The death of Michael Jackson has made its expected transition from a celebration of his life and music to an uncomfortable public autopsy of how he died. More than a month after his death, the official coroner’s autopsy has yet to be officially released, but various media outlets have sniffed out one particular drug that is expected to appear in the pop star’s toxicology report: the general anesthetic propofol.

The widely-used but little-discussed drug has provoked a number of “what is Propofol?” news segments, including a piece by ABC’s Primetime: Crime that brought a camera crew to the University of Chicago Medical Center earlier this week. That segment, reported by former MTV newsman Chris Connelly aired Wednesday night, and you can watch it here.

For 30 seconds (from -2:17 to -1:47) of the video, you’ll hear briefly about research by Avery Tung, associate professor of anesthesia and critical care for the Medical Center (you will also see a rat being anesthetized with a completely different drug, halothane). In the early part of the decade, Tung conducted an NIH-funded research project examining relationships between sleep and anesthesia, and published several papers and scientific abstracts looking at how propofol mimicked the effects of actual sleep. After Tung sat down with ABC, I spent a little more time with him discussing the anesthetic and his research.

Q: First of all, what is propofol, and how often is it used?

Tung: Propofol is given intravenously to induce anesthesia in surgical patients and to provide sedation for patients in the Intensive Care Unit. It’s the most common induction agent of anesthesia in current use. It pretty much has replaced pentothal because it has fewer side effects and it makes people feel better when they wake up.

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You could say that Janet Rowley is having a pretty good year. In March, the University of Chicago molecular geneticist stood at President Barack Obama’s right arm as he signed an executive order clearing the way for federal funding of embryonic stem-cell research. Earlier this month, she was declared the winner of the 2009 Peter and Patricia Gruber Genetics Prize, which comes with a $500,000 cash award and a gold medal.

Today, another tremendous honor was announced for the still-active 84-year-old: the Presidential Medal of Freedom, the highest award an American civilian can receive from the White House. Among the other 15 recipients are Stephen Hawking, Sen. Edward Kennedy and Desmond Tutu; very prestigious company indeed.

In typical fashion, Rowley downplayed being recognized for her important research in the early days of cancer genetics.

“I felt very humbled, but also as though I didn’t deserve it,” Rowley said yesterday about her initial reaction to the honor. (You can watch the video interview with Dr. Rowley here: Janet Rowley talks about winning the Presidential Medal of Freedom)

With all due respect to Dr. Rowley, she’s wrong. When Rowley began to investigate the mysterious relationship between chromosomal abnormalities and leukemia in the 1960’s the scientific jury was still out on the relationship between genes and cancer. It was known that patients with certain types of leukemia had unusual chromosomes — notably the shortened “Philadelphia Chromosome,” associated with chronic myelogenous leukemia (CML) — but scientists debated whether that was the cause of the cancer or the result.

After starting a laboratory at the University of Chicago with help from legendary hematologist Dr. Leon Jacobson, Rowley used the newest chromosome-staining techniques to discover that the genetic segment missing from the Philadelphia Chromosome had not disappeared, but instead traded places with a segment from another chromosome in a process called translocation. This swap was not merely cosmetic; the gene for a particular protein that promotes cell division was separated from its natural genetic brake, causing the uncontrolled cell proliferation characteristic of cancer.

Rowley’s landmark paper on CML was published in 1973, but only after rejection by at least two scientific journals unconvinced of her findings. Eventually, chromosomal translocations were found to be responsible for several different cancers, and the concept of cancer as a genetic disorder became widely accepted in medicine. Her research also led to the development of the anti-cancer drug imatinib, aka Gleevec, which acts by inhibiting the protein that is excessively activated after the translocation.

For much of the past decade, Rowley served on President George W. Bush’s Council on Bioethics, advising the White House on controversial scientific topics such as embryonic stem-cell research. Having long opposed Bush’s limitations on federal funding for such studies, Rowley celebrated Obama’s loosening of those restrictions, writing for US News & World Report that the decision “has removed a key barrier to research and discovery.”

Rowley continues her research at the University of Chicago, and is an avid swimmer, sailor, cyclist and gardener. When I interviewed her for a Chicago Tribune article on the Gruber prize in late June, she said, in her understated way, that she was flattered to receive such awards and surprised that her work was still being acknowledged.

“It’s a great honor to have one’s colleagues still recognize one’s accomplishments,” Rowley said. “I suppose it’s a great pleasure to be around to be recognized.”

Much of the latest news on the H1N1 virus, colloquially known as swine flu, indicates that the next flu season has the potential to be unusually rough. In some ways the last flu season never really ended; the Centers for Disease Control and Prevention report that 20 states are still seeing widespread or regional flu activity, with H1N1 accounting for the vast majority of cases.

The coming flu season could fall within normal ranges, but CDC planners are bracing in case it resembles an especially bad pandemic year, such as 1957. The details on how H1N1 affects patients are still coming in. Certain populations appear to be at high risk for severe symptoms and, occasionally, death. Widely covered today was a Lancet report that suggested pregnant women may be more susceptible to the virus, with a higher rate of hospitalization and an elevated death rate in the pandemic’s early days. Between mid-April and mid-June, six pregnant women (including one in Chicago) died from the novel flu strain, 13% of the 45 American deaths reported during that time period.

The authors of the Lancet paper recommend that pregnant women receive antiviral medication, such as Tamiflu, as soon as possible after developing flu symptoms - none of the six deceased patients addressed in the paper received antivirals until at least 48 hours after illness onset.

But the best way to protect pregnant women from the flu strain when it likely returns in force this fall is through vaccination. The H1N1 story of the summer has been the frantic race by governments and scientists around the world to have a vaccine against the strain ready in time for the Northern Hemisphere’s next flu season. Manufacturers told an FDA panel last week that about 100 million vaccines could be ready in the U.S. by mid-October, but with roughly 300 million Americans, not everyone is going to be immediately vaccinated and priorities will have to be set.

That sober reality set the stage for a fascinating meeting today in Atlanta, where the federal Advisory Committee on Immunization Practices - a panel of doctors, scientists and public health experts - attempted to pick and choose which groups deserved the first crack at the limited vaccine supply. Given the numbers released yesterday, it was no surprise to find pregnant women in the top priority group for this fall’s vaccinations. Also given priority in the ACIP’s recommendations were caregivers for children younger than 6 months (who cannot themselves be immunized), healthcare and emergency medical personnel, children and young adults from 6 months to 24 years old and adults with chronic medical conditions.

Added together, that’s about 150 million people, roughly half the U.S. population. But with compliance among the priority groups expected to be far below 100% (it’s only around 40% for the regular old seasonal flu), it’s thought that the initial batch of 100 million will suffice, even if each person needs two doses to be fully protected, which experts predict may be necessary. As more vaccines become available, people between 25 and 64 will get it next. Those above 65 years old, who have seemed less affected by H1N1, are in the third, lowest priority group.

Much of the debate Wednesday (helpfully webcast on the government’s flu.gov website) centered over whether the younger population targeted in the first wave of vaccinations should be capped at age 19 or age 24. The argument of some panelists: college kids are as good at spreading viruses as they are at sleeping in late. Others argued that colleges are also an excellent distribution system for getting vaccines to this particular population. So young adults will join the front of the queue for the first batch.

The effects of H1N1 on different age groups appear to vary in a striking way, according to epidemiology discussed at the meeting. With nearly 44,000 American cases of H1N1 now documented, elderly folks appear to be less susceptible to the strain than younger populations. That observation runs counter to the pattern in most flu seasons, when senior citizens are more sensitive to the effects of seasonal strains and thus are heavily encouraged to get the yearly vaccine. At a CDC press conference announcing the panel’s recommendations, Assistant Surgeon General Anne Schuchat urged American seniors to get the seasonal flu vaccine as usual this coming fall. But for the H1N1 vaccine, they’ll be at the back of the line behind their children and grandchildren.

(Not to be a scaremonger, but for a gripping tale of H1N1 overseas, see this article by New York Times reporter Sheryl Gay Stolberg and her daughter Olivia Robinson, who contracted the virus while on a school trip to China)

Now that my new job leaves less time for blogging, we’re changing the format of this site a bit and adding more voices to the mix. The biggest change is the addition this week of Rob Mitchum, who got his PhD in neurobiology here at the University of Chicago a couple of years ago before joining the Chicago Tribune as a reporter. Now Rob is back here, with a mandate to write, blog and give perspective to the biological research he knows so well. Here’s a nice sample of the science writing Rob was doing at the Tribune.

ScienceInsider, the top-notch blog by Science magazine writers, flags this case of a scientist who discovered his research grant application had been part of a Freedom of Information Act request. A physician at another university asked for the application, on the assumption that once something is submitted to a federal agency it’s fair game for a public records request.

This reminds me of the slightly shady practice among journalists of doing a FOIA for all the other FOIAs that have been submitted to a given agency. It’s a way to keep track of what your reporting competitors are up to, but it always struck me as a bit like cheating.

In this case, as the original post explains, there’s a legitimate legal case that the unpublished data in such an NIH application should be shielded from public view. And as the poster argues, a FOIA is certainly a non-collegial way of getting information. But is it unethical? Clearly it is if the intent was to get an unfair advance peek at another scientist’s methods, objectives, etc. But public records are public. I never submitted an e-mail, FOIA or other communication to a public agency that I wouldn’t have been comfortable seeing released. Grant requests are different, but it’s probably safe to assume that unless there’s a clear exemption, anything you give a government office could become public.

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.