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The most common eating disorders (EDs) according to DSM-5 are anorexia nervosa (AN), bulimia nervosa (BN) and binge eating disorder (BED). These disorders have received increasing attention in psychiatry due to rising prevalence and high morbidity and mortality. The diagnostic category "anorexia nervosa," introduced by Ernest-Charles Lasègue and William Gull in 1873, first appears a century later in a German textbook of psychiatry, authored by Gerd Huber in 1974. However, disordered eating behavior has been described and discussed in German psychiatric textbooks throughout the past 200 years. We reviewed content regarding eating disorder diagnoses but also descriptions of disordered eating behavior in general. As material, we carefully selected eighteen German-language textbooks of psychiatry across the period 1803-2017. Previously, in German psychiatry, disordered eating behaviors were seen as symptoms of depressive disorders, bipolar disorder or schizophrenia, or as manifestations of historical diagnoses noringly associated with abnormal eating behavior and are listed as important differential diagnoses of EDs in DSM-5. Moreover, there are overlaps regarding the neurobiological basis and psychological and psychopharmacological therapies applied to all of these disorders.Bullying victimization and trauma research traditions operate quite separately. [https://www.selleckchem.com/products/tas-120.html selleck] Hence, it is unclear from the literature whether bullying victimization should be considered as a form of interpersonal trauma. We review studies that connect bullying victimization with symptoms of PTSD, and in doing so, demonstrate that a conceptual understanding of the consequences of childhood bullying needs to be framed within a developmental perspective. We discuss two potential diagnoses that ought to be considered in the context of bullying victimization (1) developmental trauma disorder, which was suggested but not accepted as a new diagnosis in the DSM-5 and (2) complex post-traumatic stress disorder, which has been included in the ICD-11. Our conclusion is that these frameworks capture the complexity of the symptoms associated with bullying victimization better than PTSD. We encourage practitioners to understand how exposure to bullying interacts with development at different ages when addressing the consequences for targets and when designing interventions that account for the duration, intensity, and sequelae of this type of interpersonal trauma.<br /><br /> Previous studies have shown that high glucose (HG) induces endothelial cell (EC) damage via endothelial-to-mesenchymal transition (EndMT). Although the underlying mechanisms are still unclear, recent studies have demonstrated the role of calcium-sensing receptor (CaSR) in mediating EC damage. Therefore, the aim of our study was to investigate whether CaSR mediates HG-induced EndMT and to determine the underlying mechanism.<br /><br /> Bioinformatics analysis of microarray profiles (GSE30780) and protein-protein interaction (PPI) analyses were performed to select the hub genes. As for <br /><br /> research, the human aortic ECs (HAECs) were exposed to HG to induce EndMT. The expression of CaSR and β-catenin was determined, as well as their effects on EndMT (endothelial marker CD31, mesenchymal marker FSP1, and α-SMA).<br /><br /> The bioinformatics analysis indicated CaSR was significantly increased in HG-treated HAECs and was one of the hub genes. The <br /><br /> results showed that HG significantly inhibited the expression of CD31 and increased FSP1 and α-SMA in a concentration- and time-dependent manner. Moreover, CaSR was increased in HAECs after HG treatment. The CaSR antagonist attenuated HG-induced expression of EndMT-related markers. Furthermore, HG treatment increased the nuclear translocation of β-catenin in HAECs. In contrast, blocking the nuclear translocation of β-catenin by DKK1 could attenuate HG-induced EndMT (increased the protein expression of CD31 by 30% and decreased the protein expression of FSP1 by 15% and α-SMA by 25%). CaSR siRNA further inhibited the HG-induced nuclear translocation of β-catenin in HAECs.<br /><br /> Our research demonstrated that HG-induced EndMT in HAECs might be mediated by CaSR and the downstream nuclear translocation of β-catenin.<br /><br />Our research demonstrated that HG-induced EndMT in HAECs might be mediated by CaSR and the downstream nuclear translocation of β-catenin.Muscle strain is one of the most frequent sports injuries, having the rectus femoris (RF) muscle as the reported preferred site of quadriceps muscle strain. The decrease muscle stiffness could be an effective RF muscle strain prevention. In recent studies, a high-intensity static stretching intervention decreased passive stiffness, though no study has investigated on the effect of the different static stretching intervention intensities on quadriceps muscle stiffness. The purpose of this study was to investigate the three different quadriceps muscle stiffness intensities (120 vs. 100 vs. 80%). Eighteen healthy, sedentary male volunteers participated in the study and randomly performed three intensities. The static stretching intervention was performed in knee flexion with 30° hip extension. Three 60-second stretching intervention with a 30-second interval were performed at each stretching intensity. We measured knee flexion range of motion and shear elastic modulus of the RF muscle used by ultrasonic shear-wave elastography before and after the static stretching intervention. Our results showed that the knee flexion range of motion was increased after 100% (p less then 0.01) and 120% intensities (p less then 0.01) static stretching intervention, not in 80% intensity (p = 0.853). In addition, our results showed that the shear elastic modulus of the RF muscle was decreased only after 100% intensity static stretching intervention (p less then 0.01), not after 80% (p = 0.365), and 120% intensities (p = 0.743). To prevent the quadriceps muscle strain, especially the RF muscle, 100%, not 120% (high) and 80% (low), intensity stretching could be beneficial in sports setting application.The perivascular adipose tissue (PVAT) is an active endocrine organ responsible for release several substances that influence on vascular tone. Increasing evidence suggest that hyperactivation of the local renin-angiotensin system (RAS) in the PVAT plays a pivotal role in the pathogenesis of cardiometabolic diseases. However, the local RAS contribution to the PVAT control of vascular tone during obesity is still not clear. Since the consumption of a high-carbohydrate diet (HC diet) contributes to obesity inducing a rapid and sustained increase in adiposity, so that the functional activity of PVAT could be modulated, we aimed to evaluate the effect of HC diet on the PVAT control of vascular tone and verify the involvement of RAS in this effect. For that, male Balb/c mice were fed standard or HC diet for 4 weeks. Vascular reactivity, histology, fluorescence, and immunofluorescence analysis were performed in intact thoracic aorta in the presence or absence of PVAT. The results showed that HC diet caused an increase in visceral adiposity and also in the PVAT area.