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Why do marmosets have claws when most primates don't? What is the structure of their hands like?
The majority of primates have really thick nails, though not as broad or flat as humans'. However, marmosets have 18 claws, and only their big toes have nails. What differences in evolutionary pressures caused this? And how does the structural relationship between marmosets' germinal matrices and their distal phalanxes differ from other primates, so they can grow claws?

its not entirely clear why some primates have little spades instead of points, and why it evolved. something to do with grooming, food and trees. older  primates which are nearer to lemurs have less flat nails. search for questions about why nails evolved, there arent clear answers.

@com.prehensible is that a genuine comment, or a partial answer?

Thanks to oldchemist and com.prehensile for answering! I'm sorry I couldn't split the bounty between the two of you.

Since marmosets and tamarins are considered the most primitive primates, we can't assume that evolutionary pressure led to the development of claws. Rather, it's accepted that claws disappeared as primates adapted to an arboreal lifestyle. So the question is really "Why did marmosets not completely lose their claws?"
The clues to the answer lie in their unusually large incisors and disgestive system. The marmoset occupies an evolutionary niche where they rely heavily (20-70% of total diet) on exudates (sap, resin, etc.) from trees. Their claws, and incisors allow them to claw/chew holes in the bark to get at the exudates, while a specially adapted large intestine allows them to digest this food. The advantage of exudates is they are not seasonal, offering the marmoset a relatively stable year-round food supply.
Other primates enjoyed the evolutionary benefits of tool use by losing their claws and gaining opposable thumbs (which marmosets don't have). I've come across no papers that describe a different phlange structure for marmosets and other primates, and there doesn't necessarily need to be one.
Most of this information came from the University of Wisconsin's Primate Research Center:
http://pin.primate.wisc.edu/factsheets/entry/common_marmoset
Edited to add (since I can't comment): One way to deduce how different features evolved is to look at phylogenetic trees. There are many out there, but I pulled this one from J.R. Roede et al. Redox Biology 1 (2013) 387-393.

If you look at this simple tree, you'll see that marmosets diverged from humans on a time frame where it's possible they kept their claws instead of reacquiring this trait (it would be unusual, but not impossible, for this to happen). One thing you can do is dive deeper into the phylogeny, square this up with how primate hands evolved, and see if the split of marmosets from the rest of the primates happened when nails began to evolve.

Thanks for pointing out that "phalange structure" is vague. I didn't realize it was at the time. What I'm specifically wondering is how the relationship between marmoset's germinal matrix and their distal phalanxes differs from humans'. The only results I'm getting from Google describe how cats retract their paws. I'll update the question to be more specific.

@oldchemist Please use the terms "outgroup" or "sister groups to all other primates" but not "primitive". This term is not (or rarely) used in the scientific literature. The term "basal" is sometimes used but it is also a very misleading term.

1/2 @oldchemist Not sure why you can't comment? So, considering the trees here http://culturalanthropology.wikifoundry.com/page/Common+Marmoset%21
...To the best of my (admittedly limited) knowledge, most prosimians have nails - aye-ayes are one exception, with the same 18 claws and 2 nails on their halluxes that marmosets have; of the New World monkeys, almost all have nails, including marmosets' close relatives capuchin and squirrel monkeys; Old World monkeys have nails, Proconsul had nails (the phalanx structure wouldn't support claws) and Aegyptopithecus is assumed to have had nails.

2/2 Am I on the right track to think that this suggests either the parallel evolution of nails in prosimians and simians after a common ancestor with 20 claws, or the parallel evolution of the 18 claws and 2 nails pattern seen in aye-ayes and marmosets after a common ancestor with 20 nails?

I can comment now...need at least 50 to do so. Yes, I think this is how I would look at it. Both seem to occupy distinct niches in which their claws offer an advantage. I think it would be interesting to know on a genetic level how different the gene families are that code for nails versus claws. For instance, if they did evolve in a parallel manner we'd expect slightly different genetic makeup. I would imagine that on a genetic level claws aren't that different from nails anyhow. It could be a matter of a couple of genes being over/under-expressed during the last stages of development.

Ill try and research this later and add references, it's a bit of a draft version while im on laptop in the car, A good place to think but not to write and surf from!
It's probably best viewed as a vestigial trait, made redundant by monkey's prehensile grasp, and related to their strong social and hierarchical behaviour. Indeed the flat nails seem to be a progressive arrival transitioning from lemures/aye-ayes to larger prehensile primates.
Humans have the most vestigial nails, to protect the fingers and for fine fingertip manipulation, and earlier mammals and non-prehensile herbivores find advantage of pointy nails for grasping bark and defense, to decorticate husks rinds, to dig, and other tasks.
We can imagine if nails had become reduced vestigial tools in a different way to what they did, imagine that they had tapered into bulbous tips
We can consider other alternatives that could have evolved, but the flat shape seems most fitting for a finger protection and versatility.
Also consider that large monkeys are belligerent, for example baboons which are very fierce, and monkeys that have sharp teeth which they can use in combat. If they had claws to do demonstrative fighting, it may be less beneficial for the group, and nails would generally discourage the mostly demonstrative social competition which is found in most social and rutting creatures. It demonstrates the contrast of vestigial carnivorous traits of some primates compared to the herbivorous organs of the largest ones.
With regards to the structure, perhaps it's best to check other mammals fingernails to see that it's only a small proportional and dimensional change.
Conical nails require a different shaped matrix which doesn't fit on top of fingertips for grooming and find dexterity, to alight with the bone, the nail matrix surrounds the top of the finger bone, so it's easy to broaden and thin out.
It's matrix cells that generate keratin which is not structurally affixed to the bone, which means it can regenerate efficiently, while it has structural weakness for lifting bodyweight. For carnivores, the stress on the nail is reduced by the cutting edge. The structural difference is not very pronounced. web resources for primate nail anatomy aren't abundant but you can find trees of primate hand anatomy.

Thank you for bringing up the nail matrix. After reading oldchemist's response, I realize I wasn't clear about what I was requesting. The reason I'm asking about marmosets is because they have a nail, rather than a claw, on one of their toes. One of the sites I'd found about them cited this as possible evidence that they had once had 20 nails, just like most primates, but had re-evolved 18 claws at a later date in their evolution.


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Pain and Angina Pectoris
What causes pain in an angina pectoris? Ok, heart muscles may lack oxygen, but what is the role of pain here? Is it being beneficial? I'd like to know the physiological process of induction of pain during hypoxia.

source: Stack Exchange

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sort: votes


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law of independent assortment
Self fetilization of F1 dihybrids, following independent assortment of alleles result in:
a) 3/16 Tall-rounds ; 3/16 dwarf-wrinkled
b) 9/16 Tall-wrinkled ; 3/16 dwarf-round
c) 9/16 Tall-round ; 3/16 dwarf-round
d) 3/16 Tall-wrinkled ; 3/16 dwarf-round

This question was asked in MCAT exam in Pak for which I'm preparing this year.... no genetic arcitecture was mentioned in question... The above mentioned is original format of question.... in ans-key, the ans is D but I am confused why it can't be C.

Welcome to Biology.SE. Please do not post text as images. Images are not searcheable and pose problem to people with visual impairement.

Why do you think it could be C and not D? What is your logic?

Can you give more information about the genetic architecture underlying  these two phenotypic traits?

in my point of view, tall is dominant trait. so it can be C

The genetic architecture of these trait is not subject to a point of view. It must be defined in the question. Patterns of allele relationships must be defined, and given the choice of answer, the two loci must be linked, therefore information about their linkage must also be included. Also, your logic for answer C does not explain the round vs wrinkled part of the question.

this question was asked in MCAT Exam in Pak... but unfortunately this is the original question ..no genetic architecture was mentioned

Can you please link to this exam if available online? Also, please change your image into a text. I doubt anyone is willing to make any effort to help you if you don't show any effort.

no link is not available online... :(

@Remi.b I disagree with the fact that loci must be linked in that example, this is about phenotype not genotype, so with dominance effect we could indeed observe these 3/16 or 9/16.

Why was this upvoted. The question is unclear or incomplete (not necessarily OP's fault) and shows no effort at explaining the logic behind the suggested answer. IMO, the question should be closed either as unclear or as homework question showing no attempt at an answer.

In real life, round and tall are dominant traits in pea plants, which would make C and D both correct.  I don't think people are expected to memorize the traits of pea plants, so the question ought to tell you somewhere which traits are dominant.  There must be an error in the question as printed.

In virtual life, A is also possible if we have Tall and wrinkeld as dominant alleles. B is impossible even in virtual as Tall and wrinkled would be the dominant and dwarf-round will present 1/16 occurence. I would say like you that the question has an error in it.

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Do Pthirus gorillae remain in gorilla leaf nests after gorillas migrate and abandon them?
Gorillas build leaf nests to sleep in. Do the lice which parasitise gorillas, Pthirus gorilla, remain in gorilla leaf nests after gorillas migrate to new regions (and abandon the old nests)?

From the Wikipedia page on Pthirus gorillae: "Researchers theorize that humans acquired the parasite while butchering or scavenging on gorilla corpses, or sleeping in the abandoned sleeping nests of gorillas".
So yes, they are believed to remain.


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Why can't humans use dietary citric or acetic acid as a primary source of energy?
As the Krebs cycle is involved with the conversion of food in to citric acid, why can't eating citric acid be used as a temporary primary source of energy - in place of fat/carbohydrate/protein?? It seems like a waste of energy to convert food into citric acid if there is freely available citric acid in your diet why wouldn't that preferentially be used for energy - as it would skip a lot of steps and therefore be more efficient. And what about drinking acetic acid for similar benefits, as "it is changed to citric acid by combining with oxaloacetic acid with the help of CoEnzyme A and ATP".

how do you get citric acid in nature?

I order it online via amazon. Citric acid. ;-)
Or I can find it in lemons too.

I might be wrong, but it seems that you would need 100kg of citric acid a day for 2400 kcal diet http://www.myfitnesspal.com/food/calories/495309621

I think you mean 1kg. a day of citric acid, there are 2.5 calories per gram of citric acid. But the thing is I think that comparing equally to food calories is misleading, because if it were to be used for energy - it would be processed more efficiently than actual food which requires a lot of cellular energy to assimilate.

Please read what you have written: "If the krebs cycle is largely about converting food in to citric acid which then enters the krebs cycle." This is a conditional clause, rather than a sentence, but is obvious nonsense even if there were a main clause. How can a cycle do something to something if it is not already in the cycle in the first place? Please rewrite so it makes sense and in doing so spell Krebs with a capital K — it is the surname of Hans A Krebs who received the Nobel Prize for discovering the tricarboxylic acid cycle that bears his name.

Will do, David. There are various tiers to the Krebs and I should have been more specific.

If, as a non-scientist, you wish to post here about the Krebs Cycle you need first to learn about its place in energy metabolism. The "main" purpose of the Krebs cycle is not to produce citrate, but to oxidase acetate (from sugars or fats) to CO2, ultimately generating ATP. It is a cycle of reactions between metabolites, one of which is citrate, with entry from acetylCoA and oxaloacetate. No energy is used ("wasted") if a dietary metabolite has first to be converted to acetylCoA — quite the reverse. And your concept of efficiency bears no relation to scientific reality. I have voted to close.

Seems like a completely legitimate question to me. (there is no requirement to be knowledgeable in backgroun info for your question; just that you've done prior research, which is indicated sufficiently in the OP's post). I vote to keep open.

Why can't eating citric acid be used as a temporary primary source of energy - in place of fat/carbohydrate/protein?

No reason it can't. Citric Acid technically contains 2.5kcal/g -- which is almost half of protein/carbohydrates, almost a third of alcohol, and a fourth of fat.
So if someone needed 2500kcal/day, they'd need 1kg of straight Citric Acid. There's about 47g/L of Citric Acid in citrus fruit juice. So if you wanted it all from "natural" sources you'd need to drink 21.3L of your favorite citrus juice, though that's a bit comical.
In terms of being more efficient since Citric Acid bypasses the first two enzymatic reactions,the part where Citric Acid is processed into alpha-ketoglutarate via Isocitrate Dehydrogenase is the rate limiting step of the entire cycle. You wouldn't be saving any time by flooding your system just before the bottleneck.
Interesting question, though!

Thank you MCM! So this raises the question, how is it possible to raise the rate of the citric acid in to alpha-ketoglutarate via isocitrate dehydrogenase step?

In vivo? No idea. That would require either a lot more enzymes floating around waiting for substrate (not sure how you'd do that or maintain it), or a much more efficient enzyme -- something that could be theoretically done if you had a few hundred hours of world-class supercomputer access and the right research team, but also suffers from the "I don't know how to get it in you and keep it around" problem.
Chances are there's a better solution to whatever problem you're thinking this solves.

I'd like to try and research the idea more, I am not a scientist but would like to try form a better hypothesis and connect a few dots if possible, could you point me towards some easy to digest literature that could help a layman such as myself? Thanks!!

As far as getting citrate in to the blood stream, one idea would be a jello or an emulsion with lecithin, either with citric acid or sodium citrate, something that would slowly release it so as to optimize the transfer to the blood stream rather than the nullification by bicarbonate in the small intestine. I feel there must be a simple method to optimize the conversion of ingested acid in to cellular energy.

Another delivery idea would just be to slowly sip a citrate drink continuously throughout the day.

@ol_matty_man - I'm afraid I don't have some literature suggestions, as I don't fully understand what you wish to do. Basic metabolic processes are pretty well described via Wikipedia, and I'd suggest starting there if you're not familiar with the language. And, as I said, the problem is NOT the citrate -- it's the step going from citrate to alpha-ketoglutarate. That's the limiting step, and the bottleneck in the Krebs cycle.

Thank you. What I was trying to get at is, I think most of the citrate calories do not make it to the bloodstream, I think they are urinated out for the most part, so I was saying perhaps a way to deliver more citrate calories to the mitochondria would be to ingest citrate at a steady rate instead of all at once. I could be wrong though.

@ol_matty_man - About 95% of the citric acid we ingest goes through a metabolic process in our bodies. Unless you ingest an unusually high amount, the majority of what you eat/drink is used and not directly urinated out. That said, I still think you fail to see the problem: Getting citric acid into our bloodstream is easy. Getting more energy after doing so isn't. It is not the amount of citrate that's the problem, but the rate at which it is processed. Like a road with a stop light, the thing that determines traffic speed isn't the number of cars (the citrate), it's the stop light (enzyme).

thank you @MCM - I had read conflicting information about citric acid here: https://www.livestrong.com/article/327212-what-products-contain-citric-acid/ where it said most is urinated out.

one last thing. Is there a chance that on an extramitochondrial level that more citrate or acetate consumption can increase the output of acetyl-coa which then enters the cytoplasm, therefore providing more energy than eating equivalent calories without citric acid??

@ol_matty_man - No, in fact it's the opposite. Citrate is an inhibitor of one of the enzymes in glycolysis.


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Ribosomes producing proteins, but need proteins to be produced?
So according to my textbook:

RNA is used to create ribosomal RNA (known as rRNA) which is then combined with proteins to form the ribomsomes necessary for protein synthesis.

I'm a bit confused with this statement, as ribosomes are needed to synthesise proteins, but in order to create ribosomes proteins are needed in the first place. How does this work, does the proteins needed for the creation of rRNA come from a different source? Or by synthesising proteins via ribosomes produce more proteins than required to create the ribosomes in the first place?
Also, where are the proteins synthesised? On cytoplasmic ribosomes, or on ribosomes bound to the RER?
Thanks!

Ribosomes are the only means we know by which cells produce proteins. Consequently, all proteins are made by a ribosome, including the proteins that then become part of a new ribosome. It's never a question of "more proteins than required" because there are different types of proteins and to make a ribosome, you need those specific types of proteins known as ribosomal proteins. The process of making ribosomes is known as ribosome biogenesis.
This raises the obvious question of where a cell gets its ribosomes from when it is "born". The answer is simple: from its parent. When a cell divides, each daughter cell is made of the components of the parent. The cytoplasm also gets divided, and each daughter cell receives mitochondria, ER, etc. from the parent cell. By the time those ribosomes break down, they will have produced new ribosomal proteins for new ribosomes already.
According to this review from 2017, it appears the ribosomal proteins made in the cytoplasm (so, cytoplasmic ribosomes) get shuttled into the nucleolus, where they get assembled with rRNA to make new ribosomes, which then get exported out of the nucleus into the cytoplasm.

To clarify on the original poster's question of "does the ribosome produce more proteins than is required": maybe it's not obvious to them that a ribosome is continuously producing proteins and will produce many proteins (not a fixed quantity) over its lifetime.


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Recognition of snake (image)
I would like some help with the recognition of the snake shown in the image below. I was doing a fieldwork in a forest in Slovakia when I found it.
I was thinking it could be a water snake but I am no expert in snakes.
Does someone know what kind of snake is this?

Aesculapian snake (Zamenis longissimus). Common european species, non venomous, rodent/egg eater.
edit1: they can swim and can be found next to water bodies but are terrestrial.

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When was it understood that a male haemophilia sufferer can't pass it on to his sons?
Haemophilia A and B are both X-chromosome mutations, so a sufferer necessarily inherits the disease from his mother. She won't have serious symptoms unless both of her X chromosomes have the mutation, which is very rare. Since sons of a sufferer necessarily inherit his Y chromosome, they can't inherit the disease from him.
I'm trying to find out when it was understood that sons of a sufferer could not inherit the disease from their fathers. The relationship between chromosomes and heredity was clearly demonstrated in 1915. The idea that females were usually carriers and sufferers usually male had been understood since 1813. The XY sex-determination system was discovered in 1905.
However, it is not clear to me when this would all have been put together and become part of normal biology and medical courses. I think the crucial points are:

There are sex-linked genetic conditions.
Haemophilia is one of them, and is an X-chromosome recessive condition.
Men are XY, women are XX.

Can anyone help with when all of that became normal knowledge for doctors and biologists?
Titles and authors of biology textbooks from the 1920s to 1945 would help, since I'm quite prepared to seek out old books, if I know what to hunt for.

This page might give you some clues to follow up.

@David: Sadly not, but it has shown me how my question was unclear, and I've improved it.

Sorry about that. Chasing up these historical things is very time-consuming because there is so little on the Internet, which is in any case obsessed with the latest thing. I just wonder whether you would have had to understand the XY sex-determination system to draw the conclusion about non-transmission to sons.

Thanks for trying, it was worthwhile. Understanding XY sex-determination means you know non-transmission to sons is basically impossible, rather than just unobserved. This is for a story set in the 1940s, and the question is if it's possible to be sure that a sufferer isn't the son of someone known to be a sufferer.

Using Google Scholar, I've found the oldest publication on this item.
1911 - "The pathogenesis of hereditary haemophilia".
In this article you'll find a complete synthesis of all the works done about haemophilia till 1946.
OP adding a summary, in case of future link rot: The linked article is from 1946, based on research in the late 1930s and early 1940s into the statistics of haemophilia. It's attempting to estimate the mutation rates of X chromosomes in males and females, and to test if X-Y crossover allows the haemophilia mutation to skip generations. It assumes the knowledge that leads to the conclusion that a male sufferer can't pass it onto his sons.

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Proteomics data Vs Transcriptomics data?
I want to use either of Proteomics or Transcriptomics data for integrating it into my kinetic model. Before proceeding, I want to know what are the advantages of using either of them so that I could make an informed decision on it!
Many studies have shown that the best we can do is integrating both transcriptomics and proteomics data with our kinetic model, but I've some time constraints and have to proceed with only one of those.
My effort and findings: I've found from discussions with researchers that gathering transcriptomics data has an amplification step which increases the chance of finding a particular one whereas gathering proteomics data has no such step but has fragmentation and then rejoining which creates many problems(such as splice variants etc) and thus leads to a loss of data. But a PostDoc told me that even after the loss of that data, I'll get more information from Proteomics data.
I want to know such type of points and want to know if these are valid or not!

This is a broad question. Moreover, you should put in some research effort from your side before asking.

I've updated it @WYSIWYG

By research effort, I mean you should read thoroughly about different transcriptomics and proteomics techniques to know about their advantages and limitations (including the technical issues, cost etc). The answer to your question would be an essay and not a precise paragraph. Therefore your question is not suitable for a stackexchange format.

I sure did put efforts before posting it here. Now, I have written my points in the form of an answer. I tried pasting a table in markdown but was unable to do that. So, I posted in simple bulleted format. Please check it and add suggestions. Thanks! @WYSIWYG

This is what I found from doing some research. Comments are welcome at any point!

Capture percentage for data gathering:

Transcriptomics Data: There's an amplification step in Transcriptomics data gathering methods. Hence, it's possible to capture almost the totality of the Transcriptome using those methods(scRNA seq methods, Nanopore tech, Spatial transcriptomics, etc)
Proteomics Data: There's no amplification step in Proteomics data gathering methods. Those methods have fragmentation and a rejoining step which leads to a loss of the data.

Scalability of methods:

Transcriptomics Data: Scalable methods available
Proteomics Data: Less scalable methods for protein studies

Reference availability:

Transcriptomics Data: Fully annotated references available on consortiums such as ensembl biomart, etc
Proteomics Data: Universal and Comprehensive Human Proteome reference is still in question and because of the incomplete and inaccurate references, much of the newly generated data is being rendered useless

Uniformity

Transcriptomics Data: Lots of publications on pipelines, and their benchmarking available
Proteomics Data: Lack of uniformity across labs/research groups and lack of related literature lead to differences in protein fragmentation and solubilization and differences in algorithms to run analyses

Technical Bias

Transcriptomics Data: Many methods available to tackle cell-bias, noise in data, and batch effects, so as to capture maximum biological variability
Proteomics Data: Cell-wide Mass spectrometry has a bias towards the identification of peptides with higher concentration or contamination from other experiments

Please give your views @WYSIWYG


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How can enzymes be immobilised on glass?
I’m studying a hypothetical model for urease activity, which involves fluorescence measurement, hence the need for an optical window to which the enzyme urease is immobilised.
From my previous knowledge, immobilisation of enzymes on a solid surface is done through the covalent bonding of the enzyme (outside its active site) with a functional group on the solid surface capable of covalent bonding.
My question is, isn’t glass supposed to be inert? How can enzymes be covalently immobilised on glass? And if they can’t be, are there other materials that could be used instead of glass for an optical window?

Glass can be functionalized by organosilanization so that biomolecules can be covalently attached via some cross-linker. As an example, one might aminosilanize the glass and then cross-link their enzyme of interest with glutaraldehyde.
For what it’s worth, urease activity can be measured in solution.


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Are all mammals capable of sneezing?
I only know dogs and humans sneeze... so do other mammals sneeze as well? Is it possibly an evolutionarily-determined immunological trigger?

Are you really asking about all animals (including  jellyfish for example)  or rather about mammals, as your examples imply?

Dogs and cats sneeze. My dog sneezes of excitement every morning when we're going out. A sponge - having no nose - obviously does not sneeze.

@Marzipanherz Yes, I’m asking about all animals. I know about humans and dogs (examples of mammals) hence why I asked if “other animals sneeze as well”.

@P.SN Note that to a biologist, "animals" is quite a broad taxonomic grouping, and as Marzipanherz and Remi.b point out includes plenty of organisms that have no lungs or nose or respiratory system at all.

@Marzipanherz give the OP a break. Sponges sneeze. It's a reasonable question. This is why I like beginner questions. They aren't closed off to ideas that seem implausible to experts.

@DanHall Unclear questions are unclear. They are not open-minded because they are unclear. It is at the core of the SE format to require the question to be clearly defined by the OP. We don't want a discussion in a post, we want a clear question and a clear answer.

@Remi.b The question wasn't unclear. It was very clear. Are all animals capable of sneezing? That's a clear, interesting, answerable question. No, not all animals sneeze. Yes, some animals you might think of as not being able to sneeze can.

@Remi.b  A dog and a human both happen to be mammals, but they are also both animals. The reason the original question was interpreted as unclear was that the "savy" readers didn't think non-mammals could sneeze.

@DanHall I never doubted the question was reasonable- On the contrary, I find it very interesting. I just wanted to make sure that there is no misunderstanding due to the potential different use of the term animal by a beginner and an expert. I used to believe that this what comments are meant for.

Just curious.  Why/how did the title of the question change?  I thought the OP said all animals in the comments above.  Did the OP change their mind?

@wanderweeer Yes OP improved the post based on the comments and modified "animal" to "mammal".

@DanHall To double on what marzipanherz said, I never meant that the question was fundamentally crap. I meant that some elements of this question were unclear. OP still has not fully addressed them IMO but I removed my vote close when OP edited its post. Anyway... Let's not fight any further on it.

This national geographic post discusses many mammals that sneeze. It doesn't come right out and say all, but suggests most mammals have a cough and sneeze reflex:

Mammal coughs and sneezes come from throat and nasal passages, respectively, says Bill Milsom, a comparative physiologist at the University of British Columbia.
Mammals, he says, are the only animals that process food in the mouth by chewing. In other types of animals, like reptiles, "food is swallowed whole or by chewing, and breathing is suspended during the event."

The same expert discusses non-mammals that sneeze, marine iguanas and fish.
You don't even need nerves or muscles to sneeze, per this Cell Press article

Sponges 'sneeze' without the benefit of nerves or muscles


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Can Cas13 be used with multiple crRNAs in the same reaction?
CRISPR-Cas13 equipped with crRNA (complementary to transcripts of interest) can be designed to target ssRNA transcripts in cells.
Upon successful crRNA and ssRNA binding, a fluorescent domain on Cas13 generates a signal, indicating that target has been found.
As far as I know, this method has been used to find one ssRNA target at a time. If we use different wavelength fluorophores for distinct Cas13-crRNA targets, is it theoretically possible to mix them all in the same reaction and distinguish the presence of different targets based on the different fluorescence wavelengths generated during target binding?
In this paper one fluorescently labeled crRNA is used to detect cleavage of one RNA target through complimentary binding. So is it theoretically possible to use several crRNA, each labeled with a different fluorophore, to cleave and detect several target RNAs?

Your link to the paper is broken, is this what you mean? https://science.sciencemag.org/content/356/6336/438.abstract. Also note that you talk both about flouresently labeled CRISPR proteinn (easy to do, but always 'on') and labelled crRNA (hard to do, maybe only signal on binding possible).

As far as I understand it's not the crRNA that is fluorescently labeled, but a cleavage reporter that is mixed into the reaction. The cleavage reporter is not even the direct RNA target, but apparently gets "inspecifically" cleaved as a result of "collateral cleavage". So to me it seems this method cannot be used for multiple target detection.
Paper also at PMC: https://www.ncbi.nlm.nih.gov/sites/ppmc/articles/PMC5526198

Answer is no. Because each CRIPSR-Cas(xx) system works as a ribonucleoproteic complex, so they needs to be loaded with a crRNA in order to be working. Functionality is guaranteed while each of the Cas endonuclease domain is associated with a crRNA. You maybe could use multiple Cas13 with multiple crRNA.
In molecular diagnosis is common to use orthogonal CRISPR enzymes with different crRNA, as can be seen in this original research.

I think your answer is self-contradictory... you said the answer is no but then "maybe could use multiple Cas13 with multiple crRNA", so technically, it's a yes?! My main question was whether it was possible to use multiple crRNA that are labeled with different wavelength fluorophores, so that the signal from target binding could be distinguished based on the color signal. If you look at the paper that I just added in my question, they use one fluorophore to detect cleavage of RNA molecules complimentary to crRNA. What if we use multiple crRNA, each labeled with different fluorophores?

It should be possible, I don't see why not. Just as you can use multiple gRNAs, as long as there is an abundance of Cas13 protein you can target multiple sequences at the same time. So if you, let's say, get a green fluorescent probe for RNA 1 and a red fluorescent probe for RNA 2, you'd be able to distinguish their localization.


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Why has reproduction evolved as a choice?
From an evolutionary perspective, the purpose of an organism is to pass along its genes through reproduction. However, as humans we have a choice if we want to reproduce or not. The good feeling from climax hardly seems to be a strong enough incentive to make people want to have sex, especially when that good feeling can be achieved in many other ways.
So why did we evolve to have a choice whether we want to reproduce or not, when it's defeating our biological purpose? Why didn't we evolve a different "reward system" than a climax to goad us to have sex, and is it likely that in the far future we will acquire a different, stronger reward system?

All organisms have some level of control over reproduction. Nothing unique to humans. There are many conditions in which reproduction is costly (for e.g. food shortage). Even bacteria won't reproduce if the conditions are not favourable. The word "choice" is a very anthropocentric term.

I've voted to close your question as off-topic as any answer to either question "Why didn't we evolve (some other way)" or "Is it likely in the future…" can only be speculative. This is not a discussion site, it is a question and answer site about (single) "practical detailed questions in biology". And in any case your premise seems false — if it hadn't worked we wouldn't be here.

Ask a typical parent how they feel about their children and I think you'd realize there is more than just one reward system... If it was only orgasm, babies wouldn't survive long enough to care for themselves.

@David All hypotheses are speculative at first. My premise, that an organism's biological purpose (from an evolutionary standpoint) is to pass on its genes, is not false.

I had thought your premise was that there was a problem with the way we had evolved because it risked the survival of the species.

Possible duplicate of Why do some bad traits evolve, and good ones don't?

@P.SN, Evolution does not have a purpose or intent, it is just a description of how some structures tend to make similar replicas of themselves in certain situations that have occurred in the past.  There is no intent or purpose that an organism reproduce, it's just that some organisms inherit structures that lead to replication if conditions it finds itself in are suitable, as happened for its ancestors.

Why has eating evolved as a choice, because it is not always advantageous to eat something.

I'm actually quite curious about the many other ways to reach a good feeling equivalent to an orgasm. That is certainly interesting academically as well as practically.

Evolution happens also on the level of social groups: It may be an advantage for the survival of  a group when many of the individuals do not have own children, but support the parents of other children, leading to few strong children instead of many starving children.

Your fundamental mistake is this statement:

the purpose of an organism is to pass along its genes through reproduction

Evolution does not actually involve "purpose" in any way.  Rather, it is just the observation that populations with traits that more reliably produce descendants end up with more descendants.
With regards to humans, being really smart and flexible creatures has been extremely advantageous for us as a population (so far at least). One of the side effects of that intelligence is that we have a lot more agency in our choices than many other forms of life---and also a maddeningly huge amount of variation in our world-views and preferences (whether consciously chosen or otherwise).
That includes one's attitude toward sex and reproduction, and so it's entirely unsurprising that there are many people who choose not to have sex, or who choose to have sex but not to reproduce.
At the same time, no matter what your personal opinion on the sufficiency of our drives may be, it seems to be enough to motivate most others to have sex and children. As such, there doesn't seem to be anything selecting for that motivation to change, because the people who are insufficiently motivated to have children will not tend to have descendants, while those who are sufficiently motivated will.
Bottom line: humans are reproducing effectively and those who reproduce are evolutionary selecting for the status quo---the same drives that already motivate them to reproduce.


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What kind of beetle is this (found on landing windowsill)?
 found this beetle on my landing windowsill, would like to know what it is, very small, this was a zoomed picture on my phone.

Please provide your location. Also, please add an aproximate size if possible

Thanks, in the UK and 3mm.  Found another one yesterday, same windowsill, I've uploaded a couple more pictures.

After researching I think it's a furniture beetle or biscuit beetle?

@Angel if by "furniture or biscuit beetle" you mean a species of Anobiidae you're probably right; the third photo down shows (admittedly somewhat blurrily) that the last three antennal segments are longer than the others, which is characteristic of that family.  Which species IN that family I can't help you with; I don't know the British fauna.


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Why does music give you emotions?
Why do we feel emotions when we hear music?
Click to see video
How can a set of tones arranged in a specific order and timing make you feel sad or happy?
I read that music can somehow trigger the part of the brain which is responsible for language processing. Whatever be the mechanism of emotions, why do we feel that certain emotions are connected with certain tunes?
What may be the evolutionary origin of this?

I am voting to close this question as off topic. This doesn't concern biology on its own, it involves Neurology and Psychology. I am aware that the first one is still concerned by Biology as a whole, albeit I think it would be better to ask such question in a more specific environment, such as https://psychology.stackexchange.com/

The evolutionary origin is alleged to be recent: Other animals do not have a preference for dissonance and consonance.  (McDermott & Hauser, 2004).
Humans have new auditory regions in the brain for predicting and processing speech, and processing the emotions conveyed in the voice. The human voice mostly has harmonics in the 3rd and 4th note due to the properties of the vocal tract. There have been some basic studies of the 12 notes of the piano as represented in the human voice, which concluded that the "consonant" sounds from chords and melodies correspond to the the sound of the human voice.
This article suggests that dissonant/amusical frequencies are uncommon in natural ecology, because of the way physical objects resonate. Bird melodies are atonal and not particularly dissonant or consonant.
Some people may suggest that animal alarm calls are more dissonant than mating calls, especially those that are made to scare you like a cat hiss, a gecko scream, baby marmots which are separated from their mother, a rabbit being eaten.
Actually, many studies have identified brain regions used for emotional processing, the same that react when they see a beautiful or unnerving image, by MRI tomography and also from people who have had strokes which make them non-reactive to music, and people with amusia known as amusics.

They also
  found an increase in frontal-midline (Fm) theta power
  for consonant music, indicating greater coherence of
  neural firing in certain population of neurons. This is
  interpreted as reflecting activation in the anterior cingulate cortex (ACC), which has been implicated elsewhere in processing pleasant music (Blood & Zatorre
  2001). The ACC’s role in emotion is also supported by
  its inputs from other key emotion-related areas, such as
  the amygdala, hippocampus, and parahippocampal gyrus (Devinsky, Morrell, & Vogt, 1995).

There are a lot of studies on the topic, this is a well written summary of recent research.
Musical sensory stimulation is a fascinating topic with complex ecology and brain quirks, it's best to research the topic individually to find which aspects of music do what to the brain:
Music rhythms vs cardio/breathing/cerebral rhythms, individual sound consonance/dissonance, and complex auditive patterning of sounds found in rhythmic chords and melodies. The conflict-resolution of harmonies are what you are referring to regarding the sequence of notes, there are studies on musical expectation, it's a sub-field of consonance/dissonance neuroscience.


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Can you accelerate the growth of a plant by accelerating its surroundings?
I had this weird idea of making plants grow faster when I first visited an indoor nursery which used floodlights instead of sunlight. They turned on during the day and went off during night in cycles.

If the time period of the cycles are decreased, it would seem to the plants that the earth just switched to fast-motion. Will this trick the plants into growing faster?
If not the current generation, would the later generations of plants grown like this adapt to the new rhythm ?
(Given that the plant is provided with surplus nutrients to meet the new requirements.)
I would love to do the experiment myself if it would actually work!

Hello, This is an interesting question. I'm sure there is an effect of day-length on growth (number of hours of light). However your question is more about effect of  whole day-night cycle modification? like a cycle of 30h (15day/15night) or a shorter cycle? I would see that more like an adaptation to a whole new planet where the length of a day is not anymore 24h (climatic change won't affect that).

@Untitpoi Hello there! I meant a decrease in day-length, for your information.

How can altering the clock prevent global warming? If plants grow faster, they will also die sooner, releasing all their saved carbon to the environment. The long term effect will be close to none.

@jmster  I googled how to decelerate plant growth. It is possible with a method called Topping. So, you can slow down the growth after it has reached full growth. This should decrease global warming, or at least provide some shade!

"We can fight global warming like never before!" You have to take into account the energy and infrastructure you're expending to know how much net CO2 you're sequestring or releasing. Not to mention scaling - how much plant mass could we do this for ? What percentage of the Earth's surface would we be covering in indoor nurseries or floodlights, and how much of Earth's vegetation would we be replacing with the accelerated version ? And how much more carbon would those plants sequester than ordinary plants do in the first place?

I'm sorry but I think the idea of preventing global warming is not the principal point! The question is can we accelerate the growth using in-vitro technics (related to day-length). Whether it could be used to prevent global warming is another issue.

@Untitpoi If preventing global warming had been the principal point of the question, all those comments would have been answers! As it is, given how preventing global warming was emphasized in the question in a way that suggested a misunderstanding of the magnitude of the different phenomena involved, I think the comments were justified. I think editing that passage out of the question was a good idea, it distracted from the main question which is interesting in its own right.

they have evolved for 24/24 for billions of years. there's not a mechanical reason they perform better at 12/12.. It's been tried and studied and measured, but only to see the reaction, I don't think that the plant photosynthesized more if the same amount of light was given at different times.

@Untitpoi Don't consider it as a knowledgeable answer, but I have posted an account of the experiment  below; I don't know if it's appropriate !

This is not the best answer, but see that as a starter! Feel free to use my answer to build yours!
I have found a so-called professor speaking of advantages to go on a 24h light/12h dark cycle (36h cycle) to accelerate the growth of cannabis. I'm not sure of the reliability of this source.
I think the main problem we will encounter with that reduction of cycle would be the trouble with the circadian clock inside the plant. This clock is quite stable and I suspect some deregulation would happen if you desynchronize your day-night cycle with that clock.
See the effects we show on humans in the section Enforced longer cycles of
 Wikipedia or this stack question

Researchers are allowed to assess the effects of circadian phase on aspects of sleep and wakefulness including sleep latency and other functions - both physiological, behavioral, and cognitive.

Do you think this clock inside plants would itself get altered, in the new generations at least?

The circadian clock seems to be complex, it is highly improbable that it will change in one generation. But I think some arabidopsis mutant showing an absence of circadian clock exists and show a high suspeptibility to diseases. You could be interested in that article https://theconversation.com/studying-circadian-rhythms-in-plants-and-their-pathogens-might-lead-to-precision-medicine-for-people-84024

Note that many plants grow north of the Arctic Circle, where they get continuous sunlight for part of the summer.  (And very long days in subarctic latitudes.)  The same varieties of (domestic) plants grow in more southerly latitudes.  For instance https://sites.google.com/site/alaskafruittrees/

I'm not sure if it's right to post an answer like this but anyway, seeing is believing!
Three days ago, I (finally) gathered enough resources to do this experiment.
I'm testing on a pea plant as it comes in handy. I have set up two samples, one for the test and the other for reference.

Today's Day 3, and the results have started to show up. I thought it would be nice for you to see it yourself. The experiment is not over, it's still going on; so I would update the news every three days from now on.
Everything was done in my study room, which is not a laboratory, so the results may not be accurate. I have tried to bring uniformity in the amount and type of soil used, water content, no. of seeds in each sample, seed spacing and other parameters.
I'm providing the link here.
EDIT: Today's only day 5, but the test plant has grown out of my simulator box!
I have modified the setup and started a fresh experiment.
The updated record here.
UPDATE
Maybe I should give an update for future readers. I asked this question a couple of years ago and forgot about it. I did this experiment when I was in high school, and I am currently an undergrad in science :).
I can confirm that this experiment was seriously flawed, be it the control parameters or the theory used. The plants grew bigger just because they received more light.
My past self was too enthusiastic about the results that he forgot to think about any of these. I am not deleting this answer as I want it to serve as a reminder for myself how not to do an experiment.

Interesting input, Are you trying a 30 seconds day-length there? It seems rather fast. In your document it is not clear what is the day-length for your reference. It seems more like your control had less light than your tested peas, but I am just guessing.

@Untitpoi My reference sample is sitting in bright sunlight right now ! I am not sure of the previous days, as I was out of station.Today the seeds has just  begun to open up. But the test seeds are on its own legs already! But the initial results cannot be depended upon. I am looking forward to day 6!

Maybe I misunderstood, but your control should also be in a box similar to your test with the same length of light exposition. If you don't do that, we can't know for sure if the effect you are measuring is not due to the quality of light (sun VS articifial light) or the total amount of light.

@Untitpoi Do you mean to place the reference sample in another test environment with a 12-hour on and off period?

Yes that's exactly what I mean.

@Untitpoi I will consider that. Thank you for the input!


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Can you alter your hearing range by changing air pressure in your nose?
I caught a bad cold recently and found that increasing air pressure in my nose causes some clicks in my ear. I understood from this site that this is because ears and nose are connected. But what I didn't understand however, was that I my hearing range got completely shifted after doing so (not permanently of course). If I am right, it tends to make low frequency sounds clearer. The opposite happens when I decrease pressure. The higher frequencies become more crip and clear. I have the feeling that the answer is related to the way hearing works but would like to hear how exactly. It would be great if any of you could confirm or deny this or provide some explanations.

Questions based on personal anecdotes are hard to answer. Perceptual quality of sound may depend on a lot of things besides middle ear pressure.

Just fyi: the ear(s) and the nose are connected by the eustachian tube, not the sinuses.

@AliceD Agreed. I have also experienced the shift in audible range while travelling on a plane. This is why I think this is related to pressure.

Thanks for the info @anongoodnurse

The sound equation I = Xi^2.Omega^2.c.Rho (Xi = particle displacement, Omega = frequency, c = speed of sound, Rho = density of medium)  implies that the sound pressure (i.e. volume) changes with air pressure  and frequency- which explains the aeroplane problem, but I don't know how much effect in the small volume of an ear.


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Star-like organism seen in microscope

I found this strange star-like thing while observing a slide of onion root somatic cells. I don't know that it is; I even doubt if it is an organism. It has conical arms directed  radially outwards all over it's body. It wasn't moving. If it was indeed living,  maybe I had killed it while flaming the slide. Anyway, I am interested in knowing more about this  unexpected guest of mine. Can anyone tell me what it is ?

It may be a stellate trichome from a plant.
You can find other ones by taking swabs from the onion and nearby plants.

cool images here
wiki info about trichomes


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If fully colorblind people only see shades of white,gray, and black, does that mean that the colors black, white, gray are colors humans can’t see?
And since the brain can be tricked to thinking that objects with mostly black and grey gradients are moving, like optical illusions, does that mean motion has a color?

According to your title you should consider a repetition from optics.  But anyway it is quite interesting question.

Based on your question: if fully color-blind people see whites, blacks, and greys, that means that humans can see them colors. After all, aren't color-blind people humans?
If you actually think about it, is color just created by evolved cells? If so, should we not see just black, grey, and white?


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If crossing over did not occur, would pairs of cells after meiosis II have the same genes?
If crossing over did not occur, would there be two pairs of cells with the same chromosomes after meiosis II? This question came to my mind while I was reading through my bio textbook. After meiosis I, there are two cells with 1n chromosomes but the chromosomes have 2 chromatids. It seems to me that, if crossing over didn't occur the chromatids of the chromosomes would be identical and after meiosis II the 2 cells would divide into 2 pairs of cells with identical chromosomes. Is this right?

Your understanding is correct.
After meiosis II, you will have 4 cells: Cells 1 and 2 are identical and each have one haploid set of chromosomes; Cells 3 and 4 are identical and each have the other haploid set of chromosomes. These two sets of chromosomes are mutually exclusive. Note that these sets of chromosomes are not [necessarily] the same as the gametes that formed the organism.


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Is there an estimate of the number of enterocytes in the human body?
I've been looking for this information but I haven't been able to find it. Does anyone know if there are estimates of the number of enterocytes or epithelial cells in the intestinal tract? Otherwise, would a simple division of the volumes of the intestinal tract and of a cell work as a rough estimation?

Difficult to estimate given the considerable variation in human gut length. Related post: Does variation in human gut length vary predictably with diet of ancestors?

It might be easier to estimate the density of some small area and try scaling up based on length and other volume measures. However using such a model to do so would require density estimates from each variable segment. For example, as circular folds decrease in robustness from duodenum to ileum and eventually disappear in the colon, I would expect cell density to decline dramatically

Why are you asking? General interest (and therefore requiring low precision) or for perhaps some sort of metabolic calculation(and therefore requiring greater accuracy)?

Also, I'm not sure to what degree localized cell densities (e.g., of the duodenum lets say) vary between people. I think a more answerable question underlying yours that must be addressed in any answer you ultimately receive is whether and to what degree cell density of given anatomical regions varies between people

@theforestecologist I just want an approximate range for modeling purposes. But as the other comments have pointed out, this seems to vary significantly from person to person.

It might help if you explained why you wish to know something that on the face of it has the intellectual content of the Guinness Book of Records.


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Is inhibin hormone secreted by corpus luteum in females?
In females, I have studied that corpus luteum secretes mostly progesterone, but some of estrogen, relaxin and inhibin too. But in some of the books they say that inhibin is not secreted by corpus luteum. Can someone please explain.

In human females, inhibin is secreted by the granulosa cells of the primary oocyte which inhibit FSH secretion ,resulting in the stoppage of follicle maturation until activin ,again secreted by granulosa cells activate FSH activity .

I think this doesn't answer the question.

So inhibin is secreted by primary oocyte and not corpus luteum?


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Programs/software used to create illustrations and scientific paper ready figures
I am new to the field of molecular biology. I am finding the need to generate illustrative figures displaying interplay between proteins, DNA and various other molecular constructs at different scales of complexity and having trouble identifying tools that many use to generate their very descriptive figures. For example there are countless examples of DNA and wrapped around histones, in 2D, in 3D, in almost realistic rendered versions etc. Obviously, I can not use someone else's graphics - so I am curious where do others start? Any advice on best practices would be greatly appreciated there, in terms of tools people use to generate their molecular biology figures describing biological 3D mechanistic illustrations.
Below are 4 classes of illustrations that I have found on the web and I am including here only for the purpose of example of each type:
Type 1 has actual 3d components (histones) and DNA wrapped around for example: it's not clear if these are made in some kind of a 3D program, or they are 2D constructs somehow manipulated and put together with some clever  efforts. Are there specific 3D rendering or publishing tools/programs used for these? Perhaps one's with a library elementary blocks, somewhat akin to open-source 3D floor-map design programs many use to quickly create floor plans for their houses and apartments furnished with 3D chairs, tables and other furnishings?
Type 2: These tend to be 3D rendered constructs, like the simplified version of the chromatin ball here. Some are very realistic, and I can imagine those are done professionally by studios, and not biologists, but simpler versions like this one should be possible without a professional studio's help.
Type 3: This is more like old school hand drawn illustrations. These days, perhaps there are tools to do this with library of 2D elements that can be manipulated and placed in to create this type of illustrations?
Type 4: This type uses simpler 2D elements that are put together to create more complex biological constructs, like cells, cellular activity etc. This type is less  helpful in capturing 3D interplay and relationships between DNA and proteins but still a tool with library of objects that could be morphed to fit into the right shape(s) would be helpful.
Thank you.

Actually, you probably can use someone else's graphics, provided you obtain a license. There are many stock photo and illustration companies, and if none of the existing images match your needs, you can always commission a scientific graphic artist to produce illustrations to your specifications.

Welcome to Biology StackExchange! Can you please give an example or two of such figures so that we can give you more concrete guidances?

Thank you @Domen, I have included a few examples.

Figures 1 and 3 were drawn by professional artists, probably using Adobe Illustrator — Figure 4 probably also, but the nearest thing to that I am aware of is BioRender, as mentioned in a previous post in this general area. Any 3D proteins graphic program will output diagrams of type 2, but you need to know how to get the style and colour of picture you need. There is a learning curve.

Thank you very much @David, BioRender appears to top the list.

Stick with „vector graphic design“ applications. They enable you to open .pdfs and move around individual elements and resize them to your needs without losing resolution.

Biorender. It has a lot of ready-to use illustrations of proteins, organelles, receptors, etc. Free subscription is very limited, though. I don‘t have a lot of experience with it, but it might be the best solution for every molecular biologists. It‘s worth asking your professor if he buys one license for the whole group. Everyone loves biorender figures.
Adobe illustrator. Best vector graphic design software out there. But expensive as hell and takes a few days to learn.
Affinity publisher (My favorite!). Perfect for making posters and publication grade figures. You pay 50 bucks once and own the license forever. It‘s powerful and has more than enough features to make top-notch professional figures. Adobe illustrator is better though. Affinity publisher also takes a few days to learn.
Inkscape. Open source 100% free vector graphics. Haven‘t used it a lot, but might be a good entry point.
Microsoft powerpoint. It‘s bad, but it gets the job done in terms of placing objects next to each other. But I made big complex posters with it that look alright.
Apple Keynote. Like powerpoint but a lot better and a lot more precise. Only for mac users, though

For 3D rendering protein structures, I recommend pymol. Every structural project probably used pymol at some point. I have seen people even script some fancy animations with it, it takes some python scripting, though.


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Calculating pitch of B-DNA
From this question (How pitch of a DNA Helix is 3.4 nm?), I've learnt that for counting the number of axial rise for 10 base pairs in 1 helical turn to measure the pitch of B-DNA, we have to include the space above $1^{st}$ base pair and below $10^{th}$ base pair as per this image - https://i.sstatic.net/cZzOj.jpg
But now I'm confused as to why we include these spaces. Why do calculations fail if we were to measure starting from the base-pairs itself? Any help is valuable!

The answer is mostly that you have to use the right denominator, as suggested by @DrRadium's comment.
The crucial mistake in the other answer was measuring 9bp and dividing by 10. That's measuring the length of 0.9bp, not 1bp.
You have chosen to measure the length of 9 base pairs and divide by 9. That works! you have shown that you get the right answer. In that case you don't need to add any space on either side.
In the other question, 9 base pairs were being measured, and then they were dividing by 10- the distance between first and tenth bp is not equal to the length of 10bp. The distance between the the $n$th and first basepair will $n-1$, or in this case $10-1 = 9$.
If you take the comment suggestion and add 1/2 on either side to your distance measurement, you are then measuring 10bp truly, so you'd better divide by 10.
So if you wanted to omit the space, you could measure the distance from the 1st to an 11th base pair. That would be 11-1=10bp long.
You may be interested in reading more about 0-based vs. 1-based indexing. This is an example of a classic "off-by-one" error that arises when you mix up the two indexing styles.


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Need biological system with specific reset process
I need a biological process that can be described as a stochastic process in statistical physics. I am familiar with some processes such as birth-death or gene expression, but now I need a process where a specific reset process occurs. In this reset process, there is a counter that counts and increments an observable as the system evolves over time. The reset occurs randomly after a certain amount of time has passed, during which the counter does not count anything.Is it possible?
Thanks for your attention.

Not that I know of; most biological processes go from one state to another without reversion. What sort of reset are you after? Hard reset - counter increments up, then returns to 0 immediately or counter counts back down, or something inbetween?. If one of the latter two you might be able to use paired enzymatic reactions, such as between a DNA polymerase and a DNase.

if there counter is triggering the reset then it can't be random if it is based on a counter counting time,  maybe I am confused about what you are asking for

I guess telomere shortening is kind of like this, but I'm not sure based on the description (it's also probably noisier than what you have in mind)

stochastic processes are everywhere; I think the tricker bit is how you've specifically setup this "reset process" as being completely independent of its count accumulation. I think the best example is probably spontaneous neuron firing, but there's some controversy in the field as to just how "spontaneous" this is

I think bacterial chemotaxis may qualify, depending on how the phenomenon gets aliased into the signal and time-counter variables.
The bacterial flagellar rotor can turn in two directions. Because the flagellum is chiral, clockwise and counter-clockwise rotor directions produce two different types of movement. One type is running in which the motion is roughly linear, the other is tumbling in which the bacterium basically rotates.
It's easy to show that random switching between these modes leads, over time, to a random position in space. So, if one (say) puts a single bacterium at the center of a 2D playpen, its coordinates after an interval are random.
The ratio of runs/tumbles is set by a kind of olfactory system, so that when the bacterium is moving towards an attractant there are more runs to close the distance, and less tumbles to scramble the bearing. But even when traveling straight to an attractant, tumbles still occasionally occur. This is summarized below in a figure and its caption from 1 (with minor edits, and my boldface):

Attractants bind to the receptor-transducer proteins ( Tar, tsr, Trg, Tap) in the membrane. The receptors also mediate the response to certain repellent. This activates a CheW-dependent change in the rate of autophosphorylation of CheA and the proteins that are phosphorylated by CheA (CheB and CheY). Attractants reduce the rate of autophosphorylation, and repellents increase the rate of autophosphorylation. The phosphoryl group is transferred from CheA-P to CheY and CheB. CheY-P interacts with the switch proteins (FilM, FliN, FliG) to cause clockwise rotation of the motor and tumbling. Thus repellents increase tumbling because they increase the level of CheY-P, and attractants reduce tumbling because they reduce the level of CheY-P. CheB-P is a methylesterase whose activity results in demethylation of the receptor-transducer proteins. As CheB-P goes up, methylation goes down. Thus repellents reduce the level of methylation because they increase the level of CheB-P and attractants increase methylation because they reduce the level of CheB-P. CheB-P autodephosphorylates. CheR is a methyltransferase that methylates the receptor-transducer proteins. The more highly methylated receptor-transducer protein does not transmit the chemoattracant signal to CheA. Hence adapation to a chemoattracant is due to increased methylation of the receptor-transducer proteins. Adapation to a repellent is due to undermethylation of the receptor-transducer protein. The relative activities of CheA-P determine the level of CheY-P, hence the frequency of tumbling [3].

When a run is initiated, the protein CheY is in a dephosphorylated state. The phosphorylation of this protein is a second stochastic process driving the chemotaxis. When it is eventually dephosphorylated again, also a stochastic process, this comprises a reset of that timing system.
As a result, the time in current run or tumble is a stochastic variable that near-instantaneously resets. It could be appropriate to act as the "counter" time-index variable that could be paired with the bacterium coordinates random variable.

Thanks for your complete answer. I must read more about it. thanks.


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Does This Rock Contain A Fossil?
A couple of months ago I came across a rock which has suspicious insertions in it. It was found in southern Spain, more specificaly hiking near Zahara de la Sierra (coordinates are provided: 36.830427, -5.416054). I am curious if it could contain some sort of fossil as some of the structures are bone-ish. The rock is 40 x 40 x 10 cm (16 x 16 x 4 inches) in volume and weighs around 10 kg (22 lb) Thank you beforehand

There seem to be inclusions in a sedimentary rock, but without a clearer picture, there's no hope of identifying anything. Could you provide a few other angles including the underside - in as high resolution as possible.

think of uploading some close ups to fossil id forums

Seconding @JiminyCricket. You can't tell with this quality of photo - would need closer up of the "fossil" bits and some different angles; but look like inclusions or intrusions of some sort to me.

the stuff in the upper center of the photo is the only stuff that could possibly be a fossil, so providing a close up of that might be enough.

I added an extra picture I had in my gallery, but soon you'll get some more closeups and different angle shots. Sorry!


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Voltage-gated calcium (Ca2+) channels
My question is related to "voltage-gated calcium (Ca2+) channels". I don't really have a background in chemistry or biology other than basic elementary school knowledge so I'm a little confused about what kind of reactions need to take place (if any) to form the calcium cations that activate these channels. Do any calcium compounds that contain a calcium ion as part of the bond work to regulate the channels (such as the calcium found in milk) or do they have to be broken down into single calcium ions or form into specific calcium ionic compounds before they can be used for channel regulation?

Probably makes more sense to work on the background in chemistry and biology. In this case you want to learn what it means for an ionic compound to dissolve in water. Also voltage gated calcium channels aren't activated by calcium they are activated by voltage, that's why they're called voltage-gated.

Don't ions carry a charge? Where else does the "voltage" or potential difference come from? I'm assuming It takes a certain amount of charged ions to create the voltage levels necessary to open or close the gates.

You need a broader picture. I'd start with a neuroscience textbook like Purves Neuroscience or Kandel Principles of Neural Science. StackExchange is good for specific questions; it's not a good way to learn a topic backwards by starting with a question far from your understanding and working backwards to back fill.

If you explain why you're asking the question/what you're trying to achieve, it's possible someone can help you with that, but if you're trying to understand how neurotransmission works you should start from scratch.


text:
Why do pollen grains tend to remain in the 2 celled stage in most angiosperms?
In over 60% of angiosperms, pollen grains are shed off at 2-celled stage (Vegetative cell and a generative cell) and in the other 40% it is shed off at 3-celled stage (Vegetative cell and 2 male gametes). During the pollen pistil interaction, if the pollen grain is 2- celled, it divides to form a 3-celled stage during the growth of pollen tube in the stigma, while as the 3-celled directly goes into the ovary/ovule. I don't understand the need for the pollen grains to remain in the 2-celled stage if, ultimately, they convert into a 3-celled stage. Why don't the pollen grains remain in the 3-celled stage from the very beginning? What is the advantage of being in the 2-celled stage before pollination?
Source

This is an interesting question and I've upvoted it. It would be better if you could provide a source for your claim, so that you don't send someone (like me) on a wild goose chase. Thanks!  :)  (I like to find the answers to interesting questions, as it's fun to learn new things, but I'd like to know I'm spending time on something that's a fact.)

@anongoodnurse Thank you for the upvote. As for the source of my claim, I read that in the textbook issued to me by my school, and you can find that here. It is on page 7 and 17 (to save you some time :>).

Thanks for providing a link! As you're new here, you might not have understood that the source, a link and a quote should be edited into the question. That insures that the question is self-contained. Again, though, thanks! That chapter discusses things I never knew.

Thanks for letting me know. And, you're welcome. :)

Since, the topic itself is under research i would refrain from making bold assumptions but my hypothesis (based on evolutionary benefit; extra nutrient availability in pistil) is plausible enough and helpful for understanding your topic, but before that let me explain to you some prerequisites since you would need that understanding to think beyond as well. (Your answer is in last 2 paragraphs.)

PPI: Pollen Pistil Interaction:

As the pollen lands on the stigma (which is relatively moist) pollen absorbs some of moisture and it's metabolic activity is triggered resulting in pollen tube growth (obviously there are intermediate steps like reorientation of pollen, which in itself involves many extra cellular messengers (ECM) generaly sucrose gradient or some other peptide gradients and they trigger intra cellular signals which is the area of focus in your answer).

PT : Pollen Tube:

Consider it like a Big Long Tube (not hollow but contains actin filaments/shank actin filaments and its mechanism of extension in pollen tube is like reverse-fountain cytoplasmic streaming don't be afraid of the term it's simply like that - at axis/center of tubule its convoluted into itself while extending forward at the peripheral portion thus pushing ahead into the pistil.
Pollen tube isn't like shoot hair which is often misunderstood as similar (shoot hair is continuous projection of single cell with no blocking in between, but in PT there is callous deposit to prevent back flow) for images and further explanation refer this https://www.frontiersin.org/articles/10.3389/fpls.2020.589712/full

Progamic Phase: It is the phase between pollen landing on pistil and fertilisation. That is Period of Pollen Pistil Interaction & Pollen Tube Elongation.

Does cell while moving into pollen tube derives any nutrient from pistil? In my opinion it is very unlikely and there are rarely any conclusive research papers out there to confirm or discard that entirely BUT it might be dependent on some signaling molecules for his maneuvering and metabolic activities and it is strongly established.
Now, coming to your question

Your question is like that:
Why pollen's spermatic/generative cell divides in 'progamic phase' instead of already divided beforehand during the 'gametogenesis' phase itself.
Answer could be sought in Evolutionary benefits, why to spend so much of energy and resource in dividing all pollen cells into 3 celled stage when most of them are ultimately not going to succeed thus leaving this for the progamic phase to do so.
Also, to keep pollen 'effectively' light weighted this is beneficial, since loading pollen with vegetative cell will increase its survival time under outside environment we can not compromise on that part, thus if sperm cell is divided into the parent body itself it will lead to increase in overall weight. (Read last paragraph again).
Availability of nutrient in pistil - such hypothesis is dependent on point number 4 in prerequisites list. I could not conclude it immediately but it could be turning point to the answer.


text:
How to generate pathway fingerprints of drugs?
I have studied a paper that constructs the pathway fingerprint of a drug, which has a vector of $0$ and $1$, and they compare the pathway fingerprint using a similarity measure to assess how similar the drugs are.
But I don't know where can I download pathways and how to generate their fingerprint vector to evaluate them. I checked KEGG website but could not find anything there to download. The paper can be downloaded from: https://pubmed.ncbi.nlm.nih.gov/22426982/
I really appreciate answers that can help me to solve the problem.
Update
Since i am not familiar with DrugBank and biology science, when I parsed the xml file of drugbank, I find a tag with name pathway . But i am not sure that do these elements show the pathway of drug or not? Is it possible to use them to construct the pathway fingerprint vector for drugs? what does <uniprot-id>P00734</uniprot-id> mean?
this is the content of pathway tag for Lepirudin:
<pathways>
    <pathway>
      <smpdb-id>SMP0000278</smpdb-id>
      <name>Lepirudin Action Pathway</name>
      <category>drug_action</category>
      <drugs>
        <drug>
          <drugbank-id>DB00001</drugbank-id>
          <name>Lepirudin</name>
        </drug>
        <drug>
          <drugbank-id>DB01022</drugbank-id>
          <name>Phylloquinone</name>
        </drug>
        <drug>
          <drugbank-id>DB01373</drugbank-id>
          <name>Calcium</name>
        </drug>
      </drugs>
      <enzymes>
        <uniprot-id>P00734</uniprot-id>
        <uniprot-id>P00748</uniprot-id>
        <uniprot-id>P02452</uniprot-id>
        <uniprot-id>P03952</uniprot-id>
        <uniprot-id>P03951</uniprot-id>
        <uniprot-id>P00740</uniprot-id>
        <uniprot-id>P00451</uniprot-id>
        <uniprot-id>P12259</uniprot-id>
        <uniprot-id>P00742</uniprot-id>
        <uniprot-id>P02671</uniprot-id>
        <uniprot-id>P02675</uniprot-id>
        <uniprot-id>P02679</uniprot-id>
        <uniprot-id>P00488</uniprot-id>
        <uniprot-id>P05160</uniprot-id>
        <uniprot-id>P00747</uniprot-id>
        <uniprot-id>P00750</uniprot-id>
        <uniprot-id>P08709</uniprot-id>
        <uniprot-id>P13726</uniprot-id>
        <uniprot-id>Q9BQB6</uniprot-id>
        <uniprot-id>P38435</uniprot-id>
      </enzymes>
    </pathway>
  </pathways>

```

I know nothing about drug databases, but am familiar with Kegg. As far as I can see from the paper (and I may be wrong) The drug target database would contain the names of enzymes, the activity of which is affected by drugs. So the problem would seem to be to identify so-called Kegg ‘pathways’ in which these target enzymes occur.
(I use the adjective “so-called” as Kegg pathways are not generally what a biochemist would regard as a pathway, but areas of metabolism. However this would not matter if all one is trying to do is find a correlation.)
The poster would seem, therefore, to need to download a list of enzymes for each Kegg pathway. At one time all the Kegg information was available free of charge (I downloaded a considerable amount — although not the enzymes — to construct a relational database). However now one needs to purchase a license to do this — presumably what the authors of the paper did — at a cost of over $1000 pa.
Unless one has grant funding or is independently wealthy, it would seem to be necessary to explore alternatives, such as MetaCyc (https://metacyc.org).
Postscript
The addendum from the poster shows the UniProt IDs for the targets of the drug. These can be converted to Kegg IDs using the conversion tool on the Kegg site (https://www.genome.jp/kegg/tool/conv_id.html). The XML tag entitled “pathway” is not equivalent to a Kegg metabolic pathway as such, although the example seems to consist of proteins involved in blood clotting. If my interpretation is correct, it would be irrelevant to the procedure I suggest. However the original paper is sufficiently vague that I cannot be sure.

Thanks for your reply and your information. I added a new update section to my question which shows a tag wit name pathway in xml file of drugbank. does show the desired pathway of the drug?

@Orca — I've added a PS. If I were you I'd email the authors of the paper.

thanks for the time you spent on my question. the answers did not solve my problem, but a appreciate it with upvote


text:
What animal makes these sounds?
An animal near where I live in Austria is making these sounds. I'm thinking it is in distress, but I can't find it. Can anyone tell me what it is?
It goes quiet when you get close, but responds heavily to a cat meowing. The environment is a residential area with many rather large gardens. I haven't heard it make any noise after sundown, only throughout the day, morning til evening. There is a small stream nearby, but no larger bodies of water.
https://whyp.it/tracks/116934/unknown-animal?token=bqQEa

Welcome to the Biology Stack. Can you please edit your question with a couple of details: What sort of environment are you in (rural, urban, semi-rural)?, are there any bodies of water nearby - rivers, lakes, streams etc?, and what time of day does this happen?

@bob1 Thank you for the guidance, I have added more details.

Sounds like a kitten in distress to me. Maybe an abandoned one or if it's at particular times, maybe when it's mother leaves. I am not sure enough. Somebody please confirm.


text:
How come SSBPs in RPA don't bind primers?
I've started reading about the recombinase polymerase amplification (RPA). I'm learning that in RPA, recombinase enzyme binds to primers, then makes them anneal to the complementary target DNA strand, and the displaced strand of DNA is bound by single-strand binding protein (SSBP) to prevent reannealing and promote extension of the bound primer. But how come the primers aren't bound by SSBP thus preventing them being bound by the recombinase? How come it's not recombinase that binds the displaced DNA strand? Materials that I'm reading don't mention anything about adding some kind of recombinase-recognised tags to the primer sequences, how do these two enzymes "know" which single stranded DNA to bind to?

From a 1994 review of E.coli single-stranded binding protein (SSBP) in Annual Reviews of Biochemistry, it would appear that at least 35 nucleotides (nt) of single-stranded DNA are required for binding of SSBP to occur.
From a paper in Trends in Analytical Chemistry  describing recombinase polymerase amplification I read that the first step in the procedure (A, below) is to add the primers to the recombinase, forming a complex between the two, and that it is only at a subsequent stage (D) that SSBP is added.

As the length of primers normally used is also apparently ca. 35 nt, I presume that the length of primer available to the SSBP is less than 35 nt, and it is for this reason that SSBP is unable to bind to it. (In the cartoon there would appear to be no primer available, except, presumably, for the DNA.)
An alternative would be that the recombinase hinders the binding of the SSBP.

Thanks for the reply. Yes, I read that article, but it doesn't actually say that the SSBPs are added at a later stage. They only show up in panel D of the figure because that's where they're relevant, not because that's where they're added. Like the DNA polymerase is not added after the SSBP (panel E). Also, the manuals for commercial RPA kits do not specify that SSBPs are added after the primers, recombinase and template. However, your "less than 35nt" theory does make sense!
And thanks for the edits to my question, but they weren't necessary.

@AndrewRoots — If you found part of my answer helpful you should consider upvoting or accepting it. As regards your opinion that my edits weren't necessary, I provide an explanation of the reasons for such edits on Meta. It is, of course, your prerogative to disregard them, and I do not wish to discuss this matter further.


text:
max % of oxygen not harmful for breathing?

Is breathing pure oxygen bad for you?
Human blood is designed to capture oxygen and safely bind it to a molecule known as hemoglobin. However, if you breathe in a high concentration of oxygen, it will overwhelm the blood, disrupting the central nervous system, damaging the lungs, heart and brain.

Breathing 100% oxygen is harmful for the lungs and the brain and will cause death  under normal pressures.
link
Continuous exposure to oxygen under normal pressure leads to death , however exposure for limited amount of time or under low pressures delays death or damage to organs
The Earth's atmoshphere has around 22% oxygen.How much is the upper limit of % oxygen before it becomes harmful(death or damage to organs) to a human?

Oxygen is also harmful at 22%; like most poisons, there isn't some magic threshold at which harm begins, though you can define one and go from there. How would you like to define the threshold at which you will start calling it harmful?

@BryanKrause If it were harmful , wouldnt we be not able to live on?

We can't live forever on it, over time it causes us heart and vascular disease, cancer, etc. In the shorter term, it contributes to us needing to constantly replace proteins and other cellular components. It also almost caused the extinction of all life on earth, before life had evolved to deal with it. https://en.m.wikipedia.org/wiki/Great_Oxidation_Event

We need proteins regardless of this to feed the muscles off.And if im not mistaken , cancer doesnt come out in every human.

Muscles do not feed off protein typically, carbohydrates are the energy source. Protein is needed in diet for amino acids which build proteins, including in muscle. Cancer is sort of a chance game; things that cause cancer create more opportunities to "win" that game through damage to DNA, it is not deterministic. There is lots of DNA to potentially damage; cancer happens when the damage happens to occur in the right combination of places

You stated that at some percentage O2, be would not be able to keep on living. How are you defining death caused by O2 in excess of 22%? Are you only considering lung damage?  Must the death be acute or is chronic oxygen toxicity causing death acceptable? I know it sounds strange, but I think you need to put some kind of parameter on death by excess O2.

As a new user to SE Biology please complete the [Tour] to find out how this site works (we know you haven't as you don't have the badge). This is a site for students and professionals in Biology and posters are expected to show that they have conducted some research on the topic. Please help us to maintain our standards.

@David Been editted.

Oxygen is always harmful.  It's tearing apart your cells as we speak.  That's actually what we like about it.  It's really good at tearing apart food molecules to get at the juicy energy inside, but it will also tear apart other things in the process.  Oxygen and the oxidizing effects of it are probably a major factor in aging.  When it first appeared on the planet in any sort of concentration as a waste product of photosynthesis, it led to the world's first mass extinction event.  Since then, animals have evolved to not only tolerate it, but require it.  Doesn't mean it's not still tearing you up from the inside though.  The concentrations present in the atmosphere are the concentrations our body has become adapted to cleaning up after.  Unless you need higher concentrations for some medical reason, stick to atmospheric concentrations.

As I'm sure you know by now, this site likes objective answers that can be backed up by references. Please edit your answer with suitable references for your claims.


text:
Bone fracture and remodeling due to psychological stress?
I am reading up on this article:
click
Psychological stress causes bone fracture or the change of habits due to psychological stress cause bone fracture and remodeling?

Can you please provide a link to that article? It sounds like you're asking for medical advice rather than clarification/verification. Thanks!

Oops sorry will do!

What is your question?

The article you linked to is a review of the literature. Although your questions are related, I'll restate them as if they were independent questions. Please let me know if I'm not reading you correctly.

Can psychological stress cause bone fracture[s]?

The answer is "No." Psychological stress, which causes the release of hormones which may (over a long time) cause bone to weaken, cannot cause bone fractures. Fractures are caused by external stresses on bones obeying the laws of Physics. For example, any bone, healthy or not, will break if pressure of some kind bends or compresses it beyond it's limit to bend/compress. A very common example of this in people of all ages and bone health is a fracture of the distal radius from falling on an outstretched arm, or FOOSH (“fall on an outstretched hand"). We all reflexively stretch out our arm as we fall forwards to help break our fall. Depending on many factors, such as what surface we're falling onto, we may or may not sustain a fracture, but we've all been there. Little kids have less brittle bones, and such a fall commonly results in a "greenstick fracture", which is only partially broken, and on xray resembles the bend you see when a green twig is bent and straightened out again (hence the name). Older people don't get greenstick fractures; they have full fractures if the fall occurs on a hard surface, or under enough pressure (the FOOSH).

Does chronic psychological stress causing a change in habits cause bone fractures?

No. See above.

Does chronic psychological stress causing a change in habits contribute to bone strength and remodeling?

The answer according to the paper (and common sense) is, "In some people, most likely yes."
The paper gives a number of conditions which may well contribute to osteoporosis, a condition causing decreased bone strength. Such a decrease in bone strength means lesser external stresses can and often do cause fractures in those with the condition. Osteoporosis is most common in the elderly. Significantly decreased levels of activity over long periods of time (e.g. that may be present in depression) can contribute to the development of osteoporosis (again, multifactorial.)
I say, "...most likely, yes" because the article is not a study but a review, that is, the authors did not carry out any studies showing a direct cause and effect, but reviewed studies done by others which show a correlation between long term psychological stress (as well as the effects it has on physical behaviors) and osteporosis, which in turn predisposes people to sustain fractures which those with normal bones may not sustain. ("In some people" because it's multifactorial, e.g. sex, activity levels, genetics, and other factors contribute.)
I say "common sense" because there is much evidence in the literature about osteoporosis and fractures, but much less evidence about the effects of psychological stress causing osteoporosis, which is the subject of the review article. But common sense is not evidence.
Evidence informs us that prolonged immobilization (say, someone is in a wheelchair for a year and never uses their legs) leads to osteoporosis in those leg bones.
Evidence informs us that the incidence of fractures increases with osteoporosis.
Evidence informs us that prolonged use of glucocorticoid steroids causes osteoporosis in a percentage of those people (but not which people exactly).
Evidence informs us that psychological stress causes increased levels of glucocorticoids in people.
What evidence does not inform us of is that prolonged psychological stress causes osteoporosis.
We can infer (that is, hypothesize/make an informed guess which requires studies to obtain evidence for causation) that chronic stress may well cause ostoeoporosis in a percentage of sufferers. But a hypothesis requires "proof", through controlled studies, that our guess is correct.
That's why the paper concludes that further study is warranted. Common sense, informed guesses and hypotheses are not evidence.
I answered this question because the OP was kind enough to provide a good link, which is wonderful and fully deserves my respect. I hope that with this answer, people will understand the respective values of "common sense" and "evidence" in science, because so many of us human beings mistakenly think they are one and the same. Stepping down from the soap box now, requesting your grace for this very long... answer. Thanks.

Great answer!Thank you!

You're very welcome!


text:
What animal this bone belongs to?
I recently found this bone on the balcony of my house.

In case it helps, my house is in the northwest of Spain next to a park in a coastal city, and size is 15-20 mm.
Does anyone know what animal it could belong to and what part of it it is?

Could you please edit in the size of the bone  - it looks like it is very small, given that you appear to have it on the palm of your hand.  Size gives us important clues about what sort of animal we might be looking at.

Seems shaped like a fish jaw, are you anywhere near the ocean/sea?

Edit my question adding more info, thanks comments. There are seagulls in the park, it is possible that they bring things from the sea.


text:
In search of motivation (Examples from nature) for reaction-diffusion systems with a conservation law
I'm an applied mathematician with a huge interest in mathematical biology. While looking at  this paper, I came across with the following:

Examples of reaction-diffusion systems (1)-(2), falling into the class
of systems we are interested in, are for instance the Brusselator, the
Schnakenberg, the Gray-Scott and the Gierer-Meinhardt model coupled to
a conservation law coming for instance from ecology.

Although I googled a lot, I couldn't find any example/reference from ecology which satisfies the above. Since at the end of the day, I am simply a mathematician, I thought to ask the experts of that forum. Having a motivation can help someone gain easier intuition on the expected results, which is really important.
Question: What are some examples of reaction-diffusion systems, coupled to a conservation law, coming from biology? I'm looking for a rather simple reference or examples from daily life (if any).
Any help will be much appreciated. Thanks in advance!

Please try to use a descriptive title that makes it easy for interested people to recognize they'd be interested in your question.

Paper, Chapter

@BryanKrause You're absolutely right. I edited my title, hope that it's better now

@RoniSaiba thank you very much, I'll check that!

There is a whole book here from spatial ecology. there appear to also be some applications in biochemistry involving adsorption or consumption across a spatial gradient.

You can also look into the books "Mathemcatical Biology" (vol i and II) by J.D. Murray, which both have chapters on reaction-diffussion models, related to e.g. pattern/coat formation, spatial patterns, and (I think) some ecological examples as well. They are a couple of years old though


text:
Why does the throat close up during an allergic reaction?
I was thinking about anaphylaxis and how strange it is that exposure to an allergen, e.g. a peanut, would cause someone’s throat to close up to the point where they can’t breathe. Why does this happen, and then, why would an epinephrine injection stop it?
This page says the histamines cause the throat muscles to contract which blocks the spread. This is more of a molecular answer but I’m thinking why, on a functional level, would this happen?

Remember the requirement to show your own research when posting.


text:
What is this insect in this image?

Is it an insect coming out of its cocoon or some other type ?
It was attached on wall like a leech and was not able to detach from that because it was glued.
Location :- northern India

It's very hard to see details on your picture. Do you have something higher resolution or possibly good pictures of different parts?


text:
Which species is this short-bodied cellar spider?
It clearly belongs to the Pholcidae family and possibily the Pholcus genus, but I can't find a picture of any similar spider on the Internet.
Note that the legs of the spider in the picture are curved inside because it is dead (drowned)

(2 spider photo released under CC0 waiver)

Spider in the photo:
status: dead
age: mature
sex: likely male
location: Red River Delta, Vietnam

Creates messy and non-adhesive webs.
Abdomen vibrates when it senses danger.

EDIT: likely a male, the female's abdomen are darker and bigger

Sorry to hear the news; I once had a "pet spider" in a corer of my apartment as well. Could you add some information on the size? There's nothing in the photo that gives a clue. Is the body 1 cm long? More? Less?  Thanks, and Welcome to Stack Exchange!

Sadly i lost the spider body 2 days after taking the picture (before posting this), but the distance between to blue lines in the paper are ~3/4cm

edit previous: not ~3/4cm but ~3/4 of 1cm

This is indeed in the Family Pholcidae but you are unfortunately incorrect in thinking this is of the genus Pholcus
This appears to be a Short-bodied Cellar Spider (Physocyclus globosus) of the genus Physocyclus

Physocyclus globosus, sometimes known as the short-bodied cellar spider is a species of spider belonging to the family Pholcidae. This is a cosmopolitan species, found in caves and buildings throughout the warmer parts of the world. This is a small brown spider (body length around 6 mm), with a short, broad abdomen. A black line runs along the back of the carapace, continuing along most of the abdomen. The eight eyes are grouped close together on a raised hump on the face. Source: wikipedia.org

Image ref: inaturalist.org, Photo 26739006, (c) matthewkwan, some rights reserved (CC BY-ND), uploaded by matthewkwan

That specie have abdomen a bit too big compared to the cephalothorax, but the raised hump eyes are very interesting, i will upload a sideview photo

The photo on Wikipedia show the eyes pair and the abdomen pattern very similar, i think you are correct

@Stvkimension Thank you!