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After you have been in the habit of creationism-watching for a few years you become extremely familiar with all of the usual creationist arguments, half-baked talking points, unchecked assertions taken as obviously true, etc. If you really get into it you learn the creationist movement’s long and specific history, and you learn that whatever form of creationism you are studying at the moment inevitably traces back basically to American protestant fundamentalism, and before that to something sometimes called “naive Biblicism.”*

But there comes a point when you don’t think you can learn anything much new about the creationists. You might stumble on a new mutation of a creationist urban legend or quote mine, or a new bit of creationist history like Dean Kenyon actually being a young-earther despite this fact being carefully hidden by the ID movement for 15+ years. But basically, you don’t expect to find out much that is new.

Well, if you thought you were at this point, you would be wrong. A review article in this week’s Science magazine (with a special focus on behavioral science) shows that scholars can ring out yet another twist in creationism studies.

The PNAS Early Edition webpage has just posted a series of papers from the December 2006 National Academy of Sciences Sackler Colloquium, “In the Light of Evolution: Adaptation and Complex Design,” organized by Francisco Ayala and John Avise. The series of papers, on topics ranging from color vision to beetle horns, is now available (I will post the list below the fold). Eugenie C. Scott (aka Genie) was invited to speak at this meeting about evolution education and the history of opposition to it, and the speakers wrote papers to be published in PNAS and a forthcoming NAS volume.

Genie brought me on as a coauthor on the paper she was asked to write. This became:

The Discovery Institute’s Casey Luskin is all atwitter about a new web article from German creationist Wolf-Ekkehard Lönnig [1] about how the giraffe is some kind of massive problem for evolution. Major planks [2] include the alleged lack of transitional fossils between the different fossil giraffe genera (never mind that creationists elsewhere typically accept that the differences between mammalian genera are small, and put the “created kind” or “basic type” at a higher taxonomic level), some confusion about whether one of the giraffe vertebrae is cervical or thoracic or something in between (note to creationists: read about homeotic shifts), and the allegation that there is no evidence for a feeding advantage for tall giraffes, relying on the fact that male giraffes are taller than female giraffes and a 1996 paper in American Naturalist (Simmons & Scheepers 1996, “Winning by a Neck: Sexual Selection in the Evolution of Giraffe”) that attempted to buck conventional wisdom and suggest that sexual selection was the cause of long necks in giraffes.

Sadly, the last plank is particularly bogus, since it completely ignores and displays no knowledge of a massively relevant and quite brilliant paper, published just back in January 2007 in American Naturalist, that constitutes an experimental demonstration of the relative feeding advantage of giraffe height:

A little more than a week ago, word went around our circles here at The Thumb regarding a paper published on Public Library of Science on the use of the word evolution in medical journal articles. In essence, the authors compare the use of the word evolution in articles written by and published in journals generally read by evolutionary biologists versus physicians. Unsurprisingly, the evolutionary biologists mentioned evolution more by name, even if both groups appealed to the same concepts. Why physicians don’t use the word evolution to describe implications or the concept of evolution is the issue.

Other authors (PZ Myers, Orac, and Sequiteur, among others) have dealt with the topic, but it hasn’t appeared here on PT yet, so I thought I’d just ditto Orac’s opinion with a few thoughts of my own. Find them below, after the jump.

The control and eventual eradication of the smallpox virus from the wild is one of the most heralded success stories in all of public health. Indeed, smallpox has played a central role in the history of vaccination. Even prior to Edward Jenner’s use of the related cowpox virus to protect against smallpox disease, it was known that inoculation with materials from an infectious smallpox pustule or scab (dubbed “variolation”) could protect an individual from death due to smallpox, generally resulting instead in a mild form of the illness. Jenner’s observation that milkmaids seemed to be protected from the disease–and his use of material from cowpox pustules instead of smallpox–resulted in the development of the science of vaccination. World-wide use of the smallpox vaccine, along with a mass vaccination campaign led by the World Health Orgainzation, resulted in the end of naturally-occurring smallpox on the planet, with the exception of stores of the virus held in the United States and Russia.

This feat is being attempted currently with measles and polio viruses, but it’s been much more difficult, and eradication of these viruses may never be attainable. Below, I discuss some aspects that are critical to a campaign that seeks to eradicate a disease, and a new paper on the evolution of smallpox viruses.

(Continued at Aetiology)

Science magazine has just published the results of international polls assessing public acceptance of evolution around the world: Jon D. Miller, Eugenie C. Scott, and Shinji Okamoto (2006) “.” Science Aug 11 2006: 765-766 (Supporting Online Material)

The results are at left. Only one country beats the U.S. in the race to the bottom: Turkey, probably the only country in the list with more severe fundamentalism vs. modernism issues than the U.S. But the people in the U.K. can take heart – a BBC poll this spring (which was widely cited by creationists to support the idea that U.S. antievolutionism is not weird), said that less than half of Britons went for evolution. That result is strongly contradicted by this survey, where the U.K. ranks near the top in accepting evolution (as well they should, Darwin is on the money there).

I wrote here that pili–long, filamentous surface molecules involved in adhesion and bacterial “sex”–had recently been discovered in gram positive organisms; pecifically, in group A and B streptococci (Streptococcus pyogenes and Streptococcus agalactiae, respectively), using a genomics approach. Though this publication is quite recent, this is a fast-moving area of research, as evidenced by two new papers which extend this earlier research into pili in the group B streptococcus (GBS).

(Continued at Aetiology)

Listeria monocytogenes is a gram-positive, rod-shaped bacterium. It can be found in the environment as a soil inhabitant. However, it also can be a frequent contaminant of our food supply. As the latter, the bacterium is a significant public health concern, as it is capable of causing serious infections. Listeriosis (infection with Listeria) causes ~2500 serious illnesses and 500 deaths each year in the United States, and the hardest-hit are those with poor immune systems due to age (the very young and old), other immunocompromsing conditions (such as chemotherapy, organ transplant, or AIDS), and pregnant women. Once ingested, the bacterium is able to cross the intestine and spread throughout the body via the bloodstream, where it can attack organs and cause serious damage.

The very fact that it’s typically an environmental organism (rather than a solely pathogenic agent) likely accounts for some of its virulence and transmission. It’s able to survive a number of environmental stresses, including low temperature and high salt concentrations. Indeed, its ability to grow at relatively low temperatures is one way it evades our efforts to control it: it can grow in food even at refrigeration temperatures.

Listeria is particularly insidious as a cause of fetal death or other complications during pregnancy. Intrauterine infection can lead to preterm labor, spontaneous abortion, stillbirth, or serious–and potentially deadly–infection of the neonate. However, fairly little is known regarding exactly how this condition develops, or the mechanisms that lead to infection of the fetus. It has been thought that the increased susceptibility to infection with Listeria during pregnancy is largely due to a decrease in cell-mediated immunity that occurs as a result of pregnancy. This is a particularly attractive hypothesis for Listeria, which is an intracellular pathogen. A new paper in PLoS Pathogens examines this phenomenon in greater detail, using a guinea pig model of infection.

(Continued at Aetiology)

Those of you who have followed creationism/intelligent design literature over the years have probably felt as if you’re living in an alternate universe sometimes. In that literature, many times it seems as if “up” means “down” and “highly supported by the evidence” means “a theory in crisis.”

You may not have been following the comments to this post on AIDS denial (and lord, I can’t blame you), but if you have been, you’ve seen a similar phenomenon, where it’s suggested that mutations found in RNA viruses are just due to sloppy lab work, essentially blowing off an entire field of research.

This, of course, has implications far beyond HIV. Phylogenetic analyses based on genetic mutations are used to determine relationships for all kinds of organisms–including humans. In infectious disease epidemiology, they can be used to pinpoint the origin of a virus, or to track and predict its spread, as I’ve written about previously. A new paper in Nature uses similar methodology to examine the introduction of influenza H5N1 into Nigeria.

(Continued at Aetiology).

Last fall, Andrea wrote an excellent piece on prions, and how they “contradict century-old biological assumptions and seem to defy the expectations of Darwinian evolutionary theory.” He gives an overview of prions and discusses their potential role in heredity. My interest in them, of course, comes from the diseases they cause. Over at Aetiology, I have a post up discussing a new Lancet paper on the prion disease, kuru, and its potential to act as a model for other human prion diseases (such as “mad cow”). The authors suggest two things: one, that the incubation period of so-called “mad cow” disease may be longer than previously thought, and two, that there may be “waves” of epidemic, determined partly by host genetics.

Sometimes it’s amazing just how little we know about the microbes around us. For precious few microbes, we know a good deal about virulence factors–genes and proteins that, when present, increase the severity of disease either in animal models or in humans (or both). However, much of this research has been done investigating acute infectious diseases, where one is infected, becomes ill, and gets better in the course of a few weeks to a month. Much less is known about factors that affect long-term (or chronic) infection. A recent study addressed one gap in this research, tracking the evolution of the bacterium Pseudomonas aeruginosa in chronically infected cystic fibrosis patients.

(Continued at Aetiology)

It can’t be said often enough that “nothing in biology makes sense except in the light of evolution.” Moving from physical characteristics–color, bone shape, the form of bacterial cells–to genetic characteristics in order to classify organisms–and infer phylogenies–was a giant advance. That the molecular characteristics confirmed what was known using physical characteristics was a breakthrough, and allowed for more sophisticated analyses of organisms that don’t have bones or other easily-observable physical features that allow for simple classification into groups: microbes. I’ve previously pointed out the utility of phylogenetic analysis in tracking the spread of pathogens. A new study on the origin and evolution of HIV employs a similar approach in order to elucidate the history of the virus in Africa.

(Continued at Aetiology).

So, archaea are apparently the topic of the week. While I wrote here about the pathogenic potential of some species of these organisms, a new essay in Nature and a new review in Science focus more on their evolution (and the evolution of the other two domains of life) than any health application.

In the essay mentioned, Norman Pace discusses the eukaryote/prokaryote dichotomy. Currently the archaea are classified as prokaryotes since they, like bacteria, lack a true nucleus. However, molecular sequence analysis has shown that the archaea and eukaryotes are actually more closely related to each other than either group is to bacteria (see figure, from Pace’s Nature essay). As such, nomenclature that places the bacteria and archaea together into a group is misleading.

(Continued at Aetiology)

A new study in the journal Pediatrics suggests that a tonsillectomy may improve the condition of kids diagnosed with attention defecit/hyperactivity disorder (ADHD). I think it’s an excellent case of some true “alternative explanations” for the data that the creationist/ID types often crow about.

Creationists often try to validate their position by saying that both they and mainstream scientists start from the same data, but that creationists use their “Bible glasses” to interpret it, while scientists view it through their “evolution glasses.” In other words, they’re not wrong–it’s just a different interpretation of the same data, and where you end up depends on your initial biases and worldview. Though this is bogus when it comes to creationism, there are indeed real debates in the literature, where two hypotheses may be similarly compelling.

(Read more at Aetiology)

For once, I’m not the one writing the microbiology/evolution convergence stuff. Over at Mike the Mad Biologist, check out his post discussing Viruses, phylogeny, and Venezuela, discussing how phylogenetic analysis is used to track the evolution of Venezuelan equine encephalitis virus. As Mike notes, “This study is a really good example of how biologists use evolution to understand structure and function.”

On Aetiology, I have a discussion running about certainty, and the “I know what I know; do not confuse me with the facts” mentality that many of you accustomed to dealing with IDers/creationists will recognize.

It seems I may have spoken too soon. Quoting myself:

One historical event that has been the subject of much speculation over the decades has been the Plague of Athens, a mysterious outbreak that is thought to have changed the direction of the Peloponnesian War, and for which the cause still remains uncertain.

This plague has been attributed to bubonic plague, toxic shock syndrome and/or necrotizing fasciitis due to Streptococcus pyogenes or Staphylococcus aureus, Salmonella, yellow fever, malaria, Ebola, influenza, and smallpox, to name just a few. Typhus seems to fit the description best, but it’s likely that a cause will never be known with certainty.

Little did I know when I posted that on my old blog (just last month!) that a study had already been accepted to the International Journal of Infectious Diseases suggesting that it’s not typhus (caused by Rickettsia prowazekii), but typhoid fever (Salmonella enterica serovar Typhi) that appears to be the cause of the plague.

(Find out how over at Aetiology)

…be prepared to take some disinfectants along for the ride.

One thing that is a total geek-out for me is reading about ecology. It’s one of the areas I wish I’d taken more coursework on back in college. At the time, it didn’t much interest me–studying species interactions was boring, and molecular biology was much more interesting. I’ve pretty much flipped 180 degrees on that one. (Well, molecular biology isn’t boring, but it’s moved off its rung as a top interest). My main interest as far as ecology is concerned is microbial ecology–especially of the ecosystem we like to call human beings. I’ve discussed bacterial ecology a bit previously (see here, here, and here, for instance), and a new study is once again making us reconsider what we know about our own personal microbial flora.

A new study published in PNAS examined microbial diversity in an unusual place–the human stomach. Though it’s now accepted that bacteria such as Helicobacter pylori can live in the stomach (and cause ulcers), the image of the stomach is still a pretty sterile place: too hostile to harbor much bacterial diversity.

Well, maybe not.

(Continue reading at Aetiology)

Microbial ecology, and its relation to the development of infectious disease, is an ever-growing field of study. Of course, there are a vast number of bacterial species living amongst us, most of which do not cause us any harm. Others may infect us only when, so to speak, the stars align in a certain manner: when a number of factors collide that result in the development of a diseased state. For instance, we may already be immunocompromised due to the presence of another infection—something minor, such as a rhinovirus, or something more serious, such as HIV—and this chink in our armor allows another organism to more easily infect, and potentially damage, us.

Other agents in the environment also play a key role in the ecology of potentially pathogenic microorganisms. A recent study in Science highlighted one of these that appears to play an important role in the ecology and evolution of Vibrio cholerae, a major human pathogen of the past several centuries.

V. cholerae is the bacterial agent of cholera, a deadly water-borne disease. The bacterium itself is somewhat of a boomerang or kidney bean shape, and can be found in a number of aquatic environments of varying salinity. Cholera has killed millions over the past 200-odd years, frequently re-appearing in pandemic form after initially emerging from India in the early 1800s. Infection with the bacterium can lead to severe gastrointestinal problems, and the production of copious amounts of “ricewater stool”–even worse than it sounds, from what I understand. Death is generally due to severe dehydration. It’s also a bacterium that has played a key role in the development of the very science of epidemiology. John Snow, considered the “grandfather” of epidemiology, became famous for tracing a 1854 outbreak of cholera in London to a contaminated well, introducing the basic principles of epidemiology along the way.

More recent research has shown that in nature, the bacterium uses the polymer chitin as both a food source and an anchor. Chitin is the second most common polymer on earth (beaten only by cellulose), and is the most abundant in the marine environment, where V. cholerae thrives. Chitin can be found in a number of diatoms, in the exoskeletons and fecal material of arthropods, and in fungi, just to name a few sources.

(Continued at Aetiology)

A class of bipolar neurons, known as Von Economo neurons (VEN), are found in layer Vb of human neocortex. VEN morphology is very simple: they have a large apical dendrite as do cortical pyramidal neurons but lack the collection of basal dendrites. They possess the high-volume, elongated cell body that is typical of fast-conducting projection neurons, and preliminary tract-tracing indicates that they are such, although the array of their projections has not been elucidated. Interestingly, VENs are found in a select few cortical areas that receive inputs from numerous brain regions; the fronto-insular cortex (FI) and anterior cingulate cortex (ACC). Thus, VEN morphology and anatomical location suggest that these cells are positioned to receive an array of diverse information in parallel and then compress it for speedy processing.

Continue reading at Neurotopia…