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Be honest: Do you look at banking and other financial institutions and imagine the swishing sound of billions of dollars and euros flushing down the drain? Lies, thefts and frauds are not getting any scarcer grow among the people who handle money, so we ask:
Who takes? What gives?
The august scientific journal Nature took a stab at explaining the apparent rise in financial cheating with a study by three researchers at the University of Zurich (a banking capital!) who looked at 120 employees of an anonymous international bank. The study rested on the concept of "salience," the idea that behavior is affected by thoughts and values that happen to be present in our minds.
The question was, are bankers less honest when the thoughts and values associated with banking are running through their minds?
The study was built around a coin-flip experiment. Participants were told which side would win, and asked to report the result after each of 10 flips. Wins were worth $20 apiece. Statistics were the only way for the testers to know if the subject was being honest — in the long run, close to 50 percent of the flips should be heads, so any deviation from 50-50 marked dishonesty.
In the control situation, the bankers were asked a series of generic questions about their lives; in the experimental situation, some of the question were intended to raise the salience of banking, such as, "What is your function at the bank?"
Bankers responded honestly, essentially stating that half the throws were winners — unless the thoughts of banking were raised. But after the banking prompts, 58.2 percent of their responses were winners — a result that is not possible given the random results of flipping a coin many times. Close to 10 percent of the primed bankers reported a win on every throw, a result that would be expected in about 1 percent of the 120 cases!
Why are bankers honest — but only until they are reminded that they work in a bank? The cause seems to lie in the bank culture or values, says author Ernst Fehr, a professor of economics, who commented in a conference call that the spate of banking and financial scandals "raise question of whether the business culture in banks is favoring, or tolerating, fraud, to a larger degree than business culture in other industries."
The researchers wrote that after being reminded of their profession, subjects were significantly more likely to "endorse the statement that social status is primarily determined by financial success." That endorsement, they added, "is positively correlated with the reported number of successful outcomes." Recall that an excessive number of successes involved what we call cheating.
The authors continued that their findings "substantiate current concerns about the influence of materialistic values in the banking sector," especially since the simple recognition that one is a banker, "may have increased dishonesty through an increase in materialistic values."
It's not that bank management is telling employees to be dishonest, "it's the opposite," Fehr said. But does not seem to be getting through, he added. "I believe that … what is thought to be implicitly okay is what is showing up here."
Co-author Michel Maréchal, an assistant professor of economics at Zurich, added that "those in the experimental group who most strongly endorse the materialist statement have a positive relationship with dishonesty." Occupational norms in the banking industry, he added, "put a greater employee emphasis on dishonesty and materialism."
What can be done, given that financial businesses commonly encourage employees with financial incentives, which the authors said could play a role in the outbreak of cheating.
Recall that the study found that, until being primed to think about banking, these bank employees "are basically honest, so it's really the cultural aspect, the unwritten norms and values that prevail in the company that seem to make them more dishonest, and that is something we can change," said Fehr.
Incentives may offer one basis for fighting dishonesty, Fehr said, since any incentive "can be an incentive for being dishonest… and the stronger it is, the bigger is the problem. We don't argue for removing all incentives, but maybe we should reduce the strength of these incentives."
A second fix may reside in trying to counter the professional norms with pledges or standards, a tactic that is being tested to battle fraud among taxpayers and insurance claimants.
– David J. Tenenbaum
Rock is flowing once again on Hawaii's big island, where geologic change is not a matter of centuries and millennia, but rather of hours and days. Every square inch of these Hawaiian islands owes its existence to a hot spot that conduits molten rock from deep inside Earth to the surface.
Pelé, the god of the volcano, is a hungry god, and as volcano Kilauea oozes red-hot rock, the village of Pahoa watches the lava push closer. Families on the volcano side of town have already packed for evacuation if necessary.
Volcanoes can do much worse than ooze into the backyard and seize territory. On Sept. 27, Ontake, Japan's second-tallest volcano, erupted without warning, killing at least 56 in that island nation's worst volcanic tragedy since 1902. Earthquakes, caused by the movement of molten rock, or magma, usually precede eruptions, but little magma moved before the steam explosion at Ontake, so the government issued no warning.
Kilauea's rock chemistry is not conducive to explosive eruptions, and more inclined to slow-moving oozes. You can walk up to the molten lava. As the cherry-red surface cools to a brittle, glassy, black rock, you hear the unforgettable crinkly, crackly noise of a planet changing shape.
The rare opportunity to watch terra firma forming in Hawaii is misleading: most of the planet's crust was once rock — magma — that emerged from the deeps and cooled million or billions of years ago. Some estimates say that 80 percent Earth's cold, hard surface originated as molten rock.
Volcanoes are awesome reminders that Earth is not a boring, static hunk of rock, but rather a living planet that coalesced from a hot cloud of gas and dust about 4.5 billion years ago. The skin cooled as heat from the surface radiated to space. But the high-temperature rock inside was insulated by the crust, and actually has gained heat from radioactive decay and gravitational energy.
In short, we're sitting on a ball of fiery rock wrapped in a dozen kilometers or two of cool rock.
That's unstable. Heat rises. Hot substances are less dense than colder ones, so magma is always looking for an escape hatch through the crust. And since heat is a form of energy, rising magma brings up oodles of energy — enough to power cataclysmic explosions. Enough to reshape the face of the planet.
Volcanoes don't just appear anywhere. They require places where
* deep hot rock rises above intra-oceanic "hot spots;" these magma pipelines fuel volcanoes on Hawaii and Reunion Island; or
* water-rich ocean crust is subducted into much hotter mantle rocks at the edges of tectonic plates.
To understand volcanoes, you need to know the Ring of Fire, where most of them are located. The Ring is located where tectonic plates meet and denser ocean crust sinks beneath the lighter continental crust.
That's the process of subduction, and it's the major source of magma.
One hundred kilometers deep in a subduction zone, the sinking crust carries seawater under fantastic pressure (about 30,000 times atmospheric pressure) and temperature (1,000° Celsius) into the earth's hot mantle. When this water mixes with hot mantle rock, the rock melts. (Just as salt melts ice on your sidewalk by lowering its melting point, water lowers the melting point of mantle rock by hundreds of degrees.)
The mantle rock melts, and becomes less dense than surrounding rocks, so they rise through the surrounding solid mantle by convection, eventually reaching a magma chamber a few kilometers below the volcanic vent. As the magma continues rising, falling pressure liberates high-pressure gas that was trapped inside it, vapor bubbles expand and eventually rupture, and the volcano can erupt explosively.
Volcano structure is dependent on the geologic setting and chemistry of the emerging magma.
Composite volcanoes are built of alternating layers of ash and lava. These so-called stratovolcanoes, including Mt. Fuji in Japan, Vesuvius and Stromboli in Italy, and Villarrica in Chile, fulfill the stereotypical volcanic cone.
Shield volcanoes are born from multiple vents that emit flowing (not exploding) lava. Mauna Loa on Hawaii, standing 10 kilometers from ocean floor to summit, is a classic shield volcano. Shield volcanoes typically form over an oceanic hot spot, not at a subduction zone.
A lava dome is built by eruptions of viscous, non-explosive andesitic or dacitic lava.
A cinder cone is built from basaltic ash and lapilli — sand to golf-ball-sized ballistic fragments that pile up around a volcanic vent.
A caldera is a ring-shaped depression surrounded by steep cliffs. A caldera forms when a magma chamber spews out its molten rock, and the mountain above it collapses.
All volcanoes, in one way or another, represent a leak in the Earth's crust that allows magma to ooze or burst out. Many types of rock can be released, and some flows can threaten locations so distant that the volcano is just innocuous scenery at the horizon.
As rising populations run out of safe places to live in volcano country, sooner or later volcanoes will write headlines of havoc. The dying was already under way 2,000 years ago, when Mt. Vesuvius erupted and buried Pompeii in 79 CE. Today, three million people in Naples, Italy, live in the shadow of Vesuvius.
Plenty of other cities face grave volcanic threats. At the western edge of the Ring of Fire, for example, densely crowded Japan, Philippines and Indonesia are all studded with active volcanoes.
For example, Mexico City, the world's largest metropolis, is just 55 kilometers from Popocatépetl, a 5,465-meter giant that's erupted about 17 times since Columbus "discovered" the New World.
For perspective, eruptions like Mount St. Helens, which emitted one cubic kilometer of ash in 1980, happen every decade or so. Krakatau, Indonesia, 1883, put out about 20 times as much stuff. Such event is expectable roughly once in a century.
But consider the 3,000-cubic-kilometer eruption about 75,000 years ago of Mount Toba (also in Indonesia), which likely affected the global climate for years. These volcanic "super-eruptions" can effect the climate and economy of an entire hemisphere, yet we have no human experience of what signals volcanoes might emit before such mega-eruptions.
It's a principle of geology: What happened before can happen again. So get this straight. Gargantuan eruptions are rare. But gargantuan eruptions can happen.
Volcanoes are fascinating in their own right, but the big money is trying to anticipate, even predict, eruptions. The record is spotty, as emphasized by Ontake's unexpected and deadly eruption on Sept. 27, but steady progress in understanding the chemistry and dynamics of volcanoes should improve matters.
To reduce the surprise quotient for volcanoes, scientists look at:
* Geologic history: How regular and frequent were this volcano's past eruptions? Based on the composition of the erupted magma, how explosive were the eruptions? How did past eruptions change the landscape? How far away were the effects felt?
* Deformation of Earth's surface: Before eruption, rising magma may change the surface above the magma chamber. Broad deformation indicates deep magma, while more focused deformation signifies shallow magma that may be more likely to erupt in the near future.
* Gas emissions: Rising magma releases gases like water, carbon dioxide and sulfur dioxide. The timing and intensity of these gases hints at the magma's composition and location.
* Chemical and physical structure of the magma: Scientists are fascinated by crystals present in a "mush" in some magma reservoirs capable of super-eruptions. If the crystals vanish or change composition, could that trigger an eruption?
* Earthquakes: Rising magma must bust through rock, and the resulting quakes may be the best single indication of magma movement and near-term eruption.
* Gravity: Magma is hotter, and therefore, less dense than the same rock at lower temperatures.
* Electrical conductivity: Changes in underground electrical conductivity can reveal the presence of hot water or molten rock at shallow depths.
Although scientists do not claim that the volcano prediction problem is near solution, some incremental gains are evident. In 1991, for example, the lessons of Mount St. Helens were tested when the ground began shaking around Mount Pinatubo in the Philippines.
A collaboration of U.S. and Filipino volcanologists watched, waited, and eventually made an accurate warning. The Philippine government evacuated tens of thousands of residents, saving massive casualties. Although gigantic mud flows and ash deposits lead to the closing of two major U.S. military bases, few lives were lost during the largest eruption of the 20th century.
– David J. Tenenbaum
Many zoos and wildlife parks have replaced cages with more natural enclosures, but they may be paying less attention than they should to sound, says Suzi Wiseman, a graduate student in environmental geography at Texas State University-San Marcos.
At last week's meeting of the Acoustical Society of America, Wiseman reported on sound and the white rhinoceros at a Texas game park. She says she chose the site because it is one the few parks that can actually breed white rhinos in captivity, indicating that they are healthier and/or happier than the average captive rhino.
One reason, she says, may be the rural location of their home, the Fossil Rim Wildlife Center. But how, exactly, does that good ol' rural life help?
One possibility is sound, says Wiseman, who has just finished preliminary exams for a Ph.D. that she expects shortly.
White rhinos, natives of tropical and subtropical savannahs and grasslands, "Have the most sensitive hearing of all animals, according to animal trackers," Wiseman says.
Concerned that rhinos, which have huge territories and can run 35 mph, spend too much time standing around at zoos looking bored, Wiseman several years ago started "enrichment practices," playing audio recordings and watching for a response. "In the Texas summer," she says, "I played the sound of a storm rolling in, and they jumped up and started looking around and sniffing the air. I played a bird call, and they started poking their heads into the bushes, looking for birds. I played frog calls, and they went over to the moat and looked at the water."
But when she played zoo sounds, like a child crying, "I got a fairly disinterested response."
When we commented that these experiments seemed pretty straightforward, Wiseman responded, "I was astonished that nobody had thought to do this."
In her report last week, Wiseman described an exhaustive program to measure the full panoply of sound, stretching beyond the optimal human range of 20 to 20,000 hertz to:
Infrasound: vibrations slower than a person with perfect hearing can detect
Ultrasound: vibrations above the 20,000 limit to human hearing
Geosound: vibrations in the Earth made by wind, traffic and footfalls
We asked how low a rhino could hear, and Wiseman admitted, "It's controversial. Rhinos have been recorded in the literature vocalizing down to 4 or 5 hertz … but there are indications that it's a great deal lower than that. Some say infrasound is just a byproduct of their large size, but if an animal vocalizes at a particular frequency, and has most of the energy in their call at low frequency, I assume they can hear that frequency. The hard part is proving it."
Infrasonic noise, she points out, "tends to be pretty typical in urban areas," due to traffic and other concomitants of development.
In the future, Wiseman wants to record soundscapes at zoos and other captive environments and compare animal health in different environments. "Where they are healthier, and what is the sound like?"
Typically, acoustic studies look at volume and pitch. But Wiseman probed more deeply, saying, "I think this is the first study that used broad-based measurements to look at the whole soundscape."
She looked, for example, at entropy — a ten-dollar term for variations in sound frequency and energy. "We know humans respond poorly to a fluctuating sound, and we know animals respond to a sudden noise out of nowhere." Sirens vary quickly in pitch and intensity and are designed to grab our attention – and create an emotional response. "The point is you get stressed out if the sound moves," Wiseman says.
To gauge response to the sound, Wiseman suggests measuring stress hormones in urine. "We might be able to play back a positive sound track to rhinos and see if the stress hormones go down."
If the research continues to support the importance of sound to captive-animal health, zoos will be able to adapt, Wiseman says. 50 years ago, she notes, zoo relied on cages, but "now all of them have improved. I hope soundscapes might be another area for improvement."
Among her suggestions:
Using embankments or fences to block noise and rubber mats to insulate against severe ground vibration
Building a waterfall to create white noise that masks stressful noise
Silencing back-up alarms on zoo vehicles ("I'm sure a lot of animals don't like that")
Switching off equipment when possible
Zoos "are doing a wonderful job with the facilities they have," Wiseman says, "but if they are surrounded by freeways…."
Knowledge is power, Wiseman contends. "Are there particular frequency ranges associated with particular problems? Which species are sensitive to these frequencies? Maybe we can move them to another location with less noise."
– David J. Tenenbaum
A field long on promise and short on healing was energized on Oct. 15, 2014, when The Lancet reported on the transplant of retinal cells into 18 people who were blind because cells had died in the center of the retina.
The study focused on safety, but the hints that the transplant worked fed a desperate hunger for progress on stem cells — the long-awaited "spare parts" that may someday revolutionize medicine. Getting the story precisely backwards, CNN headlined "Stem cells help nearly blind see", then proceeded to explain that "Researchers say that human embryonic stem cells have restored the sight of several nearly blind patients — and that their latest study shows the cells are safe to use long-term."
In fact, the experts we talked to were optimistic about the safety issue — a huge hurdle for stem cells — but less sanguine about the "getting the blind to see" aspect.
So, how much progress are we making in stem cells, in the clinic and the laboratory?
The clinic part is easy: The U.S. Food and Drug Administration has not approved any non-experimental transplant of cells derived from the most versatile stem cells. These are the embryonic stem cells (ESC) that sparked all the attention 16 years ago, when they were first isolated by Jamie Thomson at the University of Wisconsin-Madison.
The laboratory part is promising, but more complex.
The cells replaced in the Lancet study, called retinal pigment epithelium, came from ESCs. The RPE provides essential metabolic support to photoreceptors — the cells that convert light into nerve impulses.
Patients in the Lancet study had either dry age-related macular degeneration (AMD) or Stargardt's macular dystrophy, which affects younger people. In both diseases, the RPEs die, which kills the photoreceptors. The dying starts at the center of vision, causing blindness exactly where detailed vision is most needed.
Each patient received three RPE-cell injections to one eye.
The diseases chosen illustrate the type of condition most appropriate to early human tests of pluripotent stem cells, says William Murphy, co-director of the Stem Cell and Regenerative Medicine Center at UW-Madison. "You need a substantial, unsolved clinical problem like AMD, ALS (Lou Gehrig's disease) or spinal cord injury."
"The new study was important from the basis of safety," says David Gamm, an associate professor of ophthalmology and visual sciences at UW-Madison, and an expert in retinal stem cell biology and cell-based therapies, "but I think it's difficult to read too much into the efficacy data."
The examiner and the patient both knew which eye was treated ("you can't fake that," Gamm says) and patients may try harder on vision tests with that eye after the transplant;
After repeated eye-chart testing, AMD patients may learn to use surviving retinal regions; and
The procedure replaced the RPE, not the photoreceptors. Because those light-sensitive cells in the center of vision are dead, the treatment at best could have "awoken photoreceptors on the edge of the lesion that are not dead but are not working because they don't have the RPE," Gamm explains.
Transplanting retinal cells may sound like a magic bullet, "But it's not like putting a new carburetor into a car," says Gamm. Eyes in advanced cases of both diseases are like "a beat-up engine. A lot of those not-so-subtle details were not discussed" in the article.
The study was more convincing on the safety issue, Gamm says, "but unfortunately that often does not get the attention it should get. The patients were followed for a median of 22 months, and nothing like the formation of tumors was seen, or cells getting to the wrong place. These are all important aspects of the study and were done well. I would flip the order of priority on the study to the safety aspect. That's the part that will advance the field."
But if the retinal cell transplant was the most impressive clinical trial to date, how much longer must we wait?
For people with untreatable disease, the 16 years since the discovery of human embryonic stem cells amounts to forever. But it's fair to say that when ESCs were first isolated, they resembled a gang of trouble-prone youths more than a disciplined cadre of bio-workers.
Their unlimited capacity to form any cell type gave embryonic stem cells plenty of potential for mischief, so the first step in putting them to work was to decipher the biochemical cues that guide stem cells into useful occupations.
For comparison, how does the timeline stack up against monoclonal antibodies, identical molecules that trigger or block specific biological processes? Monoclonals were dubbed a "magic bullet" when they were discovered in the early 1980s, but "It took 20-plus years for first therapies," says Derek Hei, director of Waisman Biomanufacturing at UW-Madison's Waisman Center.
Today, Hei says, monoclonals have finally become "a mainstay of biotechnology," used in treating cancer and autoimmune diseases like psoriasis and arthritis. "You can look for a similar timeline with cell therapy [derived from pluripotent stem cells]."
Even though biomedical technology has advanced rapidly since the 1980s, stem cells are "significantly more complex" than monoclonals, Hei says. "Cells can differentiate, integrate and replace dead cells, can secrete factors to help other cells survive, and it would not surprise me if it takes 30 years from the initial discovery, to where we have pluripotent stem cells becoming mainstream therapy."
Nonetheless, Hei was pleased with the latest results. "You don't really understand all the potential risks and technical issues until you start developing therapy. You will learn things in the first clinical trials that you can't learn in animal studies." It's safe to assume that unanticipated problems will need to be solved, he adds.
Even as Thomson's epic 1998 discovery focused attention on the blockbuster potential of "spare body parts," he and his colleagues already envisioned other jobs for the versatile stem cells.
Testing new drugs on a variety of human cells in a dish "is the immediate application" for stem cells, says Su-Chun Zhang, a professor of neuroscience at UW-Madison. Since the discovery of induced pluripotent stem cells (iPSCs) in 2007, researchers can grow cells from patients with various diseases, adds Zhang, a world expert on developing neural cells from stem cells. Having millions of cells, each carrying the donor's disease, enables use of "high-throughput" screening to test thousands of potential drugs in robotic equipment.
William Murphy, a biomedical engineer at UW-Madison, says "Industry has been ramping up screening," especially now that they can buy ready-made offspring of iPSCs. "I don't think iPSCs or ESCs have replaced the current drug-discovery system, broadly, but in particular areas, there are quite a lot of pilot studies to try understand" how to screen drugs against diseased stem cells.
Further technological development is needed to ease high-throughput screening, Zhang says. "We need ways to handle the cells in a uniform way, to put the chemical on, and do this as simply as possible." If it works, rapid screening of highly specialized cells "could be quite dramatic, can potentially shorten the process of discovery and increase the likelihood of success for a new drug."
ALS is a fatal degeneration of the motor nerves that signal muscles to contract, and Zhang has already begun screening for a drug to stop an aberrant protein that he recently discovered as a root of ALS.
But he says researchers could benefit from a more sophisticated model-in-a-dish. Since the nerves do not operate in isolation, an ideal model would include nerve cells joined to muscle cells. "That is currently not available, due to complexity," Zhang says. For one thing, when a nerve cell in a dish signals "contract!" to a muscle cell, the contraction can cause them to jump right out of the dish. "We are still trying to figure out a way to build such a system," Zhang says, "but we are not there yet.
Making life easy for the robots, he adds, is a "pure technology issue."
All of which is to say that pluripotent stem cells are a work in progress, especially in in terms of the ultimate pay-off: treating disease by replacing broken parts. Here are some critical areas for improvement:
Getting absolute control. "We know [controlling] differentiation is a challenge going forward for all applications," says Murphy. "We have to specify, standardize the target cell for transplanting; have to know what is going in. Standardization will be an ongoing area of focus for the next five to 10 years. It's a move from scientific discovery to engineering."
Cell maturity: How much is enough? Some situations require that mature cells be transplanted, says Murphy, who explains that partly developed pancreatic cells would not release insulin. But to replace cartilage in osteoarthritis, a slightly immature cartilage-forming cell is better, since very mature cells don't make that essential friction reducer. Immaturity is also valuable for neural-cell transplants, says Zhang. "If you move a mature cell, it will die. A young neuron in a hospitable location will connect to the right place. If it projects to the wrong place, that creates problems."
Getting to maturity. Even fully differentiated cells derived from pluripotent stem cells may perform like fetal cells, not adult ones. Heart muscle cells, for example, can have the pulse and pumping force of a fetal heart. "We have to find ways to rapidly mature cells so they mimic the properties of an adult," Murphy says. "It's a giant challenge facing the field, how to get a maturation process that typically takes years and do it in days or weeks in a dish. The kitchen sink is being thrown at this problem."
Getting realistic. Cells don't live in isolation and flat dishes of a single cell type are gross simplifications of a real organ. Therefore, researchers are developing "organoids" that fuse multiple cell types to screen drugs and model diseases. Gamm has generated in-dish combinations of the eye's retinal pigment epithelium and photoreceptor cells, and Murphy is developing a simple simulation of brain tissue. By recreating a disease in a dish, he says, "We can start testing the mechanism of disease progression, and compounds that influence the disease, but there are no simple technologies yet that can form organoids that are amenable to high-throughput screening."
Finally, we return our story to its roots — a study of the safety of transplanting cells to treat age-related macular degeneration. As we neared publication, Cellular Dynamics Inc., received a $1.2 million grant from the National Institutes of Health to grow retinal cells for AMD transplant experiments scheduled for 2017 or '18.
Another source of optimism is the growing recognition that developing cells heed chemical signals from their neighbors. "If you want to create a tissue structure in a dish, you might think the cells would have to be individually placed using external manipulation," says Murphy, "but it turns out for some applications, cells have the capability" to find their proper location.
"If you provide them with the right surrounding conditions, stem-cell self-assembly can build complex structures, tissues, even organs," says Murphy. "I don't think anyone would have anticipated that, but it's tremendously useful."
Bringing stem cells to the clinic has been a long struggle, but Murphy admits to "cautious enthusiasm. There remains a great deal of potential for treatment, but there are real technical and regulatory hurdles that have to be passed."
Stem cell products transplanted into the retina may or may not have restored vision in the recent study, says ophthalmologist Gamm, but the study was still a watershed. "You have taken cells derived from embryonic stem cells and put them into the retina, and did not hurt anybody; that's good. It's possible there may have been a limited positive effect on vision, and there was no negative. This was major, very positive."
– David J. Tenenbaum
A new study of lizards along Florida's Atlantic Coast shows that a long- lasting genetic change — evolution — can occur in just 20 generations. Scientists have seen evolution among microbes or fruitflies in the lab, but demonstrating a change in gene structure is more difficult for larger organisms living beyond the lab.
For decades, native Anolis carolinensis lizards have lived on islands built of sediment dredged during construction of the Intracoastal Waterway. In the 1940s, the closely related Cuban brown anole lizard (Anolis sagrei) entered Florida. Since the Cuban outcompetes the native for food and habitat, A. carolinensis lizards began moving higher into the vegetation.
The situation provided a natural experiment, says Yoel Stuart, a post-doctoral fellow at the University of Texas. Stuart is first author of new study in Science showing that this competition forced a change in native-lizard behavior and foot structure.
The behavior change started within months of the Cuban's arrival. The change in the genes that control the size and build of foot pads needed to hold onto branches happened within two decades.
Plants and animals, including the native anole lizard, took up residence after the artificial islands were created 60 or more years ago. Competition began with the arrival of the Cuban lizard in the 1990s.
During a 1995 survey, co-author Todd Campbell, an associate professor of biology at the University of Tampa, located six islands with only the native lizards, measured the height of their perches, then released Cubans on three of those islands. Within three months, the natives were roosting higher in the trees — but only on islands with the introduced Cubans.
Both lizard species eat insects and compete for territory, says Stuart. The competition "is a little bit of everything; they fight, eat one another and eat each other's food."
Was the native's choice to cede the lower elevations to the Cubans a simple behavior change, or was it associated with a genetic change — evolution? Higher branches are smaller, and higher leaves tend to be slicker, and so before investigating the genetics, the researchers predicted that the lizards would enlarge the toepads that give them such a good grip.
The observations for the new report began in 2010, when Campbell, Stuart and their colleagues compared six islands containing both species to five islands housing only natives. Again they noticed the different perching height, and also noticed that toepads on the natives were larger than before.
So far, so good. But what about genetics? After all, environment and behavior can have physical effects with no alteration of the genetic code. "Professional tennis players have a longer serving arm, likely because of tens of thousands of serves," says Stuart. With the lizards, "There might be some plastic changes that occur during growth that cause them to have different sized toepad just because they are living in trees, but this is not evolved."
To test whether the enlargement was genetic, the researchers raised individuals from both the invaded and native-only islands in a controlled environment. "We found those differences maintained in the lab, which suggests that the population has evolved," Stuart says.
Finally, using advanced sequencing, the researchers compared the displaced natives, and concluded that the larger toepads had evolved on each of the six islands they shared with the Cubans.
We remarked that 20 generations or less seemed a short time for an evolutionary change, and Stuart responded that biologists "are tending to realize that if selection is strong, it's possible to detect evolution rather quickly."
Finding a way to enter an environmental niche — like the upper branches — "is a really good way of partitioning resources, building up the number of species that can live in a community, and allowing species to coexist," Stuart says.
Stuart wrote that if the same rate of change in the standard deviation (a statistical gauge of variations in data) in the toepads were applied to men, "a back of the envelope calculation" showed that "the average U.S. male would be the height of an NBA shooting guard or small forward" after 20 generations.
UNITED NATIONS — Schools have shut down, elections have been postponed, mining and logging companies have withdrawn, farmers have abandoned their fields. The Ebola virus ravaging West Africa has renewed the risk of political instability in a region barely recovering from civil war, United Nations officials said Tuesday, hours after the World Health Organization reported that new cases could reach 10,000 a week by December — 10 times the current rate. New York Times, Oct. 14, 2014
Ebola has spread to a second Texas health care worker, and the World Health Organization has predicted a frightening climb in new infections. Health authorities are scrambling to contain a highly infectious disease that kills through massive bleeding.
In the absence of a prompt and effective response, the director of the UN's Ebola Emergency Response Mission, Anthony Banbury warned that the world faces "an entirely unprecedented situation."
As the global response lumbers onward and thousands die, we started wondering about the "classic dogma" of infectious disease: Pathogens become less virulent — less deadly — over time since live hosts spread infections better than dead ones. The rapid and mysterious disappearance of the Black Death (bubonic plague) from Europe in the middle ages helped raise the question: After killing as many as 200 million in Europe between 1346 and 1353, did the Yersinia pestis bacterium lose its "will to kill," in the interests of its own survival?
The comforting dogma is backed by some evidence — and rebutted by plenty of counter-examples, as we'll see.
Evolution is a numbers game, and this comforting dogma could allow us to think that deadly Ebola will lose its grip over time, as evolutionary pressures "persuade" the virus to sheath its claws. As many as 70 percent of West African Ebola patients are dying, far more than previously reported. The original source of infection is likely a virus-infected bat butchered and eaten by some unlucky African.
It's a nice notion that pathogens "always evolve towards less virulence," Lone Simonsen, a research professor in global health at George Washington University wrote to us. "But this is in fact not necessarily what will happen, as it depends on how the changes affect its transmissibility in the human host."
Transmissibility is the gauge of evolutionary "fitness," but the discussion of pathogen evolution can get "pretty muddy," says Caitlin Pepperell, an assistant professor of medical microbiology at the University of Wisconsin-Madison. "People tend to conflate two concepts: fitness and virulence. Virulence has to do with whether it kills you or makes you extremely sick." Fitness concerns the ability to infect others and expand its own population.
Some things have been around for a long time, and are adapted to the host," either through the host's immunity, or the development of a symbiotic relationship, says Ann Palmenberg, a common-cold expert and professor of biochemistry at UW-Madison. "Cytomegalovirus infects virtually everybody on earth, 99 percent, but it does not cause a lot of damage."
Cytomegalovirus infections are usually unnoticed, except in people with weak immune systems. Pregnant women can pass an active infection to their newborns.
A second virus with minimal symptoms is herpes simplex. "Herpes simplex causes a genital infection that will not hurt you much, but will be transmissible," says Palmenberg. "I assume it was much more virulent and killed people initially and then the virus thought, 'Hey, it's much better if I stay alive longer.'"
There are many ways that viruses can adapt to be transmissible, Palmenberg says. "You don't have to spread by lysing [dissolving] the cell; shedding a low amount over a long period [as with HIV] is a much better evolutionary strategy."
The host-microbe relationship can be unstable, Palmenberg says. Most of the countless bacteria in your gut are benign or beneficial, "but you get the occasional outbreak" of disease if they acquire disease-causing genes.
During the infection and replication process, "RNA viruses," including Ebola and HIV, insert DNA into host cells that force those cells to make new virus particles. Each human cell carries proof of an ancient stalemate between mammals and ancient RNA viruses, or retroviruses, Palmenberg says: "One-third of your genome is retrovirus," Palmenberg says. These RNA viruses infected our ancestors but instead of killing them, merged into their genome and became part of their descendants — of us.
Pathogen virulence does not always abate over time. For example, a 2013 study found that the West Nile Virus strain that reached New York in 1999 and a recently discovered "lineage 2″ version have both evolved toward greater virulence over the past 300 or 400 years. 1
West Nile, transmitted by mosquitoes, can cause fatal brain infections.
Concerning lineage 2, now found in Greece, Italy and Russia, the researchers reported, "As the virus has spread and continued to evolve, it appears to have become more virulent leading to increased numbers of cases of avian, equine and human disease."
In some pathogens, disease is almost an afterthought — harmful to the host and neutral to the virus. For example, the bacteria Streptococcus pneumoniae (the most common cause of meningitis acquired outside the hospital) is carried in the throat in healthy people. The bacterium may sit idly by as it competes with other bacteria for a niche in the throat, Pepperell says. But if its invasive genes activate, the bacteria can enter the blood stream and cause significant disease which does not, however, help it infect new hosts, which it easily achieves from its position in the throat or nose. "We probably don't really understand the driver of virulence in those organisms," Pepperell concludes. "This is not a case where it has evolved to reduced virulence."
In many cases, however, causing disease can boost fitness — measured by the number of new infections. Cholera and other diarrheal diseases, for example, are spread by infected stools that are a by-product of infection.
Similarly, the bacterium that causes tuberculosis needs to be transmitted via coughing, Pepperell says. In this case, as with cholera and Ebola, high virulence translates into high fitness.
Ebola is largely spread by contact with infected blood, and evolving toward lower virulence would reduce its frightening and frighteningly dangerous bleeding. "This is a theoretical example of lower virulence linked to lower transmissibility, and therefore not a likely evolutionary path for the virus to take," Simonsen says.
More than 30 years ago, another fearsome virus emerged from the African bush. HIV, which causes the immune disease AIDS, descended from SIV, a monkey virus. Since 1981, AIDS has killed about 36 million people.
Has the heavily-studied HIV undergone significant evolution, and if so, in what direction?
There is some evidence that some HIV strains cause varying levels of disease, says Thomas Friedrich, an associate professor of pathobiological sciences at UW-Madison, and head of virology services at the Wisconsin National Primate Research Center. "In evolutionary terms, HIV has not had a long time to evolve toward a peaceful coexistence with humans, if it is ever going to do that. If we let nature take its course, over one-half million years, the virus could or could not co-evolve with the host to make it less pathological."
HIV evolves in every patient, Friedrich said, as it struggles to survive attacks from the host immune system. "During the natural history of the infection of one person, we see evidence of adaptation to evade immune detection." This evolutionary ability also enables HIV to evade drugs.
The AIDS crisis gave a shot in the arm to all aspects of virology, and one in particular seems applicable to the Ebola crisis, says David O'Connor, a professor in the UW-Madison School of Medicine and Public Health. The drug used with some success on a few Ebola patients, ZMapp, contains three antibodies. Antibodies, delivered by the immune system or as medicine, can block the attachment points that a virus needs to infect a cell. With HIV, and likely with Ebola as well, a single antibody will quickly fail due to genetic changes in the virus — evolution. However, a "triple cocktail" of drugs, which is the standard treatment for HIV, has a better chance of success. "The three antibodies are going to synergize, and reduce the viral replication, without causing resistance to emerge," O'Connor says.
That's the case with AIDS, and the hope with Ebola. We won't know for sure until more of the difficult-to-manufacture ZMapp becomes available.
As we discuss viral evolution, we wonder: Is Ebola evolving now, and if so, in what direction? The only genetic study of the current outbreak documented variations among 300 base pairs in a genome containing 18,000 base pairs.
Whether that's a lot or a little, "is a bit like a Rorschach test for scientists," said O'Connor. "The real question is how many of these genetic changes are meaningful and are likely to rise up to dominate an individual's virus population," O'Connor says. "For example, how many of these could alter the shape of the virus to protect it from the immune system? Of the 300 base pairs ["letters" in the alphabet of RNA] with variation, there are only about 20 that could both change the shape of the virus and are found in more than 5 percent of viruses in an infected person. To me, that's not a lot of changes given how much Ebola replicates."
Pathogen evolution, in this case, is pretty straightforward: What doesn't kill them makes them stronger. The pathogens that escape the immune attack are those that have some trick to evade attack. When these viruses or bacteria multiply, their offspring are likewise resistant.
As mentioned, Ebola is composed of RNA rather than DNA, and "While we have evidence from other RNA viruses that a single base pair change can change the the structure or function of the virus," O'Connor says, "the vast majority of single base-pair changes will only modestly affect the ability of the virus to replicate, in one way or another, positive or negative."
Viruses that are unstable and frequently change shape are difficult to vaccinate against, but Ebola seems fairly stable, says O'Connor. "The issue of enormous diversity, over time, and in different populations, is probably the biggest single obstacle to a universal HIV or influenza vaccine. With Ebola, that does not seem as formidable an obstacle."
A preliminary test of a candidate Ebola vaccine on 20 human volunteers began Oct. 13 at the Walter Reed Army Institute of Research in Silver Spring, Md.
We started with the fantasy that Ebola would quickly abate, following its predecessors in its effort to stay alive, but we've learned that many factors affect whether a pathogen benefits by becoming more or less virulent, or staying pretty much as it is.
One more wrinkle: Not all changes in deadliness reflect a change in pathogen genetics; changes in medicine, the environment, host immune systems and human behavior and economics can all play a role. The recent Ebola outbreaks in Africa occurred in villages with few connections to the outside world, and they burned themselves out, says Pepperell, the tuberculosis researcher. "If you have a small, poorly connected population, the virus is going to disappear with a high mortality rate."
Once Ebola appeared in Monrovia, Liberia, and other cities in West Africa, the picture changed, she adds. "If you have a huge, well connected population, you will not run out of hosts quickly, and the selection pressure to soften the virulence is not very strong, and there is no advantage to evolving toward less virulence."
Pepperell adds that, "People who are not strong on evolutionary biology tend to think that everything that evolves is driven by advantageous mutations that increase in frequency, but many modes of evolution are neutral. Some aspects of bacterial physiology are really driven by chance."
The classic dogma is, "A vast oversimplification," Pepperell concludes. "The evolutionary strategies employed by different pathogens are different from each other, and I don't think you can make one simple rule to apply to all of them."
Edward Holmes of the University of Sydney, who has studied the evolution of viruses used to attack the hordes of rabbits that over-ran Australia in the last century, wrote us to say that the path of pathogen change, "All depends on the relationship between virulence and transmission, and which is (a) very poorly understood and (b) differs between each pathogen. In short, predicting how virulence will evolve in the long-term (or even the short-term) is very difficult and often little more than speculation."
Having heard all these criticisms of the dogma, there still is a grain of truth, says Palmenberg, a researcher into the common cold virus. "I think this is true of any host parasite relationship. If the parasite is so effective that it kill all its hosts, it will have killed itself. That has probably occurred millions and millions of times in evolution, but it's an end game."
In a sense, she adds, the pathogen will recognize, "'Oh *$&^^#%#(, we have killed ourselves!' The only examples we have in nature are those that were successful [in reducing virulence]."
None of which tells us how Ebola will end up if control efforts fail. It could simmer down, or it could run rampant. "There are Ebola-related viruses that are not as pathogenic, in the same family," Palmenberg says, "but there is no way of saying who is right and who is wrong. Ebola will be what it will be; we can't predict the endpoint. Even if Ebola kills all humans on earth, it will still have rats and bats that may count as hosts."
Moral of the story: Don't wait for evolution to save us. Unless a vaccine makes a dramatic appearance, we'll need to do the hard work of controlling this deadly virus.
– David J. Tenenbaum
By now, you know about robots that roll, fly, swim and walk, insect-like, on six legs. Are you ready for a robot that climbs a sandy hill in the fashion of the sidewinder rattlesnake?
In research in this week's Science, Daniel Goldman and company described using a robot to explore exactly how the sidewinder achieves the rare feat of climbing a steep, sandy slope.
"For years, we've spent a lot of time on problems involving animals doing interesting things in granular material, including lizards that swim in sand and turtles that run across sand," says Goldman, a professor of physics at Georgia Institute of Technology. "Then we asked what is the weirdest animal that moves on sand, and it's the sidewinder. People studied it 50 years ago, but nothing was done on a sandy slope."
The name tells it all: the sidewinder winds sideways up the hill. In tests at the Atlanta zoo, live snakes were able to climb a 31° sandy slope. That's 4° above the angle at which disturbed sand starts to avalanche. "It can get quite precarious," Goldman says. "Snakes, by doing God knows what, can ascend almost to the point where the material is cascading."
When the snake climbs a 20° sandy slope, the tracks show no signs of slippage.
The sidewinders, Goldman adds, are a "wonderful study subject. You put the snake in, and it climbs, it does what you want."
In the lab, Goldman's group sought to understand the snake's secrets by studying a robot created by Howard Choset at Carnegie Mellon University. "Our idea was to use robots … as a physical model, to test parameters that are inconvenient to test in the real world," meaning in a live snake. "We answered the questions by drag-force experiments on inclines, which had not been done before."
Goldman sees sidewinding as a hybrid of two synchronized waves: a horizontal wave down the body (best seen from above), and a vertical wave (best seen from the side). "These waves are phased, the robot and the snake both space the waves appropriately. The part of the body that contacts the ground is gently placed down, and peeled up gently."
The force that pushes the sidewinder uphill "comes from the body that is pressed down so the material is not destabilized," Goldman says. As it ascends, the snake subtly lifts sections of its body that would otherwise counter its uphill movement. "On a granular surface, there can be a small difference in how you move that dictates success or failure."
Anybody who has trudged up a steep sandy slope knows what happens to two-foots: We take two steps forward, and slide back one step (or more). Physically speaking, this occurs because sand and other granular materials "can transition from a solid to a fluid; it can slip out from under you," Goldman says.
Snakes must also avoid changing the surface to make their job more difficult. If they push away sand, they may deprive themselves of purchase. Or they may create ridges that turn into obstacles.
The live sidewinders seem to move effortlessly, especially when compared to the artificial one, but the point was not to create a cave-exploring robot but rather to figure out how flesh-and-blood sidewinders do it. "It's incredible, beautiful," says Goldman. "I'm a physicist by training. I had a love of herpetology as a kid, but I had no idea that locomotion was interesting … from the perspective of physics. I tend to think you strike a ball and it moves, but here's an internal mechanism that can manipulate the environment so it can move."
In recent years, many robot-makers, including Choset, creator of the artificial snake under study, have been fascinated with animals' astonishing ability to walk, run, climb, fly and swim. Here, the goal was different, Goldman says. "We think of it as biological physics, looking for fundamental principles. We are not using animals explicitly to inspire a better strategy in robots. We are using the robot to understand the animals at a higher level. It's a scientific enterprise, not a design or engineering enterprise."
– David J. Tenenbaum
Solar-powered photosynthesis — the creation of sugars in plants — is the basic key to virtually all life on earth. You can — and should — say a lot of good things about photosynthesis, but in terms of efficiency, there's often room for improvement.
The enzyme rubisco is at the heart of a devilishly complex process that converts atmospheric carbon dioxide into sugar. Rubisco, however, also catalyzes oxygen in a process called photorespiration that reduces the overall efficiency of photosynthesis by about 30 percent.
The ultra-efficiency of maize and other "C4″ plants is due to their ability to avoid photorespiration. Photosynthesis has been around for 3 billion years (more or less, but who's counting?), and it comes in several flavors, each with its own structures, enzymes and efficiencies. One of the most attractive comes from cyanobacteria, an ancient life form also called blue-green algae.
Photosynthesis matters because as world population grows, food production needs to keep pace. "In the last decade, we are not getting the increase in yield seen in previous decades, especially in rice and wheat," says Maureen Hanson, a professor of molecular biology and genetics at Cornell University, "so we are going to have to use biotech strategies." Such strategies include genetic engineering that boost the capture rate of solar energy.
On Sept 19, Hanson and colleagues reported the successful transfer of cyanobacteria genes into experimental tobacco plants as a major step to jump-start photosynthesis. Beyond boosting production of crops and biofuels, faster photosynthesis would also speed the removal of carbon dioxide from the atmosphere, cutting us a bit of slack against global warming.
Having said all that, the recent advance did not actually speed plant growth, since the researchers did not transfer genes for a structure called the carboxysome, which cyanobacteria evolved to concentrate carbon dioxide around rubisco.
The rubisco in most crops, you must understand, is a prisoner of its past. The enzyme evolved when the atmosphere contained little oxygen, so there was no evolutionary pressure to shape an enzyme that would tone down that wasteful oxygen reaction.
As oxygen rose from nil to about 21 percent in the atmosphere, photorespiration became more of a problem, and many plants (including the predecessors of many crops), evolved a slower form of rubsico.
Other photosynthetic organisms, including maize and cyanobacteria, responded by building "CO2 concentrating mechanisms." Cyanobacteria's concentrator is contained in a structure called the carboxysome, which pumps carbon dioxide toward rubsico.
Once it evolved the carboxysome, cyanobacteria derived nothing but advantages from its highly active rubisco variant. Because most crops never evolved a similar concentrating structure, "this was an opportunity to put it in and improve the efficiency of photosynthesis," Hanson says. Transferring the entire cyanobacteria system could, in theory, raise efficiency by 36 to 60 percent.1
Hanson concedes that her Nature experiment did not transfer the carboxysome. "This was the first step in putting the entire cyanobacteria mechanism for improved photosynthesis. Without the cyanobacteria carboxysome around the rubisco, these plants actually grow slower than ordinary tobacco plants," she says.
Hanson and others are working on the carboxysome transfer, which requires six genes, in addition to the three needed for the rubisco transfer. "With the sheer number of genes, and needing to get expression at the proper levels, it's going to be more time consuming, trickier," Hanson says.
Having watched the furor over transgenic corn and soybeans, we wondered about the acceptability of the new system. "There's no question people who don't like GMOs [genetically modified organisms] will oppose this on principle, but I fail to see how this would be harmful to anybody," says Hanson. "You can buy cyanobacteria as a food supplement."
We had to think, though, that it's also a source of neurotoxins in the environment …
Because maize is already exempt from photorespiration, Hanson expects the early work to focus on soybean. Planted on 84 million acres, it's the number-two U.S. crop.
In effect, the effort would give soybeans efficiency of maize, Hanson says. The Gates and Rockefeller foundations are funding similar genetic engineering to improve photosynthesis in rice, she adds.
– David J. Tenenbaum
If the world is seeming crowded, you ain't seen nothing yet. While many estimates foresee population growth running aground long before 2100, a new study drowns that idea by projecting that 9.6 to 12.3 billion people will cohabit the third rock from the sun by 2100.
Current population is 7.26 billion, and rising fast.
If you think more is better, that's good news. But you worry if you think population growth feeds shortages of fresh water, border wars, ethnic strife and environmental devastation. Can we feed, clothe, house and employ so many people on one planet?
A study published in Science Sept. 19 was grounded on the two main drivers of future population: life expectancy at birth and total fertility — the number of children born per woman over her lifetime. But study leader Adrian Raftery, a professor of statistics and sociology at the University of Washington, Seattle, employed them differently.
Demographic agencies have traditionally asked experts to put numbers on future life expectancy and fertility. Instead, Raftery says, he and his colleagues at the United Nations Population Division performed a statistical analysis of historic rates in all countries over the last 60 years.
Then, in a multi-layer statistical exercise, they created thousands of future scenarios through 2100. The procedure was analogous to climate models, which can be run thousands of times to help assess the probability of each particular projection.
The outcome was unmistakable: growth continues, especially in Africa (current population 1.2 billion), which has four chances in five of having a population between 3.5 and 5.1 billion in 2100. Raftery concedes these are "giant numbers… but if you project forward based on fertility and mortality, that's what you get. It's not unprecedented; it would give a population density in Africa that's about the same as China now."
Nigeria's population, currently 160 million, is projected to reach 914 million.
Why is Africa's population growing?
* Good news: declining mortality from the HIV/AIDS epidemic.
* Bad news: Only 75 percent of African women in relationships who want contraception have access to it.
* More bad news: Education for girls is lagging, even though girls in school have more opportunities and access to information about controlling fertility. "Although girl's education has improved in a lot of African countries, there are still many countries where a high proportion of girls don't complete elementary school," Raftery says.
We were skeptical that food-short Africa could survive such a dramatic increase, and Raftery told us his study did not explicitly consider war, famine or disease. Could Africa really survive with the density of China, a country that is buying land in Africa to feed its people?
We had trouble imagining African nations buying land abroad to feed themselves, but Raftery stuck by his analysis, maintaining that historic demographic data account for historic, real-world cataclysms.
If its results are widely accepted, the new study may reignite concern about what was once called "the population bomb." "Until the 1990s, population was a major global concern, then it fell off the world agenda, in favor of [matters like] HIV, climate change and terrorism," says Raftery. "People felt it was a problem that was in the process of solving itself. These new results show that was premature; there's a need to put the population issue back on the world agenda."
All of this growth, Raftery says, "will obviously present environmental, health and social challenges for these countries going forward, which would be easier to deal with if the population grew less quickly." Population feeds global warming, for example, as more people do the things that release greenhouse gases.
Aside from Africa, population growth will cease in most regions long before 2100, causing an inevitable decline in the ratio of working adults to retirees. Even Brazil, which now has almost nine workers per retiree, will only have 1.5 by century's end, says Raftery. "That's lower than Japan currently, and the same is true of India, China and Egypt. Countries we think of having young populations are going to face exactly the same problems with an aging population."
In Europe, Japan and North America, the issue is already on the table; the rising age for full U.S. Social Security benefits is one attempt to ease the imbalance.
Some suggest growing more babies way to ensure a comfortable retirement, but that will not work forever, says Raftery. "In the end, high birth rates is a pyramid scheme. Eventually the basic issue becomes, if you are going to live to 90, you are going to spend a lot of time in retirement. If you are retired for 25 years, and spend 40 years working, you are not going to have many more workers for each retiree."
– David J. Tenenbaum
Science books often tell how a scientist has explored one bit of the world. Medical stories tell how a valiant doctor struggled to cure one disease. But this scientific-medical history tells us how one courageous scientist beat the odds and saved hundreds of scientists from deportation and death.
The scene in Arthur Allen's new book was World War II Poland, a country wracked by oppression, occupation and deportation. In the city of Lwow, Rudolf Weigl's lab made vaccine against typhus, a dreaded bacterial disease that, spread by body lice, afflicts soldiers and refugees.
Lwow, now Lviv, Ukraine, was occupied by the Soviets in 1939, the Germans in 1941, and then the Soviets once again in 1944. Weigl had developed the best typhus vaccine in the world, so his skills were in great demand during the war.
Item #1 on Weigl's vaccine recipe was herds of lice to grow the typhus bacterium. Since lice feed on human blood, that entailed a herd of human blood donors. In Weigl's lab, these "feeders" strapped cages to their legs, waited 45 itchy minutes as the parasites drank their fill, and then replaced the cages with new ones.
That need for human subjects allowed Weigl to employ scientists and mathematicians, saving them from deportation (and likely death) by whichever tyranny happened to be cracking the whip at the moment.
Weigl published little on his vaccine, a departure from the scientific canon that "had an unintentionally positive effect …," Allen writes. "In the absence of a 'cookbook' on how to mass-produce the Weigl typhus vaccine, the Soviets and the Nazis alike would depend on Weigl himself to continue its production."
A contrast to Weigl's "fantastic laboratory" comes from descriptions of atrocious Nazi "medical experiments" at the death camps Auschwitz and Buchenwald, where a department of typhus and vaccine research attempted to keep the German military machine healthy.
Much of what Allen learned about the Weigl lab came from Waclaw Szybalski, who worked there with his father and brother. As Allen writes, "On two occasions, Weigl saved the Szybalskis from deportation by insisting that they were crucial to his laboratory operations."
Szybalski, who later became a noted geneticist at the University of Wisconsin-Madison, told us that Weigl "was protecting his friends, Poles, Jews, Armenians, first from the Russians for two years, then from the Germans for the next three years. He protected whoever he could, he was not afraid." Both the Germans and the Soviets "thought he was very useful. He gave a hard time to the KGB [Soviet secret police], said 'You are arresting my people and so I cannot serve.'"
Somehow, Weigl managed to survive and protect, Szybalski says. "Some people have so much personality that even your enemy is afraid to touch you."
And that, finally, expresses the heart of this book: How scientists can live in the world, instead of apart from it. When cruelty became normal under two of the most savage tyrannies of the 20th century, Rudolf Weigl had the courage, intelligence and scruples to resist.
– David J. Tenenbaum


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Create a set of these delightful Kristi Parker placemats to adorn your table every season of the year! They are quick and easy to make, using the fusible applique by machine method. Give them as gifts to all of your favorite people.
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Whoopi Goldberg 666 Park Avenue Guest Star
Whoopi Goldberg will guest star on ABC's new supernatural drama series "666 Park Avenue" on December 2.
The multi-talented performer will play Maris Elder, a woman who hypnotizes Jane, played by Rachael Taylor, and sends her traveling back in time to 1927 in a bid to find out where she disappeared down the spiral staircase, according to ABC.
Executive producer David Wilcox, said that the writers wrote the part of Maris Elder specifically for the Oscar winner. Wilcox said:
"(Whoopi will play) a mysterious resident of the Drake, who helps Jane unlock the secret of the building's true evil origins … Whoopi's an incredible actor, so when we heard that she was a horror fan, we wrote the role for her."
"Her time-travel adventures unlock secrets long hidden in Peter Kramer's apartment, where his wife was murdered, and shows Jane that her family has a dark legacy that's tangled with The Drake's history," the network said in a statement.
Goldberg is currently most popular as a co-host on the talk show "The View." However, she is a well-known American actress, comedian, singer-songwriter, author, and political activist.
She won an Oscar her role in the 1990 romantic fantasy film "Ghost," as psychic Oda Mae Brown.
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The violent and sudden end to a school trip to the Dominican Republic has not sparked a rush to keep Manitoba students at home.
Senior educators are advising against a hasty reaction after a shooting in the Dominican Republic cut short a trip there by students from two Manitoba high schools.
The educators fear an overreaction to the episode could affect dozens of international school trips from Manitoba.
"We are awaiting the conclusion of the review by the school division before determining if a province-wide review is necessary," Education Minister James Allum said in a statement Sunday.
Students from high schools in Ste. Anne and St. Jean Baptiste returned to Winnipeg at 5 a.m. Saturday after burglars shot a Dominican man they were staying with and briefly held five of the Manitobans at gunpoint early Friday morning.
"A lot of crying, but they were happy to see their families and friends. They're in good hands," Division Scolaire Franco-Manitobaine superintendent Alain Laberge said. "The families asked... to be left in peace."
The students from the school division were on an annual humanitarian mission to help an orphanage school in a rural area. None of the 26 students and adults was hurt, but the owner of their dormitory compound is in critical condition.
Laberge said he will conduct a thorough review, but said the same thing could have happened anywhere, including in Winnipeg.
"Before we throw out the water with the baby in it, I want to sit down and find out what happened," he said. "Going into some countries, you are confronted with the pain these countries are going through."
Allum issued a statement expressing confidence in the DSFM to handle the matter, and Manitoba Teachers' Society president Paul Olson urged that no one make any hasty decisions.
"It was a terrible event," Olson said. "It sounds like it was well-handled. We have home invasions in Winnipeg, but we still live here.
"Once you've guaranteed basic safety, you want the education system to respond rather than react," Olson said. "Can you learn anything? You don't want people to overreact -- school trips are an important part of a teacher's tool kit.
"You do want oversight and you do want a second look. I do worry something this frightening could get people to get cold feet."
Laberge was uncertain how many of the 18 students and eight teachers and parent-chaperones would be in school today at âcole Pointe-des-Chenes in Ste. Anne and âcole regionale Saint-Jean Baptiste.
The DSFM will have crisis-response staff in the schools today.
Students have been going to help the orphanage near Puerto Plata for several years, Laberge said. They had barely arrived Thursday when at least three gunmen broke into their compound and confronted four girls and a female teacher about 1:45 a.m. Friday.
The owner of the dorm, who Laberge was told is Canadian, intervened and was shot several times.
"It's a project we've been doing for years," Laberge said. "It's kind of a compound, four students per room, with a chaperone.
"The burglars went to the first room. They just wanted money, cameras."
Laberge said the students were not carrying much money because it was seen as "an invitation to be robbed."
"One of the girls spoke Spanish. She said, 'We have nothing,' " Laberge said.
That's when violence erupted.
"The owner (of the building) quickly stepped in between the kids and the burglars," he said. "All the students in the other rooms went into their closets, hiding."
The robbers fled and police soon arrived. DSFM officials were alerted within minutes and decided to pull the kids right away and bring them home.
They spent Friday evening in an airport in New York City and got back to Winnipeg at 5 a.m. Saturday. Since they flew out of Winnipeg at 1 a.m. Thursday for the trip, the students had not had a decent night's sleep since they were in their own homes Tuesday.
The DSFM is covering all the costs. Laberge is trying to find out the likelihood of any of the 26 in the group being called back to the Dominican Republic to testify in court -- five witnessed the shooting and saw the gunmen.
"This is where we want to ask questions," Laberge said. "They're witnesses; they might be called there again."
Out-of-country school trips in Manitoba public schools need the approval of the superintendent and school trustees. After 9/11, the province called a halt to foreign trips. Even after restrictions began to ease, some divisions were reluctant to let students go to even Minnesota or North Dakota.
School divisions generally reserve the right to cancel a trip if Ottawa issues warnings about dangerous conditions. School officials have rejected a few trips in the ensuing years, including one to Egypt, where German tourists had recently been murdered in an attack on their bus.
Olson said he can't recall anything remotely like this incident happening on a Manitoba school trip.
"Your kids go off to do the right thing -- I can't imagine the relief, once you know your kids are safe," he said.
Republished from the Winnipeg Free Press print edition February 3, 2014 A3
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Rueber Hopes For #1 in World
by KDLT Sports
June 18, 2012 6:43 PM
Very few can say they're the best at what they do.... but Stephen Rueber is just that....in the field of Taekwondo. Growing up in Canton he fell in love with martial arts....For the last 12 years he's been competing against the best in his sport.
Steve Rueber: "I train anywhere from 15-16 hours a week between my workouts here and class and my workouts at the gym as well."
As a first degree black belt.... he's known to many as the best in the world. Last year came out on top in nationals and won 7 out of 8 regional tournaments. But he's not done yet.
Rueber:"got 3rd in worlds last year..."
Rueber says he hopes his hard work pays off.
Rueber:""What drives me with perseverance and self-discipline, honor and respect to make my friends and family proud to do the best that I can."
And his determination shines through....
Rueter:"I am very very competitive… right now I'm just trying to do justice to Sioux Falls and South Dakota and represent the best I can."
But his aspirations don't stop there... Rueber wants to give back to others.
Rueter:"I'm going to be involved with martial arts and TK for the rest of my life.. maybe I wont be competing forever but I would certainly like to be involved with martial arts as an instructor and as a student."
A competitor and future instructor who has the potential of holding the world in the palm of his hands.
Betsy Jibben, KDLT News, Sioux Falls.
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Admiralty Resources' Aggressive Exploration Yields Results, La Chulula Defined As Priority Target 0 commentsJun 29, 2012 2:35 AM
Admiralty Resources (ASX: ADY) is on the right path to building its iron ore Resource base along the highly prospective Atacama Fault in the Chilean iron ore belt, with the identification of La Chulula as a high priority target.
Results from a high resolution ground magnetic survey has demonstrated the size potential of La Chulula, with the prospect shown to be 250 metres by 900 metres and to extend to depths of up to 600 metres.
The prospect is located near surface and has returned magnetic susceptibility levels higher than 0.9 S.I. units between 600 metres and surface elevations.
The results of Phase I showed the La Chulula Prospect could extend itself further south of the boundary of the surveyed lines and a 3D inversion of the results showed the potential ore body cut-off.
Phase II was carried out considering the size of the La Chulula anomaly and the potential extension of the magnetic response further south of the boundary of the Phase I survey lines.
The Phase II program was aimed at fully defining the extension of La Chulula and clearly separating it from the Mariposa Prospect.
Preliminary results from earlier exploration show the existence of three types of mineralisation at the La Chulula target - disseminated magnetite (10-15% iron), vetillas/veins (20-30% iron) and massive magnetite (50-60% iron).
A 10-hole, 2,650 metres reverse circulation drilling program began at La Chulula in early
Five holes and 1,350 metres of drilling has been completed so far, with the next five holes expected to be completed by mid-July.
Admiralty's goal
The end goal for Admiralty is to produce high quality iron from magnetite using dry magnetic separation.
The Mariposa Prospect, which is the most advanced target at Harper South, is the subject of an engineering mine plan to produce 1.2 million tonnes of 63% iron per annum over a 20 year mine life. This is expected to be completed in September 2012.
There are two types of mineralisation found in the district - magnetite style in the east and IOCG in the west.
Admiralty has confirmed seven targets in the Harper South District, with a further two anomalies identified by high resolution ground magnetic survey.
The most advanced target is Mariposa, advancing targets are La Chulula and Soberana, and early exploration targets are Negrita, La Vaca and Mal Pelo.
Strategically located
Admiralty holds a total land position of 6,800 hectares in the Chilean iron ore belt just 46 kilometres from the Guacolda and Las Losas ports.
The company's projects are strategically located 7 kilometres from the railway line owned by Ferronor S.A. and 3 kilometres from the Pan American highway, with direct access.
Harper South covers around 2,498 hectares of the total landholding and is Admiralty's most advanced exploration district with a JORC Resource of 168 million tonnes at 18% iron at the Mariposa prospect.
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3520 Wheeler St.
Dallas, TX 75209
Fax: N/A
< 5
< 500k
Hardware->Telecom Hardware
SIC Code:
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