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69, 95% CI=1.18-2.42; homozygous OR=1.99, 95% CI=1.38-2.86; respectively), and significant association was also detected between TNF-α-308G/A and DN susceptibility in type 2 DM in recessive model (OR=1.39, 95% CI=1.02-1.89). No significant association was observed between TNF-α-308G/A and DR susceptibility in total analyses and subgroup analyses by ethnicity and type of DM. TNF-α-308G/A polymorphism may enhance the susceptibility to diabetic nephropathy, especially in Asian population and in T2DM patients, but not diabetic retinopathy. © Georg Thieme Verlag KG Stuttgart · New York.Chronic active antibody-mediated rejection (CAAMR) is a particular problem in kidney transplantation, and about 25% of grafts are lost by CAAMR. Further, the pathogenesis remains unclear, and there is no effective cure or marker. We previously found that a hyper NFκB-activating mechanism in non-immune cells, called the IL-6 amplifier, is induced by the co-activation of NFκB and STAT3, and that this activation can develop various chronic inflammatory diseases. [https://www.selleckchem.com/products/CP-690550.html selleck chemicals llc] Here we show that synaptotagmin-17 (SYT17) is increased in an exosomal fraction of the urine from CAAMR patients, and that this increase is associated with activation of the IL-6 amplifier. Immunohistochemistry showed that SYT17 protein expression was increased in renal tubule cells of the CAAMR group. While SYT17 protein was not detectable in whole urine samples by western blotting, urinary exosomal SYT17 levels were significantly elevated in the CAAMR group compared to three other histology groups (normal, interstitial fibrosis and tubular atrophy, and calcineurin inhibitors toxicity) after kidney transplantation. On the other hand, current clinical laboratory data could not differentiate the CAAMR group from these groups. These data suggest that urinary exosomal SYT17 is a potential diagnostic marker for CAAMR. © The Japanese Society for Immunology. 2020. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.INTRODUCTION Quality indicators and pay-for-performance schemes aim to improve processes and outcomes in clinical practice. However, general practitioner and patient characteristics influence quality indicator performance. In Switzerland, no data on the pay-for-performance approach exists and the use of quality indicators has been marginal. The aim of this study was to describe quality indicator performance in diabetes care in Swiss primary care and to analyze associations of practice, general practitioner and patient covariates with quality indicator performance. METHODS For this cross-sectional study, we used medical routine data from an electronic medical record database. Data from 71 general practitioners and all their patients with diabetes were included. Starting in July 2018, we retrieved 12-month retrospective data about practice, general practitioner and patient characteristics, laboratory values, comorbidities and co-medication. Based on this data, we assessed quality indicator performance of procescharacteristics on quality indicator performance was surprisingly small and room for improvement in quality indicator performance of Swiss general practitioners seems to exist in diabetes care.Catatonia is characterized by motor, affective and behavioral abnormalities. To date, the specific role of white matter (WM) abnormalities in schizophrenia spectrum disorders (SSD) patients with catatonia is largely unknown. In this study, diffusion magnetic resonance imaging (dMRI) data were collected from 111 right-handed SSD patients and 28 healthy controls. Catatonic symptoms were examined on the Northoff Catatonia Rating Scale (NCRS). We used whole-brain tract-based spatial statistics (TBSS), tractometry (along tract statistics using TractSeg) and graph analytics (clustering coefficient-CCO, local betweenness centrality-BC) to provide a framework of specific WM microstructural abnormalities underlying catatonia in SSD. Following a categorical approach, post hoc analyses showed differences in fractional anisotrophy (FA) measured via tractometry in the corpus callosum, corticospinal tract and thalamo-premotor tract as well as increased CCO as derived by graph analytics of the right superior parietal cortex (SPC) and left caudate nucleus in catatonic patients (NCRS total score ≥ 3; n = 30) when compared to non-catatonic patients (NCRS total score = 0; n = 29). In catatonic patients according to DSM-IV-TR (n = 43), catatonic symptoms were associated with FA variations&nbsp;(tractometry) of the left corticospinal tract and CCO of the left orbitofrontal cortex, primary motor cortex, supplementary motor area and putamen. This study supports the notion that structural reorganization of WM bundles connecting orbitofrontal/parietal, thalamic and striatal regions contribute to catatonia in SSD patients.For most psychiatric disorders, including alcohol use disorder (AUD), approved pharmacological treatments are limited in their effectiveness, and new drugs that can easily be translated into the clinic are needed. Currently, great hope lies in the potential of psychedelics to effectively treat AUD. The primary hypothesis is that a single session of psychedelic-guided psychotherapy can restore normal brain function in AUD individuals and thereby reduce the risk of relapse in the long run. Here we applied three different treatment schedules with psilocybin/LSD in order to investigate relapse-like drinking in the alcohol deprivation effect (ADE) model. In contrast to the primary hypothesis, psychedelics had no long-lasting effects on the ADE in male and female rats, neither when administered in a high dosage regime that is comparable to the one used in clinical studies, nor in a chronic microdosing scheme. Only sub-chronic treatment with psilocybin produced a short-lasting anti-relapse effect. However, it is not a translatable treatment option to give psychedelics sub-chronically for relapse prevention. In conclusion, our results in the ADE model do not support the hypothesis that microdosing or high doses of psychedelic reduce relapse behavior. This conclusion has to be confirmed by applying other animal models of AUD. It could also well be that animal models of AUD might be unable to fully capture the therapeutic potential of psychedelic drugs and that only future large-scale clinical trials will be able to demonstrate the efficacy of psychedelics as a new treatment option for AUD.