The human vestibulo-ocular reflex (VOR) evaluated with a reactive torque helmet

The vestibulo-ocular reflex (YOR) generates eye rotations that compensate for head movements. Head movements include rotations and translations (linear displacements). Linear acceleration during translational movement, as well as the gravitational acceleration, signalling head orientation is sensed by the otolith organs. For the image of a distant object to remain upon the fovea of the retina during head rotation, an equal but opposite eye rotation must be generated. This ocular reflex, which originates in the semicircular canals, probably evolved early in vertebrate evolution, since it serves the important function of allowing animals to see and move at the same time. It was so sllccessful that it has changed vcry little since its origin, and the same basic design is fOllnd in widely divergent species of birds, mammals and fish

Dissemination of health-related research among scientists in three countries: Access to resources and current practices

Objectives. In public health and clinical settings insufficient dissemination of evidence-based practices limits the reach of new discoveries to broad populations. This study aimed to describe characteristics of the dissemination process by researchers across three countries (Brazil, United Kingdom, and United States), explore how designing for dissemination practices has been used, and analyze factors associated with dissemination. Methods. A similar online survey was used to query researchers across the three countries; data were pooled to draw cross-country conclusions. Findings. This study identified similarities and differences between countries. Importance of dissemination to nonresearcher audiences was widely recognized as important; however, traditional academic venues were the main dissemination method. Several factors were associated with self-rated dissemination effort in the pooled sample, but these predictive factors (e.g., support and resources for dissemination) had low prevalence. Less than one-third of researchers rated their level of effort for dissemination as excellent. Respondents reported limited support and resources to make it easier for researchers who might want to disseminate their findings. Conclusion. Though intentions show the importance of dissemination, researchers across countries lack supports to increase dissemination efforts. Additional resources and training in designing for dissemination along with improved partnerships could help bridge the research-practice gap

Preliminary Evidence That CD38 Moderates the Association of Neuroticism on Amygdala-Subgenual Cingulate Connectivity.

CD38 genetic variation has been associated with autism spectrum disorders and social anxiety disorder, which may result from CD38's regulation of oxytocin secretion. Converging evidence has found that the rs3796863 A-allele contributes to increased social sensitivity compared to the CC genotype. The current study examined the moderating role of CD38 genetic variants (rs3796863 and rs6449182) that have been associated with enhanced (or reduced) social sensitivity on neural activation related to neuroticism, which is commonly elevated in individuals with social anxiety and depression. Adults (n = 72) with varying levels of social anxiety and depression provided biological samples for DNA extraction, completed a measure of neuroticism, and participated in a standardized emotion processing task (affect matching) while undergoing fMRI. A significant interaction effect was found for rs3796863 x neuroticism that predicted right amygdala-subgenual anterior cingulate cortex (sgACC) functional connectivity. Simple slopes analyses showed a positive association between neuroticism and right amygdala-sgACC connectivity among rs3796863 A-allele carriers. Findings suggest that the more socially sensitive rs3796863 A-allele may partially explain the relationship between a known risk factor (i.e. neuroticism) and promising biomarker (i.e. amygdala-sgACC connectivity) in the development and maintenance of social anxiety and depression

Entropy Maximization and Instability of Uniformly Magnetized Plasma

A regime where a uniformly magnetized plasma could be unstable to a spatial perturbation in the magnetic field is explored. In this regime, a uniformly magnetized state does not maximize the entropy. The physical implication is discussed in the context of the current generation, the magnetic reconnection, and the dynamo effect

Using electronic health record data to develop inpatient mortality predictive model: Acute Laboratory Risk of Mortality Score (ALaRMS)

Objective: Using numeric laboratory data and administrative data from hospital electronic health record (EHR) systems, to develop an inpatient mortality predictive model. Methods: Using EHR data of 1 428 824 adult discharges from 70 hospitals in 2006–2007, we developed the Acute Laboratory Risk of Mortality Score (ALaRMS) using age, gender, and initial laboratory values on admission as candidate variables. We then added administrative variables using the Agency for Healthcare Research and Quality (AHRQ)'s clinical classification software (CCS) and comorbidity software (CS) as disease classification tools. We validated the model using 770 523 discharges in 2008. Results: Mortality predictors with ORs >2.00 included age, deranged albumin, arterial pH, bands, blood urea nitrogen, oxygen partial pressure, platelets, pro-brain natriuretic peptide, troponin I, and white blood cell counts. The ALaRMS model c-statistic was 0.87. Adding the CCS and CS variables increased the c-statistic to 0.91. The relative contributions were 69% (ALaRMS), 25% (CCS), and 6% (CS). Furthermore, the integrated discrimination improvement statistic demonstrated a 127% (95% CI 122% to 133%) overall improvement when ALaRMS was added to CCS and CS variables. In contrast, only a 22% (CI 19% to 25%) improvement was seen when CCS and CS variables were added to ALaRMS. Conclusions: EHR data can generate clinically plausible mortality predictive models with excellent discrimination. ALaRMS uses automated laboratory data widely available on admission, providing opportunities to aid real-time decision support. Models that incorporate laboratory and AHRQ's CCS and CS variables have utility for risk adjustment in retrospective outcome studies

Large conductance Ca²⁺-activated K⁺ (BK) channels promote secretagogue-induced transition from spiking to bursting in murine anterior pituitary corticotrophs.

This is the final version of the article. Available from Wiley via the DOI in this record.Anterior pituitary corticotroph cells are a central component of the hypothalamic-pituitary-adrenal (HPA) axis essential for the neuroendocrine response to stress. Corticotrophs are excitable cells that receive input from two hypothalamic secretagogues, corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP) to control the release of adrenocorticotrophic hormone (ACTH). Although corticotrophs are spontaneously active and increase in excitability in response to CRH and AVP the patterns of electrical excitability and underlying ionic conductances are poorly understood. In this study, we have used electrophysiological, pharmacological and genetic approaches coupled with mathematical modelling to investigate whether CRH and AVP promote distinct patterns of electrical excitability and to interrogate the role of large conductance calcium- and voltage-activated potassium (BK) channels in spontaneous and secretagogue-induced activity. We reveal that BK channels do not play a significant role in the generation of spontaneous activity but are critical for the transition to bursting in response to CRH. In contrast, AVP promotes an increase in single spike frequency, a mechanism independent of BK channels but dependent on background non-selective conductances. Co-stimulation with CRH and AVP results in complex patterns of excitability including increases in both single spike frequency and bursting. The ability of corticotroph excitability to be differentially regulated by hypothalamic secretagogues provides a mechanism for differential control of corticotroph excitability in response to different stressors.P.J.D. was supported by an MRC PhD studentship in the College of Medicine and Veterinary Medicine, University of Edinburgh. Work was supported by grants to M.J.S. and P.R. from the Wellcome Trust (082407), to M.J.S. from MRC (J008893), and to R.B. and J.T. from the National Institutes of Health (DK43200)