Sexual minority adults who are members of racial/ethnic minority groups disproportionately affected by the pandemic also have higher prevalences of several of these health conditions than do racial/ethnic minority adults who are heterosexual. Collecting data on sexual orientation in COVID-19 surveillance and other studies would improve knowledge about disparities in infection and adverse outcomes by sexual orientation, thereby informing more equitable responses to the pandemic.BACKGROUND This study was designed to explore the incompletely investigated role of the complement component 3a receptor 1 (C3AR1) in the prognosis of stomach adenocarcinomas (STAD). MATERIAL AND METHODS Using bioinformatic methods, we systematically determined the expression and prognosis value of C3AR1 in various cancers by using the TIMER (Tumor Immune Estimation Resource) database, UALCAN platform, GEPIA (Gene Expression Profiling Interactive Analysis) server, and the OncoLnc tool. The biological processes influenced by C3AR1 were determined using the GSEA (Gene Set Enrichment Analysis) software (Copyright 2004-2020 Broad Institute, Inc., Massachusetts Institute of Technology, and Regents of the University of California). The correlation between C3AR1 expression and the immune-infiltrating cells as well as the correlation analysis between C3AR1 expression and the corresponding immune-marker sets were conducted using the TIMER and GEPIA databases. RESULTS The expression of C3AR1 was significantly (P less then 0.001) differentially expressed on several tumor types, while its prognosis value could only be determined on STAD, with a high expression of C3AR1 closely correlated with a poor prognosis. The GSEA analysis revealed that the differential expression of C3AR1 profoundly affected the immune-related biological processes. The expression of C3AR1 was strongly and positively correlated with the infiltration of monocytes, tumor-associated macrophages, M2 macrophages, dendritic cells, and exhausted T cells. CONCLUSIONS Our results have revealed that a high expression of C3AR1 is positively correlated with a poor prognosis and increased tumor-immune infiltration. C3AR1 can promote the polarization of M2 macrophages and T cell exhaustion, leading to the immune escape of STAD. These findings suggest that C3AR1 could be used as a prognostic and immune-infiltration marker in the pathogenesis of STAD.BACKGROUND Primary focal segmental glomerular sclerosis (FSGS) frequently causes recurrence after kidney transplantation, leading to graft loss in half of the patients. Conservative treatment of FSGS is the main acceptable method due to the lack of randomized clinical trials. A few strategies are known to treat FSGS recurrence, such as plasmapheresis and intravenous immunoglobulin (IVIG), but failure to achieve remission may occur. In addition, some of these treatment strategies are more established in pediatric patients and lack evidence in adult patients. CASE REPORT We describe the case of a 24-year-old woman who had a kidney transplant due to FSGS and was admitted to the hospital for an evaluation of lower-limb and facial swelling. Her kidney biopsy showed segmental glomerulosclerosis compatible with recurrence of FSGS. Her FSGS relapses were further confirmed by increase in serum creatinine and proteinuria. The patient had several FSGS relapses that were treated by different combinations of plasmapheresis, pulse steroid, mycophenolic acid, tacrolimus, prednisolone, IVIG, and IV rituximab. She did not respond to conventional therapy and was eventually treated successfully using cyclophosphamide and remained in remission afterward. CONCLUSIONS FSGS has a high recurrence rate after kidney transplantation. A few options to achieve remission have been investigated. In this report, we present the case of a young woman with FSGS recurrence after a kidney transplant, achieving remission successfully with cyclophosphamide. Cyclophosphamide can be used a treatment of FSGS recurrence in a transplanted kidney when all other options have been exhausted. Additional research is needed to assess the efficacy and safety profile of cyclophosphamide in such cases.Extracellular vesicles (EVs) are implicated in the crosstalk between adipocytes and other metabolic organs, and an altered biological cargo has been observed in EVs from human obese adipose tissue (AT). Yet, the role of adipocyte-derived EVs in pancreatic β cells remains to be determined. Here, we explored the effects of EVs released from adipocytes isolated from both rodents and humans and human AT explants on survival and function of pancreatic β cells and human pancreatic islets. EVs from healthy 3T3-L1 adipocytes increased survival and proliferation and promoted insulin secretion in INS-1E β cells and human pancreatic islets, both those untreated or exposed to cytokines or glucolipotoxicity, whereas EVs from inflamed adipocytes caused β cell death and dysfunction.  https://www.selleckchem.com/products/beta-aminopropionitrile.html  Human lean adipocyte-derived EVs produced similar beneficial effects, whereas EVs from obese AT explants were harmful for human EndoC-βH3 β cells. We observed differential expression of miRNAs in EVs from healthy and inflamed adipocytes, as well as alteration in signaling pathways and expression of β cell genes, adipokines, and cytokines in recipient β cells. These in vitro results suggest that, depending on the physiopathological state of AT, adipocyte-derived EVs may influence β cell fate and function.Elevation of intraocular pressure (IOP) due to trabecular meshwork (TM) damage is associated with primary open-angle glaucoma (POAG). Myocilin mutations resulting in elevated IOP are the most common genetic causes of POAG. We have previously shown that mutant myocilin accumulates in the ER and induces chronic ER stress, leading to TM damage and IOP elevation. However, it is not understood how chronic ER stress leads to TM dysfunction and loss. Here, we report that mutant myocilin activated autophagy but was functionally impaired in cultured human TM cells and in a mouse model of myocilin-associated POAG (Tg-MYOCY437H). Genetic and pharmacological inhibition of autophagy worsened mutant myocilin accumulation and exacerbated IOP elevation in Tg-MYOCY437H mice. Remarkably, impaired autophagy was associated with chronic ER stress-induced transcriptional factor CHOP. Deletion of CHOP corrected impaired autophagy, enhanced recognition and degradation of mutant myocilin by autophagy, and reduced glaucoma in Tg-MYOCY437H mice.