This past weekend was the Montana state jazz festival. I didn't get to enjoy the music as much as in previous years, because I had the fam in tow, but it is always fun to play there and give my students a chance for a broader audience than they get on our small campus. Here's our mp3 of "Black Orpheus," for the more than passingly interested.

Plus, we all get the benefit of a half hour with a professional jazz educator who hones in the band's strengths and weaknesses and gives some great tips for taking our playing to the next level.

Those of us who play jazz consider it one of the purest forms of music, because of its emphasis on improvisation. It's tough sometimes to be directing students because of the difficulty of convincing beginners to go out on a limb and try something new. I used to have one trumpet player (sadly just for one year) who was a great player, but did not like to solo because she felt it had to come out sounding like Miles Davis on the first try. She's a Type A, overachieving excellent student, but performance is not like other disciplines. You cannot learn what you need from a book and do it perfectly the first time; or, even acknowledging some trial and error is necessary in fields such as molecular biology, failure is not a public exercise, and a perfectionist can accept that it will take a few tries to get it right because there are no public consequences.

Obviously I get the other type of student too, who is willing to take a risk. Those students improve a lot over time, because the only way to practice soloing is to do it there, with your whole band standing around you. About 80% of soloing is confidence, I think. Sure, we don't really want to hear you if you have no sense of rhythm or melody or don't understand jazz chord structure and scales at all, but that's the stuff everyone picks up as they go, even in the big bands in which they don't solo (that is if they are all interested in continuing to play, and are not there just because Mom and Dad made them). But all the wrong notes really start to sound wrong after awhile, and as time goes on everything you hear flows to your fingers, which start doing more and more of the right thing. Then you reach the point where "wrong" notes actually have a place in the structure of your solo.

This is why I love listening to Ornette Coleman. His solos stretch the form to its extreme, because he employs so many notes that are not in the chord changes, but fit in perfectly because of the way he sets them up. (This is not really an uncommen idea - most of the melody notes of the bridge of "Girl from Ipanema" are not actually in the chords, making it difficult to sing, but incredibly rich to listen to.) Coleman's classic album "Free Jazz," for which he is the most famous, explored the idea of improvisation in its purest form, by having two quartets play together without any structure at all for both sides of an LP. Each performer takes his solo in turn, and it is up to the other musicians to respond to what he is doing. Jazz is all about communication, which is why it is so fun to play when the band really clicks.

Unfortunately, at my school, it is difficult to keep students in the jazz band for longer than a year or two, so they never get the chance to see themselves really improve, and see how this connection works among musicians used to playing with each other. There tends to be a high-school mentality here that music is uncool and partying is really where it's at - all but one of my 8 or so freshmen that started the year dropped out within a few weeks, and this mentality clearly played a role. It's a shame of course, because understanding the fundamentals of music is a basic part of a liberal arts education, and because training in music is something that is much easier to keep with you throughout your life - which is what tipped the balance for me to become a biology, rather than music, major. It worked out, because I'm going strong in both fields, and realized I have only scratched the surface of what I could do in both of them.

The infinite possibilities of jazz make the same tune exciting to play over and over. Even when you have the head of the tune mastered, you can always stretch a little and try something new on your solo, with the rest of the band trying it right along with you.

Labels: education, jazz, music

This fortnight's edition of the Tangled Bank blog carnival is up at Archaeology. There is a great discussion on Nisbet and Mooney's "framing science" article in Science, so check it out.

Labels: carnivals

Arbor Day, April 27, is nearly upon us. Many of us are receiving solicitations in the mail about ordering trees through the National Arbor Day Foundation. But you should think carefully about what trees to order.

The Arbor Day Foundation remains behind the times when promoting tree-planting, because they barely mention problems with invasive trees on their site, and in none of the junk mail literature I have received. Although an entire page is devoted to invasive species that harm trees, the only reference to invasive trees is buried its FAQ:

10. Are the trees offered by the Foundation invasive?
The Foundation follows the guidelines of the National Invasive Species Information Center. Plants found to be invasive or problematic by this agency are removed from the lists of trees and shrubs offered by the Foundation. In addition, we take into consideration recommendations found in the publication entitled, Invasive Plants, Changing the Landscape of America, by the Federal Interagency Committee for the Management of Noxious and Exotic Weeds.

Naturally I'm not complaining about their policy, it shows they are at least paying some attention to the problem of invasives. What I object to is that the NADF, throughout the web site, promotes and sells trees purely by horticultural zone, as does every gardening catalog. The gardening catalogs, though, are about business, and up to this point, businesses spreading species around have not been held accountable for invasive outbreaks, so in their case this policy is understandable.

However, the NADF promotes itself as an organization that cares about ecology and the environment. Aside from fortunately not selling nasty invasive trees such as Russian olive and saltcedar, they do absolutely nothing to promote the idea that we should be cultivating local species, which is by now a standard ecological concept. Even if your exurbian front yard is hardly definable as a natural habitat, NADF should be attempting to instill in you the idea that what makes ecology important, and sustainability possible, is the recognition that certain species of trees belong in certain areas because they are used to interacting with the other species found in that area. Such a visible organization could be making great strides in promoting local habitat ecology, but they are making absolutely no effort to do so.

What difference does it make, if none of the trees they sell will become invasive? First of all, every time we move a species, or even an individual, around to where it doesn't belong, we are conducting an biological experiment. Maybe there are no problems 9,999 times out of 10,000; but the more often we do this, the more often number 10,000 comes up.

In addition, the homogenization of the planet comes with several costs. One cost is giving up the buffer that having millions of species across hundreds of ecosystem provides against our own foolhardy exploitation of resources. The honeybee "crisis" everyone is clamoring about now is a perfect example of this. Bring an alien species to a large region to replace hundreds of native species that could do the job, albeit less efficiently from a human perspective, and one disease, one environmental problem, and you are in trouble.

Another cost is to our own human sense of place. When distinctive plants and animals disappear from places - a good example here is of pacific islands, whose endemic plants and animals have been decimated, and replaced with a few ubiquitous species now found on nearly all the islands - we lose some of the wonder we have for the natural world. In fact, each successive generation has less appreciation its own corner of the planet, because fewer species remain to distinguish it from anywhere else on earth.

Perhaps these issues are just too abstract for an organization that wants to promote one simple idea, that "trees are good" - not even always true, in an ecosystem that was historically treeless, another distinction NADF fails to make in its black-and-white view of ecology. Perhaps there's no point in anything but pooh-poohing those of us who wish for a different ethic - many of these have been cultivated for generations, and some are human-created hybrids, so really what difference does it make where we plant them? I argue only that these are minor points in the greater struggle to convince humanity, especially that small portion of humanity that has the time and money to support any sort of environmental ethic that it chooses, that ecology and biodiversity are not actually words that can describe numbers of species over an entire planet. They much more aptly describe the mosaic of species assemblages that found a way to evolve in every possible environment that is found on earth. If we lose that idea, then biodiversity itself is a meaningless concept.

Labels: biodiversity, ecology, invasive species, nature

For a multitude of fascinating articles about the brain, click here for the latest edition of Encephalon at Ouroboros.

Labels: brain, carnivals

Apparently some women are actually outraged that there is finally a birth control pill that does not force us to have a period, supposedly because it is somehow "unnatural" not to have one every 28 days of our non-pregnant lives. And yet it is only due to a bizarre historical artifact that for the nearly 50 years that the Pill has been available, those of us using it have been forced to have our period thirteen times a year, even if we didn't want to.

Here's a brief summary of the human female menstrual cycle:
The first day of menstrual bleeding is arbitrarily designated as the first day of the menstrual cycle. During the first 4-5 days, during bleeding, hormones are at their lowest point. Over the next 10 days or so, an ovarian follicle develops, and once the follicle is mature, ovulation occurs. At this point, estrogen is peaking. Then, estrogen drops after ovulation and progesterone, which stimulates the uterine lining to develop in anticipation of receiving a fertilized ovum, increases. If the ovum is not fertilized, progesterone levels drop, which means the enriched lining of the uterus is not sustained, and menstrual bleeding occurs.

The birth control pill mainly contains progesterone. If you become pregnant, high levels of progesterone are maintained, which prevents further ovulation. Thus, the artificial introduction of progesterone essentially causes your body to behave as if it were pregnant, which inhibits ovulation. The traditional Pill introduces one progesterone-free week out of every four, so that menstrual bleeding will be simulated. It isn't true menstrual bleeding because we are never actually allowing our bodies to go through the cycle, we are just turning progesterone levels on and off like a switch to manipulate it.

If you ever thought about your reproductive cycle for ten minutes and asked your doctor why on earth you should be compelled to go through this ritual despite the fact that you have not even ovulated, you got some vague response about how it was not 'healthy' not to have periods. But women have been systematically misled for decades; there is absolutely no evidence whatsoever that there are health risks associated with the absence of menstruation. Certainly the lack of menstruation can be an indicator of some further health problem (such as abnormally low body fat), but it actually serves no function other than your body saying "whoops, not pregnant this time."

What furthers the outrage was the assumption that women must have 13 cycles a year to be "normal." I personally had about a six-week cycle before going on hormones, but at the time, I thought it was a reasonable trade-off to have more "periods," given that they were significantly less debilitating (of course, since I was not having natural periods). But this New Yorker article from 2000 pointed out that there is evidence that menstruating more often is a product of industrialized society, and that in pre-industrial societies, it is normal for women to menstruate as few as four times a year. The article further shows the positive correlation between lifetime number of menstrual cycles in women and cancers of the reproductive organs.

So why on earth does the traditional birth control pill force us to simulate menstruation, when for so many of us, it is a miserable few days?

Perhaps at the time the Pill was being researched and developed, in the late 50s-early 60's, people knew that the primary force behind that research and development was Dr. John Rock, who happened to be a devout Catholic. In fact, he pursued this line of research precisely because he was a Catholic, and wanted to give Catholic women more control over their reproductive lives without violating their church's rules. He reasoned that if the rhythm method was acceptable to the church, surely intervention - using the same hormones occurring naturally in the body - in order to make the cycle more regular and prevent a fertile period entirely, would be acceptable too. Of course he ultimately was wrong, and became an embittered ex-Catholic by the end of his life.

But the greatest travesty was done to women who simply wanted convenient birth control, and to have power over their own reproductive lives. A menstrual period every 28 days was arbitrarily introduced into the regimen by a Catholic doctor who thought it would appease the pope. A pope, who, eventually, decided Catholics were not allowed to use the Pill. So every woman who has used the birth control pill since is either a non-Catholic, or a "Catholic" who doesn't give a hoot what the pope thinks anyway. And yet for nearly 50 years we have been stuck with a Catholic Pill as our only option.

The one argument made in the Times article about forcing regular "periods" that made any sense to me at all was the psychological reassurance of not being pregnant. Fine, those women can use a period-forcing pill as far as I am concerned. Why should the rest of us be compelled to as well?

Here are some of my particularly favorite quotes in the article:

"It's not an easy decision for a woman to give up her monthly menses," said Ronny Gal, an analyst at Sanford C. Bernstein & Company.

There has also been a backlash among groups that celebrate the period as a spiritual or natural process, like the California-based Red Web Foundation. "The focus of our group is to create positive attitudes toward the menstrual cycle; suppressing it wouldn't be positive," said Anna C. Yang, a holistic nurse and executive director of the organization.

One [person] who attended the screening [of "Period: The End of Menstruation?"], Aviva Bergman, a 22-year-old student at Goucher College in Maryland, said she would not use products that suppressed her period because it seemed unnatural.

"I just feel that there's a reason you're getting it every month," she said.

You know what? Y'all can have as many periods as you like. You do your little spirit dances while you are washing the blood out of your underwear and popping the Advil like candy. If you believe in "natural," go live in a cave somewhere. Just don't have the gall to "backlash" against something that will make my life significantly more bearable, and that I should have already had for my entire adult life. Thank you.

Labels: gender, health, humans, nature

The Belostomatidae is a family of giant water bugs (Order Hemiptera) that has been fairly extensively studied because of the various species' unusual reproductive systems. In short, this is one of the few groups of animals that exhibit paternal care of offspring.


Probably the most well known animals with paternal care is the sea horse, who carries its mate's eggs in a brood pouch until they hatch. Belostomatids are similar because the male also takes care of the eggs, although he does it in two different ways between the two subfamilies, Lethocerinae and Belostomatinae. Above is a giant water bug in the genus Lethocerus. They are sit-and-wait aquatic predators, hanging head down on sticks or reeds underwater. An appendage extending from their abdomens remains above water and allows them to breathe. They are quite large, and much of their prey consists of tadpoles and small fish.


They have a somewhat painful bite, because they have a sharp beak with which they inject a neurotoxin which helps them control their prey. However, if one holds them just behind the head as shown it is safe to pick them up. (I was holding this particular specimen (from Costa Rica) that another student and I were studying; we were doing measurements to look for morphometric differences between males and females, and I had to do all the measuring because he was too afraid to pick one up.)

The Lethocerines are thought to be the more ancestral lineage in the family, based partly on the way they brood their young. Females lay eggs along the top of a stem sticking out of the water, but the eggs will dry out and die without care. The male stays as a sentry on that stem, periodically carrying water up to moisten the eggs and oxygenate them.


The Belostomatines are considered more derived evolutionarily, because the brooding behavior seems to be more efficient. Females lay their eggs directly on the back of the male, who must swim around with them until they hatch to keep them properly oxygenated. The picture at left shows a male with eggs.

Scientists like to study "reverse mating-system" species such as these because it gives us clues about what governs decision-making in animals. In the case of mating behavior, in nearly all animals known, females are choosy about their male mates, who often have elaborate physical features or behavior designed to attract the attention of females (or fight off other males). This is why in many species of birds, the males are more brightly colored than the females. The reverse mating-system species allow us to ask questions like, are females always the choosy ones, because they invest more resources in their gametes (eggs are a lot bigger and fewer than sperm), or is the parent with the largest investment overall the choosy one? Gamete size is an important measure of investment, but time and energy invested in a single mate are important too. In most animal species, a male has the sperm and the time to mate with many females, so he tends not to be choosy. A female not only has fewer gametes but usually invests more time in rearing the offspring than the male, so it's more important that she choose a mate with good qualities (for that species).

It has been found that in reverse mating-system species, the males actually tend to be the choosy ones - so there's nothing about being female per se that makes one choosy. Parental care of offspring is a huge investment, so when it switches to the males, they become the choosy ones. In the case of giant water bugs, a female may have enough eggs to mate with several males, and as soon as she lays them she can move on and find another mate. The male is the parent stuck taking care of the eggs for a couple weeks and thus loses opportunities for more matings in that time. Thus, accordingly, belostomatids and sea horses tend to have choosy males rather than females.

Labels: cool bugs, ecology, evolution, insects, sex

A Science Times story about the condition known as "dissociative amnesia" today jarred a memory I have of one chapter of a friend's extremely colorful life. My friend is in her 80's and was married four times; only the final marriage lasted for a significant time, and only it could be described as fairly normal. Her first marriage story can only be described as astounding.

My friend "Annie" got married for the first time near the start of the U.S. involvement in WWII. Her husband became a soldier, but never made it overseas - he was involved in a train accident in the U.S. and suffered brain damage and a long recovery. How Annie coped during this period with no money and a couple of small children is a story itself (it never occurred to her that she could get some assistance from Uncle Sam), but eventually her husband recovered enough to work for the U.S. mint as an engraver after the war. Life went on for a few years but Annie wasn't entirely happy because her husband was starting to show, in her mind, undue aggression toward her oldest son. She was concerned that sometime he might go too far and hurt her son, but didn't know what to do about it.

The problem ended up solving itself, because one day Annie's husband never came home from work. No one had a clue where he was. She tried for awhile to locate him but the effort was a bit halfhearted because in truth, she was relieved for her kids' sake. She still found it quite odd, though, that he would leave for good without even a word to her. She eventually obtained a divorce due to her abandonment, but his disappearance remained a mystery - no friends or family members knew where he went.

Something like 20 years or more passed before the mystery was solved. The ex-husband's sister was walking along in Seattle one day, and was shocked to see him on the street. She grabbed him and started talking, and it was only at that point that he himself remembered anything of his life 20 years before. The day he disappeared, he had simply forgotten everything about his life at the time, to the point of not even knowing where he was or how to get home. I know no details of how he dealt with his situation at the time, but at the time he was rediscovered, he had built an entirely new life with a wife and kids without remembering a thing about his original life until the day he saw his sister, when it came back to him.

Eventually, he travelled to visit Annie and her (fourth and final) husband, but Annie's oldest son refused to talk to him; Annie could not convince him that his father had abandoned him through no fault of his own. By that time enough years had passed that Annie, happy in her current family, was philosophical and did not feel any emotional baggage in meeting him; she did so mainly out of curiosity, and understood that what had happened was some sort of strange by-product of the train accident. She and her husband continued a friendly correspondence with her ex and his family for a number of years.

I had never heard of this type of amnesia before or since hearing this amazing story from Annie, until reading the above article. I'm sending her a copy! Here is the
Merck manual description of the disorder.

My main reaction is that this must happen more than is recognized, because Annie's ex was able to build a whole new life, and never would have known what happened to him if he hadn't happened to run into his sister - imagine the odds of that! I do not know if he ever told a doctor about his problem or not, but he coped with it rather well. Perhaps it would be harder in today's world where ID numbers are so ubiquitous. But if I ever hear again about someone abandoning their family without a trace, I would have to wonder...

Labels: behavior, brain

The monthly Oekologie carnival is up, with a wide variety of ecological posts. Check it out.

Labels: carnivals, ecology

Recent concern about apparent die-offs in bees apparently has now led to speculation that cellphone radiation is the cause for bee disappearance. Instapundit has weighed in, questioning with well deserved skepticism the validity of this claim.

Because I am a scientist, I do not try to establish validity of such reports via Google, but via Web of Science, the search engine that encompasses academic literature, both peer-reviewed and not. As far as I am concerned, until data have been published in peer-reviewed literature, any fantastic "scientific" claims are just clamors for attention.

There is no information yet in the scientific literature regarding possible causes of CCD or "colony collapse disorder" as some have tagged the syndrome of the disappearing bees. This is not too surprising, because it appears to be a fairly recent phenomenon, but I guarantee you that because the USDA supports several Bee Research Laboratories in the western U.S., this problem, if genuine, is being addressed by qualified government scientists as I write (if all the bee lab guys I used to know weren't long retired from the lab, I would call one now to get his take on it).

The mere fact that the U.S.D.A. has labs of bee scientists confirms that domesticated honey bees are indeed important to the pollination of crops in the U.S. But as I pointed out in my last post on the topic, they are by no means the only species of pollinator out there. So don't expect any food shortage panics anytime soon.

What of the cell radiation theory then? Cell radiation has been a human health concern for quite some time, and thus the literature on this topic is quite robust. Some studies (but not others) have found increased cell apoptosis (cell death that is orderly - as opposed to sudden and widespread) due to exposure to cell radiation, but even this doesn't mean we should necessarily be alarmed, because all these studies were performed on cell cultures (in vitro), not on real people using cell phones in a usual manner (in vivo). A recent paper (Valberg, P.A., van Deventer, T.E. & Repacholi, M.H. (2007) Workgroup report: Base stations and wireless networks-radiofrequency (RF) exposures and health consequences. Environmental Health Perspectives, 115, 416-424.) examines evidence that radio-frequency radiation (including cell phones) affects actual human health adversely, and concludes that there is no evidence that it does so. In fact, the authors point out (from the abstract):

The possibility of RF health effects has been investigated in epidemiology studies of cellular telephone users and workers in RT occupations, in experiments with animals exposed to cell-phone RF, and via biophysical consideration of cell-phone RF electric-field intensity and the effect of RF modulation schemes. As summarized here, these separate avenues of scientific investigation provide little support for adverse health effects arising from RF exposure at levels below current international standards. Moreover, radio and television broadcast waves have exposed populations to RF for > 50 years with little evidence of deleterious health consequences. Despite unavoidable uncertainty, current scientific data are consistent with the conclusion that public exposures to permissible RF levels from mobile telephony and base stations are not likely to adversely affect human health.

Here is a table from the paper comparing all the sources of RF we are exposed to (sorry about the low resolution):

So my advice is, chat away until further notice - with the caveat that out of caution, avoid giving cell phones to young kids because developing brains are certainly more sensitive to environmental effects than grown ones, models suggest that child heads absorb EM radiation more than adult heads (De Salles, A.A., Bulla, G. & Rodriguez, C.E.F. (2006) Electromagnetic absorption in the head of adults and children due to mobile phone operation close to the head. Electromagnetic Biology And Medicine, 25, 349-360.). Obviously, if anyone had found major health effects yet there would have been a massive response to deal with it by some country.

Back to the bees though. Different species will not necessarily be affected the same way as humans, especially such distantly related groups such as insects, but as of yet I, as an entomologist who does not specialize in bees, doubt that cell radiation is causing CCD. The article quotes some one knowledgeable about cell radiation, not insects, in asserting the likelihood that it does. Most important, bees navigate primarily via polarized light, which is in a completely different part of the EM spectrum from radio waves. How radio waves could possibly impact their use of light for navigation (any more than it does humans' use of light for navigation) is at best nonintuitive, so I would never believe it until I saw the published paper showing me the evidence. I am not holding my breath for that paper to appear.

Other references:

Erogul, O., Oztas, E., Yildirim, I., Kir, T., Aydur, E., Komesli, G., Irkilata, H.C., Irmak, M.K. & Peker, A.F. (2006) Effects of electromagnetic radiation from a cellular phone on human sperm motility: An in vitro study. Archives Of Medical Research, 37, 840-843.

Joubert, V., Leveque, P., Cueille, M., Bourthoumieu, S. & Yardin, C. (2007) No apoptosis is induced in rat cortical neurons exposed to GSM phone fields. Bioelectromagnetics, 28, 115-121.

Remondini, D., Nylund, R., Reivinen, J., de Gannes, F.P., Veyret, B., Lagroye, I., Haro, E., Trillo, M.A., Capri, M., Franceschi, C., Schlatterer, K., Gminski, R., Fitzner, R., Tauber, R., Schuderer, J., Kuster, N., Leszczynski, D., Bersani, F. & Maercker, C. (2006) Gene expression changes in human cells after exposure to mobile phone microwaves. Proteomics, 6, 4745-4754.

Thorlin, T., Rouquette, J.M., Hamnerius, Y., Hansson, E., Persson, M., Bjorklund, U., Rosengren, L., Ronnback, L. & Persson, M. (2006) Exposure of cultured astroglial and microglial brain cells to 900 MHz microwave radiation. Radiation Research, 166, 409-421.

Zhao, T.Y., Zou, S.P. & Knapp, P.E. (2007) Exposure to cell phone radiation up-regulates apoptosis genes in primary cultures of neurons and astrocytes. Neuroscience Letters, 412, 34-38.

Labels: bees, behavior, environmental toxins

I used to give blood regularly, but am now forbidden because I lived for months at a time in England from 1998-2001, where BSE (Mad Cow disease) emerged in the mid-1990's. I have scoffed at this rule; from everything that I understood, Britain has far greater monitoring of beef than the U.S. True, BSE has been found in thousands of British cattle and very few North American cattle, but then again one is unlikely to find such a sneaky pathogen if one is not looking for it. Unfortunately, the U.S.D.A., which exists to serve agribusiness interests, rather than those the American public which pays for its existence, has at best dragged its feet on increased testing of cattle, and at worst actively has prevented those who would test on their own initiative from doing so.

The U.S.D.A. itself has drastically curtailed its BSE testing in the last few months. The agency presents no data on BSE testing on its website after August, 2006. However, the new policy is spelled out based on the detection rate from the previous sampling:

Since the enhanced surveillance program began, USDA has sampled more than 759,000 animals and, to date, only 2 animals have tested positive for BSE under the program. Both cases were in animals born before the United States banned the practice of feeding recycled ruminant protein to other ruminants. In line with USDA policies, neither of the affected animals detected under the enhanced surveillance program nor the imported cow detected in 2003 entered the human food or animal feed chains.

Based on the wealth of information gained during both the enhanced surveillance program and BSE surveillance conducted in the United States in the 5 years prior, USDA recently concluded that the prevalence of the disease in this country is extremely low, less than 1 case per million adult cattle, and that the most likely number of cases is between 4 and 7 infected animals out of 42 million adult cattle. Our analysis was submitted to the scrutiny of a peer review process, and the expert panel agreed with the appropriateness of our assumptions and the factors we considered, as well as with our estimate of BSE prevalence.

The new testing protocol is as follows:

The ongoing BSE surveillance program, which will sample approximately 40,000 animals each year, will continue to sample the cattle populations where the disease is most likely to be found. The statistically valid surveillance level of 40,000 is consistent with science-based internationally accepted standards. This level allows USDA to detect BSE at the very low level of less than 1 case per million adult cattle, assess any change in the BSE status of U.S. cattle, and identify any rise in BSE prevalence in this country.

The targeted population for ongoing surveillance focuses on cattle exhibiting signs of central nervous disorders or any other signs that may be associated with BSE, including emaciation or injury, and dead cattle, as well as nonambulatory animals.

As they say, the methodology is based on standard science. But does that really protect our food supply? The unknowns about BSE are disturbing, and unfortunately the testing protocol is based on assumptions that may not be true because we still know so little about this disease.

Britain's beef supply is not currently as safe as I thought, as this 2002 report spells out in detail:

BSE: risk and regulation
A case study paper commissioned by the National Consumer Council
Prepared by Patrick van Zwanenberg & Erik Millstone
Science and Technology Policy Research, Sussex University

It turns out there are still many questions out there about how animals are contracting BSE and how to prevent it:

Indeed, to date, there have been 14 cases of BSE in animals born after August 1996; they constitute an anomaly which remains inexplicable. The mechanisms by which those animals were infected are unknown... It is therefore likely that some animals under 30 months will be sub-clinically infected with BSE and will be entering the human food chain. We cannot know how many animals under 30 months might be incubating the disease, however, because the existing short-term tests can only detect infected animals shortly before clinical symptoms appear, and the UK government has chosen not to conduct any sort of test for BSE on animals entering the human food chain. In 2001 there were 761 reported cases of BSE in the UK... A further 335 cases were also reported in that year from the, as yet uncompleted, active surveillance programme;... but in the summer of 2001, the European Commission's Food and Veterinary Office noted that "[a]s active surveillance is practically not performed [in the UK], it has to be assumed that the BSE incidence for GB has to be seen with a considerable degree of uncertainty."

This means that testing only sick and downer cattle doesn't necessarily cover the possible infected animals. Clearly we have done some things that have helped reduce the risk considerably, for example not allowing cattle to be fed mammal by-products any more. Yet there are loopholes; from the FDA itself: "In August 1997, FDA established a regulation that prohibits the use of most mammalian protein in the manufacture of animal feeds for ruminants." Apparently though it is still legal to feed chickens mammalian protein. BSE may not pass this way, but we know so little about it we cannot say for sure.

And some rules put in place in the 1990s have already been relaxed:

The U.S. Food and Drug Administration today published several amendments to the July 2004 interim final rule, "Use of Materials Derived from Cattle in Human Food and Cosmetics," that will allow the use of certain cattle-derived material in human foods and cosmetics...

As a result, FDA is amending the rule to allow use of the small intestine in human food and cosmetics, provided that the distal ileum has been removed. The U.S. Department of Agriculture is publishing today a similar amendment to its interim final rule on BSE.

The amendments also clarify that milk and milk products, hides and hide-derived products, and tallow derivatives are not prohibited for use in human food and cosmetics.

Is there any other reason for this than pressure from industry? Shouldn't the U.S. government be erring on the side of caution in the case of such a potentially devastating health issue? Those infected with BSE take decades to show their symptoms. This is not a situation where a couple people will drop dead and the FDA will say "whoops, better change that rule" as a result.

As a final note, among the real unknowns about spongiform encephalopathies is that despite what is reported in the popular press, it is clear from official and scientific documents that it is not known without doubt that prion proteins are the proximate cause. It is certainly the currently most popular idea, and most scientists are studying prion proteins based on this assumption, but there are still peer-reviewed papers in respected journals which assert alternative hypotheses, for example:

Manuelidis, L. 2007. A 25 nm virion is the likely cause of transmissible spongiform encephalopathies. Journal of Cellular Biochemistry 100:4.

The transmissible spongiform encephalopathies (TSEs) such as endemic sheep scrapie, sporadic human Creutzfeldt-jakob disease (CJD), and epidemic bovine spongiform encephalopathy (BSE) may all be caused by a unique class of "slow" viruses. This concept remains the most parsimonious explanation of the evidence to date, and correctly predicted the spread of the BSE agent to vastly divergent species. With the popularization of the prion (infectious protein) hypothesis, Substantial data pointing to a TSE virus have been largely ignored. Yet no form of prion protein (PrP) fulfills Koch's postulates for infection. Pathologic PrP is not proportional to, or necessary for infection, and recombinant and "amplified" prions have failed to produce significant infectivity. Moreover, the "wealth of data" claimed to support the existence of infectious PrP are increasingly contradicted by experimental observations, and cumbersome speculative notions, Such as spontaneous PrP mutations and invisible strain-specific forms of "infectious PrP" are proposed to explain the incompatible data. The ability of many "slow" viruses to survive harsh environmental conditions and enzymatic assaults, their stealth invasion through protective host-immune defenses, and their ability to hide in the host and persist for many years, all fit nicely with the characteristics of TSE agents. Highly infectious preparations with negligible PrP contain nucleic acids of 1-5 kb, even after exhaustive nuclease digestion. Sedimentation as well as electron microscopic data also reveal spherical infectious particles of 25-35 nm in diameter. This particle size can accommodate a viral genome of 1-4 kb, sufficient to encode a protective nucleocapsid and/or an enzyme required for its replication. Host PrP acts as a cellular facilitator for infectious particles, and ultimately accrues pathological amyloid features. A most significant advance has been the development Of tissue Culture models that support the replication of many different strains of agent and can produce high levels of infectivity. These models provide new ways to rapidly identify intrinsic viral and strain-specific molecules so important for diagnosis, prevention, and fundamental understanding.

I am not advocating a specific position on this at all; clearly, the current scientific consensus does not support this view, and I do not have the expertise in this area to judge. But I recommend that anyone who believes this is an important issue read up on it at the U.S.D.A. site and the British consumer report. In the meantime, I will be continuing my policy of avoiding factory feedlot beef (and not only because of the risk of BSE). I will also continue to update current research here because of my own interest in the topic.

Labels: brain, environment, statistics, USDA

Neurophilosophy recently posted on current research on why our brains have trouble paying attention to several stimuli presented in quick succession. While getting at the mechanisms behind these processing "bottlenecks" is an ongoing endeavor, it has actually been known for some time that what some people proudly describe as their ability to "multitask" is actually no such thing. Humans (and probably other animals as well?) are actually terrible at this, and the conceit that we are good at it is actually responsible for loss of productivity. So it's not exactly clear why an article trumpeting this as news has appeared in the popular media. Nevertheless, the article motivated me to read up a bit more on the topic. I focused on the recent paper: Sigman, M. and Dehaene, S. 2006. Dynamics of the central bottleneck: Dual-task and task uncertainty. Plos Biology 4:1227-1238.

The authors make a few relevant observations. Referencing what has been previously known:

A dynamic trace of central limitation is ... manifested at a slower time-scale (seconds to minutes) in the inability to rapidly switch the control processes that harness together independent processing modules ... This effect is most evident in task-switching paradigms, which show, using a variety of different experimental manipulations, that reaction times increase when participants change between different task configurations...

Typical result - multitasking slows us down. But why? Here is one of the authors' conclusions:

Although central processing of task 2 can be executed immediately after central processing of task 1 has been completed, the outcome of task 2 cannot be executed until the system has disengaged from the previous response-setting mode.

This means that in addition to the lag in performing a second task, due to the need to finish the previous task first, there is an added lag during which our brain has to shift gears from the first task to the next. So if you add up all the time one task takes if you focused on it completely to the time the second task takes if you focus on it, it will be less than the time you take doing them both together. Thus, as the example in the Times article suggests, shifting your attention back and forth from the road to your cell phone introduces dangerous delays in your driving response time. This probably explains why the accident rate for cell phone users is said to be equivalent to that of drunk drivers, who also suffer from impaired response time.

But what do a few seconds here and there matter for a situation in which we are not in control of a lethal weapon hurtling 75 mph down the highway? The problems go beyond time delays; there are impacts long term memory as well. For those of us in education, the problems introduced by task-switching too often are obvious. The standard university schedule of four to six classes every day, mostly lectures, pretty much could not be a worse way for students to learn. Many professors may not like this characterization; obviously we went through this system and did well enough to become professors ourselves. The problem is, the great majority of our students are not like us. They are not riveted to a lecturer's every word because they find the topic so fascinating, thinking about it in depth after class. No, most of our students attend our lectures, do their best to listen, and probably most of them genuinely understand the material at the time it is presented. When they do lousy on our tests, however, we blame their inability to apply themselves, and certainly that is a factor. Unfortunately, our system is setting up all but the brightest and hardest-working students to fail, when it comes to long term retention of the material in a class. Even many students that manage a B or C in a prerequesite might as well have not taken it when they get to the next class in the sequence.

It is known that humans possess both short-term and long-term memory. For memories to be shifted from the short-term to long-term, these memories must be retuned to and further processed. But when a student leaves my lecture and heads for the next class, what happens? Simply, the toilet flushes - all that new information sitting there in short-term memory waiting to be processed gets dumped instead, as the new information takes over. The student does not think about the material usually for two more days until the next lecture, which then is harder to follow because the student has not processed properly the previous information which is critical to the understanding of subsequent material. Even worse, the student usually does not review his or her notes until the night before a test, when they no longer make sense because the broader ideas associated with those notes have not been properly processed and stored in long-term memory. Our system is idiotic and stupid.

But there is indeed a better way, that a few colleges in the U.S. (at least) employ: block scheduling, or the taking of one class at a time. In this model, the students take one class for three hours of class time every day for 18 days, which represents the class hours necessary for a 4-credit class. Actually, many people are familiar with this format from taking summer session classes. Summer session students, though, may not have received the same benefit because for students to be able focus on the material, you can't lecture at them for 3 hours - meaning you can't take a semester class and force it into the block format as is if you want to see a real change in what the students retain from the course. Fortunately, the block format is perfect for lab exercises, field experiments, or other hands-on tasks that also do a much better job of relating concepts than the passive absorption of information spoken by a lecturer, so the students get two better ways of learning for the price of one. But more important, for three and a half weeks, students are thinking about the material in only one class, not half-listening to (or skipping) a lecture while they worry about an exam next period. They have the time to follow the connections in the material, to internalize the relevant ideas which make the material make sense, simply to think about it, not just mindlessly write down notes that they don't look at again for weeks. They come to class, because they learn quickly that to miss a day is to miss a week on the standard schedule, and miss with it a vital component of the class. They become comfortable with the terminology associated with the field of study, which in my experience rarely happens in the semester format.

So why don't more schools do this? Number one, there would basically be no point with a class of 300 students because you would be reduced to the lecture format anyway, and standard lectures are 50 minutes because that's about all our attention spans can handle as it is. Number two, this is more work for the faculty, because teaching in this environment is highly interactive when done properly. It is also much more intense to grade tests, papers, etc. in a compressed format quickly enough that students benefit from your feedback. But at a small college, it can be done when the faculty care about their students' performance.

Our big university model is basically there because it's the cheap, easy way to chunk students through and give them the degrees they have paid for. But I think most of us teaching at college and universities lament the lack of true liberal arts education that students are receiving there. Simply, most of our graduates are not critical thinkers. Were they ever? That is probably debatable, but many more people go to college now than used to, and a degree probably provided some basic measure of assessing the competence of, say, a potential employee. It's not clear to me that it does at this time.

Colleges now on the block program full time are Colorado College, Cornell College, Tusculum College, and the University of Montana-Western.

Labels: brain, education

Diachasmimorpha juglandis is a parasitoid wasp in the family Braconidae. Like other braconids, it is relatively large; while most parasitic wasps are probably less than 5 mm long, D. juglandis can get nearly up to 1 cm.

This species is categorized as a "solitary larval-pupal endoparasitoid," meaning that an egg is laid inside the host - in this case a larva (or close relative) of the walnut fly Rhagoletis juglandis, and a single adult wasp emerges from the pupal stage of the fly, having devoured it from within.


D. juglandis females, shown in these pictures, have to find their hosts without ever making visual or physical contact with them, because they are feeding within the husks of walnut fruits. Once a wasp has landed on the fruit, she walks around its surface, pausing every few seconds to feel for vibrations beneath her, caused by moving fly larvae. When she has located one, she inserts her long ovipositor through the husk (above right), and hopefully, into the body of the fly larva, where she lays a single egg.

The tiny wasp soon hatches, and bides its time as a first stage larva, cruising through the bodily fluids of its host, sustaining itself on stored fat. Interestingly, the length of the first stage is variable, depending on what stage the fly was at when parasitized; the wasp needs to wait for the fly to begin its pupation (which it does after dropping out of the walnut and digging down into the soil). At this point, the wasp molts into the next stage and begins devouring the entire body of the fly, a task made especially easy because the fly tissues have begun breaking down on their own in preparation for reassembling as an adult fly.

Notice that in the picture above and at the left, of a recently hatched wasp larva, it has a rather large sclerotized head, somewhat like a helmet with jaws. This structure is present only in the first stage; after the first molt, the wasp larva looks like an amorphous white blob.

The reason for the sclerotized head and jaws has to do with the fact that these wasps are solitary - it is only possible for one wasp to emerge from a single host. It is possible for two wasps parasitize to the same host, so that there are two first-stage larvae present at the same time. Because the host only provides enough food for one, these wasp larvae must fight to the death within the host - which all the while continues on its merry way in the walnut, eating fruit until it is full grown and ready to pupate, oblivious to the battles occuring within its body. The jaws on the wasp allow it to easily attack and kill a rival wasp in the fly.

Which wasp wins? This is a fascinating question that has been studied in several solitary parasitic wasp species. In most cases, the one that got there first has the advantage, because it has had time to feed and grow a bit, making it stronger than any subsequent intruder. But back in the early part of the last century, some biologists studying these interactions in a related Diachasmimorpha species in Hawaii (imported there for biological control of medfly and oriental fruit fly) came to a fascinating conclusion following their dissection of hundreds of parasitized flies. They found that they could distinguish how old a first-stage wasp larva was by how fat it was - newly hatched larvae were skinny, but a wasp that had been in the host for a few days had begun to get tanked up on all the fat it was feeding on in the host. When they found two wasps in a death struggle, the skinny one had killed the fat one.

So apparently, when a wasp first hatches, it swims around the host before it tanks up, perhaps looking for any other wasp larvae. When it encounters a fat larva that has been there alone for a few days, it is an easy task for the skinny and much more maneuverable wasp to pop the older one with its jaws like a balloon (upper inset on photo above right).

By the time the fly begins to pupate, it is in the soil and will not be parasitized by another wasp; at this point there is only one wasp survivor inside of it. The sclerotized head of the first stage wasp larva is no longer necessary, and when it molts to the second instar upon fly pupation, the helmet is gone.

Both the host, and thus by necessity, the parasitoid, have just one generation a year. There are a few short weeks as adults for them when the flies emerge from the soil and oviposit in ripe walnut fruits, and then the emerging adult wasps try to find them and parasitize as many as possible. Flies and wasps then diapause (a type of insect hibernation) in the soil for nearly a year until ripe walnut fruits are available again.

Labels: cool bugs, ecology, flies, insects, wasps

In my last post I explored my own thoughts about this question. This second part is a mini-review on the science that has been done in this area.

There is actually quite a bit of scientific literature on the intersection of music and language in the brain - a Web of Science search on "music brain language" produced over 600 citations, a sample of which I skimmed.

The overall gist of the papers is that there is quite a bit of overlap in brain regions that are activated during language vs. music processing, but these areas are by no means congruent. In fact it was amusing to me that many authors appeared to be arguing either that language and music matched up well, or that they did not, and both "sides" had plenty of evidence to support their case. Both music and language are complex, with several components, and the similarity between processing seems to depend on what components are compared.

Excerpts from the abstract of the first example (Brown et al., 2006. Music and language side by side in the brain: a PET study of the generation of melodies and sentences. European Journal of Neuroscience 23:2791-2803):

Parallel generational tasks for music and language were compared using positron emission tomography. Amateur musicians vocally improvised melodic or linguistic phrases in response to unfamiliar, auditorily presented melodies or phrases...Direct comparisons of the two tasks revealed activations in nearly identical functional brain areas, including the primary motor cortex, supplementary motor area, Broca's area, anterior insula, primary and secondary auditory cortices, temporal pole, basal ganglia, ventral thalamus, and posterior cerebellum. Most of the differences between melodic and sentential generation were seen in lateralization tendencies, with the language task favouring the left hemisphere. However, many of the activations for each modality were bilateral, and so there was significant overlap...

Thus the tasks of improvising a sentence (something we all do several hundred times a day) and improvising a melody (something only a subset of us do regularly) were clearly related but not identical. I assume they used amateur musicians in order to make it easier for the subjects to improvise a melody, but anyone really could do this (even if they hummed random notes that were "ungrammatical" compared to their sentences), so I wish they had done a group of nonmusicians as well, to see if there are any differences. If so, it would suggest (although obviously not prove) that experience affects musical processing.

Vuust et al. (2006. It don't mean a thing ... Keeping the rhythm during polyrhythmic tension, activates language areas (BA47). Neuroimage 31:832-841) examine a specific feature of music, especially common in jazz music - the use of a counter rhythm on top of the main rhythm of a piece - on processing of the music:

...We here demonstrate that Brodmann area 47, an area associated with higher processing of language, is activated bilaterally when musicians tap the main pulse in a polymetric context where the music emphasizes a counter meter. This suggests that the processing of metric elements of music relies on brain areas also involved in language comprehension. We propose that BA47 is involved in general neuronal processing of temporal coherence subserving both language and music.

So it appears that the rhythm associated with music and the rhythm associated with language could be related, as far as our brains are concerned. Rhythm in language is not something I have previously thought much about, but it is certainly part of the package. One reason early computer voices sounded so mechanical was the lack of cadence to the spoken word. This seems to be something that is variable not only among languages but among dialects - accents (e.g. the many accents that exist just in the U.S.) are not only about word pronunciation, but the rhythm of speech as well. So I found this result very interesting.

Slevc, and Miyake (2006. Individual differences in second-language proficiency: Does musical ability matter? Psychological Science 17:675-681) start from the question: why do some people pick up second languages so much easier than others? They hypothesize musical ability affects second-language acquisition, much as it apparently affects first-language skills such as reading in children. "Musical ability" was measured using something called the Wing Measure of Musical Talents (taken from Wing, H.D. 1968. Tests of musical ability and appreciation: An investigation into the measurement, distribution, and development of musical capacity (2nd ed.). London: Cambridge University Press). There is no attempt here to distinguish innate from learned musical ability, so the term means simply some combination of the two.

They found, essentially: "Although the link may be restricted to L2 [second language] phonology, individuals who are good at analyzing, discriminating, and remembering musical stimuli are better than other people at accurately perceiving and producing L2 sounds." The connection to musical ability is specifically the ability to reproduce the sounds associated with a foreign language (all the subjects were Japanese who began speaking English after age 11). The authors are quick to point out that musical ability is not essential for good second language acquisition, but it appears to facilitate it.

Peretz (2006. The nature of music from a biological perspective. Cognition 100:1-32) agrees with me:

Paradoxically, the musical capacity appears to be fully developed in only a minority of humans who can make music. Becoming a proficient musician requires thousands of hours of practice and, in most case, explicit transmission. This is often taken as an argument against the notion that the musical capacity is innately determined. If genes were responsible for the human musical capacity, then everyone should be able to engage in musical activities. In fact, everyone does. Nearly everyone can carry a tune (Dalla Bella, Gigue`re, & Peretz, submitted) and move to music. The problem arises from the association of music-making with an elite of professional musicians. What is usually forgotten is that music is meant for the ears of the majority. Everyone from all walks of life and all cultures is musical to some extent. Unless they are tone-deaf, all humans exhibit a precocious inclination for music. In short, music appears as natural as language is.

But what about those tone-deaf people we all know? More from Peretz: "...there are cases of musically inept individuals who have normal language and intelligence. As noted, these individuals exist and are commonly called tone-deaf...The selectivity of the musical disability is remarkable. These tone-deaf individuals can have above average language skills, and may speak several languages without accent... However, they are unable to sing, dance or recognize music, despite formal training. This condition is termed congenital amusia...illustrating exceptional isolation of musical modules in the developing brain."

This and evidence from brain-damaged people suggests that language and music are indeed quite separate in the brain, at least for some people. I suspect that the separation or overlap is variable among people; the brain is well known to be plastic in its regional specialization. People with disabilities for certain senses are known to co-opt the brain regions normally responsible for processing those senses for other tasks, such as the processing of the remaining senses.

My conclusion from my snippet of light research is that language processing and music processing are largely overlapping yet different tasks; that musical functionality is present in nearly everyone at birth, and that proficiency in music is probably due to practice. If we all practiced music skills as much as language skills, it might not be a world of Mozarts, but it might at least be a world of Salieris. We might indeed have better language skills as a consequence of exercising the relevant parts of our brains that much more.

Labels: brain, humans, music

I have thought some over the years about what makes some people music composers and others not. Obviously some sort of interest in music is a prerequesite, but is interest or ability in music truly innate? It is certainly assumed to be by many people. We love to use the word "talented" to describe someone who is good at something most people aren't good at. But supposedly - it is at least an urban myth - it rankled Michael Jordan a bit when people referred to him as talented at basketball, because what he certainly had was a great work ethic. Even knowing that, I believe most people would assume that Jordan was somehow predisposed to be good at basketball, and his work ethic is what made him great. And we all probably know people who seem so uncoordinated that no matter how much they were to practice, they would have no hope as basketball players.

These observations make it tempting to believe a certain amount of ability in specific areas such as athletics, mathematics, and music is innate. I am not so sure, however. I, for example, am a very committed amateur musician. I play several instruments and am a composer. But I hesitate to assume that any of this is due to "innate" ability. Why? Because I have very strong evidence to the contrary. I have a tape of a friend and myself playing clarinet and saxophone together in the sixth grade, when we had both been playing about a year. It is one of the most horrifying sounds you can imagine - we are close to a half-tone off in pitch, and we are clearly oblivious to this.

Ability to hear differences in pitch, then, clearly is at least partly learned, because I learned it, after being hopeless at it early in my music career. What about composition, though?

Music has always seemed to me very much like a language. If they are analagous, then all speaking humans are composers, because we rapidly composed new sentences every time we speak. Some of these may require editing to become more coherent, but in general we are able to get our point across quite well. Why should music be any different? Notes can be thought of as words, and we already use the term, "musical phrase," and music has a grammar, a syntax, which varies among cultures as do languages. In my mind the main difference is that language is an essenti