In the recent kerfuffle over the national debt, one of the rhetorical flashpoints was the $800 billion “stimulus package” pushed by the Obama administration in 2009 to fight the economic slowdown. Though the benefits of the American Recovery and Reinvestment Act on unemployment and the economy are fiercely debated, the impact upon the scientific world is just beginning to be felt. Roughly $5 billion of the stimulus money went to the National Institutes of Health for funding biomedical research - and $42 million of that sub-total came to projects involving University of Chicago researchers. Two years later, the fruits of that investment are beginning to ripen, as stimulus-funded projects reach the point of publishing results.

The largest piece of the stimulus pie awarded to UChicago researchers was the $5.6 million designated to form the EVE consortium, an unprecedented national effort to search for the genetic and environmental causes of asthma. Over 34 million Americans are diagnosed with asthma during their lifetime, and the rates are increasing every year. But the origins of this respiratory disease are still mysterious, with the relative contributions of genetics and environmental factors such as air quality and smoking still being unraveled.

One recent tool in decoding the causes of asthma has been genome-wide association studies, or GWAS, where genetic information from a large pool of patients with the disease are compared to a control pool of asthma-free people. But to find a gene or gene variant associated with a complex disease like asthma, a huge number of subjects are needed for statistical reasons. The expenses of successfully recruiting, diagnosing, and genotyping the thousands of people needed to create a sufficiently powerful GWAS were beyond the means of any one research group, frustrating the search for asthma-related genes.

“It has become clear to geneticists studying nearly every common disease that GWAS are often under-powered,” said Carole Ober, Blum-Riese Professor of Human Genetics and obstetrics/gynecology at the University of Chicago. “Unless you pull together many people doing the same thing you’re just not going to have the power to find genes.”

In the world of asthma genetics, nine groups of investigators were encouraged by the National Heart, Blood, and Lung Institute to pool their respective GWAS results to create a shared pool of data large enough to sniff out genes associated with the disease. But that collaboration was easier said than done - until the $5.6 million ARRA grant enabled the hiring of personnel to make the EVE consortium a reality.

“It would never have been possible without the grant, this was a huge amount of work,” said Dan Nicolae, PhD, associate professor of medicine, statistics, and human genetics at University of Chicago, and co-chair of the consortium with Ober. “The key was the ARRA funding that allowed us to move it faster.”

Now, just short of two years since the grants were announced, the EVE consortium has announced their initial results in the journal Nature Genetics. With a new larger data set of over 5,000 asthma cases, the group was able to pinpoint with high accuracy five genetic regions associated with asthma, including one with a very selective profile. Unlike a similar consortium formed in Europe (called GABRIEL), the EVE dataset reflected the ethnic diversity of the American melting pot with subjects of European origin, African origin, and Hispanics. That diversity proved useful, as the EVE data revealed an asthma-associated variant in a gene called PYHIN1 that only appeared in African-Americans and African-Caribbeans - ethnic groups not present in the GABRIEL sample published last year.

“Asthma rates have been on the rise in recent years, with the greatest rise among African Americans,” said Susan B. Shurin, acting director of the National Heart, Lung, and Blood Institute, which co-funded the study. “Understanding these genetic links is an important first step towards our goal of relieving the increased burden of asthma in this population.”

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In physics, there’s nothing better than an unexpected result. Wednesday, Fermilab scientists unveiled the graph at left and caused figurative rioting in the streets of the physics community, confirming months of rumors about an exciting new result from the suburban Chicago facility (You can watch video of the presentation here). It’s a big score in the final days of Fermilab’s Tevatron accelerator, which is due to close later this year due to budget cuts and the ascendancy of the more powerful CERN Large Hadron Collider in Switzerland.

The buzzworthy peak was the result of collision experiments where Fermilab scientists expected to see a W boson and two quarks, elementary particles that are part of the Standard Model of physics. But the experiments produced something additional, something unexpected, something unusual: a bump. Particle physicists spend their whole life chasing bumps, as Sean Carroll of Fermilab explains at his Discover Magazine blog, because they are “often a signature of a new particle that has been produced and then quickly decayed.” The anomaly could thus be a previously undiscovered particle that is not predicted by the Standard Model (apparently it is too large to be the elusive Higgs boson), forcing a re-write of the core theory of modern physics. Even if it’s not a new particle, some say an incorrect prediction like this one could mean that some of the rules of the Standard Model may need to be tweaked.

But despite the excitement, caution still reigns - as Dennis Overbye wrote in the New York Times, “The key phrase, everyone agrees, is ‘if it holds up.’” The chance that it is just a statistical anomaly is less than 1 in 1375, the researchers said. With that kind of data, biologists (whose 1 in 20 standards were lampooned effectively by the science comic xkcd this week) would already be popping champagne, but it’s not good enough for physicists - past findings of that strength have disappeared with further scrutiny. If additional experiments still being analyzed push the chance of error to 1 in a million, the true celebration will begin, and the finding could be the most important piece of new physics in decades.

Scientific Shutdown

Fortunately, that analysis will continue even in the face of a threatened government shutdown, the Fermilab website assures. But if a budget agreement isn’t reached by midnight tonight, business won’t continue as usual for many scientists, beginning with the 6,000 employees of the National Institutes of Health. As for extramural research that relies upon federal dollars, most ongoing clinical trials will be unperturbed, experts said. But Johns Hopkins researchers said that no new clinical trials will be able to start during the shutdown, and the Medical Center’s Richard Schilsky told MedPageToday that he’s concerned about obtaining experimental drugs from the National Cancer Institute.

“The biggest issue for us would be studies of investigational drugs being supplied by the National Cancer Institute,” he said in an email. “Many times we have to order drugs for each unique patient to be treated, and if NCI shuts down and can’t ship the drug, then we can’t treat the patient!”

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Cooking indoors over firewood and dung is a tough habit to break for billions of poor people around the world. But Sola Olopade, MD, professor of medicine and family medicine, found a way. He wanted to stop women from hunching for hours over open fires inside their houses, cooking with babies strapped to their backs. The air in such houses quickly becomes filled with toxins, and the women and children have a host of bad health consequences.

“It’s the most unclean combustion you can get,” Olopade said in his seminar earlier this month at the MacLean Center for Clinical Medical Ethics. “The women and children have coughs, headaches, runny noses, chest tightness.”

Those are just the health problems he could measure. “I wonder what kind of cognitive dysfunction people develop in spaces where the carbon monoxide is so high.”

Unfortunately, the billions of poor people who cook their daily meals over firewood and dung have few other options. Without electricity, Olopade said, “energy poverty drives people to use whatever they can get their hands on.” But Olopade was determined to see whether education and a little technology could make it less dangerous for people to breathe inside their houses.

Olopade, who is clinical director of the University of Chicago Global Health Initiative, went to two small villages in his native Nigeria, ready to distribute energy-efficient ceramic stoves. He believed the simple stoves could make an enormous improvement in the community’s health. His team measured the air quality inside 100 homes, and found heavy metals, carbon monoxide, and particulate matter more than twenty times the World Health Organization acceptable standards. The researchers also educated the community about the dangers of exposure to smoke from using firewood to cook indoors and the benefit of using the new stoves, handing out brochures about cooking in their native dialect.

“I told them without medical jargon that this was killing people,” Olopade said.

Three months after giving the stoves to the families in the villages, Olopade returned. He took the same air quality measurements, repeated the survey of symptoms and saw a remarkable improvement. Carbon monoxide and particulate matter levels were dramatically lower, much closer to the WHO standards.

“People were very happy with the stoves. They’re very simple. They’re lined with ceramic which retains a lot of heat and promotes more complete combustion of the firewood or biomass fuel,” Olopade explained.

The women were burning the same fuel - cow dung, agricultural waste, and firewood - but the stoves had kept most of the pollutants from pouring into the homes. With this small change, “you can really improve the indoor environment,” Olopade said.

The health benefits were drastic. Before the intervention, many of the children and most of the mothers suffered from dry cough, runny noses, burning eyes, breathing difficulties, chest tightness, headaches and dizziness. All of these health problems plummeted after they started cooking on the clean stoves.

“Just by engaging the community in partnership, educating them on the dangers of exposure to toxic fumes and giving people efficient stoves, without changing their lives much, the change in symptoms is dramatic,” Olopade concluded.

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Sen. Dick Durbin tours Argonne National Laboratory with Rick Stevens, Professor of Computer Science (photo courtesy of Argonne)

In Washington, the fight over budget cuts is well underway, as a Republican majority in the House and a Democratic majority in the Senate tussle over the best way to reduce a multi-trillion dollar federal deficit. The first bill of the new House, H.R.1, set federal appropriations for the rest of fiscal year 2011 (ending in September) and snipped $61 billion from the budget, predominantly from discretionary domestic spending. One target of those cuts would be the National Institutes of Health budget, which would lose roughly $1.6 billion of its $32 billion budget for funding scientific research in the United States.

As you might expect, this news was not welcomed by Chicago-area researchers, who turned up in lab coats to support a news conference by Sen. Dick Durbin last Sunday at Northwestern University’s downtown campus. Durbin vowed to fight against the cuts as H.R.1 is discussed in the Senate, saying that interrupting the funding would slow progress toward new treatments for diseases such as AIDS, diabetes, and cancer. (video here)

“When you put these research projects on hold, you can’t ask the laboratory mice to take a nap,” Durbin said. “You can’t ask the cultures to stop growing - we’ll get back to you at the end of the fiscal year. And you can’t expect the professional researchers, the men and women who have dedicated their lives to medical research, to have certainty that next year they’ll have a job.”

Researchers from each of the major Chicago academic hospitals appeared at the conference and talked about how the proposed budget cuts could harm their own projects. Michelle Le Beau, director of the University of Chicago Comprehensive Cancer Center, discussed the biomedical research underway at UChicago thanks to the nearly $300 million in NIH funding received this year and last. Le Beau focused in on her own research examining therapy-related acute myeloid leukemia - a “very cruel and ironic” cancer caused by the chemotherapy and radiation treatment of a prior tumor. Any job losses that follow from NIH cuts could break up the expert team she has formed to study causes and treatment of the disease, she said.

“A lapse in funding will result in dismantling our highly specialized research team, and this leads to a loss of capability, because it takes years to assemble these teams again,” Le Beau said. “These are individuals who have trained for years to apply their extraordinarily unique skills. They have families to support and bills to pay.”

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Welcome to pilot episode 2 of our Medical Center research news podcast. We’re keeping the water wings on for now as we continue to refine the format and discover all the technical struggles inherent in podcasting, but please do listen and give us feedback on how we’re doing - and if you have good ideas for a name.

In this episode, we talk to J. Martin Leland about the Stay in the Game event and preventing injuries for baseball, golf, and tennis season. Dianna Douglas reports on the oldest patient to ever receive Whipple surgery at the University of Chicago Medical Center, talking with Kevin Roggin and William Dale about the procedure. And Rob Mitchum reports from a news conference held last weekend by Sen. Dick Durbin about the impact of potential cuts to the National Institutes of Health budget currently being debated in Congress. Thanks for listening!

University of Chicago Research Podcast Episode #0.2 by robmitchum

[If you missed episode 0.1, you can listen here.]

From Blaxter; Science 24 December 2010

On Christmas morning this year, most people hoped to find an iPad, a puppy, or a luxury car wrapped in a giant red bow under their tree. But geneticists received their present a day early, in the form of two landmark papers published on Christmas Eve in the journal Science. The two extremely dense data sets described in the articles represent new knowledge about gene expression in two seemingly obscure animals: a roundworm and a fruit fly. But the information gained in these massive, multi-institutional projects represents the next important step after the Human Genome Project toward understanding the connection between genes and human health.

Drosophila melanogaster, a species of fruit fly, and Caenorhabditis elegans, a kind of roundworm, are two of the unlikeliest heroes in science. Both are frequently used model organisms used in laboratories around the world, prized for their short reproductive cycle and relatively small, easily manipulated genomes. Much of what we know about the mechanisms of evolution and development have been gained from studies of the fly and the worm, and the Human Genome Project was built on technologies first used on these tiny critters.

Now that scientist are beginning to search beyond the 0.5 percent of DNA that encodes for proteins, Drosophila and C. elegans are once again called upon to be pioneers. The ModENCODE consortium, short for model organism Encycolpedia Of DNA Elements, is building a library of gene expression and interaction in these species to get a better handle on the dynamics of gene function.

“These efforts in model organisms pave the way for similar annotations of the human genome,” said Kevin White, professor of human genetics and ecology & evolution at the University of Chicago, and one of the leaders of the Drosophila side of the modENCODE project.

Figuring out the billions of A, C, G, and T nucleotides that make up an organism’s genome is only the first step in understanding genetic function - the equivalent of a recipe that only lists the ingredients without giving any further instruction. The same set of genes controls the proper development and function of hundreds of different cell types, as different as the specialized cells of the retina and the strong cells of bone and muscle. To accomplish this is a matter of timing, with genetic regulators (themselves moderated by genes) turning on the right genes at the right times.

When you consider that there are 22,000 genes in C. elegans and 17,000 genes in Drosophila, figuring out which genes are turned on when is no modest undertaking. Hence the project is as much computational as biological, as enormous data sets are shaped into networks revealing the intricate genetic choreography cells use to control themselves based on internal and external signals.

“An animal cell behaves as though it contains a tiny computer, assessing the many signals that it receives from its neighborhood and then deciding whether to maintain itself unchanged (its usual fate), grow and divide, or kill itself for the good of the entire cell collective,” Science editor-in-chief Bruce Alberts writes in an accompanying editorial. “Powerful techniques such as those used in these two landmark studies can provide us with lists of all the molecules involved.”

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The structure of the agitoxin-Shaker channel complex (from Benoit Roux lab webpage)

Scientific grants are usually given out one investigator at a time, funding a single laboratory’s research. But as the questions of science grow larger, and the technology needed to answer those questions grows ever more specialized and expensive, funding collaborative grants becomes increasingly common practice. One type of multi-investigator grant has been dubbed a “glue” grant, so named because it sticks together researchers from several different institutions for the common pursuit of one important science goal.

Today, the National Institute of General Medical Sciences announced a glue grant on the topic of membrane proteins, an effort that will be led from right here on the University of Chicago campus. The grant formally creates the Membrane Protein Structural Dynamics Consortium, a team of nearly 30 scientists from 14 institutions in the United States, Germany, Canada, and the Netherlands.

“We have been able to put together almost a dream team of people currently involved in this type of research,” said Eduardo Perozo, PhD, Professor of Biochemistry and Molecular Biophysics at the University of Chicago Medical Center and the leader of the team. “There has been nothing like this project before.”

Membrane proteins are the machines on the factory floor of the cell’s surface, tasked with letting materials in and out of the cell, responding to signals from other cells, and even producing energy. The family includes ion channels that Perozo (and fellow team member Benoit Roux) study, the receptors for neurotransmitters and hormones, and various other pumps, transporters, and exchangers. Figuring out how these miniature machines function will be extremely helpful in designing new drugs, both to treat diseases caused by defective membrane proteins and for improving drugs that rely upon membrane proteins to get to their target.

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A critical step in the design of any clinical trial is picking the right primary endpoint, the result that will usually make or break the study. That’s more difficult than it sounds - one’s hope is to cure a disease or relieve a patient’s symptoms, but choosing the best specific measure for those goals is something of a guessing game. Further, the process can be made even more difficult for diseases that do not have a long history of clinical research and thus no established endpoints.

Idiopathic pulmonary fibrosis, an unexplained and very serious scarring of the lung tissue, is one such disease. Because of the extremely poor prognosis for patients with IPF, where most patients die within five years of symptoms first appearing, no large-scale clinical trials were tried until 1999, said Imre Noth, Associate Professor of Medicine at the University of Chicago Medical Center. Even today, some groups of IPF patients are still left out of clinical trials.

“The area that has been neglected by far and away are the severe patients,” Noth said. “The rationale beyond most biologics that have been looked at is you need to start early to make an impact.”

But the results of a promising clinical trial of a new treatment for severe IPF patients was published last week in the New England Journal of Medicine. The bad news? The primary outcome chosen for the study - improvement in a patient’s walking distance during a 6-minute test - failed to improve in the group treated with drug. Nevertheless, the trial was greeted with an optimism unusual for the IPF field, Noth said, thanks to a silver lining of secondary successes and promising near-misses.

“This has been a very frustrating disease for pulmonologists,” said Noth, a member of the Idiopathic Pulmonary Fibrosis Clinical Research Network, which designed and administered the trial. “The sense is, ‘Finally something we can give to our patients,’ because at least you can make them feel better, which is a great first step.”

The drug itself is an interesting story. Called sildenafil, it has already been marketed by Pfizer under the name Revatio as a treatment for pulmonary arterial hypertension. But most readers probably know sildenafil by its other commercial name: Viagra. The drug’s more famous use was actually an unintentional side effect, as it was originally developed to be a hypertension treatment. Trying sildenafil for IPF is going back to those primary intentions, capitalizing upon the drug’s ability to improve blood supply to the lungs.

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flickr photo by thepatrick

I’m spending today doing some intense video editing for pieces that will be on the site over the next two days, so here is science writer Greg Borzo with a guest post about a study released last month by University of Chicago researchers. The study proposes a new equation for calculating the survival expectations of patients with pulmonary artery hypertension, a disease sometimes observed in patients with COPD or sleep apnea. It’s also an interesting case study of how the equations doctors employ for prognosticating the course of disease or studying clinical treatments must be updated and adjusted as health care advances change the probabilities related to a disease.

Setting out to determine the survival of patients with pulmonary arterial hypertension (PAH), researchers at the University of Chicago Medical Center and their colleagues also discovered that an equation used for more than 20 years to predict survival is outdated. Accordingly, they developed and recently published a new survival prediction equation that will impact clinical practice and the drug development process.

In PAH, the pulmonary arteries, which carry blood from the heart to the lungs to pick up oxygen, become restricted, forcing the lower right chamber of the heart to pump harder. This leads to shortness of breath, limited exercise capacity, fatigue, heart failure and death. Often the condition goes undetected until it is advanced. Untreated, patients with PAH have a very poor prognosis.

That prognosis is determined using an equation developed by a landmark National Institutes of Health study published in 1987, well before there were any Food and Drug Administration approved therapies for PAH. The first such therapy was approved in 1995; today there are seven.

“Since 1987, great progress has been made in understanding and treating PAH, so a few years ago we decided that it was time to study contemporary survival,” said Mardi Gomberg-Maitland, associate professor of medicine and director of pulmonary hypertension. “Our results show that survival is vastly improved today. That led us to rework the NIH equation, which has been a standard measuring stick for more than 22 years.”

Gomberg and her colleagues at the Medical Center and Northwestern University’s Feinberg School of Medicine studied the survival of 576 PAH patients in their registry. Of these patients, 282 had idiopathic, familial, and anorexigen-associated PAH, which matches the conditions of the 187 patients in the pioneering NIH study.

Using the NIH equation, these 282 patients would have been expected to have one-, three- and five-year survival rates of 65%, 43% and 32%, respectively. In fact, their survival rates were much higher: 92%, 75% and 66%, respectively.

“This new formula is important for patients who want to know what, on average, to expect from their disease and for doctors who want to give accurate advice,” said Stephen L. Archer, Harold Hines Jr. Professor and chief of cardiology and co-author of the study. “We hope others will test our work. If it is validated by others it could be a very useful tool.”

The researchers were not able to determine why PAH patients survive longer today than in the 1980s, even though they measured the survival impact of many factors, including pulmonary function, demographics, medications, exercise treadmill, laboratory markers, echocardiography, and hemodynamics as well as the cause of the disease, which includes heart and lung disease, genetics, blood clots, connective tissue disease and other conditions.

None of these factors or causes had a significant impact on survival in multivariate analysis (when tested together statistically)-except hemodynamics. This explains why the new equation only incorporates hemodynamic parameters.

“Based on this result, physicians should stop drifting away from cardiac catherization, which is the gold standard test to determine exact hemodynamics,” Gomberg said. “Providers have been using more echocardiography and less cardiac catherization but we need to reverse that trend because until you know the hemodynamics you can’t accurately predict survival and or cure the disease.

“You can estimate hemodynamics with echocardiography but not accurately enough,” she added.

Many clinical trials in PAH used the NIH equation to suggest improvement in survival by comparing observed survival rates on a study drug versus survival rates predicted by the NIH equation, the study says. Since the NIH equation understates contemporary survival, it has led to more favorable comparisons of clinical trials testing new drugs to treat PAH, according to Gomberg.

“Our research suggests a reason that the drugs currently approved to treat PAH do not always work as well as we hope-because they were not held to a higher contemporary standard during their development and post-approval,” Gomberg said. “The new equation should ameliorate this bias.

“Although some of these drugs dramatically improve the condition of some patients, none of them improves hemodynamics to normal levels,” she added. “Therefore, we, as a medical community, have to acknowledge the fact that we have not yet cured PAH.”

As described on Monday and hinted at all week, this weekend marks the start of Neuroscience 2009, the annual mega-conference of more than 30,000 neuroscientists. After years of staging the meeting in areas with distractingly nice climates such as New Orleans, Orlando and San Diego, this year should be all business with the rainy chill of Chicago keeping people indoors. But there’s still a lot of fun to be had, with big-time speakers, immersive poster sessions, the never-ending hunt for the best vendor knick-knack giveaway and the night-time socials. Because of Neuroscience’s massive size, there are a million different ways to navigate a path through the science, but here’s a quick extremely long guide to what I’m looking forward to experiencing. Remember to tune in to ScienceLife all weekend (and through Wednesday) for coverage.

Saturday: Magicians Were the First Neuroscientists

Each year one of the most interesting lectures falls under the sober heading of “Dialogues Between Neuroscience and Society,” which basically means “we invited someone from outside of neuroscience to talk about neuroscience.” At previous meetings I’ve attended, that meant hearing public figures such as the Dalai Lama and Frank Gehry offering their own perspective on the brain, the mind and thinking - necessary reminders that the microscopic neurons those 30,000 scientists are concentrated on actually add up to some pretty amazing things in practice. 

This year’s Dialogues speakers are neuroscientists of a different sort: magicians Apollo Robbins and Eric Mead. Even though I saw a local version of this talk earlier this year with Robbins and neuroscientist Susana Martinez-Conde (which I wrote about it for the Tribune), I’m excited to see it again, because it really is a neat demonstration of how magicians have used the brain’s limitations to produce convincing illusions. Robbins, whose act is centered on his considerable abilities as a pickpocket, is a master of using diversion to direct a person’s attention one direction while he slips off their watch from another angle. As Robbins and Martinez-Conde explained back in January, this deceptively simple trick actually says a lot about how the brain shifts attention from stimulus to stimulus, and how a normal brain is “tricked” may help us learn about the neurobiological process that underlie an attentional disorder like ADHD. You can watch a video of a similar symposium organized by Martinez-Conde back in 2007 called “The Magic of Consciousness” - which includes Teller of Penn & Teller in a rare speaking role.

Also Saturday: We’re only two weeks away from the University of Chicago’s big Darwin conference, but I still will probably take in at least part of the symposium on Evolution of Brain and Behavior. Harvard’s Elizabeth Spelke caps off the day with a lecture on how the brain processes math - thankfully, it’s scheduled early in the conference, before my own brain will surely grow too tired to handle such a heavy topic.

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For information about the grants that the University of Chicago received as part of the ARRA package, click here.

If the scientists you know have an extra spring in their step today, here’s why: over $5 billion in National Institutes of Health funding was announced this week, the scientific portion of the federal stimulus package passed in the spring. In his January inaugural address, President Barack Obama made researchers’ neck hair stand up when he promised to “restore science to its rightful place,” and this was the first installment of that pledge - a much-needed boost of cash after five years of flat NIH budgets put many laboratories in jeopardy.

“We’re announcing that we’ve awarded $5 billion — that’s with a b — in grants, through the Recovery Act, to conduct cutting-edge research all across America, to unlock treatments to diseases that have long plagued humanity, to save and enrich the lives of people all over the world,” Obama said Wednesday at an NIH event announcing the grants.

A $42 million slice of that $5 billion pie was awarded to the University of Chicago, and I’ve spent the day talking to some of the researchers who snagged the biggest awards. They are all, as you might guess, thrilled to have an infusion of money to help finally launch projects that have languished unfunded or undermanned. In all, more than 100 UChicago researchers shared in the $42 million pot, with grants ranging from $10,000 to $5.6 million. After the jump is some information on the day’s big winners and the projects their new grants will fund.

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This was a busy week for biomedical news. The National Institutes of Health got a new nominee for its director, Francis Collins; the NIH finalized new rules for funding of research on embryonic stem cells; and swine flu got a new quasi-official name: “Pandemic H1N1 2009.”

Of the three events, the naming of Francis Collins as NIH chief may have the biggest long-lasting effects. Pending his confirmation, Collins will take over NIH at a time of rebounding budgets fueled by recovery funds, setting the course for the world’s most powerful research body.

But Collins’ nomination is causing more controversy than I would have thought possible.

I’ve talked with Collins in his prior capacity as director of the Human Genome Project and more recently in connection with his interest in reconciling science and religion. Collins, an evangelical Christian, has drawn heavy criticism from scientific atheists like PZ Myers and our own Jerry Coyne. Myers clearly admires Collins’ organizational skills, but describes him as a “lovable dufus” when it comes to issues of religion and some scientific principles. Coyne says he “can’t help but be a bit worried” about some of Collins’ religious views, including his conviction that the evolution of humans was in some sense inevitable. The psychologist and author Steven Pinker said he has “serious misgivings” about Collins’ appointment, calling him “an advocate of profoundly anti-scientific beliefs.”

Based on my interviews with Collins and reading of his work, most of these criticisms seem unfair.

It’s certainly true that Collins wants to reconcile religion with, for example, evolutionary biology. And this is something that naturalists such as Coyne and Richard Dawkins say cannot be done. But time and again in my lengthy talk with Collins about his book “The Language of God,” he stressed that he’s never thought religion should modify what science shows to be true. “I believe in truth, and I think we shouldn’t be afraid of truth,” he said. “If you believe in God as the creator of the universe, that can hardly be threatened by our efforts to understand how nature works.”

As Chris Wilson wrote this week in Slate, “Most of the time, Collins starts with the science and then reconciles the religion with it.” For a scientist to take issue with this approach seems gratuitous, bordering on intolerant.

On the other hand, like many of the critics I take issue with some of the content on Collins’ website for his BioLogos Foundation. The idea that God affects evolution or other natural processes through unmeasurable influences on quantum events strikes me as a game of three-card Monte - “Oops, you thought God had to act through overt miracles, but actually he was hiding with Heisenberg the whole time. Thanks for playing.”

But even on the BioLogos site, Collins and his crew make some fair points. A section called “God’s Relationship to Time” claims that as creator of the universe, God also would have created time, and would exist in some sense outside of time. This is relevant to the question of divine action, since it raises the possibility that such influence does not consist of supernatural intervention but is part of a larger scheme that was “baked into the cake” of the universe from the start. This seems to me more fundamental than a simple case of three-card monty. It’s a question that thinkers from St. Augustine to Heidegger have grappled with. It certainly doesn’t suggest an “anti-scientific” mindset.

As Wilson notes, for the most part Collins targets issues that seem by definition to be unsolvable by science; he’s not squeezing God into gaps that science has not yet solved, and he’s not challenging any facts that science has revealed. For example, Collins is understandably curious about the origins of life, but he dismisses the idea that because those origins are still murky, they require a divine explanation. When it comes to hard-core biology, Collins does not look for answers in Genesis.

This indicates a species of faith that Collins’ atheist critics share. It’s the faith that the dogged pursuit of empirically solvable questions will lead to answers we can trust, and that most of nature’s interesting mysteries will yield to rational explanations. That’s the sort of faith that should serve an NIH director well.

This announcement from the National Cancer Institute could be very big news at cancer research centers like this one. The increase, which NCI director John E. Niederhuber described in a speech at the meeting of the American Association for Cancer Research, will be part of the economic stimulus package.

Here’s an interesting passage from the story in The Scientist:

In 2009 the agency will be able to fund the top 16% of grant applications instead of only the top 12%–last year’s payline–based on budgetary increases alone, Niederhuber said. The NCI may be able to fund 25% of applications with the added $1.3 billion that the agency is set to receive as part of the $10 billion in stimulus funding for the National Institutes of Health. 

But raising the payline is only half the story. “Economic stimulus funds give us the chance to be visionary,” Niederhuber said, adding that the NCI will seek to fund more young, first-time investigators, and will emphasize prevention and early diagnosis in the research it supports in the future. “Patients still need better treatments, better prevention, and better early detection,” he said. “We must recommit ourselves to answering that call.” 

Last Friday the Obama administration published its new guidelines for federal funding of embryonic stem-cell research, ending the Bush-era restrictions on that work.

Except they didn’t end all of the restrictions. The new rules do not allow for work on cells made via research cloning (somatic cell nuclear transfer), and they require an informed consent process that may exclude some cell lines already derived with different consent procedures. Advocates at both antipodes of the stem-cell debate found something to criticize in the Obama rules. Researcher Irv Weissman of Stanford said the rules maintain an “ideological barrier” that will hinder progress, while Douglas Johnson of the National Right to Life Committee said the guidelines herald “an incremental strategy to desensitize the public to the concept of killing human embryos for research purposes.”

For now Obama seems to have struck an ideological balance, and some conservatives are giving him credit for it. Yuval Levin, a former Bush bioethics adviser who recently appeared on this blog, wrote on Friday that the new guidelines “certainly could have been worse” from a conservative’s perspective.

At the same time, the new rules mean that federally funded research can move beyond 2001-era technology. Bush’s guidelines, which restricted funds to lines derived before August 2001, allowed researchers to work with just 21 cell lines. Obama’s rules open the door to hundreds of additional lines created since 2001, many of them with genetic defects that can help scientists understand how diseases develop.

In moral terms this may even be a clearer approach than Bush’s policy, which claimed to protect nascent life but did allow some funding of research that required the destruction of human embryos. Those rules allowed fewer stem-cell lines to qualify for funding, yet the restriction was based on an arbitrary cut-off date. Why was it moral to allow funding of research on stem cells taken before August 8, 2001, but beyond the pale to allow funds for cells taken after that date?

Levin, who also served as executive director of the President’s Council on Bioethics, wrote that by keeping some limits on stem-cell research funding, Obama’s NIH has conceded “that the destruction of embryos for research is not an innocent and unproblematic practice, but must be constrained for ethical reasons.” So far, so good. As the bioethicist Art Caplan once told me in an interview, “A human embryo may not be a legally protected person, but it’s also not just any old stuff.” Levin then goes further: “These rules raise the question of why limits are necessary, and any serious answer to that question would lead us to conclude that these rules are inadequate. ”

That’s not at all clear to me. Under Bush’s old rules, an embryo’s fate might depend solely on the date when it was created. Under Obama’s new rules, the embryo’s fate is governed by something far less arbitrary - the parents’ intentions, informed by all the options available to them. It seems reasonable to trust that whatever parents decide, they will see their embryos as something more than raw material.

[Note: This post originally contained a quotation from a private classroom setting, which has been removed at the speaker's request.]

Suddenly George W. Bush is no longer the easiest target for anyone frustrated at the pace of scientific progress.

He started to occupy that position at 9 p.m. Eastern time on Aug. 9, 2001, when he went on national television to outline restrictions on federal funding for the new field of embryonic stem cell research. It seemed an arbitrary and even arrogant policy. No federal funds could be used for research on cell lines derived after the moment Bush began his speech - exactly 9:00:00 p.m. He portrayed the decision as a compromise - the original intention was to give no funds at all - but many researchers saw it as a fiat that would stifle a promising field and send a message that scientists served at the pleasure of the president. Science-related decisions in subsequent years tended to bear out that early impression.

Now there’s no obvious scapegoat for the obstacles facing researchers and patients eager for new treatments. President Obama has pledged to lift Bush’s restrictions on stem cell research, and to “put science back in its rightful place.” But we still don’t have a good sense of what that means.

This could be a rare opportunity to make a new strategy for American biomedical research. It would be a massive undertaking, centered on the sprawling National Institutes of Health, which currently lacks a permanent director. The $28 billion NIH budget supports 27 centers and institutes, and an army of researchers around the country.

A blog post last week by Stanford researcher Stephen Quake suggested that this is “the time to rethink the basic foundations of how science is funded.”  He proposed more long-term grants to scientists and better incentives to pursue creative projects. The current system has some incentives for researchers to follow the agencies’ institutional priorities, rather than give reign to their best ideas.

My op-ed last Monday in the Chicago Tribune suggested creating a new NIH institute devoted to stem cell research. Yet some of the response to that piece reflected a widespread wariness of doing anything to complicate the federal research bureaucracy. My e-mail friend Yuval Levin, a National Review writer who worked in Bush’s domestic policy office, said that if anything the NIH needs a simpler management structure, not more institutes. He echoed Quake’s point that the current system doesn’t do enough to support younger investigators or new ideas.

In the short run, how Obama handles the NIH may be a better test of his managerial success than the outcome of the stimulus plan. It’s one thing to sign a piece of paper and reverse Bush’s stem-cell policy; it would be a much greater feat to free the awesome creativity of America’s scientists.