It seems to me that constructing and justifying a moral framework... 
 
that's the problem in your argument. few few people (theist and atheist), if any, construct and justify a moral framework a priori. the construction and justification is done afterwords. you overestimate the influence parents have on how their children act.

we still need a good resumé. For the sake of convenience and for the sake of brevity. A program statement. A manifesto. A battle cry 
 
god is dead

yeah, that's a damn good essay. I'll post some excepts.

I just get annoyed at how papers coming out of his lab tend to ignore other work in the field 
 
well, this is what happens when people have wide-ranging interests-- they don't have the time to read it all. it can make you look silly if you miss essential papers (e.g. the "complex speciation of humans and chimps" paper from nature), but not always.

There's tons of data suggesting that primate protein rates are significantly affected by the latter, yet his papers always manage to trivialize this by cherry-picking the genes that are looked at. 
 
well yeah, but to defend him, he's interested in human brain evolution, not necessarily human evolution in general, so he looks at genes expressed in the brain. I don't know if I'd call that cherry-picking.

most reasonable scientists sit quite happily somewhere in the middle. 
 
agreed. and don't worry, chimpdude, lahn is a reasonable scientist, not a crackhead.

why not use this kind of analysis with allele data? 
 
I think we're talking on different time scales here. if we want to know what makes humans different from mice, one would imagine that the differences are fixed in both populations, i.e. there is no polymorphism in either species at the relevant loci.  
 
the signature of selection in polymorphism data only lasts for something like Ne (effective population size) generations, so it doesn't go back far enough to answer questions like the one above. for more recent selection, you use polymorphism data, but LD-based methods are more practical (and I think more powerful) than those based on the frequency spectrum).

Why not? 
 
if you're comparing two genome sequences--say rat and mouse--you don't have polymorphism data, just a single sequence from each species. if there are different alleles of the gene segregating in mice, you can't tell.

If the allele is both widespread and has short time-depth, then obviously it is under directional selection. 
 
this is essentially the test used by lahn to show selection in MCH1 and ASPM, except that he used haplotype length as a proxy for time.  
 
the nonsynonymous/synonymous substitution ratio is not comparing alleles, it's comparing genes between species. that is, you're comparing two genome sequences-- the time of divergence between the two is fixed, and the sequences are representative of their respective species.

Since synonymous mutations are selection-neutral, given a large enough population, their number should be a very accurate measure of time 
 
I think you're talking about sites that are polymorphic within a population. If we compare the chimp genome to the human genome, however, time is fixed (at about 5 million years) and the challenge to to sort through the sites that have become fixed.

Here we are NOT talking about ratios, but absolute numbers - this should help to distinguish between high positive selection (which would result in high ratios but low absolute numbers) and relaxed constraint (which would result in high ratios and high absolute numbers). 
 
I'm not sure. why would selection give low absolute numbers, while relaxed constraint give high absolute numbers? also, note that absolute numbers are also influenced by the local mutation rate.

Presumably the genetic component of the variance would increase if people bothered looking at normal behavior, rather than the genetic causes of suicidal behavior, on the understanding that the extreme cases like suicides are tail-cases of normal distributions along with an even stronger environmental influence. 
 
agreed. there's a trend now towards using continuous endophenotypes that underlie a binary trait in these sorts of studies now.  
 
anyone know the polymoprhic extent of BNDF in diff. populations? 
 
for the substitution associated with anxiety, I found: 
 
japan: 41% 
italy: 30% 
usa: 18% 
 
sorry to disappoint, but no data on the finns.  
 
from here:  
http://www3.interscience.wiley.com/cgi-bin/abstract/105558613/ABSTRACT

I actually just read the rakic 1988 paper as a chapter in a book, and didn't understand shit. this summary of the major points is pretty helpful.

nope. perspective is the type of article. like an opinion article.

do we know enough about recombination hot spots to say if they are heritable? 
 
hotspots aren't conserved between humans and chimps, as far as one can tell. evidence suggests they evolve rapidly. is activity at a certain hotspot heritable to some degree? probably, but it's impossible to tell (measuring the activity of a hotspot in men is plausible, as they make a ton of sperm to type, but in women you can't really look at the meiotic products to measure recombination). so the closest thing to that is jefferies et al. and their sperm studies.  
Haplotype analysis around both hotspots identified active and suppressed men sharing identical haplotypes, establishing that these major variations in the presence/absence of a hotspot and in quantitative activity are not caused by local DNA sequence variation. These findings suggest a role for distal regulators or epigenetic factors in hotspot activity and provide the first direct evidence for the rapid evolution of recombination hotspots in humans

good point, and something I hadn't though of. for sequences that form watson-crick pairing, two substitutions would have to arise for the most stable new structure to arise. that sounds like epistasis to me, and increased recombination could promote that. I hadn't seen this paper before, but it seems relevant: 
http://www.genetics.org/cgi/content/abstract/173/3/1793 
 
but here we're talking about recombination on an extremely small scale

sorry. unannotated means not marked as having a known function in the genome database.

I'll let coffee mug talk about the consequences, but epigenetics is the study of modifications to DNA (or the proteins that package the DNA). When I think epigenetics, I mostly think methylation. methylation of the DNA around a gene leads controls its expression. differential methylation of DNA in different tissues, then, leads to tissue-specific expression.  
 
something that interests me is whether, should different sperm have different methylation profiles (as they do), does this information get transmitted to the next generation, and what role does it play in the generation of phenotypes?  
 
both questions, for me, fall into the realm of epigenetics, and both are important.

When I first learned the term it was primarily in relation to the molecular modifications that can occur around the DNA 
 
that's what I'm referring to when I say epigenetics.

Tajima's D isn't useless on the HapMap data-set - you just use an empirical distribution (i.e. the genome-wide data-set) to estimate significance rather than the standard theoretical distribution 
 
like RPM says, it's not the demography that's a problem, it's ascertainment. there was no standard for including SNPs in the hapmap, so the frequency spectrum for SNPs in different regions might be variable for no reason (other than ascertainment).  
 
local variation in recombination rate creates a great deal of noise 
 
check out voight et al (2006). in plos biology. the use of the two haplotypes as internal controls is a way around this problem.  
 
I'm a big fan of outlier-based approaches--in disease genetics, the move of parameter-based to non-parametric statistics was a revolution; i predict it will be the same in popgen.

they use three statistics-- Fst, tajima's D, and the log of the ratio of heterozygotsity.  
 
to judge significance, they compare the statistics in their genes to a number of windows throughout the genome. this should probably be a decent control for demographics, but the word "ascertainment" never appears in the paper.  
 
I didn't really think this through-- I imagine using tajima's D on hapmap data is useless, but what about the other two statistics?