Wednesday, November 30, 2005 

"Face/off"...and back on again

Doctors in France perform partial face transplant
Okay, so it's not quite Travolta/Cage switching places, but it's a start.
French doctors on Wednesday claimed a world-first partial face transplant, saying a nose, lips and chin were grafted onto a 38-year-old woman disfigured by a dog bite.

The woman was in "excellent" condition and that the transplanted organs look "normal," the statement said. She wants to remain anonymous, it said.

Dr. Jean-Michel Dubernard, one of the surgeons who collaborated on the transplant, told The Associated Press when reached Wednesday that the transplant was the world's first of its kind.

Scientists elsewhere have performed scalp and ear transplants in the past. However, the claim is the first for a mouth and nose transplant. Experts say the mouth and nose the most difficult parts of the face to transplant.

The woman was disfigured by a dog bite in May that made it difficult for the woman to speak and chew, the statement said. Such injuries are "extremely difficult, if not impossible" to repair using normal surgical techniques, it added.

The organs were taken from a donor who was brain dead, with the family's consent, the hospitals said.

I'm a big advocate of organ donation, but I wonder if this would creep me out a bit if I was the donor's family. I'm curious how much she'd resemble the donor from the nose-down? I'd assume her own bone structure must play a part in that, so that it's not exactly the same as the donor. I hope they show some pictures once she heals. Since it's only the bottom half of her face, they could easily block out the top portion to conceal her identity.


Just following the cool kids...

PZ has a post up today wondering about international visitors and left/right leaning tendencies. His blog received about 57% of its visitors from the U.S., compared to the "right-leaning" blog that was compared, Powerline (94% U.S.). Mine is in the middle, with 30% international:

Just for the record, and all.

(Oh, yeah, and I totally knew my sitemeter could do that before today. Not clueless at all, nope, not me...)


Check out Tangled Bank #42

A new Tangled Bank is up at Dogged Blog, and it is giant and awesome. First, the host herself is a writer about veterinary medicine--interesting to me since I work with zoonotic diseases (diseases that are transmitted between species) and work with veterinarians myself quite a bit. Beyond that, there are a ton of great posts. I'm adding Science and Politics to my blogroll right now, just 'cause he's a disease geek like I am, as evidenced by his post about his love of malaria. Same goes for Christie at Dogged Blog, actually:
One of my favorite subjects is disease. I was happy to get so many submissions about sickness and plague and pestilence. It may be that I'm not a well woman, but it seems I am in extremely good company.
Obviously I'm biased, but I agree.

One final post to highlight: this gem from bootstrap analysis about judging a middle school science fair (hilarity ensues). I also judge a few of these every year, so the comments were familiar, but if you've not been to one of those since you were a middle-schooler yourself, stop by and see what the kiddos are up to. I guarantee a chuckle.

Tuesday, November 29, 2005 

Berenstain Bears co-creator, Stan Berenstain, dies

Link to CNN story.
Stan Berenstain, who with his wife created the popular children's books about the Berenstain Bears, has died.

In more than 200 books, the Berenstain Bears, written and illustrated by Stan and Jan Berenstain, helped children for 40 years cope with trips to the dentist, eating junk food and cleaning their messy rooms.

The first Berenstain Bears book, "The Great Honey Hunt," was published in 1962. The couple developed the series with children's author Theodor Geisel -- better known as Dr. Seuss, then head of children's publishing at Random House -- with the goal of teaching children to read while entertaining them.

I know a post about a children's book author may seem out of place on a blog mostly devoted to science issues, but I read tons of Berenstain Bears book when I was a tot, and I now have a bunch more for my own kids. They actually have a number of books with a science theme:

The Berenstain Bears' Big Book of Science and Nature
The Berenstain Bears' Science Fair
The Berenstain Bears on the Moon
The Berenstain Bears Don't Pollute
The Berenstain Bears and the Missing Dinosaur Bone
The Berenstain Bears: Brother Bear Loves Dinosaurs (for really little tykes)
Heck, even one now for the information age: The Berenstain Bears Lost in Cyberspace

Plus, they had a woman doctor, back before Barbie taught girls that "math is hard."

I wonder sometimes how much books like these and many others shaped my early interest in science. When I was a bit older, I loved Nancy Drew mom had probably 25 of them from when she was young. I'd always buy the Encyclopedia Brown mysteries from the book club in elementary school. I used to read encyclopedias, too, and now that everything is online, it's rare to even find an actual set of those. As an older child, I graduated to science fiction and "classic" literature, but I could never get into anything too romantic and stereotypically "girly." And today, I've definitely benefited from all that reading and varied interests from my childhood. My daughter is at that age where she's starting to read more independenly--I hope she learns to love it as much as I do. Thank you, Mr. Berenstain.


Grand Rounds 2.10

Best of the medical blogosphere is up and runnin' at "Over my med body" (great title!) with a Thanksgiving theme. Ones that drew my attention: antimicrobial chewing gum on the Biotech Weblog; a discussion on the issues related to VBAC (vaginal birth after Cesarean) at Red State Moron; Polite Dissent discusses a pet peeve of mine as well: ridiculous headlines; Catallarchy has more on the autopsy of HIV-denier Christine Maggiore's daughter, Eliza; and Orac lays the smack-down on chelation therapy for autism.

Additionally, it was noted that applications are being accepted for the 2005 Medical Weblog Awards. Nominate your favorite blogs in the following categories and spread some love around:
-- Best Medical Weblog

-- Best New Medical Weblog (established in 2005)

-- Best Literary Medical Weblog

-- Best Clinical Sciences Weblog

-- Best Health Policies/Ethics Weblog

-- Best Medical Technologies/Informatics Weblog
Finally, my career prospect if I don't get tenure. DB reports on a trend in drug reps: hiring former cheerleaders. Bet it pays better than academia, too.


Super-sized needles

I suppose there are stories about obesity every day, but this one caught my attention after just posting about watching "Supersize Me:"

Fatter rear ends are causing many drug injections to miss their mark, requiring longer needles to reach buttock muscle, researchers said on Monday.

Standard-sized needles failed to reach the buttock muscle in 23 out of 25 women whose rears were examined after what was supposed to be an intramuscular injection of a drug.

Two-thirds of the 50 patients in the study did not receive the full dosage of the drug, which instead lodged in the fat tissue of their buttocks, researchers from The Adelaide and Meath Hospital in Dublin said in a presentation to the annual meeting of the Radiological Society of North America.

Besides patients receiving less than the correct drug dosage, medications that remain lodged in fat can cause infection or irritation, researchers Victoria Chan said.

23 out of 25 women?? That seems too high.

I have a love/hate relationship with stories like this. Love 'em because I enjoy reading about any new findings, but hate 'em because, since this apparently was just a conference abstract, I can't comment further on the methods. Was this some kind of population that was more likely to be obese anyway? Even if you figure that 65% of the population is overweight or obese, they found that 92% of the women in their population had too much ass fat to be able to use a regular needle. It could very well be simply a sample size effect--25 ain't much of a population to generalize from. But still, it's baffling to think that only 8% of those patients received the correct dosage of drug. Shouldn't this have been noticed before?

Monday, November 28, 2005 

It’s a small world, after all

Have you ever wondered how Kevin Bacon and the lights of fireflies related to malaria and power grids? I know it’s something that’s kept me up many a sleepless night. One word: interconnections.

Many of you have probably heard of the “Six degrees of Kevin Bacon”game. This is based on the work of Stanley Milgram beginning in the 1960s, and brought up again more recently in a 1998 Nature paper, "Collective Dynamics of ‘Small-World’ Networks,” by mathematicians Watts and Strogatz. Milgram conducted a number of studies using his “lost letter technique,” in which letters were sent out and then needed to be forwarded onto reach their destination. In one instance, Milgram sent out 160 letters to individuals in the midwest, with instructions to pass them along to acquaintances who would be most likely to reach his stockbroker friend back east. Almost all of the letters that reached the stockbroker did so via one of 3 friends, and most did it within 6 steps--hence the “six degrees of separation” idea. Similarly, Duncan Watts first became interested in the “small world problem”—the idea that all of us are more closely connected than we realize—after watching fireflies flash in synchrony, and wondering how they accomplished that. What Watts, Strogatz, Milgram, and others were investigating boiled down to a series of links in a network—hubs and connectors. As Watts and Strogatz showed in their 1998 paper, all it took to make a "small world" from a regular network was the addition of a few "short cuts" (see figure from their paper, above). This elegant and seemingly simple structure of networks explains not only connections between movie stars and scientists but also cellular metabolism, ecology webs and the World Wide Web itself.

Another “small world” phenomenon is disease transmission. Social architecture affects, and explains, factors that impact the spread of disease—the people we are in contact with, and in the cases of sexually transmitted diseases, the people we sleep with. At the base of this phenomenon in infectious diseases is an idea called the "tipping point." This is something epidemiologists have discussed much in recent months regarding the potential of an avian influenza pandemic—tiny influences can have startling effects. A simple mutation may make a virus more easily transmitted between humans. Given the right environment, this may allow the virus to sweep through a population, causing a world-wide outbreak. Under different conditions, it may cause a few infections and fade away; a few factors may make all the difference. Mathematical modelers can examine these factors in computer simulations in order to determine if a disease will burn out, remain endemic in a population, or become an epidemic. A critical determining factor affecting these outcomes is the basic reproductive rate of a disease (R0). If R0 is less than 1 (each case infects less than one additional individual), a self-sustaining epidemic is not possible. If it is equal to 1, the disease will become endemic in a population. If R0 exceeds one, the disease may become epidemic; the larger the number, the more likely this outcome is. But, while this number is useful, one must keep in mind that R is an average over the population—it may be much higher or lower in subsets of the group.

Early work in this area did not take this difference into account, and assumed that individuals in a population had an equal chance of transmitting the disease. However, reality does not bear this out, leading to the proposal of the "20/80 rule," which suggests that approximately 20% of the most infectious individuals are responsible for 80% of the disease transmission. This was most recently demonstrated by an analysis of the 2003 SARS outbreak (see figure, from MMWR 52(18);405-411), but has also been seen with AIDS and other STDs. With AIDS, we recognize that "core groups" of infected individuals are often responsible for large outbreaks of disease. What we see when we examine this graphically is a "small world" network: a series of hubs and connectors, with the largest hubs—-termed "superspreaders" (the numbered dots in the picture above)--responsible for a disproportionately large number of secondary cases. This may be due to the fact that the superspreaders simply have a higher number of contacts; they may have a co-infection that leads to increased pathogen shedding, meaning the contacts they have are more efficiently exposed; they may have an undiagnosed illness, leading to an extended period of transmission; or they may have a combination of the above. For example, imagine a sex worker with both HIV and a secondary STD, such as gonorrhea. By virtue of her occupation, she will be in contact with a large number of individuals. HIV may lead to an increase in bacterial load, exposing her clients to a larger dose of N. gonorrhea than the "average" infected person; and her lack of health care means she has been treated for neither STD—potentially spreading both for years, until she is too sick to continue working. In this case, there are multiple explanations for why she would be a superspreader.

It takes careful epidemiological analysis to identify these superspreaders, however. One limitation of epidemiological analysis is that populations are generally divided into homogeneous subgroups--people of the same age, or race, or occupation, etc. This makes it possible to carry out studies comparing groups of individuals, but at the same time, it creates false divisions; life is always messier. A new paper published in Nature seeks to investigate some of this "mess," addressing the heterogeneity of transmission number among individuals and its effect on spread of disease. This new study by Lloyd-Smith et al., instead of using R0, investigates ν, the individual reproductive number. To examine this, they looked at previously published accounts of disease transmission where contacts had been traced, and determined ν for a number of different diseases and patients (see figure, below).

To sum up their findings, they suggest that disease with a high variation in ν show infrequent, but explosive, epidemics after introduction of a single case, a statement again borne out by an examination of the epidemiology of SARS, a disease which showed a high variation in ν. Indeed, many cities were exposed to SARS, but very few had explosive outbreaks. Is this universal? It will take more careful studies to determine that, but it suggests a new avenue of investigation.

Indeed, knowledge of the architecture of these outbreaks has immediate real-world applications. If the superspreaders could be identified early in an outbreak, interventions (vaccination, isolation/quarantine, treatment) could be targeted to this group. For example, another recent report highlights this same conclusion for malaria: identifying and targeting the superspreaders could reduce the disease burden enormously. Additionally, this work suggests, again, that we need better surveillance in order to detect these events while they are in progress. We can’t control superspreaders that we aren’t aware of, or only identify retrospectively, weeks, months, or years down the line.

Finally, this work—and indeed, much of the work done in the field of network theory--also points out, again, how things that appear to be “designed” can be the product of chance and circumstance. Each of these “small worlds” reveals a very similar architectural design. Each is dominated by hubs—a few extremely well-connected individuals, or web sites, etc. Additionally, this is not merely a qualitative difference: instead, they have a specific mathematical signature, which is nearly identical from one network to the next. I won’t go into the details, but Mark Buchanan has written a very layman-friendly book on the subject. (To be complete, Watts and Strogatz have also written books on the subject, but I've not read them yet). In Nexus, Buchanan notes:

What we see then is a kind of natural order that for mysterious reasons seems to well up in networks of all kinds and that does so despite the complexities of their individual histories….In biology, Charles Darwin’s idea of evolution by natural selection offers an extremely powerful organizing framework within which historical accidents take place. In the context of networks, there must also be some deeper principle at work.
Along a similar line of thought, Nobelist Herbert Simon once said, “The purpose of science is to find meaningful simplicity in the midst of disorderly complexity.” Network theory has shown how this can be done, and unlike “intelligent design,” has immediate practical applications in a vast range of fields.


China--being as forthcoming as they claim?

Saw this while I was away, but wanted to find out more details. Reports had surfaced that China was covering up H5N1 cases. The initial ProMed email report:

Dr. Masato Tashiro, a Japanese WHO consultant, believes that China has had 300 human deaths from avian influenza and is hiding the true extent of the disease from the rest of the world. Dr. Masato Tashiro, Director of the WHO Collaborating Center on Influenza at the National Institute of Infectious Diseases, Tokyo, and head of the Department of Virology of the National Institute of Infectious Disease (Japan), astonished colleagues with this information during a speech at a recent retirement dinner for a fellow virologist, Hans-Dieter Klenk.

Having just returned from the Hunan province of China on behalf of the World Health Organization (WHO), [Dr. Masato Tashiro] claimed that a reliable source had provided him with details of the true nature of the H5N1 virus in China. "We are systematically deceived," he is reported to have said.

Tashiro visited China on behalf of the World Health Organization (WHO) in Hunan province. His laboratory, at the National Institute for Infection Research in Tokyo, as one of the Asian points of contact for the United Nations, had been particularly entrusted with investigations into avian influenza in Asia and China. Dr. Masato gave his lecture in the University of Marburg Clinic before some the most outstanding virologists in the world and shocked the meeting with his unauthorized data [report] from inside China.

The Japanese virologist [said he] firmly believes in the reliability of the source and its data. The secrecy of the Peking government is still causing concern as it was at the beginning of the SARS epidemic disease, complained Tashiro. At least 5 medical co-workers who should be reporting on the situation in the provinces were arrested, and [other] publication-willing researchers were threatened with punishments [he said].
A kind-of denial was then issued (see here), but the situtation still lacks clarity. Given China's population, agriculture practices, and past history of being, err, less than forthcoming when it comes to releasing information about disease to international authorities, this doesn't bode well, even if Dr. Toshiro's comments were played up or misunderstood.



Well, this past week has been interesting. I traveled back to Ohio early to throw my sister a baby shower, then stayed with my in-laws over the Thanksgiving weekend. Saturday night my husband and I ended up watching most of "Supersize Me." My husband's reaction to the film: "I'm hungry for a Big Mac." As a public health professional, this made me weep. At least I've edumacated him about many issues in infectious disease epidemiology; guess I must now move on to nutrition epi.

Saturday, November 26, 2005 

More microbial tools

I mentioned a real "microbial machine" in this post last month. Now, they're appearing as living photographs:
Researchers at the University of California, San Francisco and the University of Texas announced in the journal Nature that they had created photographs of themselves by programming the bacteria — — best known for outbreaks of food poisoning — to make pictures in much the same way Kodak film produces images.


Voigt and colleagues took from algae light-sensitive genes that emit black compounds and spliced them into a batch of E. coli bacteria. The organisms were then spread on a petri dish that resembles a cookie sheet and placed in an incubator. A high-powered projector cast photographic images of the researchers through a hole on top of the incubator, exposing some of the bacteria to light.

The result: Ghostly images like traditional black-and-white photographs of the researchers responsible for the invention, at a resolution Voigt said was about 100 megapixels, or 10 times sharper than high-end printers.
Nature paper (vol 438, 441-442):

Synthetic biology: Engineering Escherichia coli to see light

Anselm Levskaya1, Aaron A. Chevalier, Jeffrey J. Tabor, Zachary Booth Simpson, Laura A. Lavery, Matthew Levy, Eric A. Davidson, Alexander Scouras, Andrew D. Ellington, Edward M. Marcotte and Christopher A. Voigt

Abstract:We have designed a bacterial system that is switched between different states by red light. The system consists of a synthetic sensor kinase that allows a lawn of bacteria to function as a biological film, such that the projection of a pattern of light on to the bacteria produces a high-definition (about 100 megapixels per square inch), two-dimensional chemical image. This spatial control of bacterial gene expression could be used to 'print' complex biological materials, for example, and to investigate signalling pathways through precise spatial and temporal control of their phosphorylation steps.
Very cool stuff. The MSNBC article discusses a bit of the ethics behind it (the ubiquitous "bioterrorism applications" and such), but those fears have been applied to essentially every advance in technology probably since fire. ("Put it out, Snog! That may be used against us someday!")


Influenza series from LiveScience

As the start of the influenza season is upon us, LiveScience has done a 3-part series on the virus, the disease, and the pandemic potential.

Part One: A guide to the biological basics of influenza and its effects

Part Two: Defending yourself against the flu. Vaccines and healthy habits keep harmful viruses at bay

Part Three: A pandemic primer.

Friday, November 25, 2005 

Could arsenic poisoning have led to the development of Chilean mummification techniques?

Living in the harsh desert of northern Chile's Pacific coast more than 7,000 years ago, the Chinchorro fishing tribe mysteriously began mummifying dead babies — removing internal organs, cleaning bones, stuffing and sewing up the skin, putting wigs and clay masks on them.

The Chinchorro mummies are the oldest-known artificially preserved dead, dating thousands of years before Egyptian mummies, and the life quest of the archaeologists who study them is to discover why this early society developed such a complex death ritual.

"I was reading a Chilean newspaper that talked about pollution and it had a map of arsenic and lead pollution, and it said arsenic caused abortions. I jumped in my seat and said, 'That's it,'" Arriaza said.

Arriaza says high levels of arsenic in the water in the region, which persist to this day, meant more premature births, stillbirths, spontaneous abortions and higher infant mortality among the Chinchorro.

"We've always known that the Camarones (the area where the mummies are found) had a lot of arsenic, and the first mummies were children," he said.

He posits the Chinchorro began preserving dead babies to express personal and community grief and later began mummifying adults as well, and the practice became more elaborate.
Interesting how something as seemingly minor as a trace chemical in the water could have led to a cultural revolution.


Only in America...

...could a man as incompetent as Michael Brown turn lemons into lemonade, by starting a consulting company on disaster preparedness.
“If I can help people focus on preparedness, how to be better prepared in their homes and better prepared in their businesses — because that goes straight to the bottom line — then I hope I can help the country in some way,” Brown told the Rocky Mountain News for its Thursday editions.

Brown said officials need to “take inventory” of what’s going on in a disaster to be able to answer questions to avoid appearing unaware of how serious a situation is.

Boy, I hope he's going to provide more pearls of wisdom than that. According to the article, "companies already have expressed interested in his consulting business." Hey, companies considering hiring Mike Brown--I have actual experience and education in this area, and I work cheap! I'll even throw in a money-back guarantee: no disasters bigger than the one Brown made of Katrina.

(Seriously, though, someone please tell me this is a joke...please?)


Followup to "dragons and microbes" post

I discussed here new research on venom evolution that topples some old conventional wisdom. It seems this and another study are already making large waves in that field.

Genealogy of Scaly Reptiles Rewritten by New Research
The most comprehensive analysis ever performed of the genetic relationships among all the major groups of snakes, lizards, and other scaly reptiles has resulted in a radical reorganization of the family tree of these animals, requiring new names for many of the tree's new branches. The research, reported in the current issue of the journal C. R. Biologies, was performed by two biologists working at Penn State University: S. Blair Hedges, professor of biology, and Nicolas Vidal, a postdoctoral fellow in Hedges' research group at the time of the research who now is a curator at the National Museum in Paris.

Vidal and Hedges collected and analyzed the largest genetic data set ever assembled for the scaly reptiles known as squamates. The resulting family tree has revealed a number of surprising relationships. For example, "The overwhelming molecular-genetic evidence shows that the primitive-looking iguanian lizards are close relatives of two of the most advanced lineages, the snakes on the one hand and the monitor lizards and their relatives on the other," Vidal says.

"We gave this group the new name, 'Toxicofera' because of another discovery, reported in a related paper, that some lizard species thought to be harmless actually produce toxic venom, as do some snakes--including some large monitor lizards in the same family as the giant Komodo Dragon and some large species of iguanians." Vidal, Hedges, and other researchers report this and other discoveries about the early evolution of the venom system in lizards and snakes in a paper led by Bryan G. Fry, of the University of Melbourne in Australia, published in the current issue of the journal Nature. "It's a really startling thing that so many supposedly harmless lizards actually are venomous," Vidal comments, "but their sharing of this characteristic makes sense now that our genetic studies have shown how closely they are related."

This is a great example of how science works. Important new findings have come to light, and the rest of the evidence is re-examined in that light, to see what stays and what thinking may need to be revised. No one expects it to happen overnight, and a call is put out for others to investigate and test the new conclusions:

"Because the current tree has been widely accepted for nearly a century, I think there is going to be a delay of maybe a few years before the general scientific community gets used to the new tree," Vidal says. "If other research groups working in this area find the same pattern with additional genes, then I believe the scientific community may accept these results more quickly."

Note how there are no politics involved, no pressure to teach these new results. The investigators are confident enough in their own data that they can wait for other scientists to examine it, express skepticism, test it themselves, and add their own conclusions to the scientific literature. It may take several years, but if the data stand up and are repeated by others, the way students are taught *will* change--not because anyone was lobbied to do so, but because the evidence is strong and it would be folly not to acknowledge that. I look forward to following this in the coming years.

Tuesday, November 22, 2005 

Flu and asymptomatic infections

I've mentioned many times on here reservations I have over the current avian flu numbers--how many subclinical or mild infections are being missed? Are they indeed offset by the number of serious disease cases we're also missing? There's a reason for these questions, and it's now out in electronic form in Clinical Infectious Diseases.

A bit of background. I work in Iowa as part of the Center for Emerging Infectious Diseases. One of our pet pathogens happens to be influenza virus, and we have ongoing studies looking at serological evidence of prior infection with swine and avian viruses in people who are exposed to these animals. This current paper looks at a cross-section of people who are in several of these groups: swine farmers, veterinarians, and meat-processing workers. The results:

Using multivariable proportional odds modeling, all 3 exposed study groups demonstrated markedly elevated titers against the H1N1 and H1N2 swine influenza virus isolates, compared with control subjects. Farmers had the strongest indication of exposure to swine H1N1 virus infection (odds ratio [OR], 35.3; 95% confidence interval [CI], 7.7–161.8), followed by veterinarians (OR, 17.8; 95% CI, 3.8–82.7), and meat processing workers (OR, 6.5; 95% CI, 1.4–29.5). Similarly, farmers had the highest odds for exposure to swine H1N2 virus (OR, 13.8; 95% CI, 5.4–35.4), followed by veterinarians (OR, 9.5; 95% CI, 3.6–24.6) and meat processing workers (OR, 2.7; 95% CI, 1.1–6.7).

To boil it down a bit, farmers were about 35 times more likely than the control group to react positively to the swine H1N1 virus used--indicating they'd been previously exposed. Similarly for the swine H1N2 virus--13 times more likely. It appears there is a good deal of zoonotic transmission occurring in this population--it's just not manifesting with serious clinical symptoms, so we're missing much of it.

This has implications for what's going on in Asia with H5N1 as well. How many sub-clincial or mild infections are there with that virus? We don't know yet--we need good surveillance and seroprevalence studies to address that question. Do these milder infections allow the virus more time to adapt to humans, so that human-to-human spead will become more efficient? We don't know. It's largely a black box at this point. It also is something that's largely been ignored at the response level--do we vaccinate and/or treat these groups early, along with first responders and others? Will doing so prevent a significant number of new infections, protecting not only the human population, but also domestic animals? During the 1918 pandemic, pigs also were susceptible to the virus, and suffered high mortality rates, but this isn't something that's garnered much discussion in the current pandemic plan.

This is just a pilot study, and limitations are discussed in the paper. A prospective study is ongoing, which should be able to pick up seroconversion events. Still, even though this is a small study, it hopefully will be food for thought, and will draw attention to including agriculture workers and others in contact with animals in pandemic response plans.

Edited to add other media coverage:
Des Moines Register
Cedar Rapids Gazette
NIAID press release
IDSA news release


Of dragons and microbes

Carl Zimmer has a post today about the work of Dr. Bryan Grieg Fry on the evolution of snake venom. If that name sounds familiar to those of you who aren't reptile specialists, you may have run across Dr. Fry's homepage, or you may have seen his research profiled previously on Panda's Thumb here, or you may have read comments by the good doc in this thread. Zimmer, as always, has an excellent overview of Fry et al's new paper in Nature (link ), but he didn't emphasize the one sneak peek I received from Bryan.

This tasty bit of information involved monitor lizards, such as the Komodo dragon. The conventional wisdom has been that these lizards kill by infecting their prey with bactera during a bite, featured on many sites such as this one:
[The komodo dragon] can run as fast as a dog for short stretches and prey they merely injure are brought down shortly by the deadly bacteria in their mouths.
and this one:
[The komodo dragon's] saliva is not venomous, but the mouth of a Komodo dragon is so full of bacteria that a bite from one almost always leads to infection. If untreated, the infection is usually fatal.
Only thing is, it's wrong. I can't say how much bacterial infection plays a role in the killing of a komodo dragon's prey, but the research by Fry's group shows that indeed, these lizards are capable of producing venom, via previously undescribed venom glands. (Carl Zimmer has posted a figure from the Nature paper; the komodo dragon is in the Varanidae group).

Previously, it was thought that venom production in snakes and lizards had evolved independently, since the venom glands in these lineages had a different structure. However, using new DNA sequence data, Dr Fry and his colleagues found nine venom toxin types that were shared between lizards and snakes. Seven of these were previously only known from snake venoms, including one that had only previously been reported in rattlesnake venom but was sequenced by the team from the Bearded Dragon. Looks like yet another paradigm-shattering paper; y'know, the kind all the IDists say scientists are so afraid of...


Grand rounds 2.09

This week's grand rounds is up at codeblog. Of particular interest to me is Orac's post, a response to Dean Esmay's post here. Some of you may remember the story of the death of Eliza Jane, whose mother, Christine Maggiore, is a prominent AIDS-denyer. The coroner had listed the cause of Eliza's death as AIDS-related pneumonia; of course, those in the AIDS-denial community scoffed. They had their own "expert" analyze the coroner's report, and they eventually came out with a different cause of death, detailed at Esmay's blog. Orac points out that their alternative version just doesn't add up:

1. A previously completely healthy girl developed PVB19 infection leading to both encephalitis and aplastic anemia (possible, but highly unlikely, and, even if PVB19 were found, it would be far more likely that it was able to cause anemia because of immunosuppression due to AIDS).

2. This same girl also developed an acute allergic reaction to amoxicillin that led to cardiovascular collapse and--oh, by the way--also caused steatosis of the liver within a day after starting the drug, the steatosis being something even Dr. Al-Bayati's own references do not seem to support as being likely.

3. This same otherwise healthy girl had sufficient quantity of P. carinii in her lungs to show up on Gomori methenamine silver staining at her autopsy.

4. The medical examiner and neuropathologist either botched the staining for the p24 protein (or that it was a false positive) and an experienced neuropathologist didn't know the pitfalls of the diagnosis of HIV encephalitis using brain tissue sections.

Other grand rounds posts that caught my eye include this one reminding us that heart attacks are the leading cause of death in women (with a link to the story of a near-fatal heart attack in a 37-year-old woman); posts at Parallel Universes on a connection between antibiotic use and non-Hodgkins lymphoma (and an update), and a rant on Science Creative Quarterly about people who wear their lab coats and scrubs out in public (I don't get that one, either!). Lots of good reading this week.

Monday, November 21, 2005 

Other topics

As I mentioned in the comments, I'm out of town and staying at a site without internet access, so I don't have as much time as I need online this week. As such, there are a few items I'd have liked to expand upon, but am not able to at this moment. So, check out these stories if you have a chance:

Women stay in bed for 60 days ... for science. NASA is carrying out a study on the effects of weightlessness on women. While lounging around in bed for 60 days sounds awesome initially, they are unable to even sit up--exercise is even done on a vertical treadmill. I think I'd go crazy after a few hours.

The lowdown on dog flu. Though of course "bird flu" has been getting all the big headlines, dog lovers have had a lot of questions about this influenza as well. Kim Campbell Thornton smacks down the rumors and puts minds at ease.

Viagra: not just for ED. The drug may increase exercise capacity in patients with pulmonary arterial hypertension.

Finally, Newsweek has an article on Darwin, "science vs. religion," and the new American Museum of Natural History exhibit.


40 million infected with AIDS; but, some good news

The global HIV epidemic continues to expand, with more than 40 million people now estimated to have the AIDS virus, but in some countries prevention efforts are finally starting to pay off, the United Nations says.

AIDS has killed more than 25 million people since it was first recognized in 1981, making it one of the most destructive epidemics in history. An estimated 3.1 million people died from the virus last year and another 4.9 million people became infected, according to a U.N. update published Monday.

However, for the first time there is solid evidence that increased efforts to combat the disease over the last five years have led to fewer new infections in some places, said UNAIDS chief Peter Piot.

Previously improvements had been seen in places such as Senegal, Uganda and Thailand, but those were rare exceptions.

"Now we have Kenya, several of the Caribbean countries and Zimbabwe with a decline," Piot said, adding that Zimbabwe is the first place in Southern Africa, the hardest-hit area, to show improvement.

These are all countries that have invested heavily in safe-sex campaigns and other prevention programs, with the result that prevalence of HIV among the young has declined.

"People are starting later with their first sexual intercourse, they are having fewer partners, there's more condom use," Piot said.

These are key ingredients in the "ABC"s of AIDS, a program first widely used in Uganda. A=abstinence (or delayed sexual experiences), B="be faithful", C=condoms. This simple strategy has resulted in increased awareness of disease transmission, and has resulted in a decrease in the rate of new infections diagnosed--showing just what good sex education and condom availability can do.

However, there is, of course, some bad news as well:
The epidemics continue to intensify in southern Africa. Growing epidemics are under way in Eastern Europe and in Central and East Asia. Five years ago, one in 10 new infections were in Asia. Today the number is one in four or five.

China, Papua New Guinea and Vietnam are facing significant increases. There are also alarming signs that Pakistan and Indonesia could be on the verge of serious epidemics, the report said.

Intravenous drug use and commercial sex are fueling the epidemic in Asia, where few countries are doing enough to inform people about the danger of such behavior, the report warned.

Worldwide, less than one in five people at risk of becoming infected with HIV has access to basic prevention services. Of people living with HIV only one in 10 has been tested and knows that he or she is infected.

That last part is critical. Great strides have been made, but it's not a time to rest on our laurels. Condoms and education have done so much--now we need to work to extend those services into areas where they aren't currently available. We also need to work to have more of those who are at-risk get themselves tested. This is a bit trickier, as there's not only the problem with lack of access to resources, but also stigma that comes from finding out one is HIV-positive. The latter can cause even those who may have access to tests to not take advantage of that--they'd rather not know their status, and thus don't get treatment, and potentially infect others. It's relatively easy to provide supplies; it's much more difficult to provide a shift in the cultural attitudes that will allow HIV+ patients to live a full life even after diagnosis.

Sunday, November 20, 2005 

U of Iowa faculty petition against ID released

...and has spawned some press coverage, here in the Ames Tribune and
in the Cedar Rapids Gazette, making us the first state to have faculty from all Regent universities speak out against intelligent design. I'll briefly address some of the comments.

In the first article, U of I physics professor (and signer of the DI's "Scientific dissent from Darwinism" petition) Fred Skiff elaborates one giant strawman:
"It's part of science to consider what blinders you might be wearing," Skiff said. "Materialists put conditions on science that things can only exist if they satisfy materialism. I think that is a mistake."

He said scientists need to be open to the possibility of God and the idea that the world could be "bigger than their imagination."

"They say that can't be true because it doesn't fit into their conception of the world," he said. "That's not science' that's metaphysics. It's not looking at the world around you. It's closing your eyes and saying that 'Nothing can exist except for things that can fit into my theory.'"

Skiff is using a typical Discovery Institute tactic here, equating accepting evolution with an atheistsic worldview. Too bad it's just wrong. Many scientists are, indeed, "open to the possibility of God." Many even consider themselves evangelic Christians. (Check out the "clergy letter project", where over 9,000 Christian clergy have signed seeking to "preserve the integrity of the science curriculum by affirming the teaching of the theory of evolution as a core component of human knowledge.") But they realize God just ain't something you can investigate scientifically. Additionally, even most scientists who are atheists would admit that there may be more out there--but that's not a question of science, it's a question of personal philosophy. Skiff and others try to conflate the two, despite the fact that science is a field where two people can have polar opposite personal philosophies, and yet still reach the same scientific conclusion using a materialistic *methodological* philosophy. This happens every day, and I'd assume that Skiff's own research also investigates only naturalistic phenomena.
Skiff said he believed the statement is intimidating to he and his colleagues who are open to intelligent design because it institutes the philosophy of materialism as the definition of science.
"They are saying that anyone who doesn't have our point of view isn't a legitimate scientist," he said. "That's coming on pretty strong."
That's just baloney. I don't know Dr. Skiff, and have only seen him once (and was thoroughly unimpressed, described here). He may very well be an excellent physicist, and I don't doubt for a minute he's a "legitimate scientist." I just think he's letting his religious views cloud his judgement in this matter. You can read the petitions for yourself: U of Iowa's; Iowa State's; and U of Northern Iowa's. Nowhere does it say that people who support ID aren't "legitimate scientists." The fact that he (and so many other) ID supporters feel that way is simply their own paranoia.

Speaking of which, from the Gazette article:
He [Casey Luskin of the Discovery Institute] criticized the ISU statement signed by professors opposing intelligent design as a slap at Gonzalez’ academic freedom.

‘‘This is a wonderful development,’’ he said. ‘‘It shows that people opposed to intelligent design are no longer acting like McCarthyites.’’
Again, you can read the ISU statement for yourself. Nowhere is Gonzalez targeted, and nowhere does anyone say Gonzalez can't research ID (not that he is, anyway). It simply says that it ain't science.

Also in the Gazette article:
Gonzalez said Avalos and a few other intelligent design critics have created a hostile environment for him at ISU by circulating the statement and speaking out in the media. But Gonzalez said he thinks many ISU faculty silently support teaching intelligent design as science.

‘‘It would be nice if someone took a poll to find out what the real opinions are,’’ he said.

Gonzalez said intelligent design is still too controversial to teach in high school, except as part of what he regards as the controversy over evolution. He also wouldn’t mandate that anyone teach it either. Partly, he said, because few teachers really understand it.

I find the irony here delicious. He acknowledges that few teachers understand ID. I'd wager this applies to most of the general public as well--they know ID as simply the "goddidit" argument, without a deeper understanding of exactly what ID says. Yet, Gonzalez thinks that many of these same people would "silently support" teaching ID. Does he think the faculty in general are more educated on the issue than secondary school teachers? I doubt it. One professor at ISU whose field is veterinary medicine, when the statement reached his/her department, even remarked that ID was something "for physicists to grapple with." !! They don't realize this is something ID advocates are trying to get into *every* department, by undermining the very nature of science.
Officials at the Iowa Department of Education know of no school districts in the state teaching about intelligent design, department spokeswoman Kathi Slaughter said.
In my opinion, this is the way it should be. Though I think the whole "debate" is largely a waste of time and effort (since there *is* no real "challenge to evolution,") at least here in Iowa it's largely being carried out at the university level, rather than in our secondary schools. Maybe we'll succeed at other states' expense, making Iowa a state of science. Once again, if you're in Iowa and are interested in getting involved, check out our website, or email us at iowascience AT gmail DOT com.

Edited to add: bummer, as noted in the comments, Missouri beat us to the punch.

Edited again to add: I see Dembski is claiming " ID proponents were bypassed" when we circulated this. Not true at all--I don't even know who on the faculty is an "ID proponent" besides the already-mentioned Fred Skiff (and I can't say how it was circulated within the physics department, if it went there at all). It was mostly passed along through word-of-mouth, and generally sent to entire departments or colleges at a time. The idea that we were bypassing certain people on a faculty this large is a joke.

Friday, November 18, 2005 

New malaria vaccine shows promise

Malaria is one of the world's leading infectious killers. World-wide, almost 40% of the world's population is at risk of acquiring this disease--many of them in poor countries with limited resources to control the disease. Each year, malaria causes 300-500 million infections, and up to 3 million deaths--about 5000 Africans die of the disease every day; one child succumbs every 30 seconds. Mosquito-borne, simple devices (such as mosquito nets over beds) have been shown to drastically decrease the incidence of disease. Though these only cost a few dollars each, many in developing countries lack the resources to purchase them. Additionally, evolution, as we often see, has caused both the parasites that cause the disease (one of four species of Plasmodium) and the mosquitoes that transmit it (Anopheles species) to become resistant to our efforts to stop them. The parasites have developed high levels of resistance to many of the anti-malarial drugs, and many insecticides are of little use in controlling the mosquito population due to a similar phenomenon.

Malaria is an ancient disease. Descriptions of malarial symptoms exist in Chinese literature dating back almost 5000 years. The name itself comes from 16th century Italy, meaning "bad air" (the assumed cause at that time). The disease used to be rampant in the United States. During the U.S. Civil war, troops on both sides stationed in the south suffered more than a million cases of the disease. Indeed, malaria was endemic in the southern United States until the 1940s, and continues to be a problem in the U.S. due to "imported" cases. Despite this huge burden of disease, to date, there has been no successful malaria vaccine. This is largely due to problems that arise in trying to target an organism with an extremely complex life cycle (see image, left). 1. Sporozoites in salivary gland. 2. Oöcysts in stomach wall. 3. Male and female gametocytes. 4. Liver phase. 5. Release of merozoites from liver. These enter red cells where both sexual and asexual cycles continue. As you can see, it's a bit of a mess, with different protozoal antigens being expressed at different times throughout the life cycle. What do you target? Which are the most important for immunity?

A new study may have cracked that question. Led by Pierre Druilhe of the Pasteur Institute (link to journal article), investigators focused on a malaria protein--merozoite surface protein 3 (MSP-3)--that prior research had identified as the focus of the immune systems of adults who had proven resistant to the disease.

The team injected an MSP-3-based vaccine into 30 European volunteers who had never had malaria, readministering it after one month and again after four months. Blood samples were taken one month after each injection. These blood samples were then compared to French blood samples from individuals with no immunity to malaria and African blood samples from people with immunity.

Nearly every vaccinated sample produced an immune response to malaria when it was introduced in vitro and 77 percent produced anti-MSP-3 antibodies. Plus, these antibodies proved to be as good at killing the parasite as those from immune adults and, in some cases, better, destroying up to twice as much. "This type of immune response, characteristic of immune adults living in malaria-endemic regions, requires under natural conditions 10 to 15 years of daily exposure to billions of infected red blood cells," Druilhe notes.

They didn't challenge the volunteers with Plasmodium infection to put the nail in the coffin, but they did test it in humanized mice, where it was highly effective. Additionally, they tested the blood of immunized volunteers a year after vaccination, and it still was effective in neutralizing the pathogen. A long-lasting vaccine would be critical, since as mentioned above, resources in these countries are scarce, and frequent boosters would be unlikely.

Malaria vaccine research has also recently been given a "booster" of its own, in the form of a $258 million pledge by the Bill and Melinda Gates Foundation. About 40% of that donation is earmarked for vaccine research. However, while the news seems to be positive in the fight against malaria, we want to use caution. I recently linked a discussion on the evolution of avian influenza virulence. Similarly, a group of scientists published a paper last year suggesting that inadequate vaccines could increase malarial virulence:
Vaccines are designed to protect people by boosting the immune system to kill parasites but, unless a malaria vaccine leads to the death of every single parasite, the ones that survive are likely to be the nastiest.

Initially, the Edinburgh researchers directly injected two groups of mice with infectious parasites - "immunised" mice, which had been exposed to Plasmodium and then treated with the anti-malarial drug, mefloquine, and "naive" mice, which had not. They then transferred parasites via a syringe from host to host 20 times. The parasites thus evolved in the immune or non-immune environments. The parasites that evolved in the immunised mice were more virulent than parasites evolved in the naive mice. Infection was not as severe after transmission through mosquitoes, but the effect was still there. In other words, immunity accelerates the evolution of virulence in malaria, even after mosquito transmission, making them more dangerous to their non-immunised hosts.

Dr. Mackinnon said: "How does immune selection create more virulent pathogens? One possibility is that many parasites die in immunised hosts but those that win "the race to the syringe" - or the mosquito - are probably genetically equipped to stay ahead of the advancing immune system. Since the virulent strains showed no problems transmitting infection to new hosts, it's likely that such strains would spread throughout an immunised population.
This echoes a 2001 warning in Nature magazine by 2 of the same authors, where they emphasize infection-blocking vaccines, rather than vaccines that target the agent once infection has been established. The Druilhe article doesn't cite either of these studies, so I don't know if that's a concern they'd considered or not. However, since they identified this antigen by screening those in Africa who'd been repeatedly exposed *naturally* and were already immune, it seems likely that any increase in virulence due to partial immunity would have already occurred. Overall, this is some much-needed good news in the fight against this devastating infection.

Thursday, November 17, 2005 

The ethics of avian flu response

Josh Braun (a "a card-carrying bioethicist") at Sciencegate, the official editorial blog of Seed Magazine, has posed a number of interesting questions regarding 10 topics in pandemic flu response and preparedness. Topics include many that I've considered, but don't have any definitive answers to, such as:

Is the mainstream media scare-mongering? Or is it providing a public service? If there is an eventual backlash in public support for pandemic preparedness that results in hundreds or millions of bird flu deaths, who is to blame?
and developed nations have the right to stockpile antiviral medications for treating their populations at large in the event of avian flu, when the drugs are best indicated for the control of new avian flu outbreaks - outbreaks that are far more likely to occur in developing nations?

Lots of food for thought over there. I hope our leaders are having similar "what if/what's the right thing to do" brainstorming sessions.


Video time capsule

I first ran across the thylacine (aka "Tasmanian tiger" or "Tasmanian wolf") when I was preparing to teach a summer course on vertebrate zoology for a local Catholic college during grad school. While I'd had a decent amount of organismal biology and zoology as a college undergrad, I was a bit rusty from a few years of only studying organisms lacking nuclei, so I was looking for a quick refresher as well as some interesting topics for final paper assignments for the course. Just announced around that time was a "breakthrough" in the attempt to clone the thylacine, so I introduced that to the class in a discussion of geographic isolation, and had a nice discussion of both the molecular techniques and the ethics of a Jurassic Park-type scenario.

For those of you unfamiliar with this animal, it was, like many Australian mammals, a strange critter. Though it looks like a dog or hyena (hence the nickname "wolf"), it's a marsupial. Thousands of years ago, they were main predators in Australia, until dingoes pushed them out. They stuck around longer in Tasmania, until settlers in the 1800s worked to seal their fate. The Tasmanian government began to offer a bounty for the thylacine in 1888; at least 2,268 were brought in for the reward between 1888 and 1914. Infectious disease seems to have decimated them further; an outbreak thought to be distemper (likely brought by introduced dogs) occurred in wild thylacines in 1910.

In 1936, the Tasmanian government reversed their stance and granted the thylacine protected status, but it was too little, too late: the thylacine was already gone. The last captive thylacine died in captivity that same year. The last recorded kill of a wild thylacine was recorded in 1930, and the last one captured live was caught in 1933, but died the same year in the Hobart zoo. Since then, the animal has become somewhat of a legend. A sighting was reported in western Australia in the 1980s, but has not been confirmed, and it is assumed to be extinct. However, as mentioned above, attempts have been made in recent years to clone the animal. At least 3 different animals are known to be preserved in ethanol in collections in Australia, and DNA has been extracted. Currently, it seems that the cloning project has been put on hold, but genome wiz Craig Venter has offered assistance and possible collaboration--so this may gain more steam in the future. Only time will tell if we'll ever see a live thylacine.

Anyhoo, the point of all this background was to introduce some video clips of captive thylacines I recently ran across: found here.
They don't have any sound, but they're still a haunting reminder of what we've lost, possibly forever.

Wednesday, November 16, 2005 

Tangled bank #41

Apparently it's been 2 weeks already--time flew, and I forgot to submit anything for this one. Nevertheless, lots of good stuff to read over at Flags and Lollipops. My highlights: over at Thinking for Food, Bughunter discusses his bout with pertussis (whooping cough) as an adult, a first-hand account of why new vaccine recommendations for pertussis are coming. Ruminating Dude discusses dangers besides "bird flu," featuring MRSA. And the invasive species weblog discusses giant, frog-eating hamsters and tex-mex frogs.


Human H5N1 cases confirmed in China

China confirms three human cases of bird flu
China reported its first three confirmed human cases of bird flu Wednesday as the government raced to vaccinate billions of chickens, ducks and other poultry in a massive effort to stop the spread of the virus.

The World Health Organization said two of those cases were fatal.

The Health Ministry confirmed two human cases in the central province of Hunan and one in the eastern province of Anhui, the official Xinhua News Agency reported. Both areas reported outbreaks in poultry in the past month.

The fatalities were a 12-year-old girl in Hunan and a 24-year-old female poultry worker in Anhui, said Roy Wadia, a WHO spokesman in Beijing.

Not too shocking, considering the large poultry outbreaks that had been seen there. In the meantime, China is planning to vaccinate billions of birds against H5N1, in an effort to reduce both bird and human cases.


More bacteria discovered using metagenomics strategy

I know, everyone's so sick of all the new "omics"es. But "metagenomics" is one that I don't see going away anytime soon. At its core, metagenomics is a way of looking at organisms in concert as a complex ecology, rather than as an individual, as genomic analysis has traditionally been done. Rather than isolating 10 different species of bacteria from, say, a gram of soil and analyzing them all separately, a metagenomics strategy would investigate all the organisms in the soil (or in sea water, dental plaque, or even human feces). A huge advantage to this approach is that we can get sequence data even from organisms that we're unable to culture; as such, it's not surprising that huge numbers of novel microbes are found whenever researchers tackle a new area using this strategy. Also, as you may expect, one focus of this research in humans is to discover causes and/or cofactors of diseases.

One of these diseases is bacterial vaginosis, one of the most common infections among women. Despite this distinction, scientists and doctors know little about the causes of bacterial vaginosis (BV), a usually benign disease that is also linked to serious health problems including pelvic inflammatory disease, an increase in the viral load of HIV from infected women and a two-fold increase in risk for pre-term labor and delivery. A study in the Nov. 3rd issue of the New England Journal of Medicine seeks to shed some light on this mystery.

Previous studies of this disease have been based on culture of bacterial organisms. However, this has a fatal flaw: we know that many of the bacteria that live within our bodies are not amenable to culture by traditional means. Therefore, investigators used a strategy targeting the bacterial 16sRNA gene. This is a gene present in all bacterial species that has been widely used for species identification. Their results?

Women without bacterial vaginosis had 1 to 6 vaginal bacterial species (phylotypes) in each sample (mean, 3.3), as detected by broad-range PCR of 16S rDNA, and lactobacillus species were the predominant bacteria noted (83 to 100 percent of clones). Women with bacterial vaginosis had greater bacterial diversity (P<0.001),>with 9 to 17 phylotypes (mean, 12.6) detected per sample and newly recognized species present in 32 to 89 percent of clones per sample library (mean, 58 percent). Thirty-five unique bacterial species were detected in the women with bacterial vaginosis, including several species with no close cultivated relatives. Bacterium-specific PCR assays showed that several bacteria that had not been previously described were highly prevalent in subjects with bacterial vaginosis but rare in healthy controls. FISH confirmed that newly recognized bacteria detected by PCR corresponded to specific bacterial morphotypes visible in vaginal fluid.

So, the women with BV not only had a greater diversity of bacteria, but they were also more likely to be colonized with these previously unknown species of bacteria. Obviously, if we don't even have a clue as to what these bacteria are, we don't know the best way to treat them. It still amazes me at times to contemplate how little we know about the organisms we are most intimately associated with.

Tuesday, November 15, 2005 

Cow tipping debunked

I grew up in the middle of vast swaths of northwestern Ohio farmland. My dad, the youngest of 13 kids, was raised on a farm, most of my uncles still farm to some extent, and collecting eggs and shearing sheep was something I got to do regularly as a kid on visits to Grandma's house. But I'd honestly never heard of "cow tipping" until I went to Swanky East Coast College (TM) and got asked if that was a pasttime I and my rural friends engaged in. (Obviously, it wasn't). Well, now researchers at the University of British Columbia have data to show that it's likely that all these tipping stories are simply myths.

Ms Boechler, now a trainee forensics analyst for the Royal Canadian Mounted Corps, concluded in her initial report that a cow standing with its legs straight would require five people to exert the required force to bowl it over.

A cow of 1.45 metres in height pushed at an angle of 23.4 degrees relative to the ground would require 2,910 Newtons of force, equivalent to 4.43 people, she wrote.

Dr Lillie, Ms Boechler’s supervisor, revised the calculations so that two people could exert the required amount of force to tip a static cow, but only if it did not react.

“The static physics of the issue say . . . two people might be able to tip a cow,” she said. “But the cow would have to be tipped quickly — the cow’s centre of mass would have to be pushed over its hoof before the cow could react.”


Another problem is that cows, unlike horses, do not sleep on their feet — they doze. Ms Boechler said that cows are easily disturbed. “I have personally heard of people trying but failing because they are either using too few people or being too loud.

“Most of these ‘athletes’ are intoxicated.”

I've not been around cows much--Grandma had them occasionally on the farm, but it was mostly sheep and chickens (and poor, tortured barn cats. Think Elmyra on Tiny Toons, then multiply it by about 10 because I had way too many cousins). Anyway, we now live on a farm and currently have about 15 cows quite literally in our backyard--and yeah, they are *not* heavy sleepers. The second I let my dogs out in the morning, all the cows are running away from the fence, despite the fact that neither my door nor my dogs are very noisy. I guess it's good to know that our bovine friends are (well, mostly) safe from the shenanigans of intoxicated frat boys throughout the country.

(Hat tip to SciAm Observations for the link to the study)


Doesn't look too bad for 175 years old...

Happy birthday, Harriet!

Harriet the tortoise, quite possibly the oldest living animal on Earth, celebrated her 175th birthday on Tuesday -- with a pink hibiscus flower cake at her retirement home in northern Australia.

Australia Zoo, where Harriet has spent the past 17 years, claims the Giant Galapagos Land Tortoise was collected by British scientist Charles Darwin in 1835.

More pictures of Harriet eating.


Evolution of resistance--bacteria win again

Resistance to antibiotics has been a concern of scientists almost since their widespread use began. In a 1945 interview with the New York Times, Alexander Fleming himself warned that the misuse of penicillin could lead to selection of resistant forms of bacteria, and indeed, he’d already derived such strains in the lab by varying doses of penicillin the bacteria were subjected to. A short 5 years later, several hospitals had reported that a majority of their Staph isolates were, as predicted, resistant to penicillin. This decline in effectiveness has led to a search for new sources and kinds of antimicrobial agents. One strategy involves going back to a decades-old approach researched by Soviet scientists: phage therapy. Here, they pit one microbe directly against another, using viruses called bacteriophage to infect, and kill, pathogenic bacteria. Vincent Fischetti at the Rockefeller University has used this successfully to kill anthrax, Streptococcus pyogenes, and others. Another novel source of antibiotics has come from our own innate immune system, one of our initial defenses against microbial invaders.

An enormous variety of organisms produce compounds called cationic antimicrobial peptides. A component of our own innate immune system, these are fairly short strings of amino acids (less than 100 a.a.’s) that have a net positive charge. It is thought that these peptides work primarily by disrupting the integrity of the bacterial cell wall, essentially poking holes in the wall, causing death of the cell. Since the peptides are targeted at the bacterial cell wall structure, it was thought that resistance would require a fundamental change in membrane structure, making it an exceedingly rare event. Therefore, these antimicrobial peptides might make an excellent weapon in the fight against multiply drug-resistant bacteria. Additionally, the remarkable diversity of these peptides, combined with the presence of multiple types of peptides with different mechanisms of action present at the infection site, rendered unlikely the evolution of resistance to these molecules (or so the common thinking went). However, evolutionary biologists have pointed out that therapeutic use of these peptides would differ from natural exposure: concentration would be significantly higher, and a larger number of microbes would be exposed. Additionally, resistance to these peptides has been detailed in a few instances. For example, resistance to antimicrobial peptides has been shown to be essential for virulence in Staphylococcus aureus and Salmonella species, but we didn't *witness* that resistance develop--therefore, it might simply be that those species have physiological properties that render them naturally resistant to many of these peptides, and were never susceptible in the first place.

Antimicrobial resistance is always a problem—it can render antibiotics much less useful, and make deadly infections almost untreatable. But resistance to these peptides could make us all vulnerable. The peptides of our innate immune system are one of our first lines of defense against an immense variety of pathogens, and we don’t know what the outcome may be if we compromise this essential level of protection. But realistically, could such resistance evolve within the bacterial population?

Dr. Michael Zasloff of Georgetown University was originally a doubter. In this 2002 Nature article, he states in conclusion:
Studies both in the laboratory and in the clinic confirm that emergence of resistance against antimicrobial peptides is less probable than observed for conventional antibiotics, and provides the impetus to develop antimicrobial peptides, both natural and laboratory conceived, into therapeutically useful agents.
Certainly in the short term, resistance was unlikely to evolve for the reasons I mentioned above. However, if these peptides are used over an extended period of time, could the mutations necessary to confer resistance accumulate? This was the question asked in a new study by Dr. Zasloff along with colleagues Gabriel Perron and Graham Bell. Following publication of his 2002 paper where he called evolution of resistance to these peptides “improbable,” Bell challenged Zasloff to test this theory. Zasloff took him up on the offer, and they’ve published their results in Proceedings of the Royal Society.

They tested this using strains of E. coli and Pseudomonas fluorescens. They started out growing these bacteria with low concentrations of a peptide antibiotic called pexiganan, a derivative of a peptide originally isolated from a frog. (Carl Zimmer has an excellent post on this same topic here). The experimental design was quite simple. They grew the bacteria, took a portion of the growth, and added that to a new tube with fresh media. Gradually, they increased the concentration of pexiganan in the growth medium. In all, they did 100 serial transfers of the bacteria (correlating to ~500-600 generations of bacteria), and the end result were--voilà!--bacterial populations that were resistant to the peptides.

Creationists/ID advocates (such as chemist Phil Skell) often claim that “evolutionary theory contributes little to experimental biology,” or that “evolution has little to do with almost all research in biology and biotechnology”, etc. etc. And sure, the theory of evolution didn’t *directly* result in the discovery of peptide antibiotics. But advances in biotechnology do not exist in a vacuum, and we have seen what can occur from the misapplication of these types of technologies, unguided by an understanding of underlying evolutionary principles. Peptide antibiotics have not yet been used clinically to treat human infections, but imagine if they had gone into widespread use without a thought given to the evolution of resistance to these peptides. Imagine if they had gone into widespread use prior to an investigation of the relatedness of various peptides to those produced by humans. Imagine if, as a result of not considering these implications, we had lost an ancient protection against bacteria—-which *evolved* over millions of years of host-pathogen interaction--due to a mere advancement in biotechnology. While I enjoy proving the evolution-doubters wrong, I hope it never comes down to that kind of situation in order to do so, and I hope this example is instructive to those who claim that evolution isn't useful.

Monday, November 14, 2005 

ID advocate Guillermo Gonzalez speaking in Lima, Ohio

Okay, so the fact that I've already attended one of his talks here in Iowa, coupled with the fact that the one I'm mentioning is about 500 miles away from where I live may make me look like a stalker. But I swear, I'm not. I just found out that Gonzalez is giving a talk at a church in Lima, Ohio next Saturday, the 19th.
Professor Gonzalez will be speaking on the subject of Intelligent Design, how it makes the earth a privileged planet, and why Darwinian science from the steam engine era is no longer able to keep up in the information age.

I'm from that area, and I'm heading back there this weekend to throw a baby shower for my sister. So, I'll be about 20 minutes away from Lima with time to kill and might stop by. If anyone else is planning on heading there, drop me a line.

Edited to add: I just realized he's referred to as an "astrobiologist" on the church's website. Astrobiologist, my ass...he kept saying over and over how he's "not a biologist" at his UNI talk, and his research (according to his ISU website) is on "the late stages of stellar evolution through the use of spectroscopic observations. Recent work includes spectroscopic abundance analysis of post-AGB supergiants and RV Tau variables. He has also undertaken a study of the parent stars of the recently discovered extra-solar planetary systems. The results indicate that these stars have anomalous chemical abundances, suggesting some sort of unusual formation history." Maybe I'll start calling myself a biophysicist...I have more training in physics than Gonzalez appears to have in biology.


IA and ID in the WSJ; update on CfS

Today's Wall Street Journal has an article on ID in college classrooms today.

AMES, Iowa -- With a magician's flourish, Thomas Ingebritsen pulled six mousetraps from a shopping bag and handed them out to students in his "God and Science" seminar. At his instruction, they removed one component -- either the spring, hammer or holding bar -- from each mousetrap. They then tested the traps, which all failed to snap.

"Is the mousetrap irreducibly complex?" the Iowa State University molecular biologist asked the class.

"Yes, definitely," said Jason Mueller, a junior biochemistry major wearing a cross around his neck.

That's the answer Mr. Ingebritsen was looking for. He was using the mousetrap to support the antievolution doctrine known as intelligent design. Like a mousetrap, the associate professor suggested, living cells are "irreducibly complex" -- they can't fulfill their functions without all of their parts. Hence, they could not have evolved bit by bit through natural selection but must have been devised by a creator.

"This is the closest to a science class on campus where anybody's going to talk about intelligent design," the fatherly looking associate professor told his class. "At least for now."

Overshadowed by attacks on evolution in high-school science curricula, intelligent design is gaining a precarious and hotly contested foothold in American higher education. Intelligent-design courses have cropped up at the state universities of Minnesota, Georgia and New Mexico, as well as Iowa State, and at private institutions such as Wake Forest and Carnegie Mellon. Most of the courses, like Mr. Ingebritsen's, are small seminars that don't count for science credit. Many colleges have also hosted lectures by advocates of the doctrine


At the end of the article, they present one of Ingebritsen's tactics:

On a brisk Thursday in October, following the mousetrap gambit, Mr. Ingebritsen displayed diagrams on an overhead projector of "irreducibly complex" structures such as bacterial flagellum, the motor that helps bacteria move about. The flagellum, he said, constitutes strong evidence for intelligent design.

One student, Mary West, disputed this conclusion. "These systems could have arisen through natural selection," the senior said, citing the pro-evolution textbook.

"That doesn't explain this system," Mr. Ingebritsen answered. "You're a scientist. How did the flagellum evolve? Do you have a compelling argument for how it came into being?"

Ms. West looked down, avoiding his eye. "Nope," she muttered. The textbook, "Finding Darwin's God," by Kenneth Miller, a biology professor at Brown University, asserts that a flagellum isn't irreducibly complex because it can function to some degree even without all of its parts. This suggests to evolutionists that the flagellum could have developed over time, adding parts that made it work better.

During a class break, Ms. West says that Mr. Ingebritsen often puts her on the spot. "He knows I'm not religious," she says. "In the beginning, we talked about our religious philosophy. Everyone else in the class is some sort of a Christian. I'm not." The course helps her understand "the arguments on the other side," she adds, but she would like to see Mr. Ingebritsen co-teach it with a proponent of evolution.

Ms. West and other honors students will have a chance to hear the opposing viewpoint next semester. Counter-programming against Mr. Ingebritsen, three faculty members are preparing a seminar titled: "The Nature of Science: Why the Overwhelming Consensus of Science is that Intelligent Design is not Good Science."

I think that's a *course,* not a one-time, hour-long seminar, if I'm not mistaken. Or at least, a similar one was/is in the works there. Additionally, for those of you who are in Iowa, there also will be a seminar on Feb. 2nd at ISU:

Why Intelligent Design Is Not Science - Robert M. Hazen

02 Feb 2006, 8:00 PM @ Sun Room, Memorial Union - Robert M. Hazen is the Clarence Robinson Professor of Earth Science at George Mason University, and a scientist at the Carnegie Institution of Washington's Geophysical Laboratory. He received his M.S. in geology from the Massachusetts Institute of Technology, and his Ph.D. in Earth Sciences from HarvardUniversity. Dr. Hazen is the author of over 240 articles and 16 books, including the most recent Genesis: The Scientific Quest for Life's Origin; Why Aren't Black Holes Black? and the best-selling Science Matters: Achieving Scientific Literacy, which he co-authored with James Trefil. Dr. Hazen has recorded the acclaimed lecture series, The Joy of Science, with the Teaching Company (, which provides a fresh and definitive overview of all the physical and biological sciences.

Finally, again for those of you in the Hawkeye State, the Iowa Citizens for Science group now has a website: It's still a bit rough, but I'll be updating it with events like these as I find out about them, so keep an eye on it--and drop me an email (iowascience AT gmail DOT com) if you'd like me to add you to the email list for even quicker updates.

About me

  • I'm Tara C. Smith
  • From Iowa, United States
  • I'm a mom and a scientist, your basic stressed-out, wanna-have-it-all-and-do-it-all Gen Xer. Recently transplanted from Ohio to Iowa, I've spent most of my life in the midwest (with 4 years of college spent out east in "soda" territory). My main interest, and the subject of my research, is infectious disease: how does the microbe cause illness? What makes one strain nasty, and another "avirulent?" Are the latter really not causing any disease, or could some of those be possible for the development of chronic disease years down the road? Additionally, I've spent a lot of time discussing the value of teaching evolution, and educating others about "intelligent design" and other forms of creationism. My interest in history of science and medicine is also useful as a way to tie all of the above interests together. [Disclaimer: the views here are solely my own, and do not represent my employer, my spouse, that guy who's always sitting by the fountain when I come into work, or anyone else with whom I may be remotely affiliated.]
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