Some fantastic work was presented at the press conference on stem cells, but it all fell rather flat – the only conference I was at that finished early for lack of questions.

We heard about really cool stuff from Korea. Sujeong Jang partially repaired hearing in guinea pigs whose inner ears had been injured by destroying those little hair-like cells which turn sound waves into electrical signals. She transformed bone-marrow-derived stem cells into neuron-like cells and transplanted them into the inner ear. The number of new hair cells expanded, along with restoration of hearing. The MP3 generation will be glad this work is going on now – if the trajectory continues, ways of repairing currently irreversible inner ear damage will be available to them by the time they are old enough to need it.

Michael Zuber from SUNY, Syracuse reported his work showing he could convert pluripotent cells from frog cells into all seven classes of retinal cells normally found in the eye – and that these cells could be made to form complete, functioning eyes in tadpoles.

And Australian scientists reported on some intriguing new latent stem cells in the hippocampus of mice. Tara Walker suggests that these could potentially be activated in situ in neurodegenerative diseases.

Why the journalistic lethargy? One problem is that the press conference presenters declined to comment on the broader questions posed by the journalists– how might the politics of embryonic stem cell research in the US change, why is so much low-quality adult stem cell research being brought already into the clinic? Participants conveyed an air of defensiveness that was obviously strategic but nonetheless annoying.

Secondly, perhaps in the [misguided] interests of avoiding hype, they failed to present a useful context. It is just getting really hard for journalists to sort out how they should react to new findings in adult stem cell research. There is so much that is good, so much that is trivial, and not a clear enough signal from those in the field of where the difference lies.

Posted by Alison Abbott on November 19, 2008
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Last year there was wild buzz about some new techniques predicted to transform biology. The Brainbow, of course, but even more the light-activated channel rhodopsins which allow you to activate or deactivate key proteins with the flash of light of particular wavelength - you could watch the consequences of opening membrane channels, for example, in a live animal. Yet close to nothing is being presented on this at this meeting.

Does this mean no-one is taking up the offer to transform biology? That is certainly not the case. I suspect that the problem has more to do with the fierce competition in the field. Everyone is playing their cards very close to their chest. The Neuroscience meeting is sadly not always the place for open discussion and presentation of red-hot new results.

Posted by Alison Abbott on November 19, 2008
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The History of Neuroscience lecture this afternoon was one I had been really looking forward to. McGill University’s Brenda Milner was to speak on the field of memory, which - when she began to study it in the 1950s - was rather unfashionable and certainly understudied.

Milner was recruited to the Montreal Neurological Institute to work alongside surgeon Wilder Penfield, who was performing operations to treat intractable epilepsy. The recognised procedure at the time involved taking out tissue from the brain’s temporal lobe. Of course, looking inside the brain to discern what to take and what to leave was barely possible when these operations were being carried out, and so in a couple of cases, surgeons removed far more than they bargained for. Milner tested memory in several patients who had had such surgery, and the expertise of her and her colleagues in this area led Dr Henry Scoville to get in touch when in 1953, an operation he had performed for epilepsy at a hospital in Hertford, Connecticut had left his patient with severe amnesia.

That patient was HM, whose anterograde amnesia (he cannot form new memories) has since been widely studied by Milner and subsequently her colleagues and others. Milner told his story with wit and warmth, explaining what it was like to work with him for 30 years (he was very friendly and amenable to being studied, and would try hard to perform well on the tests he was given), illustrating the challenges with anecdotes. There were many times she would give him a test to do, step out of the room for half an hour, and then go back in and have to reintroduce herself as if they had never met.

One particularly lasting contribution was her finding that although HM couldn’t tell her who the president was, or remember a number she had given him 5 minutes earlier, he could in fact form one type of new memory, and that was for motor skills. Milner described to us a set of tests on mirror drawing, where the subject must draw a figure looking not at their hand but in a mirror – something that normal subjects improve upon over time. HM also showed this improvement, but he wouldn’t remember having done the test before, and as a consequence he thought the test rather easy.

The pace with which Milner delivered her talk was pretty swift, and certainly belied her 90 years (she was born in 1918 in Manchester, UK). But to listen to such an engaging speaker talk about such a pioneering life in science - I only wished it could have gone on longer.

Posted by Kerri Smith on November 18, 2008
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Michael Ahlijanian, a vice-president of the small biotech company EnVivo, told the meeting that the company’s new compound EVP-0334 is to enter clinical trials for treating memory disorders ‘very soon’. That it has made it so far is surprising and scientifically interesting, particularly since it acts by interfering with epigenetic phenomena in the brain.

This small molecule blocks a class of enzymes called histone deacetylases. These enzymes strip acetyl groups from histone proteins surrounding tightly coiled strands of DNA. Acetyl groups mark the DNA for unwinding so that genes can be exposed for transcription. By stopping the enzymes from working, EVP-0334 promotes a looser DNA structure and thus more gene expression.

According to Ahlijanian the compound enhances long-term and short-term memory in mice – not in all memory tasks though. It’s very robust in object recognition tests, good but less robust in spatial recognition tests and it does not affect other aspects of memory like contextual fear conditioning. He also says that it showed no toxicity in the mice at high doses for 28 days.

That’s the interesting thing. Why not? Histone deacetylase inhibitors don’t feel intuitively very selective. After all, they keep open those stretches of DNA tagged with acetyl groups, exposing lots of genes. Ahlijanian said that ‘only’ 5% or fewer genes were affected by EVP-0334 – but that’s a hell of a lot. Yet the response in the mice seems to be very specific – and no-one gets close to clinical trials without good toxicology data. Ahlijanian doesn’t have the answer – he doesn’t even know for sure yet which are the relevant genes activated by the drug -- but he speculates that it may be down to regional distributions of relevant gene promoters.

Histone deacetylase inhibitors are already used in cancer therapies but those in the clinic do not get into the brain. EVP-0334 passes the blood-brain barrier. If it really does get into clinical trials it’ll be a welcome new addition to the list of hopefuls for Alzheimer’s disease and other disorders of memory, and one with a novel mechanism. That’s of course a long way off. In the meantime it will be extremely interesting to follow how the science of its mechanism unfolds.

Posted by Alison Abbott on November 18, 2008
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I’m a sucker for the rather trendy area of brain-machine interfaces, which is why I poked my nose into the symposium on Advanced Neurotechnologies for Chronic Neural Interfaces this afternoon. This is the kind of work that aims to take brain activity and use it to control prosthetics, or even to control an individual’s own limb. The first speaker was Eberhard Fetz of the University of Washington in Seattle, whose team recently published this paper (here’s the Nature News story) on controlling muscles directly with electrical activity from neurons routed through a computer.

I was interested in what he sees in the future of this technology, and the next steps he and his team are now taking to advance their recent work. While their recent Nature paper connected brain activity directly to muscles, Fetz also talked about the possibility of connecting certain parts of the brain to other parts, to induce plasticity and remapping. This could be of use in order to remodel bits of the brain to perform a function that has been lost through damage or disease, for example.

He also mentioned that his colleague Ted Berger, who is at the University of Southern California, is working on ‘cognitive prosthetics’ – computer programs that simulate the activity in a particular brain area that may have been damaged, and can therefore sub in for it in a network. For example, damage to the CA3 region in the hippocampus is devastating to memory; Berger is working on a CA3 model in order to reconnect the dentate gyrus, upstream, with with another part of the hippocampus, CA1.

Posted by Kerri Smith on November 17, 2008
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31,000 participants so far and counting. The density of humans at this meeting is unimaginable. But the programme is better than it's ever been.

New technologies, particularly imaging, have opened up fields of research that literally couldn't have been imagined twenty years ago, not least aspects of consciousness and behaviour that we thought would always remain in the private, personal and mysterious sphere. Lectures on decision-making are not one-minute-management guides, but address the very process of decision-making at the level of individual neurons deep in the brain. Symposia on the mechanisms of drug addiction, which over the decades seemed an insolvable problem, are now being profoundly linked to basic brain function. Now that we understand more about how memory works, and how important memory is in addiction, it no longer seems impossible -- just improbable.

What has surprised me most so far is the number of new techniques, for imaging living brains and cells, that have developed over the last year. I'm not a fan of such big meetings, but I'll probably go next year anyway because the stage is so well set for big things to be discovered.

Posted by Alison Abbott on November 17, 2008
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I always enjoy, as a bit of a departure from the rest of the conference, checking out the History of Neuroscience posters, typically situated in row ZZ through ZZZ of the enormous hall, and not so well-attended as the rest of the selection. Which is a shame, as many provide a really nice way to step back from calcium channel agonists or dopamine activity in area LMAN of the zebra finch brain, and take a wider-angle look at the field. Sunday's highlights: Aristotle; and a neuroscience of neuroscience.

A recent book by science writer Jonah Lehrer proclaimed in its title that Proust was a Neuroscientist. In it, Lehrer makes the point that Proust anticipated, in the early twentieth century, a lot of what neuroscientists have only recently found out about the strength of memories relating to taste and smell, and how memory depends on the time and situation of the individual.

Well, a poster today claimed that Aristotle too was a neuroscientist before his time. Aristotle talked about the psyche as a central faculty that connected up many other mental properties. A group from Nipissing University in Ontario, Canada, argue 'that psyche can be defined as neural activity', and 'our current views on consciousness, perception, sensation, and thought as neural processes may have been anticipated by Aristotle' – before anyone even had any idea what a neuron was.

Another history section favourite of mine was a poster entitled 'Circling the square: towards a neuroscience of neuroscience'. The presenter, Rutgers University's Kai Schreiber, who according to his website studies the neuroscience of vision, was not on hand to explain the (surely) tongue-in-cheek experiments, which included putting a subject (yes, just n=1) in a scanner and showing them neuroscientific articles. This apparently activiated 'their left brain'. Nice and specific. The poster's conclusion section claimed, among other things, that this neuro-neuroscience approach could lead to the creation of neural networks that could build neural networks, and that we surely aren't too far from a neuro-neuro-neuroscience, which I guess is a neuroscience of the neuroscience of neuroscience. Kai, if you're reading this, please feel free to explain. My suspicion is that it was really an anthropological observation gauging people's reactions to the neuro-neuroscience theory...

Posted by Kerri Smith on November 17, 2008
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The directors of each of the neuro-related National Institutes of Health convened for a press conference this morning. Those of us who were after hard news were a little disappointed, but I found the short talks a useful basis for the rest of the sessions, many of which I of course won't be able to get to given that the committee love to run at least six interesting things concurrently (like the Queen of Hearts, we are running to stay in the same place, but unlike her we cannot attend six impossible talks before breakfast).

Best for background was NIMH (National Institute of Mental Health) director Tom Insel, who reminded us why many of the scientists at SfN do what they do: to help understand and treat neurological and mental illness. He gave us some sobering stats too: 90% of the 30,000 suicides in the US every year are due to mental illness; the average age at death of someone with a mental illness is 25 years less than a healthy contemporary, at 56 years of age; and while only 4% of the US population have a major mental illness, they smoke 44% of the cigarettes sold, hinting at the knock-on effects of diseases of the brain and mind on health in general.

So whilst a lot of the science here is fundamental in nature, it'll be useful to remember why it's being done - and where the dollars are coming from.

Posted by Kerri Smith on November 17, 2008
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Posted on behalf of Ashley Yeager

The parasite Toxoplasma gondii causes rodents to enter the lion’s den: They go against their instincts and sniff out the scent of cat urine. Now, new research has identified the specific regions in the brain involved in this game of cat-and-mouse.

Toxo is a parasite that can only reproduce in the gut of a cat, so it “basically co-opts certain brain circuits in the rats’ amygdala to change their fear into a sexual attraction,” says Patrick House, a neuroscientist at Stanford University in Palo Alto, California.

The team scanned the brains of both healthy and Toxo-infected rats to see which neurons fired when the rats smelled scents classified as neutral, feline, or potential mates. The healthy rats exposed to cat odour show an increase in stress hormones. But infected rats showed a reduced hormone response. In fact, neurons in the same amygdala regions fire in an infected rat as they do in a male rat smelling a potential female mate.

Many people carry Toxo, usually contracted after eating under-cooked meat or unwashed vegetables, or through handling cat litter. The parasite is mostly dormant in humans, though House says some studies suggest that infected people take part in more risky behaviour. But “you can never tell if the behaviour causes people to pick up the parasite or if the parasite triggers the risky behaviour,” he says.

Those diagnosed with schizophrenia are also more likely to carry the parasite. It’s possible, says House, that Toxo carries a gene whose expression could trigger higher dopamine production in both rats and humans – thus leading to behavioural changes, he says.

More research needs to be done to understand the link, he said - which is why the Stanford team’s current research focuses on how dopamine production factors into rats’ attraction to cats.

Image: ICanHasCheezburger.com (where else? posted by Ashley's editor, she is not responsible)

Posted by Alex Witze on November 16, 2008
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The annual behemoth of a conference that is the Society for Neuroscience meeting kicks off here in Washington today. They expect about 30,000 neuroscientists to attend - probably using about that many calories each running from poster session, to symposium, to lecture througout the event. Together with Alison Abbott and Ashley Yeager, I'll be blogging about what's going on.

By the way, it hasn't escaped SfN's notice that there's some other little meeting in town this weekend too:
'G20 Summit in Downtown Washington
As Neuroscience 2008 approaches, SfN is monitoring Washington heightened security in effect due to the G20 summit meeting at the National Building Museum. No disruption of meeting activities is anticipated, but some street closures are probable, as are minor disruptions on the Washington Metropolitan Area Transit system (Metro).'

Sadly, it doesn't seem as if anyone has planned a satellite event on neuroeconomics and the neuroscience of the credit crunch to take advantage of the overlap.

Posted by Kerri Smith on November 15, 2008
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Albert LaSpada of the University of Washington in Seattle was able to reverse Huntington symptoms in a mouse model of the disease using a transgene expressing PGC1alpha. He presented details of his study on Wednesday, but gave a little additional background at a press conference this afternoon. It’s one of those lovely genetics discovery stories that not only offers promise for a devastating disease, but comes together so neatly when looked at in hindsight, I just had to relate it.

LaSpada was a grad student with Kenneth Fischbeck at the University of Pennsylvania in the late 1980s and early 1990s. Together, in 1991, they discovered the genetic underpinnings of X-linked spinal and bulbar muscular atrophy. It was caused by a gene with an abberant trinucleotide repeat. Two years later it was found that Huntington’s disease (HD) worked in much the same way, with an repeated CAG sequence in the huntingtin protein creating a long string of the amino acid glutamine. These repeats prevent huntingtin from folding properly and make it clump up in the brain -- a hallmark of many neurological diseases. The relatively high profile of HD made for a lot of excitement LaSpada says, and now there are at least nine of these so-called polyglutamine diseases known.

After he became a PI himslef, LaSpada had a trainee looking to treat HD who was going to test a cannabinoid drug in a mouse model for the disease. LaSpada predicted that the drug might interfere with temperature regulation, so he suggested that they observe temperature closely. They found surprisingly that untreated mice had very low body temperatures, leading them to speculate about the metabolic pathways that might have been contributing to this. In HD there’s the hallmark unfolded proteins, but there’s also dysregulation of transcription and mitochondrial dysfunction. But nothing linked the pathways together. Using the mouse model they were able to show how huntingtin aggregates interfered with the activity of PGC1alpha, a transcriptional co-activator involved in mitochondrial function in the brown fat by which mice maintain their body temperature. They engineered an HD model mouse to overexpress PGC1alpha and it both improved neurological function and cleared the huntingtin clumps. Screening for proteins that PGC1alpha interacts with reveals that it modulates the activity of PPARdelta. Another recent study LaSpada says, further shows that PPARdelta is involved in the response to retinoic acid, thus revealing two potential targets for drugs: ATRA, a chemotherapeutic that works like retinoic acid is already in use for promyelocytic leukemia, and GW 501516, a PPARdelta agonist has been used in clinical trials to modulate cholesterol and go after fat.

It seemed such a tidy path of discovery, definitely inspiring. Even the person following LaSpada at the press conference was a bit stunned. Before presenting his own results following humans with Gaucher disease, Hans Andersson at Tulane Univeristy in New Orleans just had to pause to say, "Cool. That's a cool story!"

Posted by Brendan Maher on November 14, 2008
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I’ve got another fabulous guest post from Chris Gunter

At the Presidential Symposium, speakers pleaded the case for personal genomes and for Philadelphia. First was Philly mayor Michael Nutter, who assured us he knew absolutely nothing about genetics but joked that geneticists must have big expense accounts and the people of Philly would be very grateful if we could leave some of that money here with them.

J. Craig Venter of the self-titled institute gave us a tour of his publication history and then of his own genome. (In an overlap with the carbon conference that Nature is also currently blogging, he announced that his J. Craig Venter Institute was building the first zero-carbon research building, on the UCSD campus.) As for his genes, he’s heterozygous in 44% of them, and he’s anxious to see this information translate into medical practice. “To me it’s not surprising that pharmaceuticals don’t work on everybody” because we are so different. In fact, “it’s amazing that they work on up to 1/3 of the population.” He reiterated his call for predictive power from the genome: “I have been arguing for some time that going to a preventative medicine paradigm is one of the few ways we have to lower health-care costs.”

Richard Gibbs of Baylor College of Medicine, the second speaker, picked up on the theme but stated that “we” –presumably meaning the genomics community – thought that there would be an orderly transition to genomic medicine, one would just walk into the doctor’s office and get genomic information and interpretation quickly. But we did not foresee the widespread distribution of direct-to-consumer tests, and the confusion that has resulted. We are driven by amazing advances in technology and therefore able to get mountains of genomic information, but we don’t really know what to do with it all. His personal experience, of course, is from sequencing Jim Watson’s genome. “We brought Watson to Houston for a genetic counselling session, which was pretty much a complete failure” because there were 320 loci with “suspicious” differences, based on the existing databases, and the counsellors were just overwhelmed.

Talk about overwhelming: In a plenary session on Wednesday David Kaufman of the Genetics & Public Policy Center told us that 60% of survey respondents would participate in genetic testing for a major medical research survey, and more than 90% of these said they would want to see their individual results (more on their survey here). So, it’s obvious the human geneticists have work to do in developing accurate but understandable interpretations of genetic tests. Any scientists out there who are not geneticists – please feel free to join the field, because we need you. All the better if you come with a big expense account.

Posted on behalf of Chris Gunter, HudsonAlpha Institute for Biotechnology

Posted by Brendan Maher on November 14, 2008
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I couldn’t leave this be. I’ll be writing more about it soon, but these numbers are just staggering. David Altshuler gave a status report on the 1000 Genomes project, which aims to plumb the depths of human variation (I'm still waiting for the 1KG handle to take off). As it nears completion of its three pilot phase projects, it's generated 3.8 trillion bases of genome sequence. Although they haven’t yet sequenced 1,000 genomes, that is technically 1,000 human genomes worth of sequence data. Altshuler said that if you take the amount of data that was in GenBank at the start of the project, they put in roughly that amount more for each week of September and October. And they’re just a tenth of the way there! It’s useful to remember, Altshuler said, that the Large Hadron Collider, which is similarly expected to heave terabytes of data at researchers, had copious amounts of planning going into its data handling and analysis. 1KG will need to catch up quickly, hence two recent requests by the NIH looking for people with a plan and a heck of a lot of computational power. See here and here.

Posted by Brendan Maher on November 14, 2008
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Before signing off for the conference, I figured I would highlight one other bit of news that cropped up yesterday. It involves a major national election and a peaceful power change that could shift a government’s policy on global warming emissions. And no, it has nothing to do with Barack Obama.

While the world’s eyes were on a sharp turn to the left in the United States, New Zealand held its own elections on Saturday - and moved sharply to the right. Apparently one of parties – ACT – that stands to gain is sceptical about global warming and has promised to pull out of the Kyoto Protocol. And all of this comes at a time when New Zealand is implementing a potentially groundbreaking cap-and-trade program designed to regulate all greenhouse gas emissions, including the difficult stuff like agriculture and development that is cutting down native forests.

I’m getting most of my information from Tim Denne, a private consultant who spoke at the conference and has been working for the New Zealand government as it develops and implements the regulations. Denne said the impacts in terms of climate policy are still unclear, but he remains optimistic. “I don’t think they will change the fundamental design, rather they will just throw around a few additional allowances,” Denne said.

“Allowances” in a cap-and-trade system are in essence permits to pollute, with one allowance equalling a tonne of carbon dioxide. If you don’t have an allowance, you can’t pollute. So by limiting the overall number of allowances, the government can limit overall greenhouse gas emissions. In other words, Denne believes the incoming government might be forced to compromise on just how onerous the regulatory system will be.

So there you go. We’ll see what happens.

Posted by Jeff Tollefson on November 14, 2008
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It's family history month, explained Ed McCabe of UCLA, president elect of the American Society of Human Genetics. This was at a press conference announcing the society's statement on ancestry testing, but he wasn't advertising for direct-to-consumer testing companies. Rather he suggested that this Thanksgiving, we should take the time to ask our elders about where we came from. Learning about the cultural richness of family history, he said, is very different from knowing that your genes say your are 40% european, for example.
I think family history month is largely recognized as October, but it's a nice sentiment, and I for one wish I had more people around to ask.

Posted by Brendan Maher on November 14, 2008
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ASHG released recommendations today about how researchers and direct to consumer companies should treat the sometimes fraught area of genetic ancestry testing. Although a seemingly innocuous area both for research and for consumer products, ancestry testing does carry with it tricky ethical, legal and social issues when one considers how people might treat such data. I did a quick Q&A with Charmaine Royal of Duke University, who co-chaired the task force on the topic (find it here).
At the press briefing today, announcing the recommendations, I got to talk briefly with Joanna Mountain, senior director of research at 23andMe, one of the companies providing such tests.
She said the recommendations were provocative, but vague. Why, she asked, if they were going to make a big deal about how people might try to use ancestry tests to claim rights in affirmative action or for inclusion into specific groups, did they fail to provide any actual policy recommendations? Royal indicated to me that they’ve just begun to scratch the surface, here. Interestingly, Native American groups are keenly aware of the issues and will not allow identification with a particular tribe based simply on a genetic test, at least that’s what I’d heard at a session yesterday on the topic.

It is important to note that ASHG’s recommendations (you can find them here) were aimed both at academic researchers and those at direct to consumer companies. Mountain says, though, that 23andMe hadn’t been contacted and she suspects the task force hadn’t consulted with any of the companies. But as Royal said, there’s still a lot to be done including consulting with a broader swath of interested parties.

Posted by Brendan Maher on November 14, 2008
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Mary Nichols, chairwoman of the powerful California Air Resources Board, just finished discussing her states efforts to curb global warming pollution in the transportation sector. California passed its own limits on greenhouse gas emissions from vehicles in 2004, but the US Environmental Protection Agency under George W. Bush has declined to issue a waiver allowing the state to proceed. It’s a long story, but suffice it to say that Nichols predicted a speedy resolution once Barack Obama takes office.

“We are operating under the assumption that we will get our waiver some time next year,” she says.

Given the sheer size of the California market and the fact that some 16 states have signed on to the California proposal, it is entirely possible that the rest of the country would follow. In fact, the Supreme Court has already ruled that EPA has the authority to do just that. EPA essentially punted on the issue earlier this year, but the next administration might be more inclined to follow up on that authority as well.

As it happens, Nichols is rumoured to be on Obama’s shortlist to head the EPA, where she previously worked under President Bill Clinton. Speaking to reporters after the session, she was certainly open to the idea. Nichols said the first thing she would do if appointed EPA administrator would be to meet with the president and the rest of the agency heads to coordinate a comprehensive federal energy and climate strategy. But has she discussed the idea with the Obama transition team? No comment.

Who knows? She might one day find herself in the unique position of fulfilling her own prediction – by granting California the waiver herself.

Posted by Jeff Tollefson on November 13, 2008
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The conference kicked off this morning with a keynote address from New York Times Columnist and green-energy guru Tom Friedman, and then moved on to a plenary panel on the United Nations effort to reach an international climate agreement in Copenhagen in 2010. In short, inspiration followed by a sharp dose of reality. Although nobody is giving up, there’s a growing feeling here in the United States that it could be quite difficult to sign off on anything significant next year.

The morning sessions are over, and I’m now in a press conference where the Massachusetts Institute of Technology and the Pew Center on Global Climate Change are releasing a series of reports covering the nitty-gritty details of cap-and-trade systems. All sponsored by the Doris Duke Charitable Foundation, the reports are intended to update the technical foundation on global warming policy for the incoming administration and Congress.

Most of this material is long and detailed, but I’ll quickly highlight one of MIT’s most basic findings: Despite constant criticism by many policymakers in the US, the European trading scheme is working. “It does reduce emissions,” says Denny Ellerman, a professor with MIT’s Sloan School of Management. “That is becoming clear.”

And if it’s not reducing emissions enough, Ellerman adds, that is because the goals are too tame, as opposed to some fundamental problem with the framework itself. Not entirely new, but it comes from a respected source on the matter and bears repeating.

Now it’s time to drop in on a couple of sessions on the afternoon sessions covering carbon offsets (which allow companies to meet their emissions caps by reducing emissions somewhere else) and international trade issues.

Posted by Jeff Tollefson on November 13, 2008
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Despite the optimism, it doesn’t take long wondering through meeting rooms here to realize that restructuring the global economy won’t be easy. I’m in a room with a few hundred other people listening to a panel of business representatives, analysts and investment bankers talk in mind-numbing detail about the intricacies of cap-and-trade systems. Terms like “additionality,” “fungibility” and “compliance eligibility risk” are bandied about with impunity.

The piece of “cap-and-trade” that most people care about and understand is the “cap,” which limits the sheer volume of greenhouse gases pumped into the atmosphere. That’s easy. Getting the “trade” piece right is difficult, and that’s what conferences like this one are all about. The goal is to set up a viable market for carbon dioxide and other greenhouse gases, which then enables one company that can cheaply reduce its emissions to sell pollution credits to another that cannot. As such, the market will help companies determine the cheapest methods of reducing emissions, and direct private money accordingly.

Sounds easy enough, but countless questions need to be answered if money is actually going to change hands. How do you verify that a carbon credit is actually linked to a tonne of carbon? How do you link various markets that are operating or under development around the world? And what about “offsets” - how many credits can be purchased abroad if the cheapest way to reduce emissions is by, say, curbing tropical deforestation?

US Senator Jeff Bingaman of New Mexico, a leading Democrat on energy and climate issues, riled the conference early on by saying offsets are “fraught with opportunity for game-playing, which will be exploited by lots of creative people.” Loaded words for a conference that is built around the notion that carbon markets can solve the climate problem, but these are the questions that politicians must deal with up-front.

Bingaman said Democrats are ready to push for a new round of energy legislation next year, which could a long-sought federal mandate for renewable electricity generation. Such a schedule likely pushes climate legislation into 2010, which naturally begs the question about whether an international climate agreement can be struck next year, as scheduled. More than one frustrated questioner raised the issue.

“I don’t know that what we are able to do domestically is going to be driven by any kind of international expectation of what we should do,” Bingaman replied.

Indeed. Barack Obama might well bring a new multilateral spirit to the United Nations climate negotiations in Copenhagen next year, but the rest of the world would be wise to remember that it is the US Senate that ratifies international treaties.

Posted by Jeff Tollefson on November 12, 2008
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As a special treat, I’ve got a guest post from former genetics editor at Nature Chris Gunter. She’s also twittering the event here. How hip!

Aravinda Chakravarti’s presidential address was, of course, thoughtful and fun. He pointed out that it’s our responsibility to educate the public about genetics. I have been coming to the ASHG meeting since 1993, and have worked directly for two ASHG presidents and with many others. I believe every single presidential address I’ve seen since 1993 has made a similar call, for us to engage the community in education. In the age of direct-to-consumer genetic testing, we all know this is more important than ever. Unfortunately, this morning’s session on “the future face of genetics education” was sparsely attended, with only about 100 people. At the risk of repeating a cliché, all geneticists need to be educators, so I wish more people would take a more active interest in the area. It didn’t help that the ASHG scheduled six (SIX!) sessions at the same time and every one was interesting. The speakers discussed introducing genetics at all levels of education (full disclosure: two are colleagues from HudsonAlpha and one is a former colleague from NPG), and ways to measure what we need to teach and how we need to teach it. Many of the scientists attending the meeting will be teaching at some point in academia, or will be talking with their family and friends about genetics. Where were the scientists this morning? Similarly, the plenary session featured a talk on public attitudes toward genetic testing. People literally streamed out in droves right before this talk; they stayed for several research talks beforehand, but didn’t want to hear a data-driven study about how we should most effectively engage the public. This brings me to ask: are we serious about education, or not? Are scientists really uninterested in hearing about education, and how do they think they can afford to feel that way?

**Update: Link fixed. Sorry Chris!

Posted by Brendan Maher on November 12, 2008
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Geneticists are taking an increasing interest in copy number variants (CNVs), genetic sequences that can be repeated or deleted from individual to individual. I might have two copies of a gene, while my wife might have three. These are a major source of genetic variation and have been implicated in contributing to important diseases. Alexandre Reymond of the University of Lausanne explained work he’s been involved with to characterize CNVs in mice. Looking at lab strains and several wild mice, they uncovered nearly 3000 of them. Then to understand how these CNVs might be affecting phenotype, they looked at gene expression in different tissue types in the mice to see if genes in and around those CNVs might be differentially expressed depending on how many copies there were. In five out of six tissue types they tested, as many as 2/3 of the CNVs they looked at were differentially expressed. The brain only showed 1/3 of CNVs affecting gene expression and generally doing so in a negative fashion. They found that genes far away from the actual CNVs could be affected, and one experiment suggested that the effects could span 10s of millions of basepairs, affecting the expression of quite distant genes. They also looked at expression during different developmental stages in the mice for brain and liver and found that while expression for 2/3 of genes in CNV regions were always affected in liver, brain CNVs appeared to be controlled differently at different developmental stages. Their findings had several people asking about how epigenetic changes like histone tail modifications might be influencing expression changes. I wonder how the brain specific differences square with discoveries linking CNVs to autism and schizophrenia in humans. Might there be a mechanism to protect the brain from CNVs that goes haywire for those affected?

Posted by Brendan Maher on November 12, 2008
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Ancestry testing can be a sensitive subject as evident in a packed morning session discussing some of the social and education aspects of ancestry and genealogical testing. While genetics has a long and sordid past with the term race, it remains a fact (possibly as a vestige of how populations have been studied) that ethnic groups show distinct genetic signatures associate with commonly delineated ethnic groups, and there could be health benefits to using this information. Esteban Gonzalez Burchard at the University of California San Francisco studies African American and Latin American groups. He talked of one project on Multiple Sclerosis that he had been collaborating with. Multiple Sclerosis is predominantly a disease affecting people of European descent. Africans are rarely affected. So his group sent out requests for African Americans affected by the disease and used ancestry specific markers to zero in on portions of the individual’s genomes that might identify a European risk factor migrating through the genome. U.S. Television talk show host Montel Williams was a volunteer.
The series of talks ended with some rather passionate debate about the value of race as a term or even as a concept. While one questioner approaching the microphone at the end of the presentations pressed the panel and all in attendence to end its "love affair with the term." "Given that science has clearly shown that humans don’t meet the biological definition for race, why can’t science provide some leadership?" A genetic counselor was equally adamant that we don't avoid such terms just in the interest of being PC if they can provide useful health information.

Posted by Brendan Maher on November 12, 2008
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I arrived at the Carbon Market Insights conference in Washington this morning to find the same sense of wonder that has pervaded the entire country for the past week. Sponsored by Point Carbon and the Pew Center on Global Climate Change, this conference caters to the believers, all of whom have been anxiously awaiting some kind of action on global warming from the United States. With the election of Barack Obama as the next president, the expectation is that the time has come.

And now for a much-anticipated word from President-Elect Obama, delivered by Jason Grumet, one of his environmental advisors, before a standing-room only hall filled with upward of 800 people: "I came here today absolutely firm in the commitment to tell you nothing at all."

Well. I guess it was to be expected, given the ongoing clamp-down on any information from the Obama camp. And it must be said that Grumet delivered his statement with a smile that drew not only laughter but applause, which speaks plenty about just how much good will and political capital the new president has in the bank as he enters office.

Grumet told everybody to keep up the good work and recommended they rest up during the holidays. "It's going to be a very, very busy 2009, and we are going to need all of you at the top of your games." He then made a prompt exit, kindly answering no questions from a gaggle of reporters at his heels and leaving everybody else to deal with the details, which are daunting indeed. But more on that later.

Posted by Jeff Tollefson on November 12, 2008
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Last night the American Society of Human Genetics meeting started in Philadelphia and kicked off with a crowded mixer featuring classic Philly fare (hoagies and pretzels). I asked Aravinda Chakravarti what he thought the major themes of the meeting would be. He said he was glad to report that the field has moved slightly away from data to new ideas. New ideas including better understanding of the genetic structure of disease and the characterization and understanding of the meaning of structure in the genome, including copy number variations (a term that appears in the abstract book more than 200 times). That’s not to say that data have taken a back seat. It’s no secret that the data are pouring out from new sequencing technologies. Illumina staged a brief press conference featuring the three papers appearing last week in Nature that presented four new full human genome sequences, those of an Asian individual, an African individual and one from a woman and from the cancer that she eventually died from.
Stay tuned for most posts from the field, and possibly some guest posts.

Posted by Brendan Maher on November 12, 2008
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Journal publishers sometimes get a bad press for making a profit from academics’ hard work without adding much value to the scientific endeavour. Although I am a journal publisher myself, I have some sympathy with that sentiment, especially when journals simply reproduce the authors’ work without helping them to improve the communication of their data by editing the paper, improving the figures, or providing help communicating with the media. However, when journals live up to their side of the bargain, it’s clear that they (we) have a huge amount to offer to the scientific community.

Many of the major papers that have been presented over the past few days here at the American Heart Association have been simultaneously published in journals like Circulation, JAMA, and The New England Journal of Medicine. The advantages to this approach are obvious. Having the published paper available helps the media report on the study accurately. And when the news breaks in the popular press, doctors, who are often faced with questions from anxious patients, are able to download the full paper to educate themselves about what the clinical study means for patients in their care.

Peer reviewing and editing a paper accurately to tight timelines is an expensive and difficult thing to do. But in my opinion it is worth the additional effort from authors, editors, and publishers to expedite papers so that they can be released to coincide with the oral presentation of the data at scientific conferences. Indeed, I wish this happened more frequently than it does now. Everyone benefits from the end result.

James Butcher is publisher of Nature’s eight Clinical Practice review journals.

Posted by James Butcher on November 12, 2008
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When I was an undergraduate, my tutor, a laboratory-based PhD-trained scientist, often complained that the medical students he tutored were incapable of thinking scientifically; clinicians are only able to learn by rote, not think logically, my tutor regularly said. It was only when I started working in medical publishing that I came to realise how misinformed my tutor was and how rigorous clinical research can be.

I am currently attending the American Heart Association’s annual scientific meeting and the quality of some of the science is simply breathtaking. Every day the results of massive randomised controlled trials are presented that are run by large collaborations of clinical researchers based all over the world.

I’ve already blogged about JUPITER, which may well turn out to be one of the most significant pieces of medical research published this year. Yesterday, another big trial was presented: I-PRESERVE, which enrolled 4218 patients from medical centres in 25 countries. The trial was negative---it showed that irbesartan does not improve the outcomes of patients with heart failure who have an ejection fraction of at least 45%---so it won’t get as much airtime as JUPITER in the popular press, but it is still an impressive piece of work all the same (see paper in the NEJM).

As is usual in clinical trials, the primary and secondary endpoints in I-PRESERVE had been prespecified in the trial protocol, leaving the researchers unable to mine the data until they found a statistically significant result. The large sample size means that the results are likely to be reproducible; indeed the negative findings of I-PRESERVE agree with two other clinical trials that have already been published.

I doubt very much that the vast majority of bench science is done to anywhere near such high standards. How many lab-based scientists do a power calculation in advance and prespecify exactly which endpoints they’re investigating in an experimental protocol that’s published in advance?

In addition, many medical journals insist that clinical trials are reported in a standardised fashion, according to the CONSORT guidelines, so that readers have all the information they need to determine whether the trial methodology is adequate and the analysis appropriate. Sure, life scientists also have publication guidelines---MIAME instantly springs to mind---but in my opinion basic scientists, like my old undergraduate tutor, could learn a lot from their clinical colleagues about how to design scientifically meaningful experimental protocols and how to publish the resulting papers in as rigorous a fashion as possible.

James Butcher is publisher of Nature’s eight Clinical Practice review journals.

Posted by James Butcher on November 12, 2008
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The biggest story to come out of the American Heart Association’s annual jamboree is undoubtedly the JUPITER randomised controlled trial, which was showcased on Monday to a packed auditorium of over 6000 cardiologists. Data from the trial suggest that even healthy people with low cholesterol may benefit from receiving rosuvastatin to prevent cardiac events, if they have high levels of high-sensitivity C-reactive protein.

The trial was due to run for 4 years, but was stopped prematurely in March after just 2 years when an interim analysis showed that patients who received rosuvastatin were approximately half as likely to have a coronary event compared with those who received placebo. The trial’s independent data and safety monitoring board decided that it would be unethical to continue giving some people placebo in light of this strong evidence of efficacy, so they voted to stop the trial.

Reducing the risk by half sounds very impressive, and many people will call for statins to be prescribed more widely as a result of JUPITER, but some cardiologists (including Mark Hlatky, who wrote an excellent editorial in the NEJM about the trial) quite rightly say that caution is needed. For the trial illustrates how important it is to make the distinction between relative and absolute risk before drawing conclusions about a study’s clinical relevance.

Closer inspection of the data reveals that 157 of the 8901 (1.9%) people who received placebo had a cardiac event compared with 83 of the 8901 (0.9%) who received rosuvastatin. So, although the relative risk reduction was about 50%, the reduction in absolute risk was only 1%. Put another way, doctors will have to treat 120 people for 2 years to prevent one cardiac event.

Since the drug costs $3.45 per day, would prescribing it to apparently healthy people be a good use of resources? (Spending ~$300k to prevent one cardiac event would be hard to justify.) It’s quite possible that generic statins, which are much cheaper than rosuvastatin, could be similarly beneficial, but I’d hazard a guess that AstraZeneca will be using the results from JUPITER to convince doctors that Crestor is the best one to prescribe. Indeed, the coffers of The New England Journal of Medicine, which published the trial, are likely to be bulging soon as highly lucrative reprint orders start to flood in.

Read Nature News's briefing on the trial results.

James Butcher is publisher of Nature’s eight Clinical Practice review journals.

Posted by James Butcher on November 11, 2008
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