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Background The use of disinfectants is crucial to preventing the spread of nosocomial infections in health care workers. As many as 25 applications of hand disinfectants is a realistic default value during a working day. However, alcohol-based hand disinfectants may weaken skin barrier function and induce dryness and eczema, which decrease their acceptance. Objective To evaluate the effect of ethanol-containing disinfectants with 5% urea on skin barrier function and on sensitivity to an irritant soap (sodium lauryl sulfate [SLS]). Methods Twenty healthy volunteers treated one of their forearms twice daily for 17 days with an ethanol-containing gel with 5% urea. Two types of gels with urea were tested. Treatment was randomized to left or right forearm, and the contralateral forearm served as untreated control. Transepidermal water loss, skin capacitance (dryness), and sensitivity to SLS were evaluated. Results Twice-daily application of the urea-containing ethanol gels lowered transepidermal water loss, prevented dryness, and reduced sensitivity to SLS compared with the untreated control skin. Conclusions Improved barrier function using this ethanol gel with urea may have relevance in daily disinfectant procedures.When studying the effect of a prenatal treatment on events in the offspring, failure to produce a live birth is a competing event for events in the offspring. A common approach to handle this competing event is reporting both the treatment-specific probabilities of live births and of the event of interest among live births. However, when the treatment affects the competing event, the latter probability cannot be interpreted as the causal effect among live births.Here we provide guidance for researchers interested in the effects of prenatal treatments on events in the offspring in the presence of the competing event "no live birth". We review the total effect of treatment on a composite event and the total effect of treatment on the event of interest. These causal effects are helpful for decision making, but are agnostic about the pathways through which treatment affects the event of interest.Therefore, based on recent work, we also review three causal effects that explicitly consider the pathways through which treatment may affect the event of interest in the presence of competing events the direct effect of treatment on the event of interest under an intervention to eliminate the competing event, the separable direct and indirect effects of treatment on the event of interest, and the effect of treatment in the principal stratum of those who would have had a live birth irrespective of treatment choice. As an illustrative example, we use a randomized trial of fertility treatments and risk of neonatal complications.Background/aims MicroRNAs (miRNAs) are short, non-coding RNA molecules that control gene expression trough negative translational regulation. MiR-623 is a tumor suppressor, and it's function and mechanism in breast cancer has not been reported. Results Exogenous overexpression of miR-623 suppressed cell proliferation, migration and invasion, meanwhile, but promoted cell apoptosis. MiR-623 knockdown displayed opposite results. Overexpression of miR-623 resulted in the downregulation of CDK4/6 as well as the inhibition of the phosphatidylinositol-3-kinase (PI3K)/Akt and Wnt/β-Catenin signaling pathways. MiR-623 knockdown displayed opposite results. Results of the reporter assay revealed that the luciferase activity was decreased in XRCC5-wt cells, suggesting that miR-623 could directly combine with 3' UTR of XRCC5. MiR-623 significantly suppressed XRCC5 expression, which is critical for miR-623-induced proliferation and migration block in breast cancer cells. Conclusion miR-623 suppressed cell proliferation, migration and invasion through downregulation of cyclin dependent kinases and inhibition of the phosphatidylinositol-3-kinase (PI3K)/Akt and Wnt/β-Catenin pathways by targeting XRCC5. find more Methods miR-623 was either overexpressed in breast cancer cell lines through exogenous transfection or knocked down by specific siRNA. Cell proliferation, migration and invasion were examined using CCK-8, colony formation and transwell assay. The direct target of miR-623 was verified using luciferase reporter gene assay.As the outbreak of coronavirus disease 2019 (COVID-19) progresses, prognostic markers for early identification of high-risk individuals are an urgent medical need. Italy has one of the highest numbers of SARS-CoV-2-related deaths and one of the highest mortality rates. Worldwide, a more severe course of COVID-19 is associated with older age, comorbidities, and male sex. Hence, we searched for possible genetic components of COVID-19 severity among Italians by looking at expression levels and variants in ACE2 and TMPRSS2 genes, crucial for viral infection.Exome and SNP-array data from a large Italian cohort were used to compare the rare-variants burden and polymorphisms frequency with Europeans and East Asians. Moreover, we looked into gene expression databases to check for sex-unbalanced expression.While we found no significant evidence that ACE2 is associated with disease severity/sex bias, TMPRSS2 levels and genetic variants proved to be possible candidate disease modulators, prompting for rapid experimental validations on large patient cohorts.Amid the coronavirus disease (COVID-19) crisis, we have witnessed true physicianship as our frontline doctors apply clinical problem-solving to an illness without a textbook algorithm. Yet, for over a century, medical education in the United States has plowed ahead with a system that prioritizes content delivery over problem-solving. As resident trainees, we are acutely aware that memorizing content is not enough. We need a preclinical system designed to steer early learners from "know" to "know how." Education leaders have long advocated for such changes to the medical school structure. For what may be the first time, we have a real chance to effect change. In response to the COVID-19 pandemic, medical educators have scrambled to conform curricula to social distancing mandates. The resulting online infrastructures are a rare chance for risk-averse medical institutions to modernize how we train our future physicians-starting by eliminating the traditional classroom lecture. Institutions should capitalize on new digital infrastructures and curricular flexibility to facilitate the eventual rollout of flipped classrooms-a system designed to cultivate not only knowledge acquisition but problem-solving skills and creativity.

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