Comparative admission rates and infection severity of COVID-19 among unvaccinated and vaccinated patients.

Vaccination efforts have limited the burden of the pandemic caused by the coronavirus disease 2019 (COVID-19) with substantial evidence showing reduced hospitalization rates among vaccinated populations. However, few studies have explored correlations between vaccination status and inpatient COVID-19 outcomes. This observational case-control study involved a retrospective chart review of adult patients hospitalized for COVID-19 infection at a medium-sized hospital in Central Michigan between May 1, 2021 and September 30, 2021. Unadjusted analyses involved t-tests and chi-square tests followed by adjusted analyses using binary logistic and linear regression models. Of the 192 screened patients, 171 subjects met the inclusion criteria. Vaccinated patients were significantly older (71.09 vs 57.45, p < 0.001), more likely to identify as white (89.4% vs 66.9%, p = 0.026), and had a lower baseline 10-year survival rate predicted by the Charlson Comorbidity Index (42% vs 69%, p < 0.001) compared to unvaccinated patients. Common symptoms between both groups included shortness of breath (50%), malaise (23%-37%), cough (28%-32%), and fever or chills (25%). Upon matching, adjusted analysis showed significantly higher rates of remdesivir administration to unvaccinated patients (41.3% vs 13.3%, odds ratio (OR): 4.63, 90% confidence interval (CI): 1.98-11.31). Despite higher intensive care unit admission rates among unvaccinated patients (39.1% vs 23.9%, OR: 1.83, 90% CI: 0.74-4.64), this difference did not reach statistical significance. Accordingly, immunization status strongly correlates with patient demographics and differences in inpatient treatment. Larger studies are needed to further assess the vaccine's impact on inpatient outcomes outside of our community.

Meet-U: Educating through research immersion.

We present a new educational initiative called Meet-U that aims to train students for collaborative work in computational biology and to bridge the gap between education and research. Meet-U mimics the setup of collaborative research projects and takes advantage of the most popular tools for collaborative work and of cloud computing. Students are grouped in teams of 4-5 people and have to realize a project from A to Z that answers a challenging question in biology. Meet-U promotes "coopetition," as the students collaborate within and across the teams and are also in competition with each other to develop the best final product. Meet-U fosters interactions between different actors of education and research through the organization of a meeting day, open to everyone, where the students present their work to a jury of researchers and jury members give research seminars. This very unique combination of education and research is strongly motivating for the students and provides a formidable opportunity for a scientific community to unite and increase its visibility. We report on our experience with Meet-U in two French universities with master's students in bioinformatics and modeling, with protein-protein docking as the subject of the course. Meet-U is easy to implement and can be straightforwardly transferred to other fields and/or universities. All the information and data are available at www.meet-u.org.

Enoxaparin attenuates doxorubicin induced cardiotoxicity in rats via interfering with oxidative stress, inflammation and apoptosis.

BACKGROUND: Doxorubicin (DOX) is commonly used in the treatment of many types of cancers but its cardiotoxicity is limiting its clinical use. Beyond its anticoagulant action, enoxaparin (ENX), a low molecular weight heparin, has been shown to exert multiple pharmacological actions including antioxidant, anti-inflammatory and antiapoptotic effects. Therefore, the current study aimed to assess if ENX could ameliorate cardiotoxicity induced by DOX. METHODS: Twenty-one adult male Wistar albino rats were randomly allocated into three groups (n = 7 each) of control, receiving 0.9% saline (i.p.), DOX, receiving 2.5 mg/kg of DOX (i.p.) thrice weekly; and DOX + ENX, receiving ENX (250 IU/kg/day i.p.) and a DOX dose equivalent to that of the DOX only group. RESULTS: DOX-induced cardiotoxicity was indicated by marked increases in cardiac troponin I (cTnI) and severe histological lesions, which significantly correlated with cardiotoxicity, oxidative stress, inflammation and apoptosis markers, compared to controls. DOX group also showed elevations in malondialdehyde (MDA), a marker of oxidative stress, and reductions in total antioxidant capacity (TAC). Cardiac inflammatory markers including tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1ß) and caspase-3, an apoptotic marker, were also elevated in the DOX group. DOX, however, did not significantly alter brain natriuretic peptide (BNP) levels. ENX significantly attenuated, but not completely reversed, DOX-induced cardiotoxicity through lowering cTnI and improving cardiomyopathy histopathological scores as compared to the DOX group. ENX also decreased MDA, increased TAC of rats' heart to levels relatively comparable to control. Significant reductions in TNF-α, IL-1ß and caspase-3 were also observed following ENX treatment relative to the DOX only group. CONCLUSIONS: Collectively, these results describe a cardioprotective effect for ENX against DOX-induced cardiotoxicity which is likely facilitated via suppression of oxidative stress, inflammation and apoptosis.