Stoutpennington0599

Gammaherpesvirus infections are ubiquitous in captive and free-ranging ruminants and are associated with a variety of clinical diseases ranging from subclinical or mild inflammatory syndromes to fatal diseases such as malignant catarrhal fever. Gammaherpesvirus infections have been fully characterized in only a few ruminant species, and the overall diversity, host range, and biologic effects of most are not known. This study investigated the presence and host distribution of gammaherpesviruses in ruminant species at two facilities, the San Diego Zoo and San Diego Zoo Safari Park. We tested antemortem (blood, nasal or oropharyngeal swabs) or postmortem (internal organs) samples from 715 healthy or diseased ruminants representing 96 species and subspecies, using a consensus-based herpesvirus PCR for a segment of the DNA polymerase (DPOL) gene. Among the 715 animals tested, 161 (22.5%) were PCR and sequencing positive for herpesvirus, while only 11 (6.83%) of the PCR positive animals showed clinical signs of malignant catarrhal fever. Forty-four DPOL genotypes were identified of which only 10 have been reported in GenBank. The data describe viral diversity within species and individuals, identify host ranges of potential new viruses, and address the proclivity and consequences of interspecies transmission during management practices in zoological parks. The discovery of new viruses with wide host ranges and presence of co-infection within individual animals also suggest that the evolutionary processes influencing Gammaherpesvirus diversity are more complex than previously recognized.Alzheimer's disease (AD) is a devastating illness affecting over 40 million people worldwide. Intraneuronal rise of amyloid beta in its oligomeric forms (iAβOs), has been linked to the pathogenesis of AD by disrupting cytosolic Ca2+ homeostasis. However, the specific mechanisms of action are still under debate and intense effort is ongoing to improve our understanding of the crucial steps involved in the mechanisms of AβOs toxicity. We report the development of a mathematical model describing a proposed mechanism by which stimulation of Phospholipase C (PLC) by iAβO, triggers production of IP3 with consequent abnormal release of Ca2+ from the endoplasmic reticulum (ER) through activation of IP3 receptor (IP3R) Ca2+ channels. After validating the model using experimental data, we quantify the effects of intracellular rise in iAβOs on model solutions. Our model validates a dose-dependent influence of iAβOs on IP3-mediated Ca2+ signaling. We investigate Ca2+ signaling patterns for small and large iAβOs doses and study the role of various parameters on Ca2+ signals. Uncertainty quantification and partial rank correlation coefficients are used to better understand how the model behaves under various parameter regimes. Our model predicts that iAβO alter IP3R sensitivity to IP3 for large doses. Our analysis also shows that the upstream production of IP3 can influence Aβ-driven solution patterns in a dose-dependent manner. Model results illustrate and confirm the detrimental impact of iAβOs on IP3 signaling.In this paper we focus on a critical component of the city its building stock, which holds much of its socio-economic activities. In our case, the lack of a comprehensive database about their features and its limitation to a surveyed subset lead us to adopt data-driven techniques to extend our knowledge to the near-city-scale. Neural networks and random forests are applied to identify the buildings' number of floors and construction periods' dependencies on a set of shape features area, perimeter, and height along with the annual electricity consumption, relying a surveyed data in the city of Beirut. The predicted results are then compared with established scaling laws of urban forms, which constitutes a further consistency check and validation of our workflow.Maternal effects on offspring growth can impact survival and evolution of natural and domesticated populations. Genetic correlation estimates often support a negative relationship between direct and maternal effects. However, the genetic underpinnings whereby this antagonism operates are unclear. In pigs, sow feeding status and body composition condition piglet development and growth. We hypothesized that variants in genes impacting these traits may be causative of maternal influences that could be antagonistic to the direct effects for piglet growth. A recessive missense mutation (C>T) in the porcine leptin receptor (LEPR) gene (rs709596309) has been identified as the possible causal polymorphism for increased feed intake and fatness. Using data from a Duroc line, we show that the TT sows exerted a negative impact on the body weight of their offspring at the end of the growing period of similar extent to the positive direct effect of the TT genotype over each individual. Thus, TT pigs from TT dams were about as heavy as CC and CT (C-) pigs from C-dams, but TT pigs from C-dams were around 5% heavier than C-pigs from TT dams. In contrast, body composition was only influenced by LEPR direct effects. This antagonism is due to a higher propensity of TT pigs for self-maintenance rather than for offspring investment. Tat-BECN1 We show that TT pigs consumed more feed, favored fatty acid uptake over release, and produced lighter piglets at weaning than their C-counterparts. We conclude that LEPR underlies a transgenerational mechanism for energy distribution that allocates resources to the sow or the offspring according to whether selective pressure is exerted before or after weaning.Restoration of the Florida Everglades, a substantial wetland ecosystem within the United States, is one of the largest ongoing restoration projects in the world. Decision-makers and managers within the Everglades ecosystem rely on ecological models forecasting indicator wildlife response to changes in the management of water flows within the system. One such indicator of ecosystem health, the presence of wading bird communities on the landscape, is currently assessed using three species distribution models that assume perfect detection and report output on different scales that are challenging to compare against one another. We sought to use current advancements in species distribution modeling to improve models of Everglades wading bird distribution. Using a joint species distribution model that accounted for imperfect detection, we modeled the presence of nine species of wading bird simultaneously in response to annual hydrologic conditions and landscape characteristics within the Everglades system. Our resulting model improved upon the previous model in three key ways 1) the model predicts probability of occupancy for the nine species on a scale of 0-1, making the output more intuitive and easily comparable for managers and decision-makers that must consider the responses of several species simultaneously; 2) through joint species modeling, we were able to consider rarer species within the modeling that otherwise are detected in too few numbers to fit as individual models; and 3) the model explicitly allows detection probability of species to be less than 1 which can reduce bias in the site occupancy estimates.