Via Jim Kalb, France is No Longer a ‘Catholic’ Country. A google translation of a summary of the original report is here. Two points:

1) In keeping my earlier contention, a decline in the dominant organized confession doesn’t mean that all defectors are turning to atheism. A vague (pan)theism remains in place (the translation summary seems to imply that some are switching from “Catholic” to generic “Christian”).

2) Muslims were 4% of respondents. I’m assuming this excludes the non-religious of ethnicities traditionally Muslim (since they form around 10% of the population).

Just an FYI for readers, lots of comments on the Heather Mac Donald interview can be found on technorati. A link from Arts & Letters Daily has resulted in a new spike of interest. Larry Auster probably has the most serious commentary. Many liberal bloggers praised her atheism but were blasphemed by Heather’s conservatism, while many conservative bloggers now seem to believe she is a crypto-liberal.

The APOE gene comes in a number of varieties in humans. The ancestral primate allele (APOE4) still hangs out in humans at a low frequency and is most famous for increasing risk for Alzheimer’s. I noted a paper a few months back suggesting that the APOE4 allele is protective for severe childhood diarrhea. I just found another paper showing an association between APOE4 and better episodic memory. So you have better memory when you’re young, but you pay for it when you get older. It seems like learning was just easier for APOE4 carriers. In the fMRI portion of the study they showed reduced hippocampal signal, interpreted as “more efficient” use of neural resources. The authors note that the memory phenotypes of humans are paralleled by LTP phenotype in an APOE4-carrying transgenic mouse strain. LTP is enhanced in young mice, but gets worse as they get old. Apparently, APOE4 is capable of stimulating CREB activation unlike other alleles. CREB is a heavily studied transcription factor thought to be important for inducing expression of genes needed for memory consolidation. At one point, the authors seem to suggest that this ability might help explain the greater hippocampal efficiency in APOE4 carriers, but the whole transcriptional activation and cellular consolidation program involving CREB is supposed to take several hours if not a whole day, while the changes in hippocampus activity took place within an hour. So maybe better LTP induction could be part of the explanation, but I doubt CREB is part of the equation. I wonder if the pattern of memory performance (young = above avg.; old = below) can be observed regardless of APOE genotype. Maybe this is more mechanical such that if your memory system is overclocked you are likely to burn it out.

Sergey Gavrilets and William R. Rice have a new population genetic model for homosexuality out. You can read the full paper over at Gavrilets’ website, while Ars Technica and Matt both have some nice commentary. I don’t have much to add, and generally share Matt’s skepticism of the utility of a one locus model, but at least it is somewhere to start. I will reiterate that the “problem” is obligate homosexuality. I don’t find facultative homosexuality as surprising or evolutionarily mysterious. Also, I am intrigued by the the older brother effect because of its implications of genomic conflict.

I rediscovered the NIH videocasting site last night. Looks like they finally made the transition to downloadable content.

This one promises to be interesting:

Issues and Approaches in Genome-Wide Association Mapping

Program date: Wednesday, December 13, 2006, 3:00:00 PM
Presented by: Nancy J. Cox, Ph.D., University of Chicago Department of Medicine

Abstract:

TALK SUMMARY:
I will air some of the “dirty laundry” in conducting genome-wide association studies with current platforms, and provide an overview of approaches that we have been developing in applying in GWA studies on type 2 diabetes. In addition, I will address some of the reasons that I believe GWA studies for complex phenotypes will be just as challenging as all other genetic studies of these phenotypes have been.

BIOGRAPHICAL SKETCH:
Nancy Cox is a quantitative human geneticist with a primary interest in the relationship between genotypes and complex phenotypes. Research in the lab focuses simultaneously on the development and extension of analytic approaches for identifying and characterizing genotype – phenotype relationships and on the application of those approaches to a variety of complex phenotypes including type 1 and type 2 diabetes and related phenotypes.

Audio or Video

Their vast library is still only available in realmedia. Some good ones should be David Amaral, Michael Hasselmo, Karel Svoboda, Paul Glimcher, and Gyorgy Buzsaki.

I just found this article by Heather Mac Donald in Slate, Send a Message to God: He has gone too far this time. She published it two years ago, and somehow I missed it!

The Inductivist has a hilarious post on obesity rates. Americans are the fattest of course….

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Mad cow disease is caused by the misfolding of a protein called the prion protein. One might imagine, then, that a cow without said protein would be resistant to mad cow. And indeed, that is the case:

Prion diseases are caused by propagation of misfolded forms of the normal cellular prion protein PrPC, such as PrPBSE in bovine spongiform encephalopathy (BSE) in cattle and PrPCJD in Creutzfeldt-Jakob disease (CJD) in humans. Disruption of PrPC expression in mice, a species that does not naturally contract prion diseases, results in no apparent developmental abnormalities. However, the impact of ablating PrPC function in natural host species of prion diseases is unknown. Here we report the generation and characterization of PrPC-deficient cattle produced by a sequential gene-targeting system. At over 20 months of age, the cattle are clinically, physiologically, histopathologically, immunologically and reproductively normal. Brain tissue homogenates are resistant to prion propagation in vitro as assessed by protein misfolding cyclic amplification. PrPC-deficient cattle may be a useful model for prion research and could provide industrial bovine products free of prion proteins.

Will it one day be considered irresponsible to produce beef that is not genetically modified?

Jason Rosenhouse has a nice post on the rate of mutation within the genome. David plumbs the depths of J.B.S. Haldane’s 2s. Peromyscus posts on the ladies looking for possible “extra-pair matings.” A**man posts on short guys.