4:15 p.m. - Of Mice and Mammoths

The last talk of the day (for me, as I had to leave before the final, final talk) made for a great reminder of how far the field of evolutionary biology, wrapped in a relatively simple story told engagingly by Hopi Hoekstra of Harvard. Hoekstra described her research quest as “the hunt for genes that make a difference,” and she uses a really nice model system - the oldfield mice of the southern United States. These mice typically are brown in color, but they have migrated in the recent (meaning thousands) of years to the gulf and atlantic coasts and taken up residence, like a retired couple, on the beach. But a brown mouse on a beach is a target, and their predators, which include birds and coyotes, find it all to easy to locate their brown fur on white sand and make a beachside snack out of them.

Cue natural selection - soon you have brown oldfield mice inland, and predominantly white oldfield mice that live on the beach. Hoekstra tested whether the fur color really does construe an evolutionary advantage with a simple experiment - make a bunch of clay mice colored brown or white, and leave them out on the beach. Sure enough, the brown clay mice quickly showed divots and bitemarks left by attacks from (presumably very frustrated) predators.

That would have been a fine experiment for the 1959 conference, but Hoekstra’s next step was pure 2009 - she took examples of brown and white mice back to the lab, bred them, and searched for the genes that determined fur color. Her laboratory narrowed the gene candidates down to three genes, and in one of them - a receptor called Mc1r - the substitution of a single amino acid flipped the switch from brown fur to white fur. Amazingly, when another group of scientists sequenced the genome of extinct mammoths in 2006, they found the same amino-acid substitution in the same gene, implying that mammoths, like the oldfield mice, came in different color varieties.

After so much high theory and methodological complexity, Hoekstra’s experiment sent all of us (or at least me) home with a warm feeling - not only was her experiments a beautiful example of evolutionary biology that would have been impossible in 1959, it was a great example of teachable science, the kind of story that a 3rd-grader could wrap their head around and begin to see the truth of evolution. The cloud hanging over Darwin/Chicago 2009 was the uneasy feeling that all this scientific progress was still losing out in the arena of public opinion, but Hoekstra’s work and charismatic speaking style (on the heels of similar ambassador figures Neil Shubin and Michael Shue) chased away some of the pessimism, and left me confident that the more examples we find of Darwin’s elegant theory at work in nature, the easier it will be to convince the world that it is true.

And with that, we’re finished. Happy Halloween to those of you who have followed me this far, and thanks very much for reading and perhaps linking to the posts. I’ll be back Monday with a digest post to help navigate the coverage of the last few days, and Jeremy Manier will be here Tuesday with his own thoughts on the conference.

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5:00 p.m. - Biomedicine and Bracketology

Here’s the final report from today’s session, join us again tomorrow for a full Halloween day of evolutionary science and philosophy! Also, continue to follow PZ Myers of Pharyngula and Skip Evans of Wisconsin Citizens for Science for their reports on the conference.

Both talks in the final session of the day focused on how the incredible advances in gathering genetic information over the last decade have done much to shake up the worlds of genetics and evolutionary biology. As we’ve written about previously, the 1959 conference helped solidify what’s known as the modern synthesis of evolution that incorporated the then-new information about DNA, genes and molecular mechanisms of inheritance, an arrangement that forever married the two fields. Well, could the participants in that conference have predicted that 50 years later we would have a reasonably complete genome for humans, not to mention 43 other vertebrate species? And did they know how much trouble it would cause?

Eric Lander, who was one of the leaders of the Human Genome Project, said he felt slightly out of place at a conference about Darwin, but the modern synthesis marriage sometimes makes strange bedfellows! Regardless, Lander’s talk was a great primer on how the dogma of genetics has been forever altered by what we learned from the HGP and the genomes of other animals: that we have far fewer genes than we thought (~20,000 vs. previous estimates of 100,000), that much of what is handed down between generations is “non-coding” DNA that doesn’t make proteins, that those “non-coding” sections may create important regulatory elements that help organisms develop. Lander, who described himself as a biomedical scientist, said much of what has been found since the explosion of genetic data has been bad news for medical geneticists - many disease-associated alleles have been found, but most have very marginal effects on the probability of a person developing that disease. But Lander said it was a glass half-full/half-empty situation:

“Those people who want to do personal genomics - take your DNA and tell you your risk of diabetes - they’re in trouble. This is not going to be the best way to do that,” Lander said. “But if I want to understand what diabetes is about…I start to get clues to the pathways that matter to diabetes.”

The final talk of the day covered how genetics has caused a similar reshuffling in the field of phylogeny - the science of organizing life into “trees” that show the evolution and relationships of species. Philip Ward, from UC-Davis, talked about the durability of the “Tree of Life” simile, which Darwin readily used in Origin of Species - the only figure in the book is an early phylogenic tree. Modern phylogeny produces beautifully complex trees that look like 10,000-team basketball tournaments run in reverse, with the winner being life’s common ancestor. But as biologists have turned to genetics to build these trees, they’ve found that they lead to completely different trees than the ones built from morphology, the physical characteristics of organisms.

One reason for this is a tricky effect called convergence - two species that are not closely related and live continents apart could form a resemblance because they evolved in similar environments. Ward studies a type of ant that is found in both Asia and America, and morphology would suggest that they are closely related species despite being so far apart geographically. However, genetic data showed the ants were more distantly related than previously could have been estimated from their looks, suggesting they evolved to look similar due to their similar environments, without a recent common ancestor.

But the Tree of Life remains a strong structural model, Ward said. So strong, in fact, that it has been adopted by creationists, who describe an “orchard of life” of animals that evolved after Noah’s flood. As with most mentions of creation “science” at the meeting, Ward’s slides about these theories drew mostly giggles from an audience decidedly on the side of Darwin, even as genetics reveals a world more complex than he ever could have imagined.

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Many thanks to PZ Myers, author of the amazing evolution blog Pharyngula, who gave us a nod last night in his ongoing live-blogging of the Darwin/Chicago 2009 conference. PZ is doing a fantastic job covering the event in real time. For other coverage, check out WMFT’s interview with conference organizer Robert Richards, and Milt Rosenberg’s interview on WGN Extension 720 with Richards and conference speaker Ronald Numbers.

Darwin/Chicago 2009 is here! Here is the lineup for tonight, our live-blog will begin below around 6:00 p.m.

6:00 p.m. Welcome by Robert Zimmer, President of the University of Chicago

6:15 p.m. Richard Lewontin (Harvard University): “Genetic Determination and Adaptation: Two Bad Metaphors”

7:00 p.m. Ronald Numbers (U. of Wisconsin): “Anti-Evolutionism in America: Scientific Creationism to Intelligent Design”

7:45 p.m. Marc Hauser (Harvard University): “From Where do Morals Come? NOT Religion!”

We’re only a few hours away from the start of Darwin/Chicago 2009, 2+ days of the world’s leading evolutionary biologists discussing the past and future of the field. Come back to this space tonight at 6:00 pm Central time for live-blog coverage of the opening event at Rockefeller Chapel, and keep coming back all day Friday and Saturday for frequent updates from the conference.

Before things get into full swing, I wanted to play armchair Linnaeus and organize the conference’s 30-some talks into a few major themes. So much is packed into Friday and Saturday, with two simultaneous programs covering “biological sciences” and “history and philosophy,” I won’t be able to see everything, but the list also contains what I’m hoping to prioritize in order to get at least a representative sample of the event.

Evolution Goes to Church

Rockefeller Memorial Chapel, the looming gothic structure on the southeast side of campus where convocations and communion services are held, has been the site of Darwin discussion before - as mentioned yesterday, Sir Julian Huxley gave a speech predicting the end of religion at the 1959 conference. Thursday night’s trio of speakers both follows that agnostic tradition and nicely previews the main threads of the more tightly-packed Friday and Saturday schedules.

Addressing the renewed vigor of the evolution vs. religion debate, Ronald Numbers of the University of Wisconsin will recap the historic path of these conflicts, emphasizing that the “young earth” element of today’s creationists is a relatively new development. Harvard’s Marc Hauser, meanwhile, will pull the rug out from under one of the main creationist arguments - that morality could not have developed under natural selection and must have been given to humans by a supernatural power. But lest you think evolutionary biologists are too distracted by the external debate to do the hard work in their own field, legendary geneticist Richard Lewontin will open the night’s proceedings talking about the challenges of directly determining how genes contribute to an organism’s fitness.

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Sir Julian Huxley speaks in Rockefeller Chapel, 1959

As discussed yesterday, the Darwin/Chicago 2009 conference marks not just the anniversary of Darwin’s birth and most famous book (The Origin of Species) but also 50 years since a landmark evolution conference was held at the University of Chicago. Like this year’s gathering, the 1959 conference was meant to both look back at Darwin’s life and ideas and look forward to the future of the field his theory created: evolutionary biology.

To commemorate this historic conference, the University of Chicago’s Regenstein Library has put together a great web exhibit with video and audio from the Darwin Centennial conference in 1959. Encylopedia Brittanica Films produced a film of the conference, and you can watch several video clips from that film and listen to audio excerpts from three presentations - in addition to songs from the Darwin musical commissioned for the meeting.

From the film footage available on the website, you can see that the style of the conference in 1959 was very different from what will occur this weekend. Instead of individual talks and Powerpoints, the scientists participated in panel discussions on topics such as The Origin of Life and Man as an Organism - the latter of which was held on Thanksgiving Day. One clip shows overflow crowds that couldn’t get into Mandel Hall (where the panels were held) sitting in other University buildings and staring off into space as they listen to the audio of the conference. This weekend’’s overflow crowd will be able to stare at their computer and follow along right here on the blog, if you’ll forgive the plug.

Then again, some things weren’t so different between 1959 and 2009. Tension between evolution and religion was intact: Sir Julian Huxley, the renowned zoologist considered to be one of the main architects of the modern synthesis of evolutionary biology, gave a lecture in Rockefeller Chapel entitled The Evolutionary Vision which, according to Regenstein librarian David Pavelich, “proposed that religion, being subject to the laws of evolution, was fast becoming obsolete and would eventually evolve itself out of existence.” The religious opposition to Darwin’s theories was acknowledged by University of Chicago chancellor and professor of philosophy Lawrence Kimpton, who likened Darwin to John Stuart Mill as advocates of free thought and liberty:

“Darwin, in his own sphere and his own action, produced an independent defiance of the pressures of his day, challenging the rigidity of thought and temper with a naturalistic theory shocking to the entrenched supernatural explanation of biology. The outrage and the distortions that erupted immediately, persisting well into this century and even in this country, are measures of Darwin’s independence.”

Also in audio clips:

• Sir Charles Galton Darwin discussing his grandfather’s legendary voyage observing and collecting specimens on the H.M.S. Beagle, including a reading of what Darwin wrote in his journal the first time he ate a banana.
• Archaeologist Louis Leakey on the search for fossils of human ancestors - “You hear people say ‘what has Africa created to the human race?’ It contributed the human race.”

In lighter fare, check out the songs from the Darwin musical, Time Will Tell, premiered at the conference. They are very 1959, and are probably the only songs you will ever hear with lyrics such as “this gastropod has quite an odd phylogeny” and “Alas, to his sorrow, he generally finds/That pre-conceived notions of various kinds/Have already helped them to make up their minds/And the facts will only confuse them.” I could see that as the theme song for quite a few evolution blogs, actually.

There has certainly been no shortage of attention on Charles Darwin this year. With the dual landmarks of Darwin’s 200th birthday and the 150th anniversary of The Origin of Species, virtually every scientific publication, museum, conference and institution has taken the opportunity to pay tribute to the life and work of the man who gave us the theory of evolution. But now that the celebrations are (mostly) over, it’s time for the field of evolutionary biology to move forward, capitalizing on new technologies and discoveries that were only a dream when Darwin drew upon decades of observation and thought to craft his revolutionary book.

That same challenge faced evolutionary biologists in 1959, when they gathered at the University of Chicago to observe the 150th and 100th birthdays of Darwin and his book. Brought together were many of the 20th century’s greatest thinkers on the subject of evolution, including legendary biologists Julian Huxley, Theodosius Dobzhansky, and Ernst Mayr, Darwin’s grandson Charles Galton Darwin, and John Scopes of Scopes Monkey Trial fame. And according to Robert Richards, professor of the history of science and medicine at the University of Chicago, the discussions that took place at that conference helped solidify what we now think of as the “modern synthesis” of evolutionary theory, the merging of Darwin’s ideas about the gradual effects of natural selection with the then-new field of genetics.

Darwin/Chicago 2009, which begins Thursday night at the University of Chicago, will try to recapture that spirit and make a similar impact upon the path of evolutionary biology. Once again bringing the field’s brightest lights to Hyde Park for an exchange of ideas, Richards and the conference’s other organizers hope that the event will do more than merely acknowledge a triple anniversary, but will instead re-evaluate evolution science in light of a world much different from the 19th century environment that shaped Darwin’s thoughts. Here, with Richards’ assistance, are three reasons why now is a great time to talk about Charles Darwin and evolution.

1) New technologies

The 1959 conference took place only six years after James D. Watson and Francis Crick published their landmark paper on the double-helix structure of DNA. And it wasn’t until 1957 that the “central dogma” of biology - that DNA encodes for RNA which encodes for proteins - was enunciated by Crick. So the ‘59 conference took place at the dawning of the genetic age, when the biological substrate that Darwin’s natural selection acts upon was finally understood.

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Studies of human disease often work from the patient backwards - doctors and scientists take the common symptoms of a particular disorder and use them as clues to figure out what first went awry to spur the disease. For neurological diseases like Parkinson’s or amytrophic lateral sclerosis (aka Lou Gehrig’s Disease), symptoms and brain images have pointed the research at particular parts of the brain, which are then studied in animal models and on the genetic or cellular level. But disease research can also work from the other direction, where a particular cellular process is identified as a potential culprit in the disorder before a patient with that defect is even found.

That’s the case with a paper published this month by a team of University of Chicago researchers studying the cellular mechanisms that underlie diabetes. There are many types of diabetes mellitus, but all can be traced back to the hormone insulin - the body’s signal that cells should soak up sugar from the blood. Most cases of juvenile, or Type 1, diabetes result from the immune system erroneously attacking and killing the Beta-cells of the pancreas, which release insulin. Type 2 diabetes, which often develops in adulthood, results from a reduced sensitivity to insulin and/or a decreased release of the hormone.

But diabetes can also have a genetic origin, in some rare cases, when one of the genes involved in the secretion of insulin is disrupted. Previously on the blog, we’ve talked about the story of Lilly Jaffe, whose diabetes was found to be caused by a rare genetic mutation in a protein called a potassium channel, critical for the release of insulin. The mutated potassium channel seen in Lilly’s case interferes with the trigger of insulin release, causing lower amounts of the hormone to circulate through her blood. Thus, Lilly was treated by daily injections of insulin, until doctors at the University of Chicago detected the mutation and prescribed her a drug that directly targeted the potassium channel.

Now researchers at the University of Chicago have found another ion channel that must function properly for the right amount of insulin to be released. Only problem: there’s no patient.

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Over the course of four days covering the Neuroscience 2009 meeting in Chicago, I wrote nearly 7,000 words between Sunday, Monday, Tuesday and Wednesday. You might say I was excited to be there. But I know not everybody has an hour to devote to reading feverish recaps of the latest neuroscience research, so here’s a post summarizing some of my favorite parts, along with some excellent posts from other websites about the conference.

Best Talks

Eric Kandel - I was charmed by this 80-year-old Nobel laureate’s undiminished enthusiasm for scientific research; even though he’s already contributed more than perhaps anyone else to our understanding of how the brain learns and remembers, he’s still forging ahead with new, ambitious experiments.

Thomas Sudhof - There is no shortage of bad science about autism, so it was refreshing to hear some good science, even if the answers aren’t as easy and reassuring as those provided by the quacks. Sudhof, who used black widow spiders to discover two proteins that help neurons find each other and communicate, spoke eloquently about how defects in these proteins could underlie many of the symptoms of autism spectrum disorder.

Hot Tech

Optogenetics - Everyone at the conference seemed to be abuzz about this technique, developed by Karl Deisseroth of Stanford, for activating or de-activating specific neurons with light. Here’s an awesome video from Deisseroth’s lab of a mouse’s activity being controlled by a fiberoptic implant, and a talk by Deisseroth describing his method and its applications.

Wikipedia - Nothing new about this tech, of course, but two Wikipedian-scientists held a fascinating workshop on how neuroscientists can help improve public understanding of science by writing and editing for the open-source encylopedia…and circumvent the media in the mean time.

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And so Neuroscience 2009 comes to an end, and it’s time to put away my badge, rest my weary feet and note-taking hand and think about biology below the neck again. Here’s the final installment of our live coverage, but come back tomorrow for a roundup of the conference with highlights, loose observations and links to other people’s thoughts on the conference. Thanks for reading!

2:30 PM - The Final Talk

The schedule may say that Neuroscience 2009 runs through the end of the day today, but judging by how many suitcase-toting scientists were jumping in airport cabs this afternoon, a small portion of the 30,000+ attendance makes it to the very end. Indeed, even the main stage ends its conference early, shutting down after a talk by Mt. Sinai School of Medicine’s Eric Nestler, an expert in the field of molecular psychiatry.

Nestler’s research focuses on the gritty details of how drugs of abuse change the expression of a person’s genes - yes, it was another addiction talk, and the former addiction researcher that I am, it was great to see the topic getting so much attention this year. In the addiction press conference I attended yesterday, Nestler hinted at a bombshell idea - frequent users of addictive drugs such as cocaine, heroin or alcohol may change the mechanics of their genes so permanently, the modifications could be passed on to their children. This “inheritable addiction” has already been observed in lab rats, Nestler said, mirroring similar results seen with the offspring of obese rats (which I talked about on Monday).

But that data must be too fresh for mass consumption, despite Nestler telling a roomful of reporters about it the day before. His talk today focused on the steps leading up to that discovery, carefully examining how repeated cocaine increases or decreases the activity of hundreds of genes in the reward pathway of the brain. Those long-lasting changes, which can cause cells of the reward pathway to actually grow and change shape, help explain why addiction is such a difficult condition to treat - it may require a complete re-re-structuring of the brain.

Much of the addiction research I’ve talked about this week has taken place in animals, but before Nestler’s talk, I came across a rare experiment that looks at the behavioral effects of a commonly-used drug in humans. It might seem strange that we know a ton about the specific genes that are up or down-regulated by cocaine, but not so much about its effects upon humans, but that’s due to procedural reasons - it’s quite hard to get approval for a study that gives illegal drugs to humans.

Michael Ballard, from the University of Chicago laboratory of Harriet DeWit, was trying to fill in at least one of those gaps in the research by testing the effects of THC (the active ingredient in marijuana) to presumably eager volunteers. Ballard then tested the subjects’ ability to judge facial expressions and determine the emotional content of pictures and personality trait words while they were under the influence of the drug. Interestingly, higher doses of THC caused the subjects to misjudge the facial expressions they were shown, suggesting an effect of the drug on social perception. The other tests were normal during the drug effect, but when brought back to the laboratory a week later, the subjects showed a decreased ability to remember neutral and negative personality traits, possibly indicating that their memories of the drug effect were biased toward happier stimuli. Ballard hopes to continue that research into other drug types - he’s currently testing amphetamine - to give the field of addiction research much-needed, laboratory-controlled human data to make sense of the flood of animal experiments.

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6:45 PM - The Opposite of a History Lesson

Eric Kandel is 80 years old, was present at the first Society for Neuroscience meeting in 1969, is 9 years removed from winning the Nobel Prize for physiology and medicine. He’s also so well known at the Neuroscience meeting, he can go by one name, “like Bono,” said SfN president Tom Carew in his introduction to tonight’s Presidental Lecture. So you might have expected Kandel’s talk to be a history lesson, a retelling of how he uncovered the cellular chain of events that underlie learning and memory in sea slugs, fruit flies, mice and, by extension, you and me.

But Kandel, looking like The Sopranos’ Uncle Junior and speaking with Woody Allen’s Brooklyn accent, had very little interest in looking back. After 75 minutes of him excitedly flashing through graphs and figures explaining recent findings in his laboratory at Columbia University, he could only narrow his talk down to four conclusions. My thesis adviser, who was sitting next to me, leaning over and whispered in amazement, “these aren’t conclusions at all, he’s still forging ahead.”

That relentless drive in someone so late in his career was infectious. Kandel said the goal of his talk was to explain how a person remembers his first love for the rest of his life, as if that was a simple quest, but his lecture portrayed science as it should be: a never-ending story, with each answer giving birth to several more questions. While some researchers settle on a single technique and pass the torch to younger researchers when the limits of that technique are reached, Kandel proved that he has stayed on the cutting edge of science, bringing fresh talent into his lab to apply new tools to his endless questions about how neurons encode memory.

As a result, almost a decade after his Nobel victory, Kandel was excitedly telling 10,000 of his colleagues about a new cellular signal, called CRB-3 in mice, which he humbly described as “a new class of functional proteins” and “an entirely new model of synaptic plasticity.” The work was backed up with the latest in genetic, cellular biology and imaging evidence, testimony to both Kandel’s ability to keep up with the fast-moving world of science as well as the sprawling world of neuroscience itself.

“One of the wonderful things that has happened in my forty years in the society, is that neuroscience, which really was quite fragmented when I entered the field…has become a unified organism,” Kandel said.

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6:30 PM - Taking Drugs Like Driving Without Brakes

The day ended with another emissary from the NIH, as Nora Volkow, director of the National Institute on Drug Abuse, gave the week’s third Presidential Lecture. I’ve heard Volkow speak a couple times now - I was actually at NIDA when she was named director in 2002 - and I’ve always found her work to be some of the most convincing data available about addictive drugs change the way the human brain works. The operative word there is human, since most studies of drug addiction (including my own work) has been performed in animals, and there are several nagging questions about the human relevance of research in animals on complex behaviors like addiction.

The directorship appears to be keeping Volkow busy with administrative duties rather than scientific work, as much of the talk was unchanged from when I saw it seven years ago. But the story is still a good one, using imaging of a particular neurotransmitter system in the brain, dopamine, to search for differences in the brains of people who habitually use drugs and people who don’t. Dopamine is increased in response to drugs of abuse, and without getting too technical, Volkow found that one type of dopamine receptor, called D2, is severely reduced in people who repeatedly use drugs such as cocaine, heroin and alcohol. Simultaneously, another region called the prefrontal cortex (PFC) shows reduced activity in drug addicts. The role of the PFC is to control people’s impulsivity - Volkow described it as the part of the brain that told her not to have a glass of wine before her talk. So repeated exposure to a drug such as cocaine can actually remove a person’s natural control of impulses, leading to more drug use and binge drug-taking behavior.

“You basically disrupt any ability to control that drive,” Volkow said, “So the person is really without brakes, and is unable to stop taking the drug.”

but the more recent data indicated an interesting flip as relatives of alcoholics, who don’t drink themselves, also show lower D2 receptors and PFC activity. So it creates a chicken and egg situation - do addicts lower their D2 receptors, or do lower D2 receptors predispose a person to become addicted to drugs. Regardless, coming closer to understanding this relationship means that improved therapies for addiction may not be far off.

And with that, I’m off to the dopamine party, made up of dopamine researchers raising their own dopamine via drinking, listening to music and social interaction. See you tomorrow.

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4:00 PM - What Makes a Man, Mr. Lebowski?

Sex differences appeared to be the unintentional theme of the day, as the press conference I sat in on focused on biology and behavior specific to males. This is an interesting scientific double-reverse - as Arthur Arnold had said earlier in his special lecture, most of neuroscience (and science in general) has experimented on males, which has created occasional problems in applying those results to females. For at least the past decade, that imbalance has been remedied, with most animal studies including both male and female subjects. But that doesn’t meant that aren’t interesting questions remaining about the male brain, and this conference brought together Arnold and four researchers working in that sub-field.

Despite the message of Arnold’s talk earlier (”sex difference is more than just hormones”), the research largely focused on how testosterone - the hormone produced by the male testes - affects behavior. Two of the studies (both from the University of Wisconsin) utilized an interesting animal model, California mice, whose males display two curious behaviors. One, presented by Matthew Fuxjager, is “the winner effect,” a phenomenon where mice that have won fights with other mice are more likely to win subsequent fights. Fuxjager found that the brains of California mice are full of triggers for testosterone, including areas normally associated with reward. “Winning can in fact change the brain,” Fuxjager concluded, a relevant message for an NFL Sunday.

Erin Gleason also uses California mice in her research, but instead of focusing on their fighting habits, she looks at their parenting. The mice are one of the few rodent species where the father and mother share in the care of their pups, and Gleason looked at the role testosterone plays in this behavior. Surprisingly, removing testosterone (by, well, castration) actually decreased the mouse fathers’ parenting skills - the same hormone so intricately involved in making a mouse a good fighter also made them a good Dad, it seems. Moreover, when Gleason looked at the offspring of those castrated dads later in life, they themselves were bad fathers despite no experimenter manipulation of their hormones. Lax parenting was inherited, and hormonal effects rippled down a generation.

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Alyssa Smith, now 21, was the first U.S. recipient of a living-donor liver transplant in 1989.

Today’s conference celebrating the 20th anniversary of the first pediatric living-donor liver transplant in the United States was many things: a history lesson, a technical discussion of surgical techniques, a reunion of dispersed colleagues, a media event. But most impressively, it was the rare medical conference that paid direct tribute to the reason everyone was there - the patients. Capping nearly 8 hours of presentations were brief remarks by Teri and Alyssa Smith, the mother-daughter/donor-recipient pair at the heart of that first procedure back in November 1989.

In their speeches, both Teri and Alyssa listed off things that they do that most of us would likely take for granted: dancing ballet, playing bass clarinet, going off to college, comparing clothes over a video chat. But in the context of hearing about a procedure that seems implausible even today, much less in 1989, these everyday activities were like a series of priceless gifts, given to the Smith family by medical science and the talent and care of the surgeons, pediatricians, nurses and medical ethicists 20 years ago.

Many of those personnel had made it to Chicago for today’s conference, and many of the speakers spoke lovingly of Dr. Christoph Broelsch, the lead surgeon on that first living-donor liver transplant. Broelsch was the other featured speaker of the day, but he found little to talk about after all the preceding talks had outlined the history of the procedure and how it has since spread around the world and been used to extend the lives of thousands of patients. Instead, Broelsch took the time to thank the surgical teams, here and at the two medical centers he subsequently worked at in Germany, and to talk movingly about a failed case in the early days of liver transplantation, and how difficult such failures were to face.

Also moving was Giuliano Testa, director of liver transplantation at the University of Chicago Medical Center who spoke about the importance of protecting the donors in these types of procedures. The pressure of potentially holding the key to saving a loved one’s life often puts the donor in a situation where they may not be able to make an honest decision, Testa said, reinforcing the need for independent donor advocates provided by the hospital. When all agree that donating an organ is the right decision, medically and ethically, for the donor, they should be emphatically saluted, Testa said.

“It is only through the courage of this mother [Teri Smith], and all mothers, brothers, sisters, and fathers that have gone under our knife, that not only have we saved lives, but become better doctors,” Testa said.

I took several videos of Alyssa and Teri Smith, Christoph Broelsch, and medical ethicist Mark Siegler (who was intricately involved in the 1989 case), that I will post on this site in the future. If you want to read a more detailed account of this event, my live-blog commentary remains below.

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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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