New and Exciting in PLoS today

So, let's see what's new in PLoS Medicine, PLoS Biology and PLoS ONE today.

First, my SciBlings Shelley, Nick and Tara just published a PLoS Biology article about science blogs:

Advancing Science through Conversations: Bridging the Gap between Blogs and the Academy:

Scientific discovery occurs in the lab one experiment at a time, but science itself moves forward based on a series of ongoing conversations, from a Nobel Prize winner's acceptance speech to collegial chats at a pub. When these conversations flow into the mainstream, they nurture the development of an informed public who understand the value of funding basic research and making evidence-based voting decisions. It is in the interests of scientists and academic institutions alike to bring these conversations into the public sphere.

DrugMonkey, John Wilkins, Razib, Nick, Tara, Chad, Mo, Sheril, Dave, Blake, John Dennehy, Larry, Carlo Artieri, Thomas and Brian have more. I expect a lot of other science bloggers to write about this article, of course.

Another blogger, Pamela Ronald, also published today in PLoS Biology:

Rice XB15, a Protein Phosphatase 2C, Negatively Regulates Cell Death and XA21-Mediated Innate Immunity:

Resistance to pathogens is critical to plant and animal survival. Plants, unlike animals, lack an adaptive immune system and instead rely on the innate immune response to protect against infection. To elucidate the molecular mechanism of plant innate immunity, we are studying the signaling cascade mediated by the rice pathogen recognition receptor kinase XA21, which confers resistance to the bacterial pathogen Xanthomonas oryzae pv. oryzae. We demonstrate that XA21 binding protein 15 (a protein phosphatase 2C) negatively regulates XA21-mediated signaling resistance. This finding provides significant insight into regulation of receptor kinase-mediated immunity.

Then, there is other interesting stuff:

Environment, Migratory Tendency, Phylogeny and Basal Metabolic Rate in Birds:

Basal metabolic rate (BMR) represents the minimum maintenance energy requirement of an endotherm and has far-reaching consequences for interactions between animals and their environments. Avian BMR exhibits considerable variation that is independent of body mass. Some long-distance migrants have been found to exhibit particularly high BMR, traditionally interpreted as being related to the energetic demands of long-distance migration. Here we use a global dataset to evaluate differences in BMR between migrants and non-migrants, and to examine the effects of environmental variables. The BMR of migrant species is significantly higher than that of non-migrants. Intriguingly, while the elevated BMR of migrants on their breeding grounds may reflect the metabolic machinery required for long-distance movements, an alternative (and statistically stronger) explanation is their occupation of predominantly cold high-latitude breeding areas. Among several environmental predictors, average annual temperature has the strongest effect on BMR, with a 50% reduction associated with a 20°C gradient. The negative effects of temperature variables on BMR hold separately for migrants and non-migrants and are not due their different climatic associations. BMR in migrants shows a much lower degree of phylogenetic inertia. Our findings indicate that migratory tendency need not necessarily be invoked to explain the higher BMR of migrants. A weaker phylogenetic signal observed in migrants supports the notion of strong phenotypic flexibility in this group which facilitates migration-related BMR adjustments that occur above and beyond environmental conditions. In contrast to the findings of previous analyses of mammalian BMR, primary productivity, aridity or precipitation variability do not appear to be important environmental correlates of avian BMR. The strong effects of temperature-related variables and varying phylogenetic effects reiterate the importance of addressing both broad-scale and individual-scale variation for understanding the determinants of BMR.

Of Mice and Men, and Chandeliers:

What makes us human? One of the most obvious answers to this age-old question lies in the structure and function of the central nervous system, particularly the neocortex, where unique human features may lie. In fact, humans have not only a proportionally much larger neocortex compared to that of other mammals, but also a huge frontal lobe, the font of higher cognition.

In seeking clues to the biological basis of being human, neuroanatomists have long compared the human brain to that of other species, leading them to develop two distinct theories. Santiago Ramón y Cajal, the father of neuroanatomy, argued that the cortex of "higher" mammals, like humans, has more classes of neurons than those of "lower" mammals, for which he used the mouse as an example [1]. Specifically, he proposed that the variety and sophistication of "short-axon" cells, i.e., GABAergic inhibitory interneurons, increases as one climbs up the evolutionary ladder [2].

It's Not How Fat You Are, It's What You Do with It That Counts:

The spiralling increase in obesity rates in the Western and developing worlds has brought with it a host of related metabolic complications including diabetes, dyslipidaemia, cardiovascular complications, and cancer. Whereas obesity itself presents its own independent health problems--such as sleep apnoea or psychological issues--the vast majority of obesity-related mortality is caused by these secondary metabolic complications. The link between obesity and such complications as insulin resistance is well established on a population level but poorly understood mechanistically. Efforts to tackle the obesity epidemic through public health initiatives and drugs have so far been notable for their lack of success. With little prospect for halting the obesity epidemic, treatment of its associated diseases becomes of paramount importance both for public health and associated costs [1].

Ethical and Practical Issues Associated with Aggregating Databases:

The goal of "personalized medicine" relies upon defining the genetic variation responsible for disease susceptibility and response to therapy [1]. For most common human diseases, the contribution of a single sequence variant to disease susceptibility is typically small, and can only be detected with data from large numbers of people [2]. Practically, this necessitates collaboration among investigators who either have DNA and phenotypic information previously collected, or have access to populations from which to recruit participants. It also requires that data be shared among the collaborators. Modern bioinformatics platforms have the capacity to combine datasets and store them for re-analysis. This is scientifically advantageous since it makes possible studies with enhanced validity in a cost-effective fashion. However, this data storage can complicate the already vexing practical, scientific, and ethical issues associated with gene and tissue banks. Research participants' data may have been collected without authorization that meets today's standards for informed consent. Research participants may not have consented to participation in genetics research in general, to inclusion in genetics databases specifically, or to use of their samples in genetic analyses that were unanticipated, unknown, or nonexistent at the time samples were collected [3]. Participants who consented to the collection of their data for use in a particular study, or inclusion in a particular database, may not have consented to "secondary uses" of those data for unrelated research, or use by other investigators or third parties [4]. There is concern that institutional review boards (IRBs) or similar bodies will not approve of the formation of aggregated databases or will limit the types of studies that can be done with them, even if those studies are believed by others to be appropriate, since there is a lack of consensus about how to deal with re-use of data in this manner.

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