Brain region-specific expression of genes mapped within quantitative trait loci for behavioral responsiveness to acute stress in Fisher 344 and Wistar Kyoto male rats

Acute stress responsiveness is a quantitative trait that varies in severity from one individual to another; however, the genetic component underlying the individual variation is largely unknown. Fischer 344 (F344) and Wistar Kyoto (WKY) rat strains show large differences in behavioral responsiveness to acute stress, such as freezing behavior in response to footshock during the conditioning phase of contextual fear conditioning (CFC). Quantitative trait loci (QTL) have been identified for behavioral responsiveness to acute stress in the defensive burying (DB) and open field test (OFT) from a reciprocal F2 cross of F344 and WKY rat strains. These included a significant QTL on chromosome 6 (Stresp10). Here, we hypothesized that the Stresp10 region harbors genes with sequence variation(s) that contribute to differences in multiple behavioral response phenotypes between the F344 and WKY rat strains. To test this hypothesis, first we identified differentially expressed genes within the Stresp10 QTL in the hippocampus, amygdala, and frontal cortex of F344 and WKY male rats using genome-wide microarray analyses. Genes with both expression differences and non-synonymous sequence variations in their coding regions were considered candidate quantitative trait genes (QTGs). As a proof-of-concept, the F344.WKY-Stresp10 congenic strain was generated with the Stresp10 WKY donor region into the F344 recipient strain. This congenic strain showed behavioral phenotypes similar to those of WKYs. Expression patterns of Gpatch11 (G-patch domain containing 11), Cdkl4 (Cyclin dependent kinase like 4), and Drc1 (Dynein regulatory complex subunit 1) paralleled that of WKY in the F344.WKY-Stresp10 strain matching the behavioral profiles of WKY as opposed to F344 parental strains. We propose that these genes are candidate QTGs for behavioral responsiveness to acute stress

Statistical mechanics of normal grain growth in one dimension: A partial integro-differential equation model

We develop a statistical-mechanical model of one-dimensional normal grain growth that does not require any drift-velocity parameterization for grain size, such as used in the continuity equation of traditional mean-field theories. The model tracks the population by considering grain sizes in neighbour pairs; the probability of a pair having neighbours of certain sizes is determined by the size-frequency distribution of all pairs. Accordingly, the evolution obeys a partial integro-differential equation (PIDE) over ‘grain size versus neighbour grain size’ space, so that the grain-size distribution is a projection of the PIDE’s solution. This model, which is applicable before as well as after statistically self-similar grain growth has been reached, shows that the traditional continuity equation is invalid outside this state. During statistically self-similar growth, the PIDE correctly predicts the coarsening rate, invariant grain-size distribution and spatial grain-size correlations observed in direct simulations. The PIDE is then reducible to the standard continuity equation, and we derive an explicit expression for the drift velocity. It should be possible to formulate similar parameterization-free models of normal grain growth in two and three dimensions

Geographical and temporal distribution of SARS-CoV-2 clades in the WHO European Region, January to June 2020

We show the distribution of SARS-CoV-2 genetic clades over time and between countries and outline potential genomic surveillance objectives. We applied three available genomic nomenclature systems for SARS-CoV-2 to all sequence data from the WHO European Region available during the COVID-19 pandemic until 10 July 2020. We highlight the importance of real-time sequencing and data dissemination in a pandemic situation. We provide a comparison of the nomenclatures and lay a foundation for future European genomic surveillance of SARS-CoV-2.Peer reviewe

Yellow fat disease (steatitis) in 20 equids : description of clinical and ultrasonographic findings

Diagnosis of steatitis can be challenging due to nonspecific clinical signs and ultrasonography might be a useful aid for making a diagnosis. The objective of this retrospective clinical case study was to describe history, clinical signs, ultrasonographic findings, treatment and outcome in equids with steatitis. The medical records of all equids presented to the Department of Large Animal Internal Medicine, Ghent University between January 2008 and December 2015 were reviewed retrospectively to identify horses suffering from steatitis. A total of 20 cases with steatitis were reviewed. History included dullness, recumbency, decreased appetite and weight loss. Fever, ventral oedema, stiff/painful gait and a painful neck were found. Low haematocrit, low vitamin E and selenium and increased levels of creatinine kinase and particularly lactate dehydrogenase were almost consistent findings. On ultrasound, ventral oedema was found. Ventral extraperitoneal, perirenal, mesenteric, coronary and caudal mediastinal fat showed homogenously increased echogenicity. The ventral extraperitoneal fat in particular was surrounded by oedema or free fluid. Increased amounts of abdominal, thoracic and pericardial fluid were often found. Fat biopsies were taken in the neck, or from the ventral extraperitoneal fat in the ventral flank. Steatitis was confirmed in all horses where a fat biopsy was taken (n = 13). Treatment consisted of selenium and vitamin E (intramuscular injection followed by oral treatment) supplementation and anti-inflammatory treatment (dexamethasone or prednisolone parenteral or oral) for at least 1-4 weeks. A total of 15 animals (75%) survived. Full recovery took about 2-6 months. In conclusion, steatitis is an uncommon disease in young horses usually seen during winter. It may be underdiagnosed because of nonspecific clinical signs. Ultrasonography is a useful aid for the diagnosis of yellow fat disease based upon the increased echogenicity of ventral extraperitoneal, perirenal, mesenteric, coronary and caudal mediastinal fat and increased amount of surrounding fluid