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Economist说我这周5个免费文章看完了,找好的一篇越障贴不过来。所以今天的越障比较简单,大家可以放轻松的读一下了。 速度还是有点意思,第二篇是上周末的breaking news。Enjoy。 [Speed1] Why Genes Don’t Predict Voting Behavior
When it comes to complex behaviors, gene variants don't count for much
Dozens of studies in the past few years have linked single genes to whether a person is liberal or conservative, has a strong party affiliation or is likely to vote reguarly. The discipline of “genopolitics” has grabbed headlines as a result, but is the claim that a few genes influence political views and actions legitimate?
We don't think so. The kinds of studies that have produced many of the findings we question involve searching for connections between behavior and gene variants that occur frequently in the population. Most of the 20,000 to 25,000 human genes come in hundreds or thousands of common variations, which often consist of slight differences in a gene's sequence of DNA code letters or in repeats of a particular segment. For the most part, scientists do not know what effect, if any, these common variants, known as polymorphisms, have on the functioning of the proteins they encode. Genes predict certain well-defined physiological diseases—such as hereditary breast cancer and the risk of developing Alzheimer's disease—but when it comes to complex human behaviors such as voting, the link is tenuous at best.
One of the most prominent papers showing a link between a few polymorphisms and political behavior was published by James Fowler and Christopher Dawes in 2008 in the Journal of Politics. They concluded that people who possess certain variants of a gene called MAOA are more likely to vote than those who do not and that people with a particular variant of a gene known as 5-HTT who regularly attend religious services are also more likely to vote. We do not believe that these conclusions are right.
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[Speed2] Like most claims that a specific gene predicts variations in a particular behavior, the findings were based on what is known as a candidate gene association study. Instead of surveying all the genes in the human genome for possible associations with a given trait, such studies look for potential links between polymorphisms for one or two candidate genes and a specific trait. This type of study can be a relatively inexpensive way to conduct research because it usually depends on large databases of information that already exist, but it can lead researchers astray.
We identified two major problems with the study of Fowler and Dawes. First, they misclassified the genes they were studying in a way that amplified the statistical significance of their findings. Second, their methods fell short of adequately taking into account population stratification, in which the frequency of polymorphisms varies from one ethnic population to another as a result of unique ancestral patterns of migration and mating practices. (This is a common problem in the field.) When we analyzed the different ethnic groups in detail, we found inconsistencies. For instance, in the case of Asians, Native Americans and nonwhite Hispanics, we saw the opposite trend—toward less voting.
Yet we have more fundamental issues with these kinds of studies. The same polymorphisms of these same two genes that have been tied to voting are also said to predict variation in other behavioral and physical traits—irritable bowel syndrome, schizophrenia and premature ejaculation. Such broad findings beggar belief. The idea that a pair of genes could be responsible for so many disparate behaviors is biologically implausible.
Recent research provides growing evidence that genetic influences on human behavior involve thousands of different genes, which influence one another and the environment in intricate ways. Differences in aggression among fruit flies, to take just one example, entails the activity of more than 4,000 genes. The chance that any complex human behavior—such as voting—might have one or two major predisposing genes is practically zero. [334]
[Speed3] NASA rover finds no methane on Mars, yet Non-detection casts doubt on previous claims of methane hotspots due to microbes.
The question of methane on Mars isn’t dead yet, but NASA’s Curiosity rover has at least put a first nail in the coffin.
On Friday, scientists on Curiosity announced that they had not detected methane with any confidence — though they left themselves some wiggle room for revision, saying that the 95% upper and lower confidence limits of the non-detection varied between -2 and 5 parts per billion.
“Bottom line, we have no detection of methane so far,” says Chris Webster, a Mars scientist at the Jet Propulsion Laboratory in Pasadena, California, and principal investigator for the Tunable Laser Spectrometer (TLS), the rover instrument central in seeking the gas. “Mars may yet hold surprises for us.”
On Earth, life is responsible for the vast majority of the planet’s atmospheric methane, which exists at levels of about 1,700 parts per billion. If methane were detected on Mars, microbes could thus be invoked as its source, though trace amounts could also be produced via comet impacts or chemical reactions underground involving rocks and hot water.
Various campaigns in the last decade have claimed to detect martian methane at levels as intriguingly high as 30 parts per billion1 and 45 parts per billion2. But more perplexing was the way that the methane signals sometimes appeared as hotspots, or plumes, and then disappeared — implying both a sudden injecton, as well as an unknown process to destroy the methane quickly, which would otherwise mix in the atmosphere and persist. Skepticism for these claims has abounded (See “Curiosity set to weigh in on Mars methane puzzle” ).
While the Curiosity result would also seem to cast doubt on previous claims, one proponent, Michael Mumma, of Goddard Space Flight Center in Greenbelt, isn’t backing down yet. The plume he detected back in 2003 was in a different part of the planet, and could have dispersed by now, nearly a decade later, at the rover’s landing site. “Gale crater is not an auspicious place to search for current releases,” he says. [332]
[Speed4] The TLS team will continue to take small gulps of Mars air in an effort to beat down their uncertainties. They have used the instrument four times, which works by firing a laser into a small mirrored chamber; if methane is present, absorption lines should appear at key frequencies. But on the first two occasions, a large methane signal of 7 or 8 parts per billion was present. The team quickly realized it was due to contamination by residual Earth air. The team has pumped out this residual air as best they can, and have also devised a workaround — but it’s a more complicated protocol that increases the systematic errors. The TLS team has another trick that it plans to use in the coming weeks or months that would make the methane show up far more noticeably. By stripping the Mars air of carbon dioxide and concentrating it prior to illuminating it with the TLS laser, Webster says the concentration of methane can be increased by a factor of 10 or more, making it stand out sharply. He says the instrument should ultimately be able to detect methane at levels as low as 100 parts per trillion.
But at that sensitivity — not as good as had been promised pre-launch — many natural processes could be responsible. Moreover, another key capability of the TLS will be mooted: distinguishing between methane with different isotopes of carbon. The team had hoped to see the slightly different absorption lines associated with methane comprised of carbon-12 — the type that microbes tend to produce — and methane made with the carbon-13 isotope, which tends to be non-biological in origin. Webster says these differences would be noticeable only if methane existed at levels of several tens of parts per billion, which is now ruled out. [296]
[Speed5]
Were Dinosaurs Destined to Be Big? Testing Cope's Rule ScienceDaily (Nov. 2, 2012) — In the evolutionary long run, small critters tend to evolve into bigger beasts -- at least according to the idea attributed to paleontologist Edward Cope, now known as Cope's Rule. Using the latest advanced statistical modeling methods, a new test of this rule as it applies dinosaurs shows that Cope was right -- sometimes.
"For a long time, dinosaurs were thought to be the example of Cope's Rule," says Gene Hunt, curator in the Department of Paleobiology at the National Museum of Natural History (NMNH) in Washington, D.C. Other groups, particularly mammals, also provide plenty of classic examples of the rule, Hunt says. To see if Cope's rule really applies to dinosaurs, Hunt and colleagues Richard FitzJohn of the University of British Columbia and Matthew Carrano of the NMNH used dinosaur thigh bones (aka femurs) as proxies for animal size. They then used that femur data in their statistical model to look for two things: directional trends in size over time and whether there were any detectable upper limits for body size.
"What we did then was explore how constant a rule is this Cope's Rule trend within dinosaurs," said Hunt. They looked across the "family tree" of dinosaurs and found that some groups, or clades, of dinosaurs do indeed trend larger over time, following Cope's Rule. Ceratopsids and hadrosaurs, for instance, show more increases in size than decreases over time, according to Hunt. Although birds evolved from theropod dinosaurs, the team excluded them from the study because of the evolutionary pressure birds faced to lighten up and get smaller so they could fly better.
As for the upper limits to size, the results were sometimes yes, sometimes no. The four-legged sauropods (i.e., long-necked, small-headed herbivores) and ornithopod (i.e., iguanodons, ceratopsids) clades showed no indication of upper limits to how large they could evolve. And indeed, these groups contain the largest land animals that ever lived.
Theropods, which include the famous Tyrannosaurus rex, on the other hand, did show what appears to be an upper limit on body size. This may not be particularly surprising, says Hunt, because theropods were bipedal, and there are physical limits to how massive you can get while still being able to move around on two legs.
Hunt, FitzJohn, and Carrano will be presenting the results of their study on Nov. 4, at the annual meeting of The Geological Society of America in Charlotte, North Carolina, USA. As for why Cope's Rule works at all, that is not very well understood, says Hunt. "It does happen sometimes, but not always," he added. The traditional idea that somehow "bigger is better" because a bigger animal is less likely to be preyed upon is naïve, Hunt says. After all, even the biggest animals start out small enough to be preyed upon and spend a long, vulnerable, time getting gigantic [418]
越障
SARS Veterans Tackle Coronavirus A recently completed genome sequence of the new virus has sped up efforts to come up with a diagnostic test to screen for it
Scientists who helped to fight the 2003 epidemic of SARS (severe acute respiratory syndrome) have sprung into action again to investigate the latest threat: a new SARS-related virus that has killed one man and left another seriously ill. Last week, the researchers reported the genome sequence of the new coronavirus and the first diagnostic tests to screen for it — two major advances that will help in efforts to control the pathogen if it turns into a wider menace. The SARS virus was identified in March 2003 as the cause of an epidemic that had emerged in China several months before, and which had spread rapidly around the world. It caused nearly 8,500 cases and 916 deaths before it was finally contained in July 2003. At the time, scientists knew almost nothing about the virus — coronaviruses had received scant attention until then because they had previously caused little more than colds.
The research and public-health networks established during the SARS epidemic — and the body of coronavirus research that followed — puts scientists today in a much stronger position to understand the latest virus and to develop countermeasures such as drugs and vaccines, should they be required. “We are all collaborating again,” says Christian Drosten, director of the Institute of Virology at the University of Bonn Medical Centre in Germany, who has been involved in developing diagnostic tests for the pathogen. “This is the old SARS club.”
So far, there is little evidence that the virus poses any major public-health threat. No one who came into contact with the two cases has fallen ill, suggesting that the virus does not spread easily between humans. Nonetheless, health authorities worldwide are not being complacent — respiratory viruses can cause pandemics, and this strain has already caused serious disease. The key question now, and one that the diagnostics will help to answer, is whether the two cases are isolated events or whether the virus could strike again and perhaps adapt to spread more easily in humans.
The first case was a 60-year-old man admitted to the Dr Soliman Fakeeh Hospital in Jeddah, Saudi Arabia, on 13 June with severe pneumonia and acute renal failure, who died on 24 June. Post-mortem tests were negative for influenza and the other usual suspect viruses, so Ali Mohamed Zaki, a microbiologist at the hospital, ran a coronavirus test at the suggestion of Ron Fouchier, a virologist at Erasmus University Medical Centre in Rotterdam, the Netherlands, who had worked on the SARS virus. On 20 September, Zaki posted his results on the Program for Monitoring Emerging Diseases (ProMED), an online disease-reporting system, confirming that the coronavirus tests were positive. A week later, Fouchier’s group, which had received an isolate of the virus from Zaki in early July, published the pathogen’s genome sequence in the GenBank database. The genome confirmed that the pathogen was a new coronavirus, the closest relatives of which are found in bats.
Two days after seeing Zaki’s ProMED post, the UK Health Protection Agency reported that it had found a second case: a 49-year-old man from Qatar who fell ill on 3 September with similar symptoms. He was admitted to intensive care in Doha on 7 September and then transferred to a London hospital, where he remains seriously ill. Comparing a fragment of the genome sequence of his virus with that of the first case showed that the two were identical. The viral genome sequence also enabled an international group of researchers, including Fouchier and Drosten, to quickly devise diagnostic tests that look for short, characteristic stretches of the virus’s RNA. The collaboration came easily, says Drosten: “The good thing here is that these are all friends from the SARS time.
Existing SARS research provides a useful template for further investigation of this latest coronavirus, adds Drosten. Scientists will use animal models such as mice, ferrets and macaques to study the pathogen’s virulence and how it spreads, for example. They will also test whether antivirals and vaccines developed since SARS to treat other coronaviruses are effective.
A key experiment, he says, will be to find where the new virus latches on to the human lung. Some scientists suspect that it might bind to the angiotensin-converting enzyme 2 (ACE2) receptor, as did the SARS virus. That could be both good and bad news. The receptor is found deep in the lungs, where infections can cause severe disease, but viruses nestling there are less apt to be coughed or sneezed into the air than are those found higher in the lungs.
“Receptor-binding properties could also be crucial to the success of potential control measures, should they be needed,” says Drosten. SARS was contained by isolating suspected cases, partly because it did not spread quickly, but also because those it infected became very ill before the virus moved into the upper respiratory system. That made cases easy to identify before the patients started spreading the virus. Flu pandemics, by contrast, are impossible to stop, largely because those infected with the virus spread it to others for days before they show any symptoms of infection.
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