Say what you will about Sarah Palin’s experience, competence and views on (to pick just two of Lab Notes' favorites) creationism and climate change, give her this: she's got that whole beauty queen thing going for her. Roll your eyes if you must, but in a finding that will further depress anyone who still thinks that voters are rational scientists, for female pols, looks really, really matter.

According to a new study, to win the votes of men as well as women, female political candidates need to be seen as attractive. “Even female voters seemed to tap into the cultural expectation that women who are attractive as well as competent are more worthy of high status roles,” said psychology researcher Joan Y. Chiao of Northwestern University, who led the study, which is being published tomorrow in the online journal PLoS One.

The research is part of the growing recognition that voting decisions do not reflect logical, rational analyses of candidates’ positions and records, but an emotional, even visceral reaction. Or as Chiao and her colleagues put it, “Contrary to the notion that people use deliberate, rational strategies when deciding whom to vote for in major political elections, research indicates that people use shallow decision heuristics, such as impressions of competence solely from a candidate’s facial appearance.”

For their study, the scientists had 73 volunteers (college students) score 106 male and female candidates in the 2006 congressional elections on a 7-point scale on several traits: competence, dominance, attractiveness and approachability, all based on their looks (face only). Then the volunteers saw the same candidates, in pairs, and were asked to say which one they would vote for for president. (The scientists made sure than the volunteers did not recognize any of the candidates; no Nancy Pelosi pictures, for instance.)

All of the volunteer voters were more likely to vote for candidates who looked more competent. (I guess that's good news, except that the assessment of "competence' was based purely on looks.) But more-attractive female candidates got more votes than homelier ones, especially from men, and the difference in vote-getting ability between attractive and less-attractive candidates was greater for female candidates than for males. Perhaps it is no coincidence that more men than women have favorable views of Palin.

What’s “attractive”? For men, faces with “mature” features (thick eyebrows, square face, large chins), which are associated with strength and assertiveness, traits that society expects from men. For women, immature features (thin eyebrows, round face, small chins), which are considered signs of less physical strength and assertiveness and of a more nurturing and sensitive nature, traits that society expects from women.

The scientists put it this way in their conclusion: “Good looks was almost all that mattered in predicting men’s votes for female candidates. And, true to prevailing stereotypes, competence was almost all that mattered in predicting men’s votes for male candidates.” Chiao gives campaign managers credit for “understanding that image really matters,” she said. “They know that, contrary to popular notions, people are not necessarily using deliberate and rational strategies in deciding who to vote for, especially when it comes to women.”

Other research has also found that appearance plays a role in how voters judge candidates. A 2005 study found that people’s impressions of the competence of a candidate based solely on their facial appearance predict the outcomes of recent U.S. congressional elections, while a 2007 study found that differences in facial shape predict which candidate will win an election.

Oh, and if this seems like some empty academic exercise, consider this. In the actual 2006 congressional races, candidates perceived as more attractive by men in this lab experiment were more likely to win. So let’s forget all this high-minded talk about how undecideds will break and how Reagan Democrats will vote, and focus on the question that can really predict next Tuesday’s outcome: who’s cuter, McCain or Obama?

Let's not kid ourselves: an endorsement by scientists is unlikely to sway many voters next week. But the decision by 76 American Nobel laureates—including all three of the Americans who won one of the science prizes this year—is notable for one thing: if you think ordinary Americans believe the last eight years have been a nightmare, you should see how scientists feel. As documented over and over, especially by Rep. Henry Waxman’s House Committee on Oversight and Government Reform, the politicization of science by this administration has set records. Scientists are furious and can’t wait for it to end.

The letter by the 76 Nobelists (only 47 endorsed John Kerry in 2004) argues that the nation needs “a visionary leader who can ensure the future of our traditional strengths in science and technology and who can harness those strengths to address many of our greatest problems: energy, disease, climate change, security, and economic competitiveness,” concluding that “Barack Obama is such a leader.” The scientists are particularly dismayed that, under Bush, America’s “once dominant position in the scientific world has been shaken and our prosperity has been placed at risk. We have lost time critical for the development of new ways to provide energy, treat disease, reverse climate change, strengthen our security, and improve our economy.”

I have spoken at a couple events recently where scientists asked me why scientific issues—stem cells, research spending and the like—have played such a small role (make that “no role”) in the 2008 campaign. I am always sorry to tell them that science issues hardly matter to most Americans, especially compared to the imploding economy. It would be foolish to think that scientists’ view on politics carries any weight with most Americans either. But the letter, organized by Scientists and Engineers for America, underscores one thing. For much of what ails this country, from international competitiveness to energy independence (by which I mean independent not only of OPEC but of fossil fuels), science is the key to a solution.

King Solomon, who assumed the throne of the kingdom of Israel after the death of his father King David, was renowned for his great wealth no less than for his great wisdom. But as always with the Bible, scholars have a field day arguing over the account’s historical accuracy. On one count, at least—the story of King Solomon’s mines—archaeologists think they have evidence that the story was more than a legend.

An excavation led by Thomas Levy of the University of California, San Diego, and Mohammad Najjar of Jordan’s Friends of Archaeology has unearthed what they identify as an ancient center for copper production at Khirbat en-Nahas. Located in the lowlands of a desolate, arid region south of the Dead Sea in what was once the Kingdom of Edom, which the Old Testament describes as a foe of Israel, it is now the Faynan district of Jordan. As they are reporting in the Proceedings of the National Academy of Sciences, radiocarbon analysis dates the site as from the 10th century BCE, when David and Solomon would have ruled and about 300 years earlier than scholars thought. It is by no means certain that Solomon (or David) controlled the mines, but at least the dates now match.

Earlier work by Levy and Najjar, The New York Times reported in 2006, “len[t] credence to biblical accounts of the rivalry between Edom and the Israelites in what was then known as Judah. . . . [T]his supported the tradition that Judah itself had by the time of David and Solomon, in the early 10th century, emerged as a kingdom with ambition and the means of fighting off the Edomites.”

The current work finds that metallurgic activity at the site spiked during the 9th century BCE, which is in agreement with the idea of the strength and power of the Edomites. Biblical archeologists have been torn over whether the Edomites were sufficiently organized by the 10th to 9th centuries BCE to threaten the neighboring Israelites. But with the new excavations, said Levy, “we have evidence that complex societies were indeed active in 10th and 9th centuries BCE and that brings us back to the debate about the historicity of the Hebrew Bible narratives related to this period.”

Ancient Egyptian artifacts—a scarab and an amulet—were found in a layer of the dig that coincided with a serious disruption in copper production, at the end of the 10th century BCE. That was also the time when Pharaoh Sheshonq I, whom the Bible calls Shishak, mounted a military campaign after Solomon’s death to crush economic activity in the area.

“We can’t believe everything ancient writings tell us,” Levy said. “But this research represents a confluence between the archaeological and scientific data and the Bible.” It remains to be seen whether other scholars in the notoriously disputatious field of biblical archaeology agree, of course, but for now Levy and his team are pressing on. They hope to figure out who actually controlled the copper industry at Khirbat en-Nahas: David and Solomon, or Edomite leaders?

Memo to tennis players: because of the way the human visual system works, referees are more likely to call “out” a ball that actually lands in, rather than call “in” a ball that in fact lands outside the line. Now that professional players are permitted to challenge calls, therefore, they would do well to focus on balls that are called “out,” since they are more likely to be wrong.

So concludes a neat little study published online today in Current Biology. Scientists led by David Whitney of the University of California, Davis, started from the fact that the human visual system consistently misperceives moving objects as shifted in the direction of their motion, making them appear to be farther along their path than they are.

To see what effect this might have in a tennis match, Whitney and his colleagues analyzed 4,457 randomly-selected points from the 2007 Wimbledon tournament, focusing on those where the ball landed close to the line. Using video from the matches, they uncovered 83 incorrect calls. Of those, 70 were balls that were called out when they actually fell inside the line. Only 13 were called in when they were actually out. Prediction confirmed: the brain thinks a moving object is farther along in its path that it really is.

Under the new rules for challenges, players get two (in the U.S. and Australian Opens) or three (at Wimbledon) incorrect challenges per set. Given the bias in incorrect calls, it is clearly to a player’s advantage to focus on balls that are called “out” in their opponents’ court rather than balls called “in” on their own side of the net: the former challenges are more likely to be upheld, while the latter count against the two or three incorrect challenges a player is allowed. As long as a player continues to challenge incorrect referee calls, he or she is allowed to continue making challenges. (At Wimbledon in 2007, there were about 140 challenges, resulting in 25% of the calls being overturned.) Players can improve their odds of challenging only incorrect calls if they focus on balls called “out.”

In our gene-obsessed society, whenever one group differs from another on some measure of health, laypeople as well as experts reflexively leap to a genetic explanation. Higher rates of hypertension among African-Americans than Caucasian Americans? It must be their genes. That assumption is behind race-based medicine, too—the idea that different medications will work better for people of different races.

Next time someone hands you that line, send them to a paper published in the November issue of the journal Social Science and Medicine.

In it, scientists led by Roland James Thorpe of the Bloomberg School’s Hopkins Center for Health Disparities Solutions, while not ruling out genetic or other inherent biological factors, find that social environment is a big reason for the black-white hypertension disparity. “Our study found that nearly 31 percent of the hypertension disparity among African Americans and non-Hispanic whites is attributable to environmental factors,” Thorpe said. “These findings show that ethnic disparities could be linked to a number of factors other than race. Careful review of psychosocial factors, stress, coping strategies, discrimination and other personality characteristics could play a large role in reducing or eliminating the disparity.”

Translation: Not to put too fine a point on it, but living in a society where security guards at high-end stores eye you suspiciously, where cab drivers refuse to pick you up, where fellow students and work colleagues let you know in subtle and not-so-subtle ways that they think you’re where you are because of affirmative action—well, let’s just say that any and all of these are excellent ways to raise your blood pressure. Hypertension, in turn, can damage the heart and blood vessels, raising your risk of stroke, heart failure, heart attack and kidney failure. It affects some 65 million people in the U.S.

In a nutshell, the Hopkins scientists compared data from a study called the Exploring Health Disparities in Integrated Communities-SWB (EHDIC-SWB) Study, which was run in a racially-integrated community where income did not vary by race, with data from a broad-based national survey called the National Health and Nutrition Examination Survey. They focused on hypertension, defined as systolic blood pressure of 140 or more, or diastolic blood pressure of 90 or more. Comparing the two data sets, the scientists found that race alone elevated blood pressure about one-third less in the racially-integrated community than nationally.

“These findings support our theory that the disparity [in rates of hypertension] is likely caused by environmental factors along with several external factors, and not biological differences among race groups, as previously suspected,” said co-author Thomas LaVeist.

It's great to live in an integrated (and presumably less racist than the national average) community as an adult, but biological changes triggered by social experiences kick in long before adulthood. So, here’s the next question: what would happen to race-based health disparities if children grew up in a race-blind society, never feeling the blood-pressure-elevating sting of racism? Just wondering.

Photo: Virginia-Maryland Regional College of Veterinary Medicine

Which brings us back to animals. Are the minds of horses, dogs and cats sophisticated enough that when they see someone approach with needles, and gently swirl them around various entry points, the beast thinks, “ah, this smart person is trying to help me,” and presto—placebo effect?

Dr. Mark Crisman, a professor in the Department of Large Animal Clinical Sciences in the Virginia-Maryland Regional College of Veterinary Medicine at Virginia Tech, administered acupuncture therapy to a horse named Gypsy, who had an infection in her ankle. Crisman was using acupuncture (plus traditional therapy) to help strengthen her bones and immune system, and relieve pain--successfully, apparently. The college offers acupuncture to animals large and small, for conditions from skin disorders to musculoskeletal issues to neurological problems.

A number of recent studies have been finding that people who score lower on intelligence tests (notice how careful I am not to say “smarter people”) tend to die earlier than those who score higher. The effect doesn’t seem to arise from socioeconomic factors (well-off people score higher on IQ tests and also tend to be healthier), leaving scientists to reach for hypotheses. Maybe high-IQ people smoke less? eat healthier? follow doctors’ advice more?

Now a new study, reported in the September issue of the journal Psychological Science, finds an even more intriguing connection. The first to examine whether IQ and dependability in childhood together are associated with risk of death by age 67, it comes to a stark conclusion: “brighter, more dependable children live longer,” write Ian J.Deary of the University of Edinburgh and colleagues.

The scientists studied 1,181 Scots who were born in 1936. Almost everyone born in Scotland in that year took the “Scottish Mental Survey of 1947” when they were 11, were assessed by teachers for dependability at age 14, and then were tracked from 1968 through early 2003 (when there were 193 deaths). These are the data that Deary combed.

The results should strike dread in the hearts of the intellectually challenged and non-conscientious. People who were smarter than 67% of the population when tested as children had a 30% lower chance of dying from 1968 to 2003; people who are smarter than 95% of the population have a 40% lower chance of dying. People who were more dependable than 67% of the population when tested as children had a 22% lower risk of dying by age 67, and the truly conscientious—more so than 95% of their peers—had a 46% lower mortality risk. Children in the bottom half of the distributions for intelligence and dependability were more than twice as likely to die by age 67 than those in the top half for both.

For IQ, there was a “dose-response” relationship for the top 75%: the smarter they had been as kids, the lower their risk of dying starting at age 32 and through age 67. (The lowest 50% had basically the same mortality risk.) For dependability, there was also a dose-response effect, with lower mortality the more dependable the participants had been at age 14.

These numbers are in the same ballpark as established risk factors such as cholesterol, blood pressure, and smoking in middle age. How can your smarts at age 11 and your dependability at age 14 have such a powerful effect on something as fundamental as when you die?

Neither education levels, socioeconomic status or other factors known to influence mortality risk explained it, the scientists find. Other studies have found that dying before age 65 is linked to childhood intelligence and that early intelligence predicts later cardiovascular disease and death, but again it’s not clear why. And there is no obvious way that being smart and diligent should reduce the risk of dying of cancer, except maybe by keeping you from smoking and getting you to be screened for the disease. Ideas, anyone?

As of a few minutes ago, you could buy a lovely carving made of African-elephant ivory on eBay for $1,100, an ivory mermaid for $300, an ivory napkin ring for $99 and more: all of the ivory is described as “pre-ban,” meaning it was “harvested” (such a benign word for ripping tusks out of slaughtered elephants) before the international community banned the sale of elephant ivory in 1989. It’s illegal to sell any ivory harvested after that, and illegal to sell any ivory, pre-ban or not, internationally. As for whether the "pre-ban" claims are all accurate, well, if you believe that perhaps I can interest you in a nice bridge we have here in New York.

The sale of questionable ivory may finally be coming to an end, however, at least on eBay. Last night, the company announced that as of January 1, 2009, it will institute a global ban on ivory sales. That was interesting timing, coming as it did on the eve of the release of a report today by the International Fund for Animal Welfare. The report, Killing With Keystrokes, was based on a six-week investigation that tracked some 7,000 wildlife-product listings on 183 Web sites in 11 countries. eBay was the worst offender, responsible for almost two-thirds of the online trade in wildlife products globally.

The most common product was elephant ivory, with some 4,000 listings or 73% of all product listings that IFAW tracked. Exotic birds were second, at 20% of the listings. You can even find primates and big cats—both live animals and wildlife products, including turtle shells and leopard, cheetah, ocelot, lizard and crocodile skins.

The 1989 quasi-ban on ivory sales—grandfathering in pre-ban ivory—left a hole big enough to drive a tusk through, and animal rights groups have been charging that eBay did a lot of the driving. A year after the company said, in June 2007, that it would take down any ivory items that sellers offered to ship internationally, which is illegal, IFAW said it had found 678 ivory items for sale on eBay one week last spring, up from 440 nine months earlier. (Sellers said then, as they still do, that the ivory was obtained before the 1989 ban.)

eBay told Scientific America that it was trying to get control of illegal ivory sales on its site, but conceded that it did not verify that ivory listed for sale was harvested prior to the global ban.

By going further and instituting the total ban on ivory sales, eBay takes a big step to clean up its image. “IFAW congratulates eBay on this very important step to protect elephants,” said Barbara Cartwright of IFAW. “With these findings and eBay’s leadership, there is no doubt left that all Internet dealers need to take responsibility for their impact on endangered species by enacting and enforcing a ban on all online wildlife trade.”

“Internet dealers profit off of every piece of elephant ivory sold on their Web sites, and every piece of that ivory came from a dead elephant,” said Jeff Flocken, Director of IFAW’s Washington office. Every year, more than 20,000 elephants are illegally slaughtered in Africa and Asia for ivory. And as we reported earlier this year, an alarming amount of illegal trade in wildlife is being carried out not only by the usual criminal gangs but also by terrorist groups such as the Janjaweed, responsible for the genocide in Darfur. The least companies like ebay can do is not make it ridiculously easy for them to move the goods.

Add another group to the growing list of those who realize that if we wait around for the current way of doing biomedical science to produce cures for disease, those cures will forever be “10 years off,” as researchers in cancer, Alzheimer’s, Parkinson’s and just about everything else have assured me (and everyone else) for years and years.

This time it is a group focused on ALS (amyotrophic lateral sclerosis), or Lou Gehrig’s disease, that has decided the traditional way of finding cures just isn't working. So the non-profit group Prize4Life has taken a page from the X Prize Foundation: today it is announcing a $1 million prize for discovery of a drug that can extend life in lab animals with ALS.

Prize4Life, founded by a group of Harvard Business School students when their friend Avi Kremer was diagnosed with ALS at the age of 29 in 2004, is the first disease-oriented group to use a prize approach for biomedical research. But prizes to foster discovery and innovation have been gaining in popularity. The X Prize Foundation offers $10 million windfalls for a spacecraft able to fly a crew 60 miles up and back (it was won in 2004), for genomics (for development of technology to accurately sequence 100 human genomes at a cost of no more than $10,000 each), and for other achievements.

ALS, a rapidly progressing neurodegenerative disease, typically kills within two to five years of diagnosis. Most commonly striking people between 40 and 70, it affects men slightly more than women and is caused by the degeneration of motor neurons. About 30,000 Americans have it at any one time, and there is no known cure.

All of which makes ALS ripe for a prize approach, Prize4Life’s chief scientific officer and neuroscientist Melanie Leitner told me. It has only one FDA-approved treatment (Riluzole, which extends life only two or three months and costs $7,000 to $10,000 a year). U.S. foundations and other non-profits spent only $29 million on ALS research last year, and the National Institutes of Health is spending only $39 million this year. Even worse, the field has seen one clinical trial after another flame out, and there is concern that the mouse model of ALS has been leading scientists astray: mice thought to be genetically identical, Leitner explained, turn out to have different levels of expression of a key protein involved in ALS, called SOD1. High levels of expression are associated with shorter survival, and lower levels with longer survival. So when an experimental drug extended survival, scientists thought they were on the right track. But it turned out, in many cases, that they just happened to have given the drug to a mouse that, for genetic reasons, was destined to live longer anyway. No wonder that when the drug was tried in people it bombed. (The list includes Pfizer’s Celebrex, which failed in a 12-month double-blind, placebo-controlled efficacy study in 300 people; creatine, topiramate/Topamax and . . . .well, it is a sad list of failure.)

The first $1 million prize that Prize4Life dangled in front of scientists was for a biomarker of the disease—some measurable protein or other biochemical that scientists can measure and that indicates whether an experimental drug is having an effect on ALS. That should reduce the cost of clinical trials, “de-risking” them somewhat and thereby attracting more biotech or pharma companies to the field. It has attracted about 50 teams, Leitner says, including those pursuing “out of the box” ideas.

The prize announced today is for the discovery of a compound that extends life in mice with two different mouse versions of ALS by 25 percent. “An effective treatment for ALS is desperately needed, and the existing mouse model is the primary gateway to clinical trials. The identification of a treatment capable of meeting the high survival bar set forward in this prize should attract the attention of those with the resources necessary to move a potentially effective ALS therapy into the clinic," said Tom Maniatis, Professor of Molecular and Cellular Biology at Harvard, an ALS researcher and member of Prize4Life’s Scientific Advisory Board. “The Kremer prize will only be awarded for a therapy that makes a major difference in the disease, the kinds of therapies that ALS patients really need.”

Time will tell whether a prize approach can work in biomedicine. Something better.

When oil was $147 a barrel and money was sloshing through the financial system like water, renewable energy seemed like a slam dunk: wind and solar projects attracted bank loans and private-equity money, and the higher cost of generating electricity from green sources compared to fossil fuels seemed like it might soon be a thing of the past.

All that, of course, was back in the good old days. July.

A mere three months later, green-energy backers are “assessing the risks and opportunities in renewable energy in the new economic climate,” as a symposium I attended this morning put it. Organized by the law firm Chadbourne & Parke, the meeting began with a provocative panel on how the financial upheaval is affecting the development of renewable energy projects such as wind farms and solar installations. As former New York governor George Pataki, now of counsel at Chadbourne, put it with understatement, “A little bit has changed. But there is still tremendous opportunity in green energy going forward. I think we’re going to see increased government investment in renewables and efforts to require the transformation of our transportation and auto industry.” Translation: with a new administration, we’re not going to keep up the insanity of importing 10 million barrels of crude oil a day. As Obama said in this week’s debate, “we’ve got to stop sending $700 billion a year to countries that don’t . . . like us very much,” such as Venezuela and Saudi Arabia.

You think small business owners are having trouble getting bank credit to meet their payrolls, finance expansions and the like? Try pitching a wind farm to bankers these days. “There is some money” available to renewables projects, said Brian Goldstein, managing director of BNP Paribas Securities. “But the challenge is, as capital becomes available again [with the federal bailout], where will banks allocate it? . . . Smaller is better” for energy projects, since “we’re seeing a reluctance to underwrite” big projects.

Steve Cheng, managing director of Credit Suisse, said that “some institutions have liquidity and will do deals. But it’s different today than two years ago,” most starkly in what rate backers are demanding to lend money: since loans in the secondary market are treading at 65% to 70% of their face value, reflecting fear that the borrowers will not repay them, they have an effective yield of 16% to 18%. For a new loan for a new renewables project to be attractive to a banker or investor, the rate will clearly have to be high. “There are still people with liquidity, with money they need to put to work,” Cheng said. “They will definitely come into the market and make loans, but what borrowers will have to pay will be much higher.”

Paul Ho, a principal at Hudson Clean Energy Partners (a private equity firm that invests in green projects), didn’t sound like he intended to keep his wallet closed, in part because the $700 billion bailout bill extended tax credits for solar and wind power. “We were all pleasantly surprised that renewables got bundled into the [bailout] package,” he said, though in the short term he said he expects “a serious slowdown” in the financing of projects.

“There has been a whole repricing of risk,” added Rahul Advani, vice-president of Energy Capital Partners, another private equity firm that invests in renewable energy. “Lenders are now saying they need a premium” to make a loan attractive. “Maybe we’re now living in a 9%, 10% or 12% world.” (And you think your mortgage rate is high?) “But at the end of the day, good projects are going to get financed. Relative to a lot of assets in the energy sector, renewables are a good investment.” But not as good as they were at $147-a-barrel oil.

It wouldn’t be early autumn without the annual “Arctic report card,” which tracks recent changes at the top of the planet. Produced by the National Oceanic and Atmospheric Administration, part of the U.S. Commerce Department, this year’s report card documents a continued decrease in the extent of summer sea ice, which experts call “a dramatic illustration of the pronounced impact increased global temperatures are having on the Arctic regions.” The scientists also found autumn temperatures  “a record 5º C above normal, due to the major loss of sea ice in recent years which allows more solar heating of the ocean. Winter and springtime temperatures remain relatively warm over the entire Arctic, in contrast to the 20th century and consistent with an emerging global warming influence.” Sea-ice retreat is associated with warmer temps because dark, liquid water absorbs more solar energy than white ice does; that warming of the ocean affects land and atmosphere temps as well as marine life, and reduces the amount of winter sea ice that lasts into the following summer.

These drastic changes in the physical world have, not surprisingly, had an impact on the biological world. The scientists report that the retreat of sea ice has already led to poorer health “and reduced survival of polar bears in western Hudson Bay. . . . With the record summer sea ice retreats of 2007 and 2008, walruses, in some regions of the Arctic, were forced to haul out along shores in unusually large numbers, triggering increases in trampling deaths . . . Recent estimates of wild caribou and reindeer indicate that these populations may be entering a period of declining numbers.”

In this year’s report card, three of the six areas (atmosphere, sea ice, and Greenland) are coded red, meaning the changes are strongly attributed to warming. Biology, ocean and land changes are coded yellow, meaning they may partly, or also, reflect natural variations. Last year’s report card had two red areas (atmosphere and sea ice) and four yellow.

Of course, as we all know, climate change has nothing to do with human activities, as Sarah Palin told an interviewer in August (“I'm not one, though, who would attribute [climate change] to being man-made."). Phew.

*"I'm melting, I'm melting . . . "

I spent yesterday afternoon and evening at the annual meeting of the New York Stem Cell Foundation, at Rockefeller University, where the organizers were firm taskmasters: the scientists presenting studies had to focus not on esoterica but on translational research—that is, the kind that promises to help patients.

Two presentations stood out. Pete Coffey of University College London described the work he is doing as part of the London Project to Cure Blindness, which has made remarkable progress using human embryonic stem cells (donated by couples using IVF who had "extra" embryos they did not wish to implant) to treat the blindness caused by macular degeneration). You read it here first: in the magazine’s “global literacy” issue in July I argued that the first clinical use of stem cells would be to treat blindness. The work Coffey described makes that seem more and more likely: he and his team have improved the vision of several patients who had gone blind. One of them was even able to drive again.

But Coffey was quite circumspect: the surgery so far works on only 25 percent of patients. He and his team continue to refine the technique and define the patient populations that would most benefit from the surgery.

That good news stood in stark contrast to the talk by Jeffrey Kordower of Chicago’s Rush Presbyterian Medical Center, where he is a leading neurologist. His task was to describe progress on using stem cells to treat Parkinson’s disease, which on paper looks like an excellent candidate for the stem-cell approach. Scientists know what has gone wrong in PD. Neurons in the brain’s substantia nigra die or do not work; either way, they fail to produce dopamine, leading to the tremors and other symptoms of PD. Solution: replace them with neurons derived form stem cells, or with stem cells themselves that you coax to differentiate into the lost/damaged neurons.

I’ve blogged before on the growing realization that using stem cells, or cells derived from stem cells, to repair neurological diseases is going to be really, really hard. But I’d never heard someone of Kordower’s stature put it quite so starkly: “In my opinion it will take a major miracle for stem cells to make a difference in Parkinson’s disease,” he said.

In fairness, as he went on to say, the field of PD has already had two miracles: the discovery that the drug levo-dopa and the technique of deep-brain stimulation both dramatically reduce the movement symptoms of PD. But attempts in the 1990s to transplant fetal brain cells into PD patients produced awful side effects (uncontrolled movement, called dyskinesia), for no-one-knows-what reason. “No one should do clinical trials with stem cells [for PD] until we understand the cause of the dyskinesia,” Kordower warned. Another cautionary note: in earlier studies, the transplanted cells eventually show the same kind of awful changes that the patient’s own brain cells did, such as loss of dopamine transporter and development of Lewy bodies, a cause of dementia. In other words, whatever went wrong in the brain originally to produce Parkinson’s was still going wrong, ravaging the transplanted cells. Very bad news for Parkinson’s patients who have pinned their hopes on stem cells—and ironic given the prominent, courageous role Michael J. Fox and his foundation have played in drumming up public support for stem cell research.

The animals that humans share the planet with are and have been reservoirs for all sorts of nasty diseases (deer ticks and Lyme disease; mosquitoes and malaria; Ebola and lord-knows-what wildlife reservoir), but here’s one case where the beasts were accused unjustly. It had long been thought that humans contracted tuberculosis, which currently infects an estimated 2 billion of us, from cattle. But in a clever new study, scientists conclude that humans got it first, and only later did the pathogen Mycobacterium tuberculosis mutate and jump into cows.

Scientists led by Helen Donoghue of University College London and Mark Spigelman of UCL and Hebrew University in Jerusalem (a surgeon-turned-archaeologist who has done fascinating work tracing the prehistoric origins of disease, such as hepatitis B in mummies have discovered what they say are the earliest known cases of human tuberculosis in human bones. Found in the ruins of the village called Alit-Yam, a 9,000 year-old Neolithic settlement that has been submerged off the coast of Haifa for millennia, the bones appear to be of a mother and baby and have lesions characteristic of TB; the disease likely killed them.

A submerged settlement is a jackpot for archaeologists because of the excellent preservation: Atlit-Yam was in a marshland, and the graves were encased in clay. As the sea rose they were “eventually covered by thick layer of sand and later by salt water,” the scientists write, “thus providing anaerobic conditions that retard degradation” and caused “excellent preservation of the skeletal remains”--and of ancient DNA.

Analysis of those remains revealed DNA and other fragments of Mycobacterium tuberculosis, showing that the human disease is at least 9,000 years old—3,000 years older than previously thought. “This is the earliest report of [TB] in humans that has been confirmed by molecular means,” the scientists write. And here’s where the cows get acquitted: examination of the ancient DNA confirms that bovine TB evolved later than human TB.

“What is fascinating is that the infecting organism is definitely the human strain of tuberculosis, in contrast to the original theory that human TB evolved from bovine TB after animal domestication,” Donoghue said. “This gives us the best evidence yet that in a community with domesticated animals but before dairying, the infecting strain was actually the human pathogen.”

Score one for the crystal-ball gazers at Thomson Reuters Scientific! As I blogged last week, every year the editors and researchers there forecast the Nobel Prize winners, and although they struck out on physics and medicine they nailed chemistry: Roger Tsien of UC San Diego shares this year’s chem Nobel with Osamu Shimomura of the Marine Biological Lab and Martin Chalfie of Columbia University for discovering and developing green fluorescent protein.

As Tsien and two co-authors of a key paper explained last year, with the technique for tagging cellular proteins in living things “the possibilities are endless. The probes can be used to study proteins on many levels: in live or fixed specimens; in vitro or in vivo; to study localization, activity, or modify function; and to be seen by light and electron microcopy.”

Bruce E. Bursten, president of the American Chemical Society, called the selection of the the three “a wonderful choice! This year’s Nobel Prize in Chemistry showcases chemistry’s critical but often-invisible role in fostering advances in biology and medicine. Green fluorescent proteins allow scientists quite literally to see the growth of cancer and study Alzheimer’s disease and other conditions that affect millions of people. This is chemistry at its very best, improving people’s lives.”

If you look on the bright side, when you think of the health effects of climate change you probably think of fewer sub-zero spells and, therefore, fewer cold-related illnesses and deaths. Maybe. But in a warmer world, as I wrote last year, poison ivy and ragweed will get more prevalent and more toxic, and tropical diseases such as malaria and dengue fever will reach toward the poles. Those, it turns out, are only the tip of the (melting) iceberg.

This morning, the Wildlife Conservation Society released a report listing 12 disease-causing microbes that threaten to spread into new regions as a result of climate change. What does a wildlife organization have to do with this? By monitoring wildlife, scientists will be able to detect these spreading pathogens before they cause a human epidemic. Or so they hope. As Steven E. Sanderson, President and CEO of the WCS, said, “The health of wild animals is tightly linked to the ecosystems in which they live and influenced by the environment surrounding them, and even minor disturbances can have far reaching consequences on what diseases they might encounter and transmit as climate changes. Monitoring wildlife health will help us predict where those trouble spots will occur and plan how to prepare.” Think avian flu which, with other livestock diseases that have reemerged since the mid-1990s have cost the global economy an estimated $100 billion.

The report’s “deadly dozen”:

Avian influenza: The highly pathogenic H5N1 strain is deadly to domestic and wild birds, as well as humans, and could evolve into a strain that can spread from human to human. Climate changes such as severe winter storms and droughts can disrupt normal movements of wild birds, bringing avian flu to new regions and bringing domestic birds into greater contact with wild, disease-harboring ones at water sources if rainfall declines.

 

Babesiosis: Becoming more common in humans in Europe and North America as climate change alters the distribution of the ticks that transmit this disease.

 

Cholera: This water-borne diarrheal disease, caused by the Vibrio cholerae bacterium, is highly temperature dependent, so rising global temps are expected to increase its incidence.

 

Ebola: Outbreaks of this hemorrhagic fever (and the related Marburg fever) are related to unusual variations in rainfall/dry season patterns, which climate change disrupts.

 

Intestinal and external parasites: Their prevalence is expected to rise as temperatures and precipitation levels shift.

 

Lyme disease: As tick distributions shift as a result of climate change, Lyme disease will reach new regions.

 

Plague: One of the oldest infectious diseases known, it is spread by rodents and their fleas, whose distribution will change with shifts in temperatures and rainfall.

 

“Red tides”: These algal blooms are deadly to both humans and wildlife, and may become more common as the climate changes.

 

Rift Valley Fever: Potentially fatal in people, it is carried by mosquitoes, which threaten to reach into cooler climes and proliferate as the world warms.

 

Sleeping sickness:  Trypanosomiasis is caused by a protozoan and transmitted by the tsetse fly, whose distributions could change as climate does.

 

Tuberculosis: The bovine form exists worldwide, infecting humans in southern Africa through the consumption of un-pasteurized milk. Droughts caused by climate change are likely to increase the contact of wildlife and livestock at limited water sources, increasing transmission of the disease between livestock and wildlife and livestock and humans.

 

Yellow fever: The disease-causing virus is also carried by mosquitoes, which will spread into new areas as temperatures rise and precipitation patterns shift.

In 2005, John P. A. Ioannidis of Greece’s University of Ioannina School of Medicine and Tufts University School of Medicine in Boston shook up the world of science with his provocatively-titled, and frighteningly-well reasoned, paper, “Why Most Published Research Findings Are False” in PLoS Medicine. Now he’s back, no more sanguine about the state of biomedical science. Bottom line: when it comes to “the latest studies,” take what you read with a grain of salt.

Make that a shaker of salt.

In a paper published this evening, he and his co-authors—Neal S. Young of the National Institutes of Health and Omar Al-Ubaydli of George Mason University in Virginia—argue that “the current system of publication in biomedical research provides a distorted view of the reality of scientific data that are generated in the laboratory and clinic.” Negative results are not reported, statistical flukes are not caught, and the result is a distortion of biomedical reality.

Example: A 2005 study in the Journal of the American Medical Association found that “initial clinical studies are often unrepresentative and misleading." Of the 49 most-cited papers on the effectiveness of treatments for various diseases, published in top journals from 1990 to 2004, one-quarter of the randomised trials and five of six non-randomised studies had already been contradicted or found to have been exaggerated by 2005.

Lesson: if a finding is important, it will be replicated. Until it is, don’t believe it. How long might you have to wait? “The delay between the reporting of an initial positive study and subsequent publication of concurrently performed but negative results is measured in years,” the scientists write.

In general, small studies are less likely to be true, as are studies that find only a small effect (of, say, a treatment for disease, or of a disease-causing compound or behavior), studies in which the scientists have a financial interest and studies in a field where many teams are chasing statistical significance.

In one of the more disturbing examples, which I blogged on in January, scientists found that the public and even doctors have gotten a distorted view of the effectiveness of anti-depressants. Why? Because “among 74 FDA-registered studies, 31% . . . were not published.” Simply put, manufacturers flood the scientific literature with studies that make their drug look good, and bury the other ones. Of 37 positive studies on anti-depressants given to the FDA, one was not published; of the negative studies of anti-depressants given to the FDA, 22 were not published and 11 were twisted to convey a positive outcome. That made it seem that 94% of the studies were positive, whereas only 51% of studies submitted to FDA were.

As I said, make that a shaker.

It may not pack quite the excitement as betting on the presidential race, but for science enthusiasts there is nothing like predicting the winners of this year’s Nobel prizes. An excellent cheat sheet is to be found at Thomson Reuters Scientific, which since 1989 has developed a list of likely winners in medicine, chemistry and physics (economics, too, but we’ll focus on the original science prizes).

The list is based on the number of citations a scientist has accumulated (citations are references that a new study makes to earlier studies, sort of a tip of the hat to one’s intellectual forbears) and how many high-impact papers he or she has had (if you publish a lot but no one notices, your impact is low; if you have just a few powerhouse papers, it’s high). It also reflects a sense of which fields are hot, since the Nobel committees often work by first identifying an important scientific breakthrough and then figuring out whom to honor for it. “In choosing our ‘picks’ for the Nobel Prize in 2008 (or thereafter) we looked first at citation counts and at number of high-impact papers, but then also at discoveries or themes that might be considered worthy of special recognition by the Nobel Committee,” explains Thomson Reuters’ David Pendlebury in an online essay.

So who makes the cut this time? You can see the whole lists at the link above, but a few stand out as particularly interesting:

In chemistry, if you think it’s time for the Nobel to honor nanotechnology, then place your bet on Harvard’s Charles Lieber, a leader in the race to turn this science from gee-whizardry into something useful. If you think the chem committee is more impressed with a technique to attach fluorescent probes to proteins within living cells, allowing biologists to study cellular processes live and in living color, then bet on UC San Diego’s Robert Tsien, who pioneered the technique.

In physics, there is no cooler new material than graphene, which is a sheet of carbon atoms a mere one atom thick. Its creation, by Andre Geim of the University of Manchester in Britain, has revolutionized materials science and condensed-matter physics. I confess that I’m rooting for Geim partly because of his sense of whimsy: in 1997 he used a magnetic field to levitate a frog, winning himself an Ig Nobel (a spoof Nobel, from the Annals of Improbable Research) in 2000. But I also have a soft spot for Vera Rubin of the Carnegie Institution of Washington. She discovered dark matter, the mysterious invisible stuff that lurks around and between galaxies and makes up more of the universe’s mass than the matter that does emit electromagnetic radiation (visible, x-ray, radio, whatever). Astronomers haven’t won their fair share of Nobels, it seems to me, despite revolutionizing our understanding of the cosmos.

In physiology/medicine, the handicappers like micro-RNAs. Discovered by Victor Ambros of the University of Massachusetts Medical School and Harvard’s Gary Ruvkun, m-RNAs regulate gene function in a way never before imagined. An even more interesting pick in this category are the epidemiologists who pioneered meta-analysis, the statistical technique in which you pool many studies—on, say, the association between eating meat and developing cancer, or a drug and disease—and analyze them as one. For this achievement, the handicappers like Oxford University’s Richard Peto and Rory Collins. Collins explained the need for meta-analyses this way: “The studies being done were too small to detect the sort of modest but medically worthwhile—humanly worthwhile—differences in mortality or major morbidity that are likely produced by the treatments being tested.”

Since Thomson Scientific started making predictions in 1989, there were only two years—1993 and 1996—when they failed to correctly predict at least one winner, and in some years they nailed two. So get your bets down soon: the Nobel committees will announce the physiology/medicine prize on Oct. 6, physics on Oct. 7 and chemistry on Oct. 8.

Control freaks have a bad name, but they shouldn’t. When you feel you have some control over your work, you feel less stress even when the actual tas