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Introduction Coronavirus disease 2019 (COVID-19) is a global pandemic. Governments have implemented combinations of 'lockdown' measures of various stringencies, including school and workplace closures, cancellations of public events, and restrictions on internal and external movements. These policy interventions are an attempt to shield high risk individuals and to prevent overwhelming countries' healthcare systems, or, colloquially, 'flatten the curve'. However, these policy interventions may come with physical and psychological health harms, group and social harms, and opportunity costs. These policies may particularly affect vulnerable populations and not only exacerbate pre-existing inequities, but also generate new ones. Methods We developed a conceptual framework to identify and categorise adverse effects of COVID-19 lockdown measures. We based our framework on Lorenc and Oliver's framework for the adverse effects of public health interventions and the PROGRESS-Plus equity framework. To test its applican help in three ways (1) identifying areas where a policy intervention may generate inequitable adverse effects; (2) mitigating policy and practice interventions by facilitating the systematic examination of relevant evidence; and (3) planning for lifting COVID-19 lockdowns and policy interventions around the world.Background There is a pressing need for evidence-based interventions to address the devastating clinical and public health effects of the Coronavirus disease 2019 (COVID-19) pandemic. The number of registered trials related to COVID-19 is increasing by the day. Objectives To describe the characteristics of the currently registered clinical trials related to COVID-19. Methods We searched the World Health Organization (WHO)'s International Clinical Trials Registry Platform (ICTRP) on May 15, 2020. We included any entry that is related to COVID-19. We abstracted then descriptively analyzed the following characteristics of the registered trials study design, status, phase, primary endpoints, experimental interventions, and geographic location among other qualifiers. PI3K inhibitor Results We identified 1,308 eligible registered trials. The majority of trials were initially registered with ClinicalTrials.gov (n= 703; 53.7%) and the Chinese Clinical Trial Registry (ChiCTR) (n= 291; 22.2%). The number of participants to be enrolled across these trials was 734,657, with a median of 110 participants per trial. The most-commonly studied intervention category was pharmacologic (n=763; 58.3%), with antiparasitic medications being the most common subcategory. While over half of trials were already recruiting, we identified published peer-reviewed results for only 8 of those trials. Conclusion There is a relatively large number of registered trials but very few results published so far. While our findings suggest an appropriate initial response by the research community, the real challenge will be to get these trials completed, published, and translated into practice and policy.Background Baohuoside-1 is a flavonoid compound isolated from Epimedium koreanum Nakai. This study tried to systematically explore the potential anti-cancer functions of Baohuoside-1 in Hepatocellular Carcinoma and study related molecular mechanism. Moreover, as a potential candidate anti-cancer agent, Baohuoside-1 has relatively low toxic side effect. Methods The anti-cancer function including proliferation, invasion and migration of Baohuoside-1 in liver cancer was systematically assessed via colony formation, transwell assay and migration assay. Moreover, the anti-cancer functions of Baohuoside-1 was confirmed based on the nude mouse transplantation tumor experiment. The potential targeted signaling pathway was tested via flow cytometery and western blot analysis. Results In this study, we present the anti-HCC activity of Baohuoside-1 isolated from Epimedium through examing the effect of Baohuoside-1 on two different human liver cancer cell lines (HuH-7 and HepG2). Baohuoside-1 significantly inhibited the proliferation, invasion and migration of two liver cancer cell lines. Furthermore, the anticancer activity of Baohuoside-1 was confirmed via inhibiting liver tumor growth in nude mice in vivo. Additionally, the influence of Baohuoside-1 on liver cancer apoptosis was examined by analyzing the expression of pro/anti-apoptotic proteins (BAX, Bcl-2, caspase-3, and caspase-8). The potential targeting signaling of Baohuoside-1 was determined via testing key members' expression changes of mTOR and JAK2 signaling. Conclusion The inhibition of liver cancer by Baohuoside-1 is through targeting mTOR signaling not JAK2 signaling to induce apoptosis. Our study indicates that Baohuoside-1 is a potential candidate drug for therapy against liver cancer.Objective Regular consumption of n-3 polyunsaturated fatty acids is associated with decreased cardiovascular morbidity and mortality. This study assessed the therapeutic effect of docosahexaenoic acid (DHA) in palmitic acid (PA)-induced cytotoxicity in vitro and in rats fed a high-fat diet (HFD). Methods H9C2 cells and rat primary cardiomyoblasts were exposed to PA or PA + DHA for 24 h. PA-induced lipotoxicity and mitochondrial dysfunction were evaluated by immunostaining, real-time PCR, cardiomyocyte contraction and transmission electron microscopy. The effects of dietary DHA on diabetic cardiomyopathy were evaluated in male Sprague-Dawley rats fed a reference diet rich in DHA, an HFD, or an HFD with added DHA for 16 weeks. Oxidative stress and lipotoxicity in rat heart tissue were assayed by Masson staining, immunohistochemistry, and TUNEL. Results In vitro studies showed that dietary DHA reduced the occurrence of cardiomyopathy and improved cardiac responses to PA. In the rat model, dietary DHA reduced mitochondrial oxidative stress in HFD-induced diabetic cardiomyopathy. Conclusion Dietary DHA reduced mitochondrial oxidative stress and ameliorated PA-induced lipid toxicity. DHA consumption may have had direct effects on cardiovascular risk via myocardial protection.Clear cell renal cell carcinoma (ccRCC), the most frequent subtype of renal cell carcinoma (RCC), is characterized by high relapse rate and mortality. Long non-coding RNAs (lncRNAs) are critical participants during cancer development. LncRNA DARS antisense RNA 1 (DARS-AS1), a newly-found lncRNA, is not specifically reported in ccRCC. However, Gene Expression Profiling Interactive Analysis (GEPIA) and starBase databases revealed the up-regulation of DARS-AS1 in ccRCC. Current study investigated the function and mechanism of DARS-AS1 in ccRCC. Functional assays including colony formation assay, EdU assay, caspase-3 activity detection, flow cytometry analysis and JC-1 assay were implemented to identify the role of DARS-AS1 in ccRCC. As a result, silencing of DARS-AS1 retarded proliferation and facilitated apoptosis in ccRCC cells. Moreover, mainly a cytoplasmic localization of lncRNA DARS-AS1 was verified in ccRCC cells. Then, we demonstrated that DARS-AS1 positively regulated its nearby gene, aspartyl-tRNA synthetase (DARS), by sequestering miR-194-5p.
Homepage: https://www.selleckchem.com/products/GDC-0980-RG7422.html
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