Hmm, I usually do this on Fridays, but I was busy. So here is a Saturday sampler of papers from all seven PLoS journals published last week. 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.
Light affects sleep in two ways: indirectly through the phase adjustment of circadian rhythms and directly through nonvisual mechanisms that are independent of the circadian system. The direct effects of light include the promotion of sleep in night-active animals and of alertness in diurnal species. We analyzed sleep and the electroencephalogram (EEG) under various light-dark regimens in mice lacking melanopsin (Opn4â/â), a retinal photopigment crucial for conveying light-level information to the brain, to determine the role of melanopsin, as opposed to rod and cones, in mediating these direct effects of light. We show that melanopsin mediates the direct effects of light during the subjective dark period, whereas rods and cones contribute to these effects in the light period. Our finding that "sleep-active" (i.e., galanin-positive) neurons of the anterior hypothalamus are not activated by light in Opn4â/â mice suggests that these neurons are part of the circuitry whereby light promotes sleep. Also, the alerting effects of transitions into darkness were less pronounced in Opn4â/â mice judged on the reduced increase in EEG theta and gamma activity. Finally, and unexpectedly, the rate at which the need for sleep, quantified as EEG delta power, accumulated during wakefulness was found to be reduced in Opn4â/â mice both during baseline and sleep deprivation conditions, implicating a photopigment in the homeostatic regulation of sleep. We conclude that melanopsin contributes to the direct effects of light and darkness, and in interaction with circadian and homeostatic drive, determines the occurrence and quality of both sleep and waking. If confirmed in humans, our observations will have applications for the clinical use of light as well as for societal lighting conditions.
Background to the debate: After the failure of three large clinical trials of vaginal microbicides, a Nature editorial stated that the microbicide field "requires a mechanism to help it make rational choices about the best candidates to move through trials" [1]. In this month's debate, James Lavery and colleagues propose a new mechanism, based on stopping trials early for "opportunity costs." They argue that microbicide trial sites could have been saturated with trials of scientifically less advanced products, while newer, and potentially more promising, products were being developed. They propose a mechanism to reallocate resources invested in existing trials of older products that might be better invested in more scientifically advanced products that are awaiting clinical testing. But David Buchanan argues that the early stopping of trials for such opportunity costs would face insurmountable practical barriers, and would risk causing harm to the participants in the trial that was stopped.
Echinococcus multilocularis is a tapeworm of the red fox, which represents a considerable health threat to respectively infected humans. Main endemic areas are located in China, Siberia, and central Europe. Alarmed by an emerging or reemerging situation in Europe, the question of how the parasite gets spatially and temporally spread and transmitted becomes essential to prepare appropriate control programs. The question was tackled by using genetic data on a large sample size of E. multilocularis adult stage tapeworms, combined with geographical site location data input. The historically documented endemic area, represented by the northern Alpine arch, was shown to harbour the highest genetic richness and diversity, as compared to surrounding areas in northern and eastern Europe. The spatial and temporal spread of different E. multilocularis genotypes in Europe seems to be ruled by a founder event, linked to exportation of parasites from the central core to newly identified (western and eastern) areas or subregions, where these parasites could subsequently disseminate under geographical separation from the original foci.
Modeling the Impact of Lesions in the Human Brain:
Every year, millions of people suffer the consequences of brain damage, as a result of stroke, traumatic brain injury, cancer or degenerative brain disease. The cognitive and behavioral symptoms of focal lesions of the brain are highly variable and in many cases depend on the location of the lesion site. Can we predict the functional impact of such lesions on the basis of a computational model of the brain's structure and dynamics? Numerous other systems that form complex networks have been analyzed for their vulnerability to structural damage. In many cases, the degree to which such systems are perturbed depends on network attributes of the deleted nodes and connections. We apply this network approach to investigate the structural and functional impact of localized lesions of a model of the cerebral cortex. When we delete nodes that occupy, in the intact brain, a highly central position, we find that the dynamic interactions between nodes in the remaining brain are greatly disturbed. In contrast, deletion of less central nodes has relatively little effect. In the model, some of the most disruptive lesion sites correspond to locations in the brain where lesions produce complex cognitive disturbances. Our modeling approach aims towards linking disturbances of structural brain networks to specific clinical outcomes.
Reproductive health (RH) and related needs during conflict and post-conflict situations are massive, acute, and complex to meet [1]-[4]. RH indicators for conflict-affected and post-conflict countries are worse than for least-developed countries (LDCs) not directly affected by conflict. Despite studies showing that funding for sexual and reproductive health programmes have consistently not met agreed-upon financial targets, little is known about the actual RH funding required to meet these needs in conflict-affected countries. A new study by Preeti Patel and colleagues published in this issue of PLoS Medicine addresses this knowledge gap [5]. This study is important because it attempts to quantify the direct and indirect RH disbursements to conflict-affected countries compared with overall official development assistance (ODA) by country, donor, and different RH activities. It also examines RH disbursements and ODA to non-conflict-affected LDCs.
In the life cycle of sexual organisms, a specialized cell division--meiosis--reduces the number of chromosomes from two sets (2n, diploid) to one set (n, haploid), while fertilization restores the original chromosome number. In contrast, mitosis produces two identical daughter cells. Basically, three features distinguish meiosis from mitosis. Meiosis has: (i) a succession of two rounds of division following a single replication, (ii) recombination, and (iii) co-segregation of sister chromatids at the first division. In this study, we identified a gene that controls one of these three features-- entry into the second meiotic division--in the sexual plant Arabidopsis thaliana. By combining a mutation in this gene with two other mutations--one that eliminates recombination and another that modifies chromatid segregation--we created a genotype (called MiMe for mitosis instead of meiosis) in which meiosis is totally replaced by mitosis. As a consequence, MiMe plants produced diploid male and female gametes that are genetically identical to their parent, and ploidy doubles at each generation. The replacement of meiosis by mitosis is a key component of apomixis, or clonal reproduction through seeds, which has potential revolutionary application in crop improvement.
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