Tuesday, June 17, 2008

Tree Species Robustness: Animals vs. Wind Dispersal

And evidently the winners are animals, according to a new report in last week's Science.

I am first impressed by this big number: they took 89,365 forest survey plots of 34 tree species. But since I don't know how difficult the methods are to enact, I don't actually know if that's impressive or not. On the other hand, it's in Science, it must be pretty impressive.

However, getting into the data, there are also other important numbers to consider: 12 species are wind dispersed and 22 are animal dispersed. Almost double the amount are animal dispersed? And when you look at their chart, 8 animal-dispersed species are filling out the well-dispersed end of the chart, but everything else seems pretty evenly matched. One animal-dispersed sits at the end of the chart pretty high above all the rest, and two wind-dispersed species sit in the middle, but within the range of most of the animal-dispersed species. So, if we had more wind-dispersal species, would we find them falling in the range of the higher-end animal-dispersal trees?

Perhaps part of the point is that there simply aren't more wind-dispersed trees of canopy-dominant trees, but that's not data.

Why am I talking about this on a blog about primates? Well, I got really excited about it to see if they could differentiate between the animal species dispersal, (say tell the difference between whether certain trees were dispersed by primates or birds or butterflies, etc) which could support or refute the Angiosperm theory of primate evolution. Before I got so excited, I should have recalled this paper which showed primates aren't species-specific dispersers, but diffuse dispersers.

Still a cool study though.

Monday, June 16, 2008

fMRI Studies as the new Phrenology?

A NewsFocus in Science last week on the influence of fMRI images in studies-regardless of data, led me to a more in-depth article stressing the limitations of interpreting fMRI data. Russell Poldrack, a brain-imaging researcher from Wash-Univ. St. Louis was interviewed for the article, and he clearly came down on the side that the limitations of fMRI data obscure most interpretations, and compared it to phrenology. I was reluctant to believe it, in this day-and-age? A method that is steeped in confounding variables and current societies hegemony? Come on now, fMRI can't be that bad. After all it's super expensive, technological, and fancy!

Until I read from the second article:

The general public may be easily seduced by pretty images generated by fMRI (see sidebar), but even neuroscientists sometimes seem to fall under the spell and overlook the method's limitations. One constraint is the narrow sliver of the human experience that can be captured when a person has to keep his or her head still for long periods inside an fMRI scanner. Another is the resolution. Using fMRI to spy on neurons is something like using Cold War-era satellites to spy on people: Only large-scale activity is visible. With standard fMRI equipment, the smallest cube of brain tissue that can be imaged is generally a few millimeters on a side. Each such "voxel" (a mashup of volume and pixel) contains millions of neurons. And although neurons can fire hundreds of impulses per second, the fMRI signal--which indicates an increase in oxygenated blood bringing energy to active neurons--develops sluggishly, over several seconds.

Holy crap. That's a lot of variation just waiting to happen. Who knows whether there are different patterns of neurons that can be laid down, how they are laid down (genetic, epigenetic, or part of nurturing, part of the individual's personality, etc).

I am also reminded of something my high school physics professor said. Granted this was 8-9 years ago, but basically much of our understanding of the human brain is based upon something being broken in the brain and seeing what goes wrong. He likened it to having a TV, but not knowing how the parts work. So you go in and break something, and then see what goes wrong. His point was that a lot of things can go wrong and give the same output, but they all have entirely different functions and parts!!

My point, therefore, is that while investigating it is teh awesome, we've still got a far way to go. And no amount of pretty pictures will get us there without more resolution and an understanding of what that resolution means.

Monday, June 2, 2008

VLDLR: Back to Quadrupedalism

A number of years ago, the children in a Turkish family were found to be obligate quadrupeds. All of a sudden, researchers were fascinated by what they saw as people having reverted the supposed primitive state of quadrupedalism. Since then, a few other families and individuals also have been found to exhibit quadrupedalism.

I'll disregard all the problems with that for a moment.

A recent study by Ozcelik et al (2008), published in PNAS, has now proposed VLDLR, a gene involved in lipoprotein reception, to be a gene necessary for human bipedalism.

And you know what? They're probably right. But they're wrong that this is evolutionarily interesting. As the authors note, VLDLR influences many phenotypes, and when nonfunctional results in
cerebrocerebellar hypoplasia, specifically vermial hypoplasia, accompanied by mental retardation, and dysarthric speech all in addition to quadrupedalism. It is quite possible that some of these mental defects may be what is causing the quadrupedal gait, and so any gene that influences that portion of the brain will induce quadrupedalism.

As Herz et al (2008) note:

Clinical, evolutionary, and molecular evidence refutes their hypothesis. Quadrupedal locomotion is more likely an adaptation to the severe truncal ataxia present in all VLDLR-deficient patients, resulting from a combination of uneven, rough surfaces in rural areas, imitation of affected siblings, and lack of supportive therapy. Conclusions about the role of VLDLR in the transition from quadrupedal to bipedal locomotion are uninterpretable and untenable in the presence of such extensive structural cerebellar defects.

So the authors, then, have found one gene among many that, when changed will produce a negative effect on many traits including quadrupedalism. But they have no idea what the mechanism for that relationship is.

I will say that they do note that they want to look into families B and C, of which a mutation in VLDLR does not exist but do exhibit quadrupedalism to see what other neurological mechanisms may influence gait. But will it really tell us that much about locomotion? Not likely.

Least favorite sentence:

Quadrupedal locomotion was first reported when Tan (9, 10) described a large consanguineous family exhibiting Unertan syndrome, an autosomal recessive neurodevelopmental condition with cerebellar and cortical hypoplasia accompanied by mental retardation, primitive and dysarthric speech, and, most notably, quadrupedal locomotion.

Why is "quadrupedal locomotion" the most notable of these disorders? Because it is the easiest to have a metric for? Because it is a rarer disorder? Because it is the one they are covering in this paper?