Search

Background: Despite an increase in the familiarity of the medical community with the epidemiological and clinical characteristics of coronavirus disease 2019 (COVID-19), there is presently a lack of rapid and effective risk stratification indicators to predict the poor clinical outcomes of COVID-19 especially in severe patients. Methods: In this retrospective single-center study, we included 117 cases confirmed with COVID-19. The clinical, laboratory, and imaging features were collected and analyzed during admission. The Multi-lobular infiltration, hypo-Lymphocytosis, Bacterial coinfection, Smoking history, hyper-Tension and Age (MuLBSTA) Score and Confusion, Urea, Respiratory rate, Blood pressure, Age 65 (CURB65) score were used to assess the death and intensive care unit (ICU) risks in all patients. Results: Among of all 117 hospitalized patients, 21 (17.9%) patients were admitted to the ICU care, and 5 (4.3%) patients were died. The median hospital stay was 12 (10–15) days. There were 18 patients with MuLBSTA score ≥ 12 points and were all of severe type. In severe type, ICU care and death patients, the proportion with MuLBSTA ≥ 12 points were greater than that of CURB65 score ≥ 3 points (severe type patients, 50 vs. 27.8%; ICU care, 61.9 vs. 19.0%; death, 100 vs. 40%). For the MuLBSTA score, the ROC curve showed good efficiency of diagnosis death (area under the curve [AUC], 0.956; cutoff value, 12; specificity, 89.5%; sensitivity, 100%) and ICU care (AUC, 0.875; cutoff value, 11; specificity, 91.7%; sensitivity, 71.4%). The K–M survival analysis showed that patients with MuLBSTA score ≥ 12 had higher risk of ICU (log-rank, P = 0.001) and high risk of death (log-rank, P = 0.000). Conclusions: The MuLBSTA score is valuable for risk stratification and could effectively screen high-risk patients at admission. The higher score at admission have higher risk of ICU care and death in patients infected with COVID.

Ubiquitin-specific protease 5 (USP5) is a deubiquitinating enzyme that functions as an oncoprotein in a variety of human cancers. However, the expression and role of USP5 in the metastasis of non-small cell lung cancer (NSCLC) have not been addressed. In this study, we examined the expression and prognostic significance of USP5 in NSCLC. The results revealed that USP5 was overexpressed and correlated with metastasis and overall survival in NSCLC tissues. A further in vitro study revealed that the levels of USP5 protein in NSCLC cells were associated with epithelial-mesenchymal transition (EMT) markers. Furthermore, USP5 overexpression significantly enhanced, whereas USP5 silencing significantly decreased the expression of EMT proteins and migration and invasion of NSCLC cells. In addition, the results from western blotting demonstrated that USP5 regulated EMT via the Wnt/β-catenin signaling pathway. Further immunohistochemical analysis revealed that USP5 was significantly associated with the expression of β-catenin and EMT markers in NSCLC tissues. Overall, USP5 upregulation is associated with tumor metastasis and poor prognosis in patients with NSCLC. USP5 promotes EMT and the invasion and migration of NSCLC cells. Therefore, USP5 may serve as a novel prognostic biomarker and provide a potential target for the treatment of metastasis in NSCLC.

Active adult neurogenesis produces new functional neurons, which replace the lost ones and contribute to brain repair. Promoting neurogenesis may offer a therapeutic strategy for human diseases associated with neurodegeneration. Here, we report that endogenous neuronal nitric oxide synthase (nNOS) for neural stem cells (NSCs) or progenitors positively regulates neurogenesis. nNOS repression exhibits significantly decreased neuronal differentiation and nNOS upregulation promotes neurons production from NSCs. Using a quantitative approach, we show that instructive effect, that is instruction of NSCs to adopt a neuronal fate, contributes to the favorable effect of endogenous nNOS on neurogenesis. Furthermore, nNOS-mediated instruction of neuronal fate commitment is predominantly due to the reduction of histone deacetylase 2 (HDAC2) expression and enzymatic activity. Further investigation will be needed to test whether HDAC2 can serve as a new target for therapeutic intervention of neurodegenerative disorders.