Background-Inhibitory control or regulatory difficulties have been explored in major depressive disorder (MDD) but typically in the context of affectively salient information. Inhibitory control is addressed specifically by using a task devoid of affectively-laden stimuli, to disentangle the effects of altered affect and altered inhibitory processes in MDD.

Preterm birth and fetal demise are likely the direct result of toxin-induced damage and inflammation rather than differences in efficiency of ascension into the upper genital tract. These data demonstrate a distinct contribution of βH/C to GBS chorioamnionitis and subsequent fetal infection in vivo and showcase a model for this most proximal step in GBS pathogenesis.

The integration of visual, lexical, and oculomotor information is a critical part of reading. Mr. Chips is an ideal-observer model that combines these sources of information optimally to read simple texts in the minimum number of saccades. This model provides a computational framework for interpreting human reading saccades in both normal and low vision. The purpose of this paper is to report performance of the model for conditions emulating reading with normal vision--a visual span of nine characters, multiplicative saccade noise with a standard deviation of 30%, and texts based on three full-length children's books. Comparison of fixation locations by humans and Mr. Chips revealed: (1) that both exhibit very similar word-skipping behavior; (2) both show initial fixations near the center of words, but with a systematic difference suggestive of an asymmetry in the human visual span; and (3) differences in the pattern of refixations within words that may uncover non-optimal lexical inference by human readers. A human context effect--30% difference in mean saccade size between continuous text and random sequences of words--was very similar to the 25% effect for the model associated with a corresponding difference in the predictability of text words. Overall, our findings show that many of the complicated aspects of human reading saccades can be explained concisely by early information-processing constraints.

BackgroundNext-generation sequencing of transposon-genome junctions from a saturated bacterial mutant library (Tn-seq) is a powerful tool that permits genome-wide determination of the contribution of genes to fitness of the organism under a wide range of experimental conditions. We report development, testing, and results from a Tn-seq system for use in Streptococcus agalactiae (group B Streptococcus; GBS), an important cause of neonatal sepsis.MethodsOur method uses a Himar1 mini-transposon that inserts at genomic TA dinucleotide sites, delivered to GBS on a temperature-sensitive plasmid that is subsequently cured from the bacterial population. In order to establish the GBS essential genome, we performed Tn-seq on DNA collected from three independent mutant libraries—with at least 135,000 mutants per library—at serial 24 h time points after outgrowth in rich media.ResultsAfter statistical analysis of transposon insertion density and distribution, we identified 13.5 % of genes as essential and 1.2 % as critical, with high levels of reproducibility. Essential and critical genes are enriched for fundamental cellular housekeeping functions, such as acyl-tRNA biosynthesis, nucleotide metabolism, and glycolysis. We further validated our system by comparing fitness assignments of homologous genes in GBS and a close bacterial relative, Streptococcus pyogenes, which demonstrated 93 % concordance. Finally, we used our fitness assignments to identify signal transduction pathway components predicted to be essential or critical in GBS.ConclusionsWe believe that our baseline fitness assignments will be a valuable tool for GBS researchers and that our system has the potential to reveal key pathogenesis gene networks and potential therapeutic/preventative targets.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-016-2741-z) contains supplementary material, which is available to authorized users.

Lens apoptosis plays a central role in cavefish eye degeneration. Heat shock proteins (hsps) can regulate apoptosis; therefore, we examined the relationship between constitutive hsp70 and hsp90 expression and lens apoptosis. The model system is Astyanax mexicanus, a teleost species consisting of an eyed surface-dwelling (surface fish) form and numerous blind cavedwelling (cavefish) forms. Optic primordia are formed in the cavefish embryo but they subsequently undergo lens apoptosis, arrest in development and degenerate. Astyanax hsp90 and hsp70 DNAs were isolated to use as probes to compare gene expression during surface fish and cavefish development. Hsp90β β β β β, which encodes one of two hsp90 isoforms, was not expressed in the surface fish or cavefish lens, whereas hsp70 was expressed in the lens of both forms, suggesting that neither is directly involved in lens apoptosis. In contrast, hsp90α α α α α, the other hsp90 isoform, was expressed in the cavefish but not the surface fish lens. Hsp90α α α α α expression peaked shortly before the beginning of lens apoptosis in three convergent cavefish populations, suggesting a close relationship with lens apoptosis. The absence of hsp90β β β β β in the lens allowed us to use geldanamycin and radicicol, specific inhibitors of hsp90 chaperone function, to determine whether lens cell death requires hsp90α α α α α expression. Both inhibitors blocked TUNEL labeling in the cavefish lens, suggesting that hsp90α α α α α is required for apoptosis. In contrast to their effects on the lens, these inhibitors induced TUNEL labeling in the surface epidermis, presumably due to effects on hsp90β β β β β function, implying that the two-hsp90 isoforms may have contrasting roles in cell survival. We conclude that hsp90α α α α α plays a novel role in lens apoptosis and cavefish eye degeneration.