Usually on Thursday nights I take a look at all seven PLoS journals to see what strikes my fancy. As always, you should rate the articles, post notes and comments and send trackbacks when you blog about the papers. You can now also easily place articles on various social services (CiteULike, Mendeley, Connotea, Stumbleupon, Facebook and Digg) with just one click. Here are my own picks for the week – you go and look for your own favourites:
By preventing urogenital schistosomiasis in sexually active females through simple and low-cost methods, we have an innovative and timely opportunity to reduce and possibly interrupt HIV/AIDS transmission throughout many rural areas of sub-Saharan Africa.
Everyday tasks seldom involve isolate actions but sequences of them. We can see whether previous actions influence the current one by exploring the response time to controlled sequences of stimuli. Specifically, depending on the response-stimulus temporal interval (RSI), different mechanisms have been proposed to explain sequential effects in two-choice serial response tasks. Whereas an automatic facilitation mechanism is thought to produce a benefit for response repetitions at short RSIs, subjective expectancies are considered to replace the automatic facilitation at longer RSIs, producing a cost-benefit pattern: repetitions are faster after other repetitions but they are slower after alternations. However, there is not direct evidence showing the impact of subjective expectancies on sequential effects. By using a fixed sequence, the results of the reported experiment showed that the repetition effect was enhanced in participants who acquired complete knowledge of the order. Nevertheless, a similar cost-benefit pattern was observed in all participants and in all learning blocks. Therefore, results of the experiment suggest that sequential effects, including the cost-benefit pattern, are the consequence of automatic mechanisms which operate independently of (and simultaneously with) explicit knowledge of the sequence or other subjective expectancies.
Amphibian species are facing a current global extinction crisis of unprecedented magnitude. The major factors causing their decline are the emerging disease chytridiomycosis and habitat destruction. Chytridiomycosis is caused by the aquatic fungus Batrachochytrium dendrobatidis and has been linked to species extinctions and population declines in montane regions including Australia, Panama, North America, and Spain. Currently, it is debated whether the recent emergence of the pathogen is largely the result of environmental factors triggering an outbreak of an endemic pathogen or if the epidemic has been caused by widespread introduction of the pathogen into naïve host populations (“pathogen pollution”). We studied the population genetics of chytridiomycosis using DNA sequences from a global panel of strains. These data showed evidence of a strong genetic bottleneck in the history of the pathogen, and the epidemic appears traceable to the widespread dispersal of a single genotype. Populations were not structured by host-origin, and the same lineage was detected in populations of both resistant and highly sensitive species. The data suggest that the chytridiomycosis epidemic is caused by the emergence of a novel pathogen but that disease outcome is contingent on host resistance and environmental factors.
Horses are unusual in producing protein-rich sweat for thermoregulation, a major component of which is latherin, a highly surface-active, non-glycosylated protein. The amino acid sequence of latherin, determined from cDNA analysis, is highly conserved across four geographically dispersed equid species (horse, zebra, onager, ass), and is similar to a family of proteins only found previously in the oral cavity and associated tissues of mammals. Latherin produces a significant reduction in water surface tension at low concentrations (≤1 mg ml−1), and therefore probably acts as a wetting agent to facilitate evaporative cooling through a waterproofed pelt. Neutron reflection experiments indicate that this detergent-like activity is associated with the formation of a dense protein layer, about 10 Å thick, at the air-water interface. However, biophysical characterization (circular dichroism, differential scanning calorimetry) in solution shows that latherin behaves like a typical globular protein, although with unusual intrinsic fluorescence characteristics, suggesting that significant conformational change or unfolding of the protein is required for assembly of the air-water interfacial layer. RT-PCR screening revealed latherin transcripts in horse skin and salivary gland but in no other tissues. Recombinant latherin produced in bacteria was also found to be the target of IgE antibody from horse-allergic subjects. Equids therefore may have adapted an oral/salivary mucosal protein for two purposes peculiar to their lifestyle, namely their need for rapid and efficient heat dissipation and their specialisation for masticating and processing large quantities of dry food material.
Mitochondrial disorders are a group of heterogeneous diseases. It has been estimated that the prevalence of mitochondrial diseases in humans, due to mutations of the mitochondrial genome (mtDNA), is approximately 1 in 8000 in a Caucasian population. Since the late 1980s, when the first disease-causing mutation in human mtDNA was identified, approximately 250 pathogenic mtDNA mutations have been described. Sensory ataxic neuropathy (SAN) is a recently identified neurological disorder in golden retriever dogs that is maternally transmitted. Affected dogs are ataxic, have postural reaction deficits, and exhibit reduced spinal reflexes. They have no pronounced muscle atrophy nor do they seem to be in pain. In this study, we report the identification and characterization of the mutation causing SAN, a single base pair deletion in the mitochondrial tRNATyr gene. The identification of this mutation makes it possible to eradicate the disease in golden retrievers. SAN constitutes a new animal model for mitochondrial disorders in humans.
The frequency with which scientists fabricate and falsify data, or commit other forms of scientific misconduct is a matter of controversy. Many surveys have asked scientists directly whether they have committed or know of a colleague who committed research misconduct, but their results appeared difficult to compare and synthesize. This is the first meta-analysis of these surveys. To standardize outcomes, the number of respondents who recalled at least one incident of misconduct was calculated for each question, and the analysis was limited to behaviours that distort scientific knowledge: fabrication, falsification, “cooking” of data, etc… Survey questions on plagiarism and other forms of professional misconduct were excluded. The final sample consisted of 21 surveys that were included in the systematic review, and 18 in the meta-analysis. A pooled weighted average of 1.97% (N = 7, 95%CI: 0.86-4.45) of scientists admitted to have fabricated, falsified or modified data or results at least once -a serious form of misconduct by any standard- and up to 33.7% admitted other questionable research practices. In surveys asking about the behaviour of colleagues, admission rates were 14.12% (N = 12, 95% CI: 9.91-19.72) for falsification, and up to 72% for other questionable research practices. Meta-regression showed that self reports surveys, surveys using the words “falsification” or “fabrication”, and mailed surveys yielded lower percentages of misconduct. When these factors were controlled for, misconduct was reported more frequently by medical/pharmacological researchers than others. Considering that these surveys ask sensitive questions and have other limitations, it appears likely that this is a conservative estimate of the true prevalence of scientific misconduct.
Worldwide, the World Health Organization estimated that in 1999 there were 340 million new cases of curable sexually transmitted diseases (STDs)–syphilis, gonorrhea, chlamydia, and trichomoniasis–in men and women aged 15-49 years . Although in Western countries curable STDs may not seem a major threat to public health, these diseases disproportionately affect the poor, young people, and ethnic minorities, and can cause acute illness, disability and death, pre-term or low birth-weight babies, congenital birth defects, female infertility, and increased HIV transmission. High-income countries are by no means exempt from the burden of STDs: there are 19 million new cases of STDs each year in the United States, at an estimated cost of US$15.9 billion annually to the US health care system .
Currently, one of the major debates about the American peopling focuses on the number of populations that originated the biological diversity found in the continent during the Holocene. The studies of craniometric variation in American human remains dating from that period have shown morphological differences between the earliest settlers of the continent and some of the later Amerindian populations. This led some investigators to suggest that these groups–known as Paleomericans and Amerindians respectively–may have arisen from two biologically different populations. On the other hand, most DNA studies performed over extant and ancient populations suggest a single migration of a population from Northeast Asia. Comparing craniometric and mtDNA data of diachronic samples from East Central Argentina dated from 8,000 to 400 years BP, we show here that even when the oldest individuals display traits attributable to Paleoamerican crania, they present the same mtDNA haplogroups as later populations with Amerindian morphology. A possible explanation for these results could be that the craniofacial differentiation was a local phenomenon resulting from random (i.e. genetic drift) and non-random factors (e.g. selection and plasticity). Local processes of morphological differentiation in America are a probable scenario if we take into consideration the rapid peopling and the great ecological diversity of this continent; nevertheless we will discuss alternative explanations as well.
The availability of an accurate genome sequence provides the bedrock upon which modern biomedical research is based. Here we describe a high-quality assembly, Build 36, of the mouse genome. This assembly was put together by aligning overlapping individual clones representing parts of the genome, and it provides a more complete picture than previous assemblies, because it adds much rodent-specific sequence that was previously unavailable. The addition of these sequences provides insight into both the genomic architecture and the gene complement of the mouse. In particular, it highlights recent gene duplications and the expansion of certain gene families during rodent evolution. An improved understanding of the mouse genome and thus mouse biology will enhance the utility of the mouse as a model for human disease.
In 2002, the publication of the genome of Plasmodium falciparum, the most malignant agent of malaria, generated hopes in the fight against this deadly disease by the opportunities it offered to discover new drug targets. Since then results have not lived up to the expectations. The development of comparative genomics to further understanding of P. falciparum has indeed been hindered by a lack of knowledge of closely related species’ genomes. Only one species, P. reichenowi, infecting chimpanzees, was hitherto known as a sister lineage of P. falciparum. Here we describe a new Plasmodium species infecting chimpanzees in Africa. Based on its whole mitochondrial genome, we demonstrate that this species is a relative of P. falciparum and P. reichenowi. The analysis of its genome should thus offer the opportunity to explore P. falciparum specific adaptations to humans. Our results bring new elements to the debate surrounding the origin of this lineage. They suggest that it may have been present in early hominoids and may have experienced a radiation congruent with that of its hosts. Our discovery highlights the paucity of our knowledge on the richness of Plasmodium species infecting primates and calls for more research in this direction.
Networks of interconnected brain regions coordinate brain activities. Information is processed in the grey matter (cortex and subcortical structures) and passed along the network via whitish, fatty-coated fiber bundles, the white matter. Using maps of these white matter tracks, we provided evidence that higher intelligence may result from more efficient information transfer. Specifically, we hypothesized that higher IQ derives from higher global efficiency of the brain anatomical network. Seventy-nine healthy young adults were divided into general and high IQ groups. We used diffusion tensor tractography, which maps brain white matter fibers, to construct anatomical brain networks for each subject and calculated the network properties using both binary and weighted networks. We consistently found that the high intelligence group’s brain network was significantly more efficient than was the general intelligence group’s. Moreover, IQ scores were significantly correlated with network properties, such as shorter path lengths and higher overall efficiency, indicating that the information transfer in the brain was more efficient. These converging evidences support the hypothesis that the efficiency of the organization of the brain structure may be an important biological basis for intelligence.
Stochastic resonance is said to be observed when increases in levels of unpredictable fluctuations–e.g., random noise–cause an increase in a metric of the quality of signal transmission or detection performance, rather than a decrease. This counterintuitive effect relies on system nonlinearities and on some parameter ranges being “suboptimal”. Stochastic resonance has been observed, quantified, and described in a plethora of physical and biological systems, including neurons. Being a topic of widespread multidisciplinary interest, the definition of stochastic resonance has evolved significantly over the last decade or so, leading to a number of debates, misunderstandings, and controversies. Perhaps the most important debate is whether the brain has evolved to utilize random noise in vivo, as part of the “neural code”. Surprisingly, this debate has been for the most part ignored by neuroscientists, despite much indirect evidence of a positive role for noise in the brain. We explore some of the reasons for this and argue why it would be more surprising if the brain did not exploit randomness provided by noise–via stochastic resonance or otherwise–than if it did. We also challenge neuroscientists and biologists, both computational and experimental, to embrace a very broad definition of stochastic resonance in terms of signal-processing “noise benefits”, and to devise experiments aimed at verifying that random variability can play a functional role in the brain, nervous system, or other areas of biology.