The objective of the study is the identification of racial differences in characteristics and comorbidities in patients hospitalized for COVID-19 and the impact on outcomes. The study design is a retrospective observational study. Data for all patients admitted to seven community hospitals in Michigan, United States, with polymerase chain reaction confirmed diagnosis of COVID-19 from March 10 to April 15, 2020 were analyzed. The primary outcomes of racial disparity in inpatient mortality and intubation were analyzed using descriptive statistics and multivariate regression models. The study included 336 Black and 408 White patients. Black patients were younger (62.9±15.0 years vs 71.8±16.4, P<.001), had a higher mean body mass index (32.4±8.6 kg/m vs 28.8±7.5, P<.001), had higher prevalence of diabetes (136/336 vs 130/408, P=.02), and presented later (6.6±5.3 days after symptom onset vs. 5.4±5.4, P=.006) compared with White patients. Younger Black patients had a higher prevalence of obesity (age<65 years, 69.9%) than older Black patients (age>65 years, 39.2%) and younger White patients (age<65, 55.1%). Intubation did not reach statistical significance for racial difference (Black patients 61/335 vs. 54/406, P=.08). Mortality was not higher in Black patients (65/335 vs. 142/406 in White patients, odds ratio 0.61, 95% confidence interval 0.37 to 0.99, 2-sided P=.05) in multivariate analysis, accounting for other risk factors associated with mortality. Higher prevalence of obesity and diabetes in young Black populations may be the critical factor driving disproportionate COVID-19 hospitalizations in Black populations. Hospitalized Black patients do not have worse outcomes compared with White patients.Higher prevalence of obesity and diabetes in young Black populations may be the critical factor driving disproportionate COVID-19 hospitalizations in Black populations. Hospitalized Black patients do not have worse outcomes compared with White patients.Oxidative stress injury (OSI) occurs in many cardiovascular diseases, and the OSI of endothelial cells is the main pathological basis of these diseases. Tectorigenin has an effect on oxidative stress in fibroblasts, keratinocytes, and neuroblastoma. This study attempted to reveal the effect of Tectorigenin on OSI in endothelial cells. An OSI cell model was firstly established by treating human umbilical vein endothelial cells (HUVECs) with H2O2. The H2O2-induced HUVECs were further pre-treated with Tectorigenin or PI3K inhibitor. Then the viability and apoptosis of HUVECs were evaluated using MTT, Hochest 33258 staining and TUNEL staining. Lactate dehydrogenase (LDH) leakage, enzyme activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and malondialdehyde (MDA) level were measured through colorimetric assays. The expressions of apoptosis-related factors and the activation of the PI3K/Akt pathway in HUVECs were detected by RT-qPCR or Western blot. Tectorigenin had no inhibiting effect on the viability of HUVECs at the concentrations of 0.1, 0.5, 0.5, 1, and 10 μmol/L. Tectorigenin reversed the H2O2 induced-destruction of HUVECs morphology. Tectorigenin increased the viability and decreased the apoptosis of H2O2-induced HUVECs. Tectorigenin increased Bcl-2 expression and the enzyme activities of SOD and GSH-Px, but decreased LDH leakage, MDA level, and the expressions of Bax and Cleaved Caspase-3 in H2O2-induced HUVECs. Furthermore, Tectorigenin increased the ratios of p-PI3K to PI3K and p-Akt to Akt in H2O2-induced HUVECs. PI3K inhibitor had an opposite effect of Tectorigenin on the OSI in H2O2-induced HUVECs and its effect was further reversed by Tectorigenin. read more Tectorigenin protected HUVECs against H2O2-induced OSI via PI3K/Akt pathway.The aim of the study is to expand information on the histological aspect, presence, and distribution of cytoskeletal proteins smooth muscle alpha-actin (α-SMA), desmin and vimentin in ovaries of three lizards Leiosauridae. In all analysed species, the ovaries were paired organs, located inside the coelomic cavity, covered in a simple cubic epithelium. Below the surface was the tunica albuginea. The organs can be divided into two regions the cortex and the medulla. The pre-vitellogenic follicles consist of an oocyte surrounded by the pellucid zone periodic acid schiff positive, the granulosa layer consisting of three cell types small, intermediate, and large and the theca layer. The vitellogenic follicles presented only a single layer of cubic granulosa cells. In the three lizards, α-SMA microfilaments (MFs) were verified along the theca layer and in endothelial cells of the blood vessels of the analysed follicles. Researchers have observed desmin intermediate filaments immunostaining exclusively muscle fibers of the albuginea and the ovarian stroma of Enyalius perditus. There was no immunostaining for vimentin in the ovaries of all the lizards studied. Results obtained revealed that the MFs of α-SMA could be responsible for a contractile activity present in the lizards assessed.Azanone (HNO/NO-), also called nitroxyl, is a highly reactive compound whose biological role is still a matter of debate. A key issue that remains to be clarified regarding HNO and its biological activity is that of its endogenous formation. Given the overlap of the molecular targets and reactivity of nitric oxide (NO•) and HNO, its chemical biology was perceived to be similar to that of NO• as a biological signaling agent. However, despite their closely related reactivity, NO• and HNO's biochemical pathways are quite different. Moreover, the reduction of nitric oxide to azanone is possible but necessarily coupled to other reactions, which drive the reaction forward, overcoming the unfavorable thermodynamic barrier. The mechanism of this NO•/HNO interplay and its downstream effects in different contexts were studied recently, showing that more than fifteen moderate reducing agents react with NO• producing HNO. Particularly, it is known that the reaction between nitric oxide and hydrogen sulfide (H2S) produces HNO. However, this rate constant was not reported yet. In this work, firstly the NO•/H2S effective rate constant was measured as a function of the pH. Then, the implications of these chemical (non-enzymatic), biologically compatible, routes to endogenous HNO formation was discussed. There is no doubt that HNO could be (is?) a new endogenously produced messenger that mediates specific physiological responses, many of which were attributed yet to direct NO• effects.