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Monday, July 31, 2006
Not quite, but interesting article in the Minnesota Star Tribue. Skip all the sentiment and hand-wringing and just jump to the statistics. Also, this is eye-opening: "By the year 2000, no large U.S. city anywhere other than on the intensely multiracial Pacific Coast had a higher share of multiracial children than Minneapolis." Of course, the Upper Midwest and the Pacific Northwest are whiter than average regions of the country, reinforcing Steve Sailer's point that overly large minority communities retard assimilation.
John Hawks and Tara Smith both have posts on a New York Times article describing the role of events during development on health later in life. A recent article pushed for the development of a framework to describe these kind of effects.
The basic concept is simple: during development (development in utero), the fetus recieves signals that allow it to "predict", as it were, the environment where it will live. For example, there may be some way to sense whether the environment will be nutrient-poor or nutrient-rich. Based on this information, development proceeds in a way to favor adaptation to the predicted environment. However, if the prediction is wrong, for whatever reason, disease may result later in life. Importantly, the mother acts as the conduit for the environmental information, and may alter it to suit her needs. The main example given in the article concerns metabolic disease like type II diabetes and obesity. The argument goes like this: due to basic physics, a fetus can't exceed a certain size (or couldn't, before the C-section). Thus, in a nutrient-rich environment like we have today, where a fetus would "want" to get much bigger, the mother limits the environmental signal )so as not to have a giant child), leading to a fetus that "predicts" an environment much poorer than what really exists. Once developed, the grown individual is then predisposed to gain weight. The authors put is thusly: We argue that it is this differential rate of change between the limitations imposed by maternal constraint (which set the fetal prediction) and the reality of the enriched modern postnatal environment that has created the current high incidence of cardiovascular and metabolic disease in humans. This is a broader framework for what some have called the "thrifty phenotype" hypothesis for the prevelance of type II diabetes, an alternative to the "thrifty genotype" hypothesis.
A comment that crossed my screen via that series of tubes:
There is a perception, alluded to in the discussion above, that while Gould was a remarkably adept and influential writer of popular science, his work as a scientist per se was less notable and much less influential/respected. This is not a view universally held, as a historian of science his contributions are widely described as being outstanding, and he is said to have been very well respected in his own field of paleao biology. However I have tried to establish how influential his science was by establishing how often his scientific papers (not his popular works) have been cited in the scientific literature, through the ISI databases. For comparison, Richard Dawkins' most highly cited scientific paper has 100 citations, Ernst Mayr's has 173, CG Williams' has 253 and D Tutyama's has 394. Gould's most highly cited paper (in Proc R Soc 1979) has 1,613 citations, and the next eight have 863, 609, 291, 169, 138, 121, 121, and 109 citations - the last of these published in 1974 is on antler size. I do not think that any claim that Gould was not highly influential as a scientist is objectively sustainable. His citation record is exceptional by any standards. Informative and thoughtful comments welcome.
Sunday, July 30, 2006
I don't blog much politics anymore because I think most of it is trivial epiphenomena. That being said, I want to point to Dick Lamm's recent comments. Lamm says that this country is "overdue for a candid dialogue on race and ethnicity." No shit sherlock! Back in 1996 when Lamm tried to get nominated on the Reform Party ticket I was pretty supportive because he seemed like he wasn't much of a bullshitter. I didn't agree with everything that Lamm promoted (Lamm changed his mind on free trade to become a skeptic, I still support free trade in the generality as a good for this nation), but his candid manner and "straight talk" (before that term was trademarked by John McCain) appealed to me. Lamm is not your typical "straight talker" on race. He is an old style environmentalist, and as a Unitarian Universalist he isn't a rock-ribbed right-winger in the style of fellow Coloradoan Tom Tancredo (I'd be willing to bet money he's not a theist but a humanist). Only Nixon could go to China, and only sincere progressives in the old style can transcend the excessive sentiment which seems to the consensus as exemplified by the Democratic party and the George W. Bush wing of the Repulican party when it comes to quality of life and civilizational issues. I don't really read "political" books anymore, but I've just ordered Two Wands, One Nation. You'd figure with a name like Dick Lamm someone would think up a better title, but sometimes I guess we've got to go with substance.
I just posted this on my own blog last night and thought I'd cross-post it here, as there have been a few posts lately about neurotransmitters, neurons, and behavior.
About a month ago I saw this article about the role of the dopamine transporter in cocaine reward. For those that don't know, the modified amino acids dopamine, norepinephrine, and serotonin, collectively known as monoamines, are neurotransmitters that are released by specific neurons in the brain and activate receptors on other neurons, sending a message from one cell to another. There are "pumps" in the membranes of the neurons that release these transmitters, which "clean up" the released monoamines so that they don't keep activating receptors for too long. These pumps are blocked by many psychotherapeutic and recreational drugs, producing a change in brain function. While each neurotransmitter has multiple effects in the brain, the transmitter dopamine in particular is believed to participate in the behavior-reinforcing properties of both natural (food, sex, etc.) and pharmacological (drug) stimuli. Among many scientists dopamine is still believed to be a kind of "pleasure chemical" whose concentration determines the degree of positive subjective sensation produced by the environment, regardless of the specific nature of the stimulus. This idea has been called into question especially lately, though, for a number of reasons, many of which have nothing to do with this article. For instance, the effect of drugs that directly activate dopamine receptors is not euphoric in humans. The finding that concerns us here is one made by Sora et. al. in 1998. To understand the significance of this study, it is important to know that the stimulant cocaine blocks the transporters ("pumps") for all three monoamines. Given the assumed responsibility of dopamine for reinforcement, it has long been assumed that the block of the dopamine transporter (DAT) produces the euphoric effect of cocaine by allowing dopamine to sit around and activate its receptors longer. To test this, Sora et. al. deleted ("knocked out") the gene encoding DAT from mice, and showed that they still prefer to spend time in a chamber in which they have previously received cocaine. This so-called conditioned place preference suggests that cocaine can act as a reward even when it cannot block DAT (because DAT doesn't exist in these mice). Knocking out the serotonin transporter (SERT) also left cocaine reward intact (This SERT is the same as the 5-HTT mentioned in the Caspi and Moffitt study-geneticists seem to like the name 5-HTT and biochemists SERT, and some use the alternative SLC6A4 occasionally). A follow-up study showed that knocking out both DAT and SERT makes mice that do not prefer an environment they associate with cocaine. Sora et. al. took this to mean that blocking SERT is rewarding as well, which flies in the face of the fact that blocking SERT with drugs like fluoxetine (Prozac) does not produce signs of euphoria. An obvious caveat here is that the brains of DAT knockout mice are flooded with dopamine and the animals are very hyper even when they aren't on any drugs, so findings may not generalize to normal mice. The new study by Chen et. al. took a different approach. They found that by mutating part of DAT, they could prevent cocaine from binding to it without breaking the pump. When this mutant DAT was added back into DAT knockout mice, cocaine no longer made the mice hyperactive like normal or DAT knockout mice (paradoxically, it even calmed them) and was not rewarding. This confirms what I--and probably many other researchers--suspected was going on: the mice with DAT knocked out only showed a response to cocaine because it slightly amplified the effect of the high baseline dopamine. Possible explanations are that increased activation of serotonin receptors overcomes some negative feedback mechanism limiting dopamine levels, or that lack of DAT induces a form of plasticity in the reward pathway such that SERT blockade becomes rewarding. This still doesn't explain other results questioning the idea of dopamine as a "pleasure chemical", but at least it shows that cocaine, and probably methylphenidate (Ritalin) and amphetamines, do produce their reinforcing effects through inhibition of dopamine reuptake. *I just corrected the links. For some reason the first time I posted the URLs got all messed up, even though it worked perfectly fine for my own blog when I cut and pasted from the same file on my computer.
Saturday, July 29, 2006
This month Nature Reviews:Neuroscience published an opinion piece "Gene-environment interactions in psychiatry: joining forces with neuroscience" by Avshalom Caspi and Terrie E. Moffitt who follow-up on their well-cited 2002 article in Science "Role of genotype in the cycle of violence in maltreated children." In the opinion piece the authors present a broad overview of the opportunities and challenges present in studies that address the gene-environment interactions that exist within nature. In their earlier earlier paper they:
It's quite plausible that as this science develops it will enter into the social and legal arena where it will be useful in questions dealing with Indefinite Commitment Laws. David Rose tackles this subject, and provides a useful historical overview on "genetic determinism" scaremongering, in the latest issue of Prospect (UK). I want to add to the topic, but first a little background. Indefinite Commitment Laws are designed to keep dangerous individuals from being released from prison after they've completed their terms of incarceration, have been passed in 16 U.S. States and have passed through Constitutional challenges by claiming that the commitment is a medical treatment, rather than a double-jeopardy penalty of continuing incarceration. The case law can be sampled here, here and here. The impetus for these types of laws clearly centers on fears of high recidivism probabilities of the ex-convict. Because the legal proceedings are dealing with civil commitment rather than criminal commitment, the standard of evidence must only meet a clear and convincing threshold, rather than the higher bar of beyond a reasonable doubt. Due in large part to this lower evidenciary standard the adjudicating authority becomes a de facto actuary and much of the focus deals with probability of recidivism. To gauge the boundaries of the probability estimate there are prescribed protocols which must be followed by the State. More details in this Handbook for "Sexually Violent Predator Assessment Screening Instrument for Felons: Background and Instruction" and in this Memorandum on "Civil Commitment of Sexually Violent Predators" that was prepared for Virginia Circuit Court Judges. But what are the actual probabilities of recidivism that have spurred on this legislation? In their meta-analysis of recidivism studies, Predicting Relapse: A meta-Analysis of Sexual Offender Recidivism Studies, R. Karl Hanson and Monique T. Bussiere find:
Margaret A. Alexander performed a meta-analysis of 79 studies that looked at recidivism rates after the criminals participated in various treatments regimes in her study, Sexual Offender Treatment Efficacy Revisited and found the following recidivism rates: Rapists (treated 20.1%, untreated 23.7%); Child Molestors (treated 14.4%, untreated 25.8%); Exhibitionists (treated 19.7%, untreated 57.1%) and the by far largest group, Types not specified (treated 13.1%, untreated 12.0%). The last entry isn't a typo, the untreated did in fact have lower recidivism rates. I thought it would be useful to survey the probability universe that we're dealing with when we deprive people of their freedom via Indefinite Commitment Laws for they do work on the basis of probabilities rather than certainties and it's quite likely that genotypic information will significantly improve the accuracy of assessments, especially when such information is combined with data on the life history of the subject. Rose summarizes the 2002 Caspi and Moffitt paper:
Notice that the rate for conviction of violent crime was 50 percent greater in the low-activity genotype group than in the high-activity genotype group. In absolute terns the former group has a conviction rate that is 10 percent greater than the latter group. Compare these rates to the the recidivism rates for rapists (18.9%), child molestors (12.7%) and violent offenders (12.2%.) When we're dealing with probabilities of recidivism it seems that genotypic information will only serve to improve the decision process underlying indefinite commitment proceedings. An added benefit of developing this research will be the likely erosion effect on the Axiom of Discrimination as it pertains to the question of race and crime. We already have studies which have charted monoamine oxidase activity across demographic groups:
Note that the groups most prone to low enzyme activity are males, the young, and black subjects. Another study makes the implication more explicit:
Of course, a research design that broaches the sensitive topic of race, genetics, and criminality is certain to dissuade many scientists from getting involved, for as Stanford's David Botstein remarks about genetic causes of violence:
We need look no further than Rose's essay for a sampling of what the future portends:
For most of the regular readers of this blog these types of frothing-at-the-mouth attacks are old hat. Just a few weeks ago we saw Stanford's Barres preparing the ground for classifying science he didn't like as hate crimes:
The Leftist Creationists who believe that humans are immune to evolutionary processes will not go down without a fight. Unfortunately, these types of creationists are a monolithic bloc within Academia and they can indeed put up impediments to research or simply resurrect the tactics used during the Sociobiology Wars. However, even if they can groom an obscurantist of Gouldian proportions, they're going to have a difficult time refuting the work of good scientists, work which been replicated many times over. In the end these new insights should aid society in furthering the cause of justice, just as DNA testing has been instrumental in setting unjustly incarcertated people free and helping to convict those who are guilty of crimes. The science and technology are neutral but they do aid in guiding the decisions made by our arbitors of justice.
Never ever let a n* ride if you think he's gonna slide pop'em in the spine...fo' the money. - Bone Thugs N Harmony
The Genius is dead. Genius Re-post: Your standard neuron in the cortex is called a pyramidal neuron. It generally has on big apical dendrite sticking out the top and a few basilar dendrites radiating around the bottom. Here's a glowing one:  This one comes from a somewhat troublesome paper from the lab of Karel Svoboda who as far as I can tell is a guru of new imaging techniques who happens to have an interest in the details of dendrites as well. The reason why the paper was a little vexing is because the results seemed to run against a large literature showing that the major identifiable morphological problem with neurons in Fragile X Syndrome brains has to do with dendritic spines. Let me back up. Your standard neuron in the cortex has dendrites and an axon. The axon is the output structure that goes and pokes at another neuron and can fire action potentials that release neurotransmitters from its tip to send signals. The dendrites are the parts that receive signals from axons. Where an axon and a dendrite meet is called a synapse. Dendrites are studded with these little knobby-doos called spines. Spines are where most excitatory synapses in the cortex are made. Spines go through a maturation process whereby they initially come out as long wormy things called filopodia and then kind of settle back into a variety of shapes often resembling the power-up mushrooms in Super Mario Bros. or like a large kind of extended comma. The fat part at the end is referred to as the spine head and the thin part connecting to the dendritic shaft is the spine shaft. Spine shapes change in the lifespan of the spine, but also change over the lifespan of the organism. And along side the changes in shape come changes in the number of spines per dendrite (the spine density). Since people had looked at adult human Fragile X brains and seen abnormalities with regard to spine morphology and density it seemed clear that something must be occurring during development. Nimchinsky et al (2001) wanted to see what happens in development so they got some normal mice and some mice lacking fragile X mental retardation protein (FMRP) that are a pretty good model for what's happening in humans with the disorder. When the mice were one, two, or four weeks old they injected a particular part of the cortex with a fancy shmancy virus that lights up a good portion of neurons (anyone who reads science crap knows about GFP the magical jellyfish protein, that's how they're doing this). This allowed them to use laser microscopy to do detailed quantitative analysis on the spine lengths and density. The troublesome bit is that while they found the expected differences between FraX mice (the fragile X model) and wild-type (read: normal) mice at one week (shown below), the differences disappeared by 4 weeks. How can this be?!  They offered up a number of considerations including that they were looking at a different chunk of cortex than other people usually do and that perhaps there were some limitations to their visualization technique. The most important limitation, as it turns out, is that they can't use their technique past about 6 weeks of age because the virus they used is too bad at infecting neurons after that. A more recent paper from the Greenough group in Illinois, who were some of the major reporters of these fragile X spine abnormalities in the first place, arrived at a resolution to this conflict. Galvez and Greenough (2005) took basically the same tack as the Svoboda group except they chose a couple of different ages. They used 25-day old mice to map onto the 4-week time point previously reported and they took another sample at age 73-76 days old. For those of you who have trouble dividing by 7, that's about 10-11 weeks. The reason for doing this is that it is understood that a major developmental process called pruning might be at play here. Initially developing brains produce huge amounts of connections during a period of widespread synaptogenesis. They don't need all of these connections. So they have to be 'pruned' back. There are lots of tree metaphors when talking about dendrites that can make it very pleasant for a neuroscientist to contemplate a tree in the park on a summer afternoon. This apparently happens in mice some time after one month of age. The Greenough paper used a more rudimentary staining procedure so they could look at spines in the older brains. They managed to replicate for the most part the finding that FraX mice and wild-type mice don't differ at 4 weeks with regard to spine shape and density. But at the much later time point they differ pretty radically as illustrated here:  It appears that the major malfunction with Fragile X spines then isn't that they can't grow out right or anything like that. Its that they can't be eliminated after the fact. Notice how much more bare the adult wild-type dendrite (Figure 1C from the paper) looks compared to the FraX dendrite (Fig 1D). This is awfully nice to see for two reasons. One, because it clears up an apparent discrepancy in the literature and it turns out that everyone was right which ought to make all the labs involved feel marvelous. It's also nice because it indicates that the real neurological problems in Fragile X development start later than expected in development. I'm not quite clear on when this massive pruning event is supposed to happen in human development, but it opens a window whereby if we ever get the means to replace this protein we might ameliorate some of the effects of the syndrome. References: Nimchinsky EA, Oberlander AM, Svoboda K (2001). Abnormal development of dendritic spines in FMR1 knock-out mice. J. Neurosci. 21:5139-5146. Galvez R, Greenough WT (2005). Sequence of abnormal dendritic spine development in primary somatosensory cortex of a mouse model of the fragile X mental retardation syndrome. Am. J. Med. Genet. 135A:155-160.
Friday, July 28, 2006
For those of you who are, or in my case, were, into professional sports, this site lists their political donations. I was surprised that Joe Theismann or Barry Switzer gave mostly Democrats. Also, the African Americans were more Democratic than I had expected (I'd assumed that their wealth would have worn away their cultural orientation in regards to politics).
A paper in Nature Genetics describes a mutation in a tomato gene that leads to fruits that don't ripen. This would be an important discovery in itself--the ripening of fruits is certainly an economically interesting trait--but a further twist makes it even more interesting. The twist: the mutation is actually an epimutation. That is, the two alleles--the non-ripening allele and the wild type allele--have no difference is sequence, but rather a difference in the methylation status of the promoter. The methylated allele is expressed at a lower level, leading to an inhibition of ripening.
Also interesting is that the methylation status of the allele seems to be fairly stable-- they claim to have seen a tomato revert from the non-ripening phenotype to wild type three times in 3000 plants grown since 1993. So this epimutation acts essentially in a Mendelian fashion. Whether this will be a common occurrence in plants (or other taxa) remains to be seen. Related: epigenetics in humans
The NYT has an article up about how supposedly malleable IQs are by a professor trying to get more money for early childhood education programs. Aside from the arguments about funding a program that is not that effective , the merits of the NYT article are questionable.
Kirp's argument is based on two studies by the same researcher: Michel Duyme. Before anything is stated about the studies, I'll point out that while the participants in these studies may be new, the theory and designs are not. Herman Spitz's masterful work goes over many of these types of studies, and the overall result is not too impressive for those thinking IQ is easily changed. If your educational psychology professor didn't make that book a required reading, join Questia and read it, or snag it from the local library. Now on to the NYT article....... About the first study, Kirp writes: Regardless of whether the adopting families were rich or poor, Capron and Duyme learned, children whose biological parents were well-off had I.Q. scores averaging 16 points higher than those from working-class parents. Yet what is really remarkable is how big a difference the adopting families' backgrounds made all the same. The average I.Q. of children from well-to-do parents who were placed with families from the same social stratum was 119.6. But when such infants were adopted by poor families, their average I.Q. was 107.5 - 12 points lower. The same holds true for children born into impoverished families: youngsters adopted by parents of similarly modest means had average I.Q.'s of 92.4, while the I.Q.'s of those placed with well-off parents averaged 103.6. These studies confirm that environment matters - the only, and crucial, difference between these children is the lives they have led. Darth Quixote has already deeply delved into this study, and there is no need to repeat him here. I will add: So where does leave us? Capron and Duyme sum it up best: Although these findings clearly indicate that the biological parents' background contributes to observed differences in IQ between extreme groups, as does that of adoptive parents, more detailed interpretation is difficult (p. 553) which is a far cry from Kirp's interpretation: the only, and crucial, difference between these children is the lives they have led. About the second study, Kirp writes: A later study of French youngsters adopted between the ages of 4 and 6 shows the continuing interplay of nature and nurture. Those children had little going for them. Their I.Q.'s averaged 77, putting them near retardation. Most were abused or neglected as infants, then shunted from one foster home or institution to the next. One has to do some digging elsewhere, but the study he is referring to is from PNAS. Since the study is free to read, I'll only go over the major points: As to a critique, first the selection criteria is loaded. No one with any sense about them would think that being abused/neglected from birth so bad that the legal system has to intervene would not decrease cognitive functioning. This is not at all what is meant when discussing "Average Expectable Environment." So right off the bat we know that these kids are not at all the same as a regular Joe (or Jane) off the street who has Borderline IQ. Thus, right off the bat we would expect that after any semblance of stability, the kids' cognitive functioning would improve (i.e., return to its normal state). Second, while there is some difference between the IQs across groups, it isn't major (max: Low SES PIQ vs High SES PIQ, d = .9 [r2=.17]; min: Low SES VIQ vs. High SES VIQ, d=.5 [r2=.06]), indicating SES explains somewhere between 6 and 17 percent of the variance in post-adoption IQ scores. While there is definitely an effect, given the extreme nature of the study's categories, it does not appear to be much of one. Third, it is very difficult to say with much certainty that IQ scores from scale, developed with one set of theoretical guidelines and one set of 1950s norms are directly comparable other IQ scores from a different scale, developed with a totally different theoretical orientation that uses a set of 1970s/1980s norms. This is even more so when the Bayley scale is used. For those of you that have given the Bayley (all 2 of you!), you know it is an extreme pain to administer and that it is about as unlike the Wechsler instruments as you can find a test that still measures cognitive ability. Fourth, while there was an overall mean increase in IQ, in addition, there was a universal gain in variance (stnd. dev. increased approx 9 IQ points). Thus, assuming that the before and after IQs were directly comparable, the majority of the scores fell into these ranges:
A few things to notice. 1. There were at least some kids in both categories who, pre-adoption, were in the average range. Given the stark conditions of their pre-adoption upbringing, that is amazing - and likely has little to due with a nurturing environment. 2. There were at least some kids in both categories who, post-adoption, were in the Mild to Moderately Deficient range. Meaning - they still were classified as MR. If the environment is so powerful, why didn't their IQ rise also? 3. It is a fair assumption that even the Low SES households were much better off for the kids than their abusive/neglectful original home. If the environment is so powerful, then why are some children doing worse, IQ-wise, post-adoption? Fifth, buried in the next to last paragraph of the study, we find this statement: This study shows that stability for rank can be found following a marked environmental change after 4 years of age regardless of the SES of adoptive families. The factors explaining this stability are undoubtedly different from those explaining the gains in mean IQs. Interpretation: the worst performers before the adoption tended to be the worst performers after the adoption. The only thing that happened was a linear transformation of scores (i.e., post-score ≈ a*pre-score + b) across all SES groups, which could be due to many things, including: changing IQ scales and/or many years of living in an "average expectable environment." So, what we end up with is a picture much more complex and intricate than Kirp allows. What we can definitely conclude is that abusing or neglecting your children so bad that the government has to take them away tends to produce lower IQs (although some kids will still be in the average range), but was this really in question? What we can also conclude is that for some children in the MR range, adoption into high SES environments will not significnalty improve thier IQ. If the environment is so powerful to change cognitive abilities, then how did this happen? Last, I think we can conclude that Kirp's attempt to glorify the ability of the environment to change IQ is not much more than the wheel, reinvented. [1.] I did it using the bootstrap feature in AMOS. I can go into more detail by email or in the comment box.
Thursday, July 27, 2006
That northern Europeans are different from southern Europeans, that Ashkenazi Jews are more like southern Europeans than northern Europeans, and that Finns are really strange. From this paper, European Population Substructure: Clustering of Northern and Southern Populations. Of course, this is Jaakko Tuomilehto. Anyway:
This is in PLOS Genetics, so you can read the whole thing for free. Do so. And then comment! (via Dienekes)
Of course, you knew this, but now so do others.
TangoMan Adds: See the related post - Intelligence in UK declining?
Steve has already reported on the issues that New Jersey State Police are having with an ever rising number of women and minority applicants who are applying for positions but who are disproportionately failing the background checks, physical exams and written tests. But what happens when some of these applicants do pass the tests? Another case of a woman officer being overpowered by a handcuffed suspect has made the news:
Also, recall the case of the black police officer who sued for racial discrimination because the police force promoted him beyond his level of competence and his incompetence led to disciplinary action:
Wednesday, July 26, 2006
Allelic introgression between populations:horizontal gene transfer between bacteria. Does it work?
Great juxtaposition of Monty Python storyline with Star Trek clips, but how much time do you think it must have taken to cull through 3 years worth of Star Trek episodes looking for just the right snippets to fit in with the Monty Python sketch? Congratulations to the creators for their imagination and most of all their patience.
Okay, this is my first post, and I must admit it has no interesting science news in it. However, I think many on here will find this funny.
A few days ago I took a look at Mendel's Garden #3, and among the featured posts is a discussion of the work of Japanese biologist Susumu Ohno. He took a part of the gene encoding the large subunit of RNA polymerase II and converted it into music, considering both the base sequence itself and the properties (size and charge) of the encoded amino acids. He thought that this piece sounded like a Chopin nocturne, so he took the nocturne and "reverse translated" it to a DNA sequence. He proceeded to demonstrate that this sequence contains a 160-codon open reading frame (see this site for more), and went on to make lots of philosophical speculations about how DNA sequences and music evolve in the same manner. The probability that any given sequence of 160 base triples would start with a start codon and not contain stop codons is a little less than 1/130,000. However, this could be artificially raised by many orders of magnitude by assigning the start and stop codons to sequences of notes that are very frequent and rare, respectively, in the nocturne, which shouldn't be difficult to find with the right software. Perhaps most interesting is the musician Colin Angus of the group The Shamen, who teamed up with biologist Ross King to create the piece "S2 Translation" containing the full sequence of a serotonin receptor. The program they used for this, called ProteinMusic, is available as a free download. I got the program and tried some random gene sequences, making sure to trim off any bases before the start codon (ProteinMusic doesn't do this automatically). The program went straight through the stop codon at the end of the transcript, calling it "Z". I could not hear any difference in the sound between the actual polypeptide and the 3' UTR. The poly(A) tail was easy to recognize because of its repetitiveness, but that's about it. Someone commented that "It may be possible for somebody who has heard the pattern of a calcium-binding site or an enzyme active site to recognize its occurrence in a novel protein." Yeah right. I doubt 1% of bioinformatics scientists could identify the seven transmembrane helices in that serotonin receptor by ear, something that is typically easy to do by eye using hydropathy plots. This isn't to say that the idea of turning DNA sequences into music isn't neat in a purely fun sense, just that it doesn't do anything for science except maybe increase popularity.
I'm sure many here are familiar with the prairie vole - montane vole story regarding mammalian monogamy. Prairie voles are more monogamous than montane voles. The two types have different distributions of Arginine Vasopressin Receptor 1a (avpr1a) expression in the brain. In a Science paper a little over a year ago, Hammock and Young reported that the DNA upstream of the avpr1a gene in prairie voles contains a bunch of short tandem repeats (STRs), and that the number of these repeats tracked with receptor distribution and with monogamous behavior. They also took a look at the DNA upstream of human, chimp, and bonobos and found repeat elements in common between humans and bonobos (more monogamous) that aren't found in chimps (less monogamous). The implication is that tandem repeats work the same way in primates as in voles, and that polymorphisms here are directly linked to the complex behavior of monogamy. It was a damn fine story, and it's a shame to see it go, but check this PNAS paper out: Mammalian monogamy is not controlled by a single gene. The paper makes two major points:
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