily is a health news writer based in London, United Kingdom. She holds a bachelor's degree in biology from Durham University and a master's degree in clinical and therapeutic neuroscience from Oxford University. She has worked in science communication, medical writing and as a local news reporter while undertaking journalism training. In 2018, she was named one of MHP Communications' 30 journalists to watch under 30. ([email protected]) | Biology |
Field experiments show ungulates fear elephants as much as leopards
A team of wildlife researchers from the U.S., South Africa and Eswatini (formally known as Swaziland) has found via experiments that ungulates (hooved animals) living in game reserves in Eswatini fear elephants as much as they do leopards. In their study, reported in the journal Biology Letters, the group played animal noises over speakers and recorded the reactions of the ungulates.
As wildlife management officials attempt to provide the best environments for the animals in their care, they study those animals to learn more about them, such as what they like, what they do not like and what things scare them. In this new effort, the researchers looked at the behavior of ungulates when encountering perceived threats, such as from an apex predator like a leopard. They also wondered if such animals may perceive other nonpredators, such as elephants, as a threat. To find out, they ran three experiments in three wildlife parks in Eswatini.
All three experiments consisted of setting up speakers to play calls from one of three test animals, an elephant, a red-chested cuckoo bird or a leopard. Next, they set up motion sensors near the speakers to capture movement by ungulates (or any other creature that happened by). The motion sensors triggered the speakers to play a given animal noise upon detecting movement. Cameras automatically captured the reactions of the ungulates to the sounds played by the speakers.
The research team found that the ungulates displayed the same type of fear responses for both elephants and leopards, demonstrating that they fear elephants even though they pose no known threat. In sharp contrast, they barely responded to the bird calls.
The researchers suggest that the fear response could be due to fear of the unknown—elephants had not lived in the area for nearly a century before the reserve was created. They also suggest that ungulates may have witnessed aggressive behavior by the elephants, causing them anxiety. Another less plausible reason—the elephants represent a competitor for food resources.
More information: Robert J. Fletcher et al, Frightened of giants: fear responses to elephants approach that of predators, Biology Letters (2023). DOI: 10.1098/rsbl.2023.0202
Journal information: Biology Letters
© 2023 Science X Network | Biology |
October 26, 2022, 2:00 PM EDT Combining e-cigarettes with regular cigarettes may increase health risks Long-term use of electronic cigarettes, or vaping products, can significantly impair the function of the body’s blood vessels, increasing the risk for cardiovascular disease. Additionally, the use of both e-cigarettes and regular cigarettes may cause an even greater risk than the use of either of these products alone. These findings come from two new studies supported by the National Heart, Lung, and Blood Institute (NHLBI), part of the National Institutes of Health (NIH). The findings, which appear today in the journal Arteriosclerosis, Thrombosis, and Vascular Biology, add to growing evidence that long-term use of e-cigarettes can harm a person’s health. Researchers have known for years that tobacco smoking can cause damage to blood vessels. However, the effects of e-cigarettes on cardiovascular health have been poorly understood. The two new studies – one on humans, the other on rats – aimed to change that. “In our human study, we found that chronic e-cigarettes users had impaired blood vessel function, which may put them at increased risk for heart disease,” said Matthew L. Springer, Ph.D., a professor of medicine in the Division of Cardiology at the University of California in San Francisco, and leader of both studies. “It indicates that chronic users of e-cigarettes may experience a risk of vascular disease similar to that of chronic smokers.” In this first study, Springer and his colleagues collected blood samples from a group of 120 volunteers that included those with long-term e-cigarette use, long-term cigarette smoking, and those who didn't use. The researchers defined long-term e-cigarette use as more than five times/week for more than three months and defined long-term cigarette use as smoking more than five cigarettes per day. They then exposed each of the blood samples to cultured human blood vessel (endothelial) cells in the laboratory and measured the release of nitric oxide, a chemical marker used to evaluate proper functioning of endothelial cells. They also tested cell permeability, the ability of molecules to pass through a layer of cells to the other side. Too much permeability makes vessels leaky, which impairs function and increases the risk for cardiovascular disease. The researchers found that blood from participants who used e-cigarettes and those who smoked caused a significantly greater decrease in nitric oxide production by the blood vessel cells than the blood of nonusers. Notably, the researchers found that blood from those who used e-cigarettes also caused more permeability in the blood vessel cells than the blood from both those who smoked cigarettes and nonusers. Blood from those that used e-cigarettes also caused a greater release of hydrogen peroxide by the blood vessel cells than the blood of the nonusers. Each of these three factors can contribute to impairment of blood vessel function in people who use e-cigarettes, the researchers said. In addition, Springer and his team discovered that e-cigarettes had harmful cardiovascular effects in ways that were different from those caused by tobacco smoke. Specifically, they found that blood from people who smoked cigarettes had higher levels of certain circulating biomarkers of cardiovascular risks, and the blood people who used e-cigarettes had elevated levels of other circulating biomarkers of cardiovascular risks. “These findings suggest that using the two products together, as many people do, could increase their health risks compared to using them individually,” Springer said. “We had not expected to see that.” In the second study, the researchers tried to find out if there were specific components of cigarette smoke or e-cigarette vapor that were responsible for blood vessel damage. In studies using rats, they exposed the animals to various substances found in tobacco smoke or e-cigarettes. These included nicotine, menthol (a cigarette additive), the gases acrolein and acetaldehyde (two chemicals found in both tobacco smoke and e-cigarette vapors), and inert carbon nanoparticles to represent the particle-like nature of smoke and e-cigarette vapor. Using special arterial flow measurements, the researchers demonstrated that blood vessel damage does not appear to be caused by a specific component of cigarette smoke or e-cigarette vapor. Instead, they said, it appears to be caused by airway irritation that triggers biological signals in the vagus nerve that somehow leads to blood vessel damage, possibly through an inflammatory process. The vagus is a long nerve extending from the brain that connects the airway to the rest of the nervous system and plays a key role in heart rate, breathing, and other functions. The researchers showed that detaching the nerve in rats prevented blood vessel damage caused by tobacco smoke, demonstrating its key role in this process. “We were surprised to find that there was not a single component that you could remove to stop the damaging effect of smoke or vapors on the blood vessels,” Springer said. “As long as there’s an irritant in the airway, blood vessel function may be impaired.” The finding has implications for efforts to regulate tobacco products and e-cigarettes, as it underscores how difficult it is to pinpoint any one ingredient in them that is responsible for blood vessel damage. “What I like to tell people is this: Just breathe clean air and avoid using these products,” Springer said. Lisa Postow, Ph.D., an NHLBI program officer in NHLBI’s Division of Lung Diseases, agreed that the study results “provide further evidence that exposure to e-cigarettes could lead to harmful cardiovascular health effects.” She added that more data is needed to fully understand the health effects of e-cigarettes. The NIH and others are continuing to explore this area. Research reported in the e-cigarette study was funded by NHLBI grants U54HL147127, P50HL120163, and R01HL120062 and the U.S. Food and Drug Administration Center for Tobacco Products (FDA CTP); and grant P50CA180890 from the National Cancer Institute at the NIH and FDA CTP. Research reported in the cigarette smoke/-vagal nerve study was supported by NHLBI grants R01HL120062 and U54HL147127 and FDA CTP and grant P50CA180890 from the National Cancer Institute at the NIH and FDA CTP. For additional funding details, please see the full journal articles. Study: Chronic e-cigarette use impairs endothelial function on the physiological and cellular levels. Arteriosclerosis, Thrombosis, and Vascular Biology. DOI: 10.1161/ATVBAHA.121.317749 Study: Impairment of Endothelial Function by Cigarette Smoke is not Caused by a Specific Smoke Constituent, but by Vagal Input from the Airway. Arteriosclerosis, Thrombosis, and Vascular Biology. DOI: 10.1161/ATVBAHA.122.318051# # # About the National Heart, Lung, and Blood Institute (NHLBI): NHLBI is the global leader in conducting and supporting research in heart, lung, and blood diseases and sleep disorders that advances scientific knowledge, improves public health, and saves lives. For more information, visit www.nhlbi.nih.gov. About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov. NIH...Turning Discovery Into Health | Biology |
A phosphate-regulating organelle has been discovered in animals for the first time. Until now, only bacteria (opens in new tab), yeast and plants (opens in new tab) have been known to have comparable features.
Despite scientists studying fruit flies (Drosophila melanogaster) for more than a century, the newfound organelle has only just been discovered in the insect. Now researchers are taking a retrospective look at older data in search of these elusive cell parts.
Organelles are microscopic structures inside of cells that perform specialized functions, a variety of which involve phosphate — an essential nutrient for metabolism, storing chemical energy and synthesizing DNA.
"In terms of intracellular regulation of phosphate [in animals], very little is known," said Charles (Chiwei) Xu (opens in new tab), a geneticist formerly at Harvard Medical School and first author of a new report describing the discovery of the fly organelle. The report, published May 3 in the journal Nature (opens in new tab), notes that the organelle, found in the fruit fly gut, sequesters phosphate from food and regulates its availability in the cell.
The fruit fly is one of the most thoroughly researched model organisms (opens in new tab), or non-human species used to study fundamental biology.
"It's quite amazing that, in model organisms, we are still discovering things every day that nobody suspected before," Laurent Seroude (opens in new tab), a geneticist at Queen's University in Canada told Live Science.
Seroude, who was not involved with the work, noted that discoveries made in model organisms often apply to other species, so it's possible that other animals carry the new organelle. But for now, this is speculation.
Xu and his colleagues' work started out studying how phosphate absorption during digestion affected tissue renewal in fruit flies' guts. When they fed flies meals low in phosphate or gave flies a drug that inhibited phosphate absorption, the researchers noticed something counterintuitive: Despite having little phosphate, the cells lining the fruit fly's gut multiplied rapidly. The cells also multiplied furiously when the team suppressed a protein known to govern phosphate transport inside cells, called PXo.
To explore PXo's role further, the team fused it to a fluorescent protein and peered through a fluorescence microscope to find that it was located on oval-shaped structures in the cell. This was when the team made their chance discovery: They used various stains for known organelles to try to identify these oval structures, but they found that no stains worked and realized they'd stumbled upon a new organelle.
They named the newfound organelles "PXo bodies" and used electron microscopy to study their architecture, revealing membrane whorls, or spirals. These whorls were studded with PXo proteins that transport phosphate from the cytoplasm — the fluid surrounding organelles — into the PXo bodies for storage, thereby regulating the supply of phosphate available for cellular functions.
"The gut is a prominent tissue for nutrient absorption," which may explain why PXo bodies were mainly found there, where they could control phosphate supply to the rest of the body, said Xu.
Seroude said the results were rigorous because the team "systematically used different approaches to show the same thing," namely, that the PXo protein was inextricably linked to the newly discovered organelles. However, he was not convinced that cell division speeds up when an essential nutrient for growth is limited and argued that this hypothesis needs more testing. Xu argued, however, that cell renewal may help boost phosphate absorption when there's a deficit.
"I wouldn't say that we found this organelle from out of nowhere," Xu remarked, but new research techniques allowed his team to characterize the membrane whorls that had previously been overlooked.
Since the Nature report, researchers have reached out to Xu to share images of organelles that resemble PXo bodies.
One such researcher was Leslie Gartner (opens in new tab), a retired cell biologist who emailed Xu about an old study of his (opens in new tab): "My study occurred more than 50 years ago, so it was dead and buried beneath the thousands of Drosophila research articles and it would have been almost miraculous had you been able to discover it." Gartner added that he hasn't seen anything like these structures in the fly gut until now.
Xu and his colleagues have identified several proteins that interact with PXo and they plan to decipher what roles they play in regulating phosphate transport into the newly named organelle.
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Kamal Nahas is a freelance contributor based in Oxford, U.K. His work has appeared in New Scientist, Science and The Scientist, among other outlets, and he mainly covers research on evolution, health and technology. He holds a PhD in pathology from the University of Cambridge and a master's degree in immunology from the University of Oxford. He currently works as a microscopist at the Diamond Light Source, the U.K.'s synchrotron. When he's not writing, you can find him hunting for fossils on the Jurassic Coast. | Biology |
Testing of wind sensing in rats shows sub-orbital whiskers play a role in assessing direction
A team of neurobiologists and neuroscientists at the Woods Hole Marine Biological Laboratory has found that sub-orbital whiskers play a role in helping rats determine which direction air movement is coming from and to respond accordingly. In their paper published in the open-access journal PLOS Biology, the group describes their study of rat whiskers.
The work began after team members noted that little research has been done regarding wind sensing in mammals. To learn more, they opted to focus a research effort on rats and their whiskers. Prior research has shown that rats use their whiskers for a variety of purposes, one of which is to sense air movement. The team on this new effort noticed that the sub-orbital whiskers had not been included. Sub-orbital whiskers are those located above the eye. In rats, such whiskers are few but quite long. To learn more about their purpose, the researchers tested them in several ways.
The first test involved anesthetizing several rats and then exposing them to different amounts of airflow (wind). This allowed the team to analyze and measure the movement of the whiskers under various conditions. They found that the sub-orbital whiskers behaved somewhat differently than the nose whiskers. Due to their length, they were more displaced under low wind conditions. They also found that the sub-orbital whiskers tended to bend upward more than other whiskers on the face.
Next, the team conducted micro-CT scans on the rats, focusing most specifically on their sub-orbital whisker follicles. They found that they were slightly different than follicles of other whiskers—the nerves were arranged in a way that would allow for finer sensing of direction change. This would allow the rats to accurately note which way air was moving around them.
The research team then created simulations to show how rats might use their whiskers to keep track of wind direction and how hard it was blowing. They found that response to wind was much more acute in the sub-orbital whiskers.
The team concludes by noting that prior research has shown that rats almost always spontaneously turn their faces toward a wind source blown at them, even in complete darkness. They suggest that rat sub-orbital whiskers are used for air movement sensing.
More information: Matias Mugnaini et al, Supra-orbital whiskers act as wind-sensing antennae in rats, PLOS Biology (2023). DOI: 10.1371/journal.pbio.3002168
Journal information: PLoS Biology
© 2023 Science X Network | Biology |
Engineered Tobacco Plants Produce Sex Perfume To Trick Pests
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By using precision gene engineering techniques, researchers at the Earlham Institute in Norwich have been able to turn tobacco plants into solar-powered factories for moth sex pheromones.
Critically, they’ve shown how the production of these molecules can be efficiently managed so as not to hamper normal plant growth.
Pheromones are complex chemicals produced and released by an organism as a means of communication. They allow members of the same species to send signals, which includes letting others know they’re looking for love.
Farmers can hang pheromone dispersers among their crops to mimic the signals of female insects, trapping or distracting the males from finding a mate. Some of these molecules can be produced by chemical processes but chemical synthesis is often expensive and creates toxic byproducts.
Synthetic biology applies engineering principles to the building blocks of life, DNA. By creating genetic modules with the instructions to build new molecules, Dr Patron and her group can turn a plant such as tobacco into a factory that only needs sunlight and water.
“Synthetic biology can allow us to engineer plants to make a lot more of something they already produced, or we can provide the genetic instructions that allow them to build new biological molecules, such as medicines or these pheromones,” said Dr Patron.
In this latest work, the team worked with scientists at the Plant Molecular and Cell Biology Institute in Valencia to engineer a species of tobacco, Nicotiana benthamiana, to produce moth sex pheromones. The same plant has previously been engineered to produce ebola antibodies and even coronavirus-like particles for use in Covid vaccines.
The Group built new sequences of DNA in the lab to mimic the moth genes and introduced a few molecular switches to precisely regulate their expression, which effectively turns the manufacturing process on and off.
An important component of the new research was the ability to fine tune the production of the pheromones, as coercing plants to continuously build these molecules has its drawbacks.
“As we increase the efficiency, too much energy is diverted away from normal growth and development,” explained Dr Patron.
“The plants are producing a lot of pheromone but they’re not able to grow very large, which essentially reduces the capacity of our production line. Our new research provides a way to regulate gene expression with much more subtlety.”
In the lab, the team set about testing and refining the control of genes responsible for producing the mix of specific molecules that mimic the sex pheromones of moth species, including navel orangeworm and cotton bollworm moths.
They showed that copper sulphate could be used to finely tune the activity of the genes, allowing them to control both the timing and level of gene expression. This is particularly important as copper sulphate is a cheap and readily-available compound already approved for use in agriculture.
They were even able to carefully control the production of different pheromone components, allowing them to tweak the cocktail to better suit specific moth species.
“We’ve shown we can control the levels of expression of each gene relative to the others,” said Dr Patron. “This allows us to control the ratio of products that are made.
“Getting that recipe right is particularly important for moth pheromones as they’re often a blend of two or three molecules in specific ratios. Our collaborators in Spain are now extracting the plant-made pheromones and testing them in dispensers to see how well they compare to female moths.”
The team hope their work will pave the way to routinely using plants to produce a wide range of valuable natural products.
“A major advantage of using plants is that it can be far more expensive to build complex molecules using chemical processes,” said Dr Patron. “Plants produce an array of useful molecules already so we’re able to use the latest techniques to adapt and refine the existing machinery.
“In the future, we may see greenhouses full of plant factories - providing a greener, cheaper and more sustainable way to manufacture complex molecules.”
Reference: Kallam K, Moreno-Giménez E, Mateos-Fernández R, et al. Tunable control of insect pheromone biosynthesis in Nicotiana benthamiana. Plant Biotechnol. J. 2023. doi: 10.1111/pbi.14048
This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source. | Biology |
They are known for living in packs and being sociable animals. Now meerkats are being investigated to see if they can also pick up on human emotions.
Researchers and psychologists from Nottingham Trent University are studying meerkats in zoos to see if they can detect emotions such as happiness, sadness or anger from people, and whether they then adapt their behaviour accordingly.
The team want to better understand the potential effect people have on zoo animals. They will be monitoring the behaviour and interactions of meerkats with zookeepers, whom they see regularly, and with zoo visitors, with whom they are unfamiliar.
The study will investigate how the animals react to different people and whether they demonstrate empathy by mirroring their emotions.
Dr Samantha Ward, a zoo animal welfare researcher at Nottingham Trent University’s school of animal, rural and environmental sciences, said: “Wild animals housed in zoos undergo daily interactions with familiar and unfamiliar people and this presents an ideal opportunity to see if they recognise human emotions and in a sense ‘catch’ them.
“We’re keen to know whether these abilities might be influenced by the frequency of human-animal interactions, as might be the case with strangers, or familiarity with known people such as zookeepers. For example, if zookeepers influence the behaviour of meerkats but the visitors do not, then this could impact the management of the animals.
“If it’s the people rather than the zookeepers, then that could be considered when undertaking measures such as enclosure design.”
Experts already believe that domesticated animals such as cats, dogs and horses are able to understand how people feel, but less is known about wild animals housed in zoos.
Meerkats are highly attentive to their surroundings, including to zoo visitors, and commonly interact with both familiar and unfamiliar people as part of animal-visitor experiences. For these reasons, they are considered the perfect species on which to focus.
Dr Annika Paukner, associate professor in comparative psychology at Nottingham Trent University’s school of social sciences, said: “Our study combines expertise in zoo biology and human-animal interactions with psychology and comparative cognition. The recognition of others’ emotions is vital for effective interactions across social animals, including humans.
“People are so sensitive to others’ emotions, for instance that interacting with an anxious person may increase one’s own anxiety. It is important that we understand how common this ability is among animals, and what the implications are for human-animal interactions.”
Nottingham Trent University has received funding from the Leverhulme Trust for the three-year project. | Biology |
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