Bill Gates walks across the University of Chicago campus April 20, 2010. (Photo by Jason Smith)

A College Dropout Returns to Campus

The per capita income of Hyde Park experienced a brief spike on Tuesday as Microsoft founder/billionaire philanthropist Bill Gates paid a campus visit as part of his three-day college tour. After meeting with students and professors - including a walk-and-chat with Kevin White, pictured at left - Gates spoke and answered questions in a building named for another ultra-wealthy benefactor, the Rockefeller Chapel.

As Gates’ first college tour since resigning from Microsoft to focus full-time on his Bill & Melinda Gates Foundation, the focus was less on technology and more on the humble task of solving the world’s problems. With only a limited amount of time to speak, Gates focused on two priority areas for his foundation: child mortality and education. On the former point, Gates highlighted the vast differences between the wealthy world and the poor world in childhood death rates, with less than one percent of children dying before the age of 5 in rich countries while the death rate for young children remains around 20 percent in the third world. Vaccines are a big part of that change, Gates argued, which is why his foundation recently sunk another $10 billion into vaccination efforts around the world.

Interestingly, Gates said he once worried whether reducing infant mortality in developing countries could lead to more problems in terms of overpopulation and resource scarcity. But in fact, Gates said, studies have found that better health leads to smaller families, as parents choose to have fewer children when the chances of them living to adulthood increases.

You can find more coverage of Gates’ visit at the University of Chicago News Office.

A Year of Swine Flu

Hard to believe it was only one year ago that the world first learned to be afraid of the collection of letters and numbers known as H1N1. As a newspaper reporter at the time, I recall being impressed by the speed of the outbreak - not the virus outbreak, mind you, but the outbreak of media hysteria over the virus. For sure, there was reason to be alarmed about the novel H1N1 influenza, especially in the early days when the epidemiology was sketchy at best and seemed full of dire warning signs. But the leap from “new mysterious flu strain” to “1918 Pandemic Redux!!!” happened almost overnight, and spread far more quickly than the actual virus. I found myself writing “calm down, everybody” articles almost from the time I was put on the story, as the flu experts I interviewed balanced their concerns with a healthy dose of scientific skepticism.

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Expanding the Human Family, One Cave at a Time

A couple weeks back on the blog, Callum Ross debunked a lemur-like creature, Darwinius masillae, purported by some to be a very distant human ancestor. If you were feeling sad about this contraction of the human family circle, you may have been cheered by news this week about the potential debut of a new, more human-like human ancestor. There is no fancy Latin name for this relative yet, because even the authors of the paper announcing its existence are unwilling to declare that an entirely new species has been found. But it’s enough to dream up some not entirely unscientific (and somewhat unsettling) daydreams of a time when what we know today as humans were not the only two-legged tool-using primates on the scene.

The uncertainty surrounding the finding published in Nature by Johannes Krause, Svante Paabo and colleagues is that the discovery was made with a little bit of paleontology and a lot of genetics. The human ancestors or cohabitants we’re more familiar with - like Neanderthals or Homo erectus - were discovered in skeleton form, the classical way scientists learn of extinct creatures. But Krause & company’s fossil findings are limited to a pinky bone discovered in a Siberian cave, dated to 40,000 years ago. Because you can’t tell much anatomically from a pinky bone, the researchers instead harvested DNA from the bone; specifically, mitochondrial DNA (mtDNA), a smaller stretch of genes inherited entirely from one’s mother. When compared to mtDNA from modern humans and Neanderthals, it was dramatically different from both species - roughly twice as different as the gap between humans and Neanderthals.

The authors (and most of the outside scientists I’ve come across online) reason that the most likely explanation for that difference is that the pinky belongs to a very old human-like species, one that may have branched off from modern humans 1 million years ago. There are other theories - Carl Zimmer proposes one alternate theory built on the rather salacious premise of interspecies lovin’ - but analysis from the nucleus DNA of the proposed new species is necessary to decide. In the meantime, it’s fascinating to think about a time when humans sort of like us had to compete with Neanderthals and whatever this new ancestor may have looked like for resources, much like different species of birds will fight over territory and food.

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A radiograph of Darwinius masillae, aka "Ida"

It was the fossil infamously hyped as the scientific discovery “THAT WILL CHANGE EVERYTHING.” But one year after its controversial press conference debut, Darwinius masillae has come under increased scrutiny from a scientific community already skeptical about the 55-million-year-old primate fossil’s Hollywood roll-out. When scientists from Norway, Germany and Michigan published the original Darwinius paper (oh, and also released a book and a TV show), they argued that the tiny, lemur-like Ida was the earliest known primate ancestor of humans. But in October, a paper in the journal Nature used computer analysis of Darwinius’ physical features to place it about as far away from humans as possible on the primate evolutionary tree.

Last week, another blow was struck against the claim of Darwinius as an ancestor of humanity, this time in a direct reply to the original paper that was published in the Journal of Human Evolution. The JHE paper is a straightforward, business-like rebuttal that dissects the arguments used to place Darwinius in the lineage that eventually begat humans, employing additional anatomical evidence to reverse the original conclusions. But no punches were pulled by Callum Ross, one of four authors of the reply paper and a scientist already on record calling the original article “a travesty,” in our conversation about the controversy.

Ross emphasized that he does not question the scientific integrity of the authors who originally described Darwinius, even commending them for a “great” description of the specimen. But it’s their interpretation of that description, and their placement of Darwinius in the phylogenetic “tree of life,” that Ross has quarrel with - an analysis based on cherry-picking anatomical features.

“That aspect of it, the reconstructing evolutionary relationships part, is based on a 19th-century way of doing science,” said Ross, associate professor of organismal biology and anatomy at the University of Chicago. “You select the attributes of the organism that you think reflect the relationships, and that’s what you use.”

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A brain from a person with mad cow disease, caused by prions (compared to a normal brain).

A Place for Prions

We previously discussed the bizarre infectious proteins called prions in the context of kuru, the disease of muscle tremors and uncontrollable laughter spread by cannibalistic rituals in Papua New Guinea. In diseases such as kuru or mad cow disease, abnormal prion proteins wreak havoc by binding to native prions and other cellular elements, creating clumps that kill off cells in the nervous system. But one important thing I didn’t mention in the kuru article - nobody’s really sure what the native, normal prions actually do!

That mystery may have been somewhat dispelled by an article published by Nature Neuroscience last weekend from a team of scientists in Sweden and Germany. Those researchers knocked out or interrupted the gene for prions in a number of different mouse strains, a strategy that had previously yielded a pretty normal mouse without much to say about the prion’s purpose. But for the current experiment, the researchers were patient, allowing the mice to live to the grand old age of 60 weeks (mice typically live for about two years) before looking for deficiencies related to their lack of prions.

What they found in their elderly mice links back to another ScienceLife post - peripheral neuropathy, a motor disorder marked by the demyelination of peripheral neurons. The nerve cells running from the spinal cord to muscles of the prion-free mouse’s body were normal, save for a thinned-out sheath of myelin along the axon. As discussed previously for multiple sclerosis (where central nervous systems neurons are demyelinated), this loss of myelin leaves cells less insulated and like a frayed power cable, unable to transmit signals at optimum speeds. Hence, the motor difficulties associated with peripheral neuropathy, which in humans manifests itself as twitching, paralysis, and loss of dexterity.

That could be a promising finding for not just one field but two. Recall that motor difficulties are usually one of the first symptoms of prion diseases - “kuru” is the word for “shiver” in the Fore language of Papua New Guinea’s Eastern Highlands. Prion gene knockout mice may have their issues, but have the small consolation of being resistant to prion diseases. And the study of peripheral neuropathies (plural, because the term covers several different diseases) could benefit from the new identity of the prion as a mediator of myelin maintenance.

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Videogame Learning & Brain Size

Many a member of the older generations will tell you how video games are rotting our children’s brains, turning kids into button-pushing, drooling zombies. Such warnings linger on despite the fact that my generation - the one that desperately wanted a Nintendo for Christmas - turned out pretty okay…though obviously I’m a little biased. Heard less often are whispers that video games might actually be beneficial to players, helping them fine-tune hand-eye coordination, spatial learning and perceptual tasks. But such research is out there; last year, I wrote about research showing that video games and other parental bogeymen such as Facebook and texting might actually be improving people’s brains rather than destroying them.

Some new research in that community was released this week in the journal Cerebral Cortex, in a study that was rapidly misunderstood as merely Bigger Brains Mean Higher Video Game Scores. That’s not a false headline, but it does miss the subtle point. The authors, from 4 different schools including the University of Illinois and MIT, trained people without video game experience to play the vintage game Space Fortress. In those who learned the game faster (i.e. had achieved higher scores by the end of the training day), a brain area called the striatum was found to be larger on average than the slower learner’s striatum.

The striatum is actually a pretty interesting area, implicated in both movement (and movement disorders such as Parkinson’s and Huntington’s diseases) and addiction. The ventral striatum, including a region called the nucleus accumbens, is the focus of many addiction studies because it is the “reception area” for dopamine, the neurotransmitter increased by all drugs of abuse. With video games, the size of the ventral striatum correlated with early stages of learning, lending support to the idea that learning is enhanced by activities that are rewarding - or to put it more simply, fun.

That could explain why video games are powerful tools for improving a person’s attention and pereception, a phenomenon that researchers such as Daphne Bavelier at the University of Rochester are trying to corral to facilitate education. The study’s findings also may explain the limitations of that approach - some people appear to be resistant to the beneficial effects of video games, a fact that could be explained by brain architecture limiting their ability to learn the game. So next time I’m cursing these new-generation games for being so much harder to play than Super Mario Bros., perhaps I should blame my striatum instead of the developers.

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Illustration from BMJ by Brendan Halyday

Is Santa Claus a risk factor for obesity, swine flu and drunk-driving? And if you saw such a headline, would you think it was a joke?

That’s the cautionary tale floating about on this (admittedly slow) science news week, as a scientific article in the esteemed British Medical Journal entitled “Santa Claus: a public health pariah?” kicked up a bit of a storm. An AP story on the paper, which describes it as “light-hearted research” deep in the story, nevertheless seemed to play the findings of epidemiologist Nathan Grills straight, amusingly when it contained conclusions such as “Santa is a late adopter of evidence-based behavior change and continues to sport a rotund, sedentary image.”

The actual paper is, sadly, subscription-only and unlinkable, but from the text excerpted on the BMJ website, it’s hard to believe that people weren’t tipped off by the author citing Fast Food Nation and Super Size Me in the second paragraph. The AP article, hilariously, cites Grills’ finding of a “very high Santa awareness,” his suggestion that Santa should swap out fireplace cookies for carrots, and his personal experience with the disease-spreading potential of traditional Santa visits.

More disturbingly, Grills said Santa’s close-up contact with sniffling, coughing kids made him a one-man outbreak waiting to happen, with swine flu the biggest seasonal concern.

“Unsuspecting little Johnny gets to sit on Santa’s lap, but as well as his present, he gets H1N1 influenza,” Grills warned.

Grills said he donned a Santa suit himself - and deemed the experience a public health nightmare. “I was kissed and hugged by snotty-nosed kids at each performance and was never offered alcohol swabs to wipe my rosy cheeks between clients,” he wrote.

Okay, so maybe the AP was in on the joke, but according to this Newsweek article, many commentators skimmed over the “light-hearted research” part and wrote scathing replies to Grills’ “findings,” inevitably lumping it in with the ridiculous “War on Christmas.” The bulk of that punditry seems to have been written off the press release (or the AP story), without bothering to check the clearly marked-as-satirical original journal article - another example of a troublesome trend in a journalism industry with fewer and fewer specialized science journalists. Missing some sly Australian humor in a British science journal is harmlessly embarrassing, but relying on intermediaries with an agenda to explain a science finding related to climate change or health care costs is a whole different animal.

Hopefully, the whole silly episode is a holiday lesson for journalists twice over: 1) always check the original article and 2) yes, Virginia, scientists do have a sense of humor.

Will Saletan of Slate gave this new blog a very gracious shout-out yesterday - many thanks. He also replied to my earlier post taking Will to task a bit about “designer dogs.” I’d suggested that dog breeding is a bad analogy to bring home the problems of genetic trait selection in humans, because the former is so familiar and non-threatening. Will replied that he used a familiar example on purpose, and wondered what other analogies might work better.

To answer that, it helps to think a bit about what’s troubling in the first place about genetic trait selection for people. Breeding dogs with 25-year-old frozen sperm from a former champion doesn’t quite get at what disturbs me about human trait selection. Some people already have done a version of the dog trick with the now-defunct “Nobel Prize sperm bank” - the moral equivalent of breeding a former dog show champion. The Nobel bank was creepy, but it remained something of a fringe practice, even though it offered an easy route to instant eugenics.

One reason it stayed a fringe phenomenon may have been the lack of control prospective parents had over the outcome. You couldn’t really be sure your Nobel offspring would be an Einstein, and the child might lack good looks and social graces altogether. The Nobel bank may have boosted the odds that your child would have the desired traits, but it still relied on old-fashioned, largely unsupervised egg-sperm unions.

Pre-implantation screening of traits gets you more control, and that kind of control is what worries me most. Babies should be a little surprising - as in, “Whoa, red hair! Where did that come from? Loves art - who knew?” Having a child has always meant opening yourself up to something new and unpredictable. But meticulously screening out the traits you don’t want would bring a level of control that the Nobel bank never offered.

Maybe gambling is a better analogy for the problem than designer dogs. Reproduction the old way amounted to an honest roll of the dice. Now the dice could be loaded to prevent novelty.

That idea doesn’t make me sick - sorry, Will - but it does violate my parental sense of fair play. And if children lose their power to surprise, it will drain a bit of wonder from the world.

A confession: as much as I like the idea of bloggingheads.tv, I often find the thing itself unwatchable. Too much chit-chat, not enough substance. One longs for an irritating Chris Matthews-like presence, badgering everyone to stay on topic.

But this is a worthwhile exchange between two very good science bloggers - biology blogger Carl Zimmer and astronomy blogger Phil Plait. The question is whether science blogs might do a better job of covering science than traditional media sources, which are constantly cutting back on many specialties, including science coverage. Plait in particular believes that the rise of blogs powered by real scientists offers something as good or better than the coverage from newspapers or CNN.

The idea has some appeal, and it’s one of the reasons why we started this site. In terms of sheer science knowledge, the researchers and physicians at this university would beat any news desk in the country. If we can unleash more of that expertise, it can benefit medical consumers and the broader conversation about science.

Yet I would hate to see newspapers fade as providers of reliable science coverage. Plait is right that many scientists are excellent writers, and blogs like his can cover some stories more effectively than traditional media (his recent real-time coverage of the “Texas fireball” - probably a meteor - is a great example). But science stories benefit immeasurably from good editors, along with teams of photographers and graphic artists who can pull together complicated information into a package that any reader can digest in a few minutes (see Zimmer’s engrossing Times package from last November on changing ideas about the role of genes). Scientists excel at producing knowledge, but only some can make good sense of their field for a general audience. Newspapers ought to help fill that need.

Of course, fewer and fewer papers or networks have the resources to do that. It’s a problem not just for science journalism, but for science in general.