Blakesmith2972

Although women and men differ in psychological and endocrine stress responses as well as prevalence rates of stress-related disorders, knowledge on sex differences regarding stress regulation in the brain is scarce. Therefore, we performed an in-depth analysis of data from 67 healthy participants (31 women, taking oral contraceptives), who were exposed to the ScanSTRESS paradigm in an fMRI study. Changes in cortisol, affect, heart rate, and neural activation in response to psychosocial stress were examined in women and men as well as potential sex-specific interactions between stress response domains. Stress exposure led to significant cortisol increases with men exhibiting higher levels than women. Dependent on sex, cortisol elevations were differently associated with stress-related responses in striato-limbic structures Higher increases were associated with activations in men but with deactivations in women. Regarding affect or heart rate responses, no sex differences emerged. Although women and men differ in their overall stress reactivity, our findings do not support the idea of distinct neural networks as base of this difference. Instead, we found differential stress reactions for women and men in identical structures. We propose considering quantitative predictors like sex-specific cortisol increases when exploring neural response differences of women and men.Despite the importance of the Parelaphostrongylus tenuis infection for moose (Alces alces) and white-tailed deer (Odocoileus virginianus) management, only one peer-reviewed study has evaluated the relationship between deer and moose densities and the potential for parasite-mediated competition between the species. Using polynomial-regression modeling, that study identified a deer-density threshold above which moose populations declined; however, the nature of the data and apparent outliers suggests the approach used to develop that threshold may not have been appropriate. We used the data from the original study to test whether alternative models, including linear models and negative binomial models would be less sensitive to outliers and could better explain that relationship. We found no evidence that moose density decreases as deer density increases. We concluded that, although the proposed moose-deer-P. tenuis relationship could be partially density dependent, additional factors, such as frequency dependence of disease transmission, gastropod abundance, and shared use of resources by moose and deer should also be considered.Incidence of chronic wasting disease infection showed strong, positive correlation (r≥0.944) with apparent prevalence among female and male mule deer (Odocoileus hemionus) in seven herds previously studied in Colorado and Wyoming, US. With attention to monitoring method consistency and context, inferring that observed prevalence trends reflect underlying epidemic dynamics in mule deer herds appears justifiable.Adenoviruses are common pathogens infecting a wide range of vertebrates. Few cetacean adenoviruses have been described in the literature, and their pathogenicity is still unclear. Using PCR-based viral and bacterial pathogen surveillance in Bering-Chukchi-Beaufort seas bowhead whales (Balaena mysticetus) legally harvested 2012-15 during Alaskan aboriginal subsistence hunts, six of 59 bowhead whales (10%) tested positive for adenovirus DNA in the spleen. We found a high degree of sequence divergence from other mastadenoviruses, suggesting these may represent a novel species, tentatively named bowhead whale adenovirus. The sequences detected are distinct from adenoviruses previously identified in bottlenose dolphins (Tursiops truncatus) and harbor porpoises (Phocoena phocoena), forming two distinct clades in the cetacean hosts. The clinical impact is unclear, since no histopathologic evidence of adenovirus-associated disease was found. Furthermore, detection of adenovirus DNA in the spleen, contrary to other cetacean adenoviruses detected in the intestinal tract, may suggest a broader tissue tropism. Our study demonstrates adenovirus infection in bowhead whales and the usefulness of molecular diagnostics to discover and genetically characterize novel viruses in marine mammals.Syntaxin-binding protein 1 (STXBP1; also called MUNC18-1), encoded by STXBP1, is an essential component of the molecular machinery that controls synaptic vesicle docking and fusion. De novo pathogenic variants of STXBP1 cause a complex set of neurological disturbances, namely STXBP1 encephalopathy (STXBP1-E) that includes epilepsy, neurodevelopmental disorders and neurodegeneration. L-Histidine monohydrochloride monohydrate ic50 Several animal studies have suggested the contribution of GABAergic dysfunction in STXBP1-E pathogenesis. However, the pathophysiological changes in GABAergic neurons of these patients are still poorly understood. Here, we exclusively generated GABAergic neurons from STXBP1-E patient-derived induced pluripotent stem cells (iPSCs) by transient expression of the transcription factors ASCL1 and DLX2. We also generated CRISPR/Cas9-edited isogenic iPSC-derived GABAergic (iPSC GABA) neurons as controls. We demonstrated that the reduction in STXBP1 protein levels in patient-derived iPSC GABA neurons was slight (approximately 20%) compared to the control neurons, despite a 50% reduction in STXBP1 mRNA levels. Using a microelectrode array-based assay, we found that patient-derived iPSC GABA neurons exhibited dysfunctional maturation with reduced numbers of spontaneous spikes and bursts. These findings reinforce the idea that GABAergic dysfunction is a crucial contributor to STXBP1-E pathogenesis. Moreover, gene expression analysis revealed specific dysregulation of genes previously implicated in epilepsy, neurodevelopment and neurodegeneration in patient-derived iPSC GABA neurons, namely KCNH1, KCNH5, CNN3, RASGRF1, SEMA3A, SIAH3 and INPP5F. Thus, our study provides new insights for understanding the biological processes underlying the widespread neuropathological features of STXBP1-E.Rabbit hemorrhagic disease, a notifiable foreign animal disease in the US, was reported for the first time in wild native North American lagomorphs in April 2020 in the southwestern US. Affected species included the desert cottontail (Sylvilagus audubonii), mountain cottontail (Sylvilagus nuttallii), black-tailed jackrabbit (Lepus californicus), and antelope jackrabbit (Lepus alleni). Desert cottontails (n=7) and black-tailed jackrabbits (n=7) collected in April and May 2020 were necropsied at the US Geological Survey National Wildlife Health Center and tested positive for Lagovirus europaeus GI.2, also known as rabbit hemorrhagic disease virus 2 (GI.2/RHDV2/b), by real-time PCR at the US Department of Agriculture's Foreign Animal Disease Diagnostic Laboratory. Gross and microscopic lesions were similar to those reported in European rabbits (Oryctolagus cuniculus) and other hare (Lepus) species with GI.2/RHDV2/b infection; they included epistaxis (12/13; 92%); massive hepatocellular dissociation (14/14; 100%) and necrosis or apoptosis (11/11; 100%); pulmonary congestion (12/12; 100%), edema (12/13; 92%), and hemorrhage (11/12; 92%); and acute renal tubular injury (3/8; 38%).