Hammerschmidt and colleagues (2009) recently published an empirical investigation of optimal host switching. Parasites that must infect multiple hosts to complete their life cycle face a complex set of challenges. One of these is determining the timing of the switch. The authors of this paper look at the trade-off involved in staying in an intermediate host so as to become larger and more fecund in the next host and the increased chance of mortality in the current host. The authors conduct two different experiments with a tapeworm parasite, Schistocephalus solidus. In one experiment they examined the behavior of the first intermediate host, cyclopoid copepods (Macrocyclops albidus). In the second experiment they directly measured differences in fecundity among different host switch timing between the first and second intermediate hosts (in this case the three-spine stickleback, Gasterosteus aculeatus). The authors also build an optimality model and use the data from these experiments as well as some previously published data to confirm that the switch from the first to second host occurs at an optimal time for parasite fecundity.What was most novel about this paper to me was the modification of the host behavior that had the effect of reducing parasite transmission, at least in the short run. Since the parasite was transmitted trophically, the next host eats the previous host, predation enhancement or avoidance directly influences the rate of transmission. The authors found some evidence of predation enhancement after the optimal switch time, but the stronger evidence was at least a shift in behavior of the current host. Before the parasite is mature in the first intermediate host, or before the optimal switching time to the second intermediate host, there was a reduction in movement which translates into predator avoidance behavior. Manipulating the host so as to allow the parasite a longer time to grow is a very clever strategy. In hosts that have a high potential mortality, this strategy may be found among a diversity of trophically transmitted parasites.ReferenceHammerschmidt, K., K. Koch, M. Milinski, J. C. Chubb, and G. A. Parker. 2009. When to go: Optimization of host switching in parasites with complex life cycles. Evolution 63:1976-1986.Hammerschmidt, K., Koch, K., Milinski, M., Chubb, J., & Parker, G. (2009). Whe to go: Optimzation of host switching in parasites with complex life cycles Evolution, 63 (8), 1976-1986 DOI: 10.1111/j.1558-5646.2009.00687.x... Read more »
Hammerschmidt, K., Koch, K., Milinski, M., Chubb, J., & Parker, G. (2009) Whe to go: Optimzation of host switching in parasites with complex life cycles. Evolution, 63(8), 1976-1986. DOI: 10.1111/j.1558-5646.2009.00687.x
More than 50 years ago, the first antipsychotic medications appeared in the United States. While these drugs -– fluphenazine, haloperidol, chlorpromazine, and others — were effective in treating a variety of psychiatric conditions, their safety and tolerability presented many drawbacks. It was not until the 1990s when a new class of antipsychotic medications emerged that [...]... Read more »
Bishara, D., & Taylor, D. (2008) Upcoming Agents for the Treatment of Schizophrenia. Drugs, 68(16), 2269-2292. DOI: 10.2165/0003495-200868160-00002
Peritogiannis, V., Stefanou, E., Lixouriotis, C., Gkogkos, C., & Rizos, D. (2009) Atypical antipsychotics in the treatment of delirium. Psychiatry and Clinical Neurosciences. DOI: 10.1111/j.1440-1819.2009.02002.x
Chemical Abstracts Service (CAS) will announce the 50 millionth registered chemical substance in its Registry, tomorrow (8th September).
According to the email I received from a CAS spokesman, “The number itself represents an important milestone both for researchers and CAS, but even more significant is the pace of scientific discovery around the world.” Roger Schenck, Manager [...]50 Million Chemicals and Counting is a post from: Sciencebase Science Blog
... Read more »
Lipkus, A., Yuan, Q., Lucas, K., Funk, S., Bartelt, W., Schenck, R., & Trippe, A. (2008) Structural Diversity of Organic Chemistry. A Scaffold Analysis of the CAS Registry. The Journal of Organic Chemistry, 73(12), 4443-4451. DOI: 10.1021/jo8001276
As many know, this is the 150th anniversary of the publication of On the Origin of Species. If I may be so bold, one of the things that might distinguish our thinking about evolution in the last 50 years from the first hundred years might be the speed at which natural selection can operate. For a long time, we thought of evolution taking long times: millions of years would be needed to see the gradual accumulation of changes. We learned in the past few decades that we can see the effects of selection over the course of a few decades.
There are a few fast changing situations that press should press the fast forward button on natural selection. Invasions are one. That’s why they’re invasions, not slow expansions. Boronow and Langkilde look at how the invasion of red fire ants are affecting fence lizards.... Read more »
Boronow, K., & Langkilde, T. (2009) Sublethal effects of invasive fire ant venom on a native lizard. Journal of Experimental Zoology Part A: Ecological Genetics and Physiology. DOI: 10.1002/jez.570
Today’s post is a review of a recent meta-analysis looking at the accuracy of clinical tests for meniscal lesions from our friend Dan Lorenz, MS, PT, ATC/L, CSCS. RESEARCH UPDATE: Clinical Tests for Meniscal Lesions Dan Lorenz, MS, PT, ATC/L, CSCS It has been estimated that approximately 27% of all outpatient physical therapy visits are for knee pain.1 Of the many possible lesions causing pain, one common source is from a meniscal lesion. Recently, Meserve et al2 did a meta-analysis summarizing the accuracy of clinical tests for assessing meniscal lesions of the knee. Previous researchers have performed meta-analyses on clinical tests for meniscus tear, but failed to account for the variability and in test sensitivity and specificity due to differences in methodological quality among the studies.3-5 Because of that, diagnostic accuracy could be skewed. Clinicians should select tests with the highest sensitivity or negative likelihood ratio to rule out meniscal injury, or conversely, rule in meniscal injury with tests having high specificity or positive likelihood ratios.1 The purpose of this update is to provide a synopsis of what was found in their review. Eleven studies satisfied the authors criteria of sixty-four total considered for potential review. Joint line tenderness, Apley’s, and McMurray’s were reviewed based on them being the most common tests utilized. Ege’s and Thessaly tests were also evaluated, but the quality of the studies was not good based on small sample sizes. Of note, diagnostic tests findings were interpreted without considering whether the lateral or medial meniscus was torn. The researchers ultimately found that: Joint line tenderness was found to be the superior test in terms of sensitivity, followed by the McMurray’s and then Apley’s. Specificity values were larger with Apley’s compared to joint line tenderness and McMurray’s. Ege’s Test and the Thessaly Test,6-7 tests that have either compression with weight bearing or clinician-applied axial rotation, were found to have the strongest diagnostic accuracy, but with smaller samples in the studies. Based on this review, like any other special test used clinically, a combination of a thorough history along with a physical exam will help the clinician differentially diagnose conditions that are presented to them. As with many other tests used for other pathologies, it appears that using several tests to detect meniscal lesions is supported by the literature. EDITOR’S NOTE: The results are interesting and clinically applicable. Anecdotally, I have always observed that joint line pain and pain with deep knee flexion, either with weightbearing or passively, where the most indicative of meniscal pathology in my hands. Conversely, passively extending the knee into hyperextension seems to be uncomfortable in patients with anterior horn tears. One test that just doesn’t seem to work well for me is the Apley’s test. Sounds like the test may still useful as the specificity is high. What has your experience been? What other tests you feel are helpful in detecting a meniscal lesion? Thanks for the review Dan. References Jette AM, Delitto A. Physical therapy treatment choices for musculoskeletal impairments. Phys Ther. 1997; 77: 145-54. Meserve BB, Cleland JA, Boucher TR. A meta-analysis examining clinical test utilities for assessing meniscal injury. Clinical Rehabilitation. 2008; 22: 143-161. Jackson JL, O’Malley PG, Kroenke K. Evaluation of acute knee pain in primary care. Ann Intern Med. 2003; 139: 575-88. Scholten RJ, Deville WL, Opstelten W, et al. Accuracy of physical diagnostic tests for assessing meniscal lesions of the knee: a meta-analysis. J Fam Pract. 2001; 50: 938-44. Solomon DH, Simel DL, Bates DW, et al. The rational clinical examination. Does this patient have a torn meniscus or ligament of the knee? Value of the physical examination. JAMA. 2001; 286: 1610-20. Akseki D, Ozcan O, Boya H, et al. A new weight bearing meniscal test and a comparison with McMurray’s test and joint line tenderness. Arthroscopy. 2004; 20: 951-58. Karachalios T, Hantes M, Zibis AH, et al. Diagnostic accuracy of a new clinical test (the Thessaly test) for early detection of meniscal tears. J Bone Joint Surg Am. 2005; 87: 955-62. Meserve BB, Cleland JA, & Boucher TR (2008). A meta-analysis examining clinical test utilities for assessing meniscal injury. Clinical rehabilitation, 22 (2), 143-61 PMID: 18212035 ***************************
View my collection of all the latest journal abstracts as they are published.
View my list of favorite recommended rehab books and products.
Sign up for my FREE newsletter for even more great content!
... Read more »
Meserve BB, Cleland JA, & Boucher TR. (2008) A meta-analysis examining clinical test utilities for assessing meniscal injury. Clinical rehabilitation, 22(2), 143-61. PMID: 18212035
Contrary to popular sentiment and science fiction clichés, human evolution hasn’t stopped. If anything, we’re actually evolving faster than ever according to research published in 2007. Moving into new environments and an explosion in our populations drastically increased the rate at which our genomes are changing and being selected. Compared to our prehistoric ancestors, we [...]... Read more »
Based on two psychiatric assessment procedures, a computer program investigating the presence of a psychotic disorder and a personality questionnaire, Salvador Dali was found to have a personality disorder for DSM Cluster A and B. He was also found to meet the diagnostic criteria for psychotic illnesses.
You can’t diagnose psychiatric illness without doing a face [...]... Read more »
Murphy, C. (2009) The link between artistic creativity and psychopathology: Salvador Dalí. Personality and Individual Differences, 46(8), 765-774. DOI: 10.1016/j.paid.2009.01.020
Recently I tried to make this case that a mutation in my mitochondrial DNA
didn't make me so very different than the rest of you:
Our typical conception of mutation is drawn from the tragic effects of those
relatively rare mutations, induced in our bodies or passed on through germ
cells, that lead to diseases (or, in movies to super powers). In fact, we
are, each of us, mutants. DNA replication is not perfect, we are born with about
6 or 7 new mutations...
Well, a paper published last week proved my general point while proving me wrong
on the detail by a factor of 20 or so. A team of British and Chinese
researchers that work with a family that has a unique Y-chromosome linked
hearing disorder sequenced the entire sequence of the Y-chromosome from two
men and found four mutations. Scaling up from the Y-chromosome to the whole
genome then dividing by the combined 13 generations that separate the two men
they arrived a mutation rate of 3 x 10-8 changes per nucleotide per
generation. That would give us between one and two hundred new mutations.
This finding isn't actually a revelation. We had an idea of the rate of
mutation in the human genome before we even knew what a gene was made of. JBS
Haldane, one of the founders of evolutionary genetics and perhaps the only
person to have enjoyed the First World War, used his theory of mutation
selection balance to estimate new haemophilia causing mutations occur about
once in every 105 generations. When you consider that the gene
responsible for Haemophilia A contains about 7 x 103 nucleotides
and changes to many of those won't cause Haemophilia Haldane's estimate looks
In fact, the Cool New Stuff in this paper isn't really the number that
they've produced - that number is similar Haldane's esimate and to the
measurble error rate of the enzymes that replicate our DNA and to the
rate inferred by comparing our genome to that of the cimpanzee *. What's really neat is the fact they directly measured the rate by resequencing the whole Y-chromosome - that's more than 10 million bases to sequence, 35 at a time, and put together to check for mutations. The sort of project that would only have been possible as part dedicated genome sequencing projects a couple of years ago. With only two people and four mutations the estimate has
wide error bars but it does pave the way to more accurate estimates for
particular areas of the genome (including those underlying for diseases) and
particular lineages of organisms (which is important for us evolutionary
I can't revel in my earlier post being confirmed in the broad sense without
apologising for misleading you in the details. I was just flat out wrong when I
claimed we all have 6 or 7 new mutations - I used a number that I had in my
head and didn't bother to look it up. You can see where my number came from
once you consider that only about 4% of the genome is functional DNA - 150
mutations in your genome will lead to about 6 mutations in functional regions.
Still, the original is (about to be) modified and I am suitably shamed.
* As Larry Moran points out taken together these studies tell us something
about the way evolution works. If the observed rate of mutation in DNA
replication is not wildly different than the inferred rate of mutation in a
pedigree or between closely related species most mutations aren't being
selected against - more evidence for the importance of neutral theory in
molecular evolution. back to the story ^
 Xue, Y., Wang, Q., Long, Q., Ng, B., Swerdlow, H., Burton, J., Skuce, C., Taylor, R., Abdellah, Z., & Zhao, Y. (2009). Human Y Chromosome Base-Substitution Mutation Rate Measured by Direct Sequencing in a Deep-Rooting Pedigree Current Biology DOI: 10.1016/j.cub.2009.07.032
J. B. S. Haldane (1935). The rate of spontaneous mutation of a human gene Journal Of Genetics DOI: 10.1007/BF02717892... Read more »
Xue, Y., Wang, Q., Long, Q., Ng, B., Swerdlow, H., Burton, J., Skuce, C., Taylor, R., Abdellah, Z., & Zhao, Y. (2009) Human Y Chromosome Base-Substitution Mutation Rate Measured by Direct Sequencing in a Deep-Rooting Pedigree. Current Biology. DOI: 10.1016/j.cub.2009.07.032
In their most recent article, Sommer, Dantas and Church have hit upon the craigslist for antibiotic resistance used by bacteria living in the human body. The basic genomic material needed for antibiotic resistance is readily available at your local bacterial community. Resistance genes are everywhere, and it is clear that, despite transmission barriers between species, they are transmitted. Bacteria have a large pool form which to draw new resistance genes. The arms race between drug developers and bacteria just got this much tougher.... Read more »
Sommer, M., Dantas, G., & Church, G. (2009) Functional Characterization of the Antibiotic Resistance Reservoir in the Human Microflora. Science, 325(5944), 1128-1131. DOI: 10.1126/science.1176950
The recent emergence of study into ‘pacing’ or activity regulation in pain management is a welcome addition to our knowledge of this coping strategy. Although pacing has been described and included in many self-help books as well as clinical texts as an effective strategy for people with chronic pain to use, the research base [...]... Read more »
Karsdorp, P., & Vlaeyen, J. (2009) Active avoidance but not activity pacing is associated with disability in fibromyalgia. Pain. DOI: 10.1016/j.pain.2009.07.019
As a medical association in Spain has recently communicated to the press, more than anything there seems to be an epidemic of fear going on. As I am currently living in Portugal, I do not know what the situation is in other countries, but I can tell you how the situation is here. Every news bulletin starts with more news about the flu, even though no one has died here yet. It then finishes with a previously recorded warning on how one should wash hands frequently and keep 1m away from other people while talking to them, quite an ordeal in a country where the common greeting is a couple of kisses in the cheek. In addition, we have ambulances going around with the paramedics dressed as in the photo, right out of films like ‘Outbreak’. Now, most people seem to assume that because I have just graduated with a Biology degree that I should know everything there is to know about the current flu. Besides the generic question ‘So, what do you think about this flu thing?’, I have had some more specific questions, from ‘I heard that it is impossible for this combination of genes to happen in nature, surely this must have been created by evil scientists with corporative interests?’ to ‘This virus is called H1N1, the 1918 pandemic virus was also H1N1, are we all going to die of Spanish flu?’. I try to explain people that at uni we are taught how to get informed about things, rather than becoming specialist on every single biological problems; and that frankly I am so fed up of hearing about this flu that I couldn’t be bothered to look it up. However, I think the hysteria might be affecting me, probably because I’ve just read the book Blindness (if you have read it/watched the film you will know why). So I decided to interrupt my holidays-away-from-science to read a bit about this topic, and thought I would tell you some of my findings.My first port of call was the website of the World Health Organisation, usually a reliable source for information. I was pleasantly surprised by the lack of over-dramatic information. There is of course a whole section dedicated to this flu, right in the home page, but the answers given in the FAQs seem quite sensible. It tells us that 2009 A(H1N1) is spread as the normal flu, and that the current worries as based on the fact that being a virus which never circulated in humans before, there is no, or very little, immunity. In addition, as stated in their website, the virus is spreading fast in young people (10-45), from a majority of mild cases to some serious illnesses, the majority of which in patients with underlying conditions. The recommendations of the WHO are to take pain killers and drink loads of fluids if you have the flu. And only contact the medical services if you have serious symptoms like shortness of breath, or if the fever lasts for longer than 3 days. Quite unlike what recently happened in Portugal. When a man who had travelled to Britain was diagnosed with this flu, he saw his house invaded by doctors who quickly took him away to a hospital and confined the whole family to their house. Without telling them what to do or when they could leave.Anyway, I then thought it would be a good idea to read some information from journals, a bit more scientific and hopefully less dramatic source of news. However, as you know, I am currently unable to access most papers, as I am in between universities and am yet to be provided with a username in my new institution. So what follows is based on a couple of papers I could access, and is by no means comprehensive.As an introduction, some information from the Virology handouts we were given last October. Influenza viruses are RNA viruses that have a segmented genome (8 segments/genome). The glycoprotein spikes, haemagglutinin (HA) and neuraminidase (NA) are important in the entrance of the virus in the host cells. There are 15 known HA and 9 NA serotypes, and their combination provides the name that we see for the viruses such as H1N1. Birds and pigs are important reservoirs for genetic and antigenically diversity and reassortment in these viruses. In particular pigs, as their cells can be infected by both avian and human influenza viruses, making them nice ‘mixing pots’.In July this year Garten et al., published a paper in Science in which they characterised the 2009 A(H1N1) virus both antigenically and genetically. They start the paper by giving a small introduction on the influenza pandemics of the last century, and how we got from those to the current 2009 A(H1N1). Then it goes on to characterise the actual viruses. The closest ancestral gene for each of the eight segments seems to have a swine origin, although having originally come from avians and sometimes humans in different occasions. This is quite interesting, as swine influenza viruses had not, until now, caused much disease or been incredibly good at human-human transmission. As the authors point out, this virus probably had been circulating for a while in pigs, unnoticed due to lack of monitoring.Analysis of the virus genome showed that none of the molecular signatures of increased transmissibility or virulence of A(H1N1) viruses can be found in this strain, and that functionally important receptor binding sites on HA do not differ from classic swine influenza viruses. No markers were also found that indicate adaptation to the human host or features of previous pandemic virus. The main important difference seems to be a genetic marker for resistance to adamantine antivirals, but the virus still seems to be sensitive to the other type of antivirals, the neuraminidase inhibitors. So, this study concludes, we must be worried about this virus firstly because we don’t really know what makes it good at replicating in humans, and secondly because it has a genetic composition not seen before, so we don’t really know what to expect.I then went on to read a couple of papers regarding studies done in mammal models such as ferrets (apparently classic models for influenza studies) and mice.The first study was published in Science also in July, by Maines et al. This post is becoming quite long already, so I’ll just summarise their results (based on 3 independently isolated 2009 A(H1N1) viruses as compared with a seasonal influenza strain). They basically inoculated 106 p.f.u in ferrets and monitored different indicators such as body weight, viral titres, direct and indirect transmissibility, etc. The main conclusion from the study was that 2009 A(H1N1) caused higher morbidity (weight loss, etc, depending on which virus isolate), showed, unlike seasonal flu, high viral titres in the lower respiratory tract or the intestine, but that it was less efficient at indirect transmission (putting healthy ferrets in cages near to inoculated animals).The second animal study I looked at was published online by Nature, in what they call a ‘near final version’. They also used virus isolated from infected humans, though not all of which were the same as in the Science paper. They studied the effect of these viruses in mice, macaques, ferrets and pigs, though not all of the virus isolates seem to have been used in all of the experiments. They also looked at more indicators, such as pro-inflammatory cytokines, lung pathology, etc. In ferrets the results were similar to those of the Science paper, except that this time indirect transmission was successful. In mice and macaques, the 2009 A(H1N1) virus seems to be worse than the seasonal virus (at least one of the isolates that they seem to mostly use throughout, CA04) although according with which criteria varies with the model. The inoculated pigs were asymptomatic, explaining why the virus had not been noticed before in this animal.So, what are the conclusions I could get, overall, from these three studies? Overall it seems that the 2009 A(H1N1) virus is worse than the seasonal influenza viruses in mammalian models. However, how much worse is probably hard to say. I am not familiar at all with viral studies, so it is hard for me to critically analyse these studies, but it seems to me that in most cases the n numbers were quite small (n=3 in some cases in the Nature study), but this is perhaps not surprising, as they must have been quite quick studies, considering the current need to understand this new virus. And, as it is probably the case in most animal studies in general, I reckon the doses used were probably much higher than what humans would be exposed to in the real world. In addition, there is always the question on how well do these animal models really reflect what happens in humans.In any case, it seems that so far these studies indicate that 2009 A(H1N1) is, in these models, worse than seasonal flu. Whether it is as bad as some of the pandemics that have been affecting us in the last 100 years it is unknown. The other worry is of course that the virus might evolve i... Read more »
Garten RJ, Davis CT, Russell CA, Shu B, Lindstrom S, Balish A, Sessions WM, Xu X, Skepner E, Deyde V.... (2009) Antigenic and genetic characteristics of swine-origin 2009 A(H1N1) influenza viruses circulating in humans. Science (New York, N.Y.), 325(5937), 197-201. PMID: 19465683
Garten, R., Davis, C., Russell, C., Shu, B., Lindstrom, S., Balish, A., Sessions, W., Xu, X., Skepner, E., Deyde, V.... (2009) Antigenic and Genetic Characteristics of Swine-Origin 2009 A(H1N1) Influenza Viruses Circulating in Humans. Science, 325(5937), 197-201. DOI: 10.1126/science.1176225
Maines TR, Jayaraman A, Belser JA, Wadford DA, Pappas C, Zeng H, Gustin KM, Pearce MB, Viswanathan K, Shriver ZH.... (2009) Transmission and pathogenesis of swine-origin 2009 A(H1N1) influenza viruses in ferrets and mice. Science (New York, N.Y.), 325(5939), 484-7. PMID: 19574347
Itoh, Y., Shinya, K., Kiso, M., Watanabe, T., Sakoda, Y., Hatta, M., Muramoto, Y., Tamura, D., Sakai-Tagawa, Y., Noda, T.... (2009) In vitro and in vivo characterization of new swine-origin H1N1 influenza viruses. Nature. DOI: 10.1038/nature08260
Nearly everyone seems to carry a mobile phone these days. What if social scientists could exploit this technology to spy on our social behaviour: who we speak to and who we spend time with? It turns out they already are. Nathan Eagle, named recently as a leading young innovator by Technology Review, and his colleagues, have published one of the first studies into social network analysis using spy software loaded onto Nokia smartphones.For nine months, Eagle's team recorded data from the phones of 94 students and staff at MIT. By using blue-tooth technology and phone masts, they could monitor the movements of the participants, as well as their phone calls. Their main goal with this preliminary study was to compare data collected from the phones with subjective self-report data collected through traditional survey methodology.The participants were asked to estimate their average spatial proximity to the other participants, whether they were close friends, and to indicate how satisfied they were at work.Some intriguing findings emerged. For example, the researchers could predict with around 95 per cent accuracy who was friends with whom by looking at how much time participants spent with each other during key periods, such as Saturday nights.There were also discrepancies between the two data sets. For example, participants tended to overestimate how much time they spent with friends, and underestimate how much time they spent with non-friends. Also, the accuracy of the self-report proximity data tended to peak over the previous seven days (at which point it correlated highly with the phone records), but then it's accuracy tailed off. This provides useful information about the validity of survey records over time, and an interesting insight into people's memories for their social interactions.As regards satisfaction at work, it turned out that people who were in closer proximity to their friends during work time, tended to be happier at work, whilst participants less happy at work tended to make more phone calls to friends during work hours."Data collected from mobile phones have the potential to provide insight into the underlying relational dynamics of organisations, communities and potentially societies," the researchers said._________________________________Eagle, N., Pentland, A., & Lazer, D. (2009). Inferring friendship network structure by using mobile phone data. Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.0900282106
... Read more »
Eagle, N., Pentland, A., & Lazer, D. (2009) Inferring friendship network structure by using mobile phone data. Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.0900282106
Here are two stories involving recent psychological/anthropological/biological research:In Future, Science Could Erase Traumatic Memories (NPR)The Culture of Being Rude (Smithsonian Magazine)As to the first, while describing an interesting study, the story itself is characteristically media. We can pinpoint the amygdala as being the "source" of the flight-or-fight (ie, fear) response, and we have now learned that as we (or, at least, as rats) grow, a "protective molecular sheath" coats the cells of the amygdala, which seems to also "protect" the memories contained within. So baby rats can forget "traumatic" experiences which would otherwise elicit the fear response. This doesn't mean, however, that chemically (or otherwise) removing this molecular cell coating would actually "erase" memories. Baby rats forget past fears, adult rats do not; adult rats with the molecular coating removed recover "their early ability to erase fearful memories." This is not the same as actually erasing the memories themselves. Current phobia and post-traumatic stress disorder therapies aim to "reprogram" the person's fear response - such that, as the story says, a soldier who survived being in a car bomb can "learn to believe that a car ride doesn't have to end in violence." The advent of drug therapies which would dissolve this chemical sheath on amygdala cells would still need to be in tandem with psychological treatment. This, of course, also assumes that human beings would react as rats do to the removal of this molecular layer. Though we are similar, we are not the same. And, in the end, is it so bad that fearful memories are "erasure-resistant," as the study itself (ref 1) says? We may not wish to remember, but is that cause enough to warrant forgetting?The second story is also quite interesting. Several biologists from the University of New Mexico and UBC in Vancouver argue that one thing - disease - basically shapes who we are and how we behave, anthropologically speaking (ref 2). The article in Smithsonian Magazine does an excellent job of explaining the main points; to quote the author, Rob Dunn's, summary:Their theory is simple. Where diseases are common, individuals are mean to strangers. Strangers may carry new diseases and so one would do best to avoid them. When people avoid strangers—those outside the tribe—communication among tribes breaks down. That breakdown allows peoples, through time, to become more different.Differences accumulate until in places with more diseases, for example Nigeria or Brazil, there are more cultures and languages. Sweden, for example, has few diseases and only 15 languages; Ghana, which is a similar size, has many diseases and 89 languages. Cultural diversity is, in this view, a consequence of disease.Then Fincher and colleagues go even further. Where people are more xenophobic and cultures more differentiated from one another, wars are more likely. Democratic governments are less likely because the tribe or group comes first; the nation and individuals in other tribes within the nation come second. And finally, poverty becomes nearly inevitable as a consequence of poor governance, hostility between groups, and the factor that triggered this cascade in the first place—disease.It's a rather convincing argument, but, as we all know, everything looks like a nail when one has a spiffy new hammer. First and foremost, correlation does not necessarily imply causation. Many of those who commented on the article pointed out weaknesses in the study's theory, in addition to citing counter-examples:"Wouldn't this behavior eventually prove maladaptive? While disease-induced xenophobia might ensure a group's survival over the course of a few generations, wouldn't that group eventually become inbred if its members cannot curb their distrust of outsiders?" - Matthew Graybosch"The only way this theory works is if the researchers can demonstrate that indigenous theories of death and disease act identically to the modern germ theory they are using in this model." - heteromeles"Much as we are an animal, our society is far more complex and our behavior is, biologically looking, often times irrational and likely governed by more than biological factors, at least as we understand them now (although they do provide neurological and hormonal framework)." - Marko Pecarevic"...a small, genetically-homogeneous population may have particular reason to fear stranger's diseases, since these may wipe them out. The way out of this trap is to outbreed. But this exposes you to more diseases." - Peter H. ProctorWhile "rudeness" specifically isn't actually explained by the theory (but who reads articles titled "Pathogen prevalence predicts human cross-cultural variability in individualism/collectivism" anyway?), it would seem that, in the end, biology cannot alone explain the behavior of human beings, no matter how pretty a theory might appear (biology isn't like physics, sorry boys!). There has been, and perhaps always will be, a continuing argument over nature versus nurture (as Dunn eloquently wrote, "Somewhere, probably, a cultural anthropologist is writing and rewriting a thorough and vehement response."). Perhaps this is somewhere "true" religion can help - not the xenophobic, cultish religion, but the "love your neighbor as yourself," good-Samaritan, "heal the sick" kind of religion. We are taught to always extend our hand, even to the sick and leprous, and in light of the theory, this encouragement of sociological "mixing" would, in the end, bolster our immunity, both to disease and to fear of cultural diversity.References:(1)Gogolla N, Caroni P, Lüthi A, & Herry C (2009). Perineuronal nets protect fear memories from erasure. Science (New York, N.Y.), 325 (5945), 1258-61 PMID: 19729657(2)Fincher CL, Thornhill R, Murray DR, & Schaller M (2008). Pathogen prevalence predicts human cross-cultural variability in individualism/collectivism. Proceedings. Biological sciences / The Royal Society, 275 (1640), 1279-85 PMID: 18302996... Read more »
Gogolla N, Caroni P, Lüthi A, & Herry C. (2009) Perineuronal nets protect fear memories from erasure. Science (New York, N.Y.), 325(5945), 1258-61. PMID: 19729657
Fincher CL, Thornhill R, Murray DR, & Schaller M. (2008) Pathogen prevalence predicts human cross-cultural variability in individualism/collectivism. Proceedings. Biological sciences / The Royal Society, 275(1640), 1279-85. PMID: 18302996
The model of fear extinction originated from the Pavlovian classical conditioning paradigm in the early 1900s. Defined as a reduction in a conditioned fear response following a non reinforced exposure to a feared conditioned stimulus, fear extinction is known to involve the amygdala and medial prefrontal cortex (mPFC). It's also a frequently striven-for goal in cognitive behavioral therapy during the treatment of various phobias including arachibutyrophobia; the fear of peanut butter sticking to the roof of the mouth, or barophobia; the fear of gravity. Unfortunately, extinguished fear responses sometimes reappear with the passage of time (spontaneous recovery), through a shift of context (renewal), or by unsignaled presentations of the unconditioned stimulus (reinstatement). However, the likelihood of these events happening after a few intense sessions of fear exposure may differ significantly depending on the age of the patient according to a new study published in this weeks Journal of Neuroscience.Kim, Hamlin, and Richardson investigated the role of the mPFC during fear extinction among postnatal 24 day rats (P24) and postnatal 17 day rats (P17). They found that temporary inactivation of the mPFC during extinction training blocked extinction retention the following day in P24 rats but not in P17 rats. Furthermore, through immunohistochemical analyses they observed that extinction of conditioned fear involved an increased number of phosphorylated MAPK-immunoreactive (pMAPK-IR) neurons in the mPFC and amygdala in P24 rats, but an elevation of these neurons was only seen in the amygdala of P17 rats. The results show that the mPFC has no part in the neural circuitry underlying fear extinction in P17 rats. The authors suggest that fear extinction is essentially the process of unlearning for the younger rats. In other words, they're "erasing" their fear altogether! These important findings may significantly impact the future treatment of phobias; targeting and treating fears earlier rather than later in life. Perhaps one day we can teach little barophobic Johnny why the force of gravity isn't really such a scary thing after all. Kim JH, Hamlin AS, & Richardson R (2009). Fear extinction across development: the involvement of the medial prefrontal cortex as assessed by temporary inactivation and immunohistochemistry. The Journal of neuroscience : the official journal of the Society for Neuroscience, 29 (35), 10802-8 PMID: 19726637... Read more »
Kim JH, Hamlin AS, & Richardson R. (2009) Fear extinction across development: the involvement of the medial prefrontal cortex as assessed by temporary inactivation and immunohistochemistry. The Journal of neuroscience : the official journal of the Society for Neuroscience, 29(35), 10802-8. PMID: 19726637
Japan kills over a hundred minke whales each year under the guise of “scientific whaling”, and much of the meat ends up in the commercial markets destined for Japanese dinner plates. Now a study just published in Animal Conservation indicates that a similar number of whales are killed as “bycatch” in Japanese coastal waters, [...]... Read more »
Lukoschek, V., Funahashi, N., Lavery, S., Dalebout, M., Cipriano, F., & Baker, C. (2009) High proportion of protected minke whales sold on Japanese markets is due to illegal, unreported or unregulated exploitation. Animal Conservation. DOI: 10.1111/j.1469-1795.2009.00302.x
Does this look like a religious woman to you? According to a study by Prof Richard Wiseman in the New Scientist in February this year (hey, I've only just read it, OK?), this is a typical face of a religious person in the UK.What they did was to ask readers to send in photos of themselves, along with a rating of their personality. They digitised the key features, and produced an average of each personality type. When other people were asked to guess the personality based on face alone, they were pretty accurate for religious women - 73% got it rate.There was lots of stuff in the article about why this might be (androgens or other genetic linkages, for example), but no mention of one blindingly obvious explanation.You see, the most striking difference between the 'religious' face and the 'non-religious' one is that the non-religious face is smiling.In fact, the same goes for all the pairs of female faces that the raters were able to identify correctly. The lucky face and the trustworthy face are both smiling.The raters couldn't get the male faces right. And sure enough, neither pair of male faces are smiling. It seems that it's the smile that gives the game away. In a letter in the 21 March issue, a reader points this out:Our brains seem to be hard-wired to interpret smiling positively. Nearly all of your data can be explained by it, yet the experiment does not control for smiles. Only the paired female images gave positive results, and those were the pairs that exhibited greater differences in their smiles. For example, both composite faces under the "Humorous?" heading are smiling to a similar extent, and there was no difference found between them. In the "Religious?" category, we might suppose that people would consider those who are religious to be more serious, and the image with the smaller smile is indeed chosen by the majority. Wiseman responds by conceding that smiling might explain 'some' of the results. But points out that religious people are supposed to be happier than the non-religious.This study doesn't show that you can identify religious people by the shape of their faces. But it does suggest that, in the UK at least, religious people are thought of as unsmiling.That would explain why the religious people didn't smile. They knew, of course, that the photograph was going to be linked to their personality traits. And that knowledge would undoubtedly change their behaviour.Interestingly, both religious and non-religious, and the raters, knew the rules of the game. Religious people in the UK aren't supposed to be smiley!_______________________________________________________________________________________This work by Tom Rees is licensed under a Creative Commons Attribution-Share Alike 2.0 UK: England & Wales License.
... Read more »
Rees, TJ. (2009) Is Personal Insecurity a Cause of Cross-National Differences in the Intensity of Religious Belief?. Journal of Religion and Society. DOI: http://moses.creighton.edu/JRS/2009/2009-17.html
The authors report that in 2106 consecutive patients 65 years or older admitted for syncope, "Postural blood pressure (BP) recording, performed in only 38% of episodes, had the highest yield with respect to affecting diagnosis (18%-26%) or management (25%-30%) and determining etiology of the syncopal episode (15%-21%)...... Read more »
Mendu ML, McAvay G, Lampert R, Stoehr J, & Tinetti ME. (2009) Yield of diagnostic tests in evaluating syncopal episodes in older patients. Archives of internal medicine, 169(14), 1299-305. PMID: 19636031
Lasers which can control the movement of particles are still confined to the microscopic world, but if you have an over-reactive imagination, you might wonder just what the limits are on the size of bodies which these devices can control and whether science fiction's tractor beams are becoming a reality. Today's technology may not be capable of producing force fields that lock on to starships and guide them in to land, but the size of particles which can be manipulated by light are getting larger.
read more... Read more »
Applegate Jr., R., Marr, D., Squier, J., & Graves, S. (2009) Particle size limits when using optical trapping and deflection of particles for sorting using diode laser bars. Optics Express, 17(19), 16731. DOI: 10.1364/OE.17.016731
Google-like algorithm pinpoints key species in food web
... Read more »
Allesina, S., & Pascual, M. (2009) Googling Food Webs: Can an Eigenvector Measure Species' Importance for Coextinctions?. PLoS Computational Biology, 5(9). DOI: 10.1371/journal.pcbi.1000494
Can biologists and mathematicians accomplish more together than working separately? My answer to that question has always been a resounding yes but today I am backing up that statement with a piece of research: the result of a collaboration involving mathematicians and biologists (and a pathologist) in Tampa, Nashville and Houston.
Basanta, D., Strand, D., Lukner, R., Franco, O., Cliffel, D., Ayala, G., Hayward, S., & Anderson, A. (2009). The Role of Transforming Growth Factor- -Mediated Tumor-Stroma Interactions in Prostate Cancer Progression: An Integrative Approach Cancer Research, 69 (17), 7111-7120 DOI: 10.1158/0008-5472.CAN-08-3957
The paper, of which I am one of the authors, studies the role of stromal-tumour interactions in prostate cancer progression. It introduces a computational model, developed as a result of extensive conversations with Vanderbilt’s Hayward Lab and the results have led to interesting biological experiments and observations of relevance in pathology. Hope you guys will find it an interesting read.
... Read more »
Basanta, D., Strand, D., Lukner, R., Franco, O., Cliffel, D., Ayala, G., Hayward, S., & Anderson, A. (2009) The Role of Transforming Growth Factor- -Mediated Tumor-Stroma Interactions in Prostate Cancer Progression: An Integrative Approach. Cancer Research, 69(17), 7111-7120. DOI: 10.1158/0008-5472.CAN-08-3957
Do you write about peer-reviewed research in your blog? Use ResearchBlogging.org to make it easy for your readers — and others from around the world — to find your serious posts about academic research.
If you don't have a blog, you can still use our site to learn about fascinating developments in cutting-edge research from around the world.
Research Blogging is powered by SMG Technology.
To learn more, visit seedmediagroup.com.