Tutorial Education Program at a dental school in Southern Brazil: A transforming experience.

BACKGROUND: The Tutorial Education Program (PET), regulated in 2005 by Law no. 11.180/2004, in addition to transforming higher education in Brazil, has been an essential component for the development of academic students, expanding the education perspective. AIMS: This article aims to report the actions developed regarding these three pillars and the experience of undergraduate dentistry students, who are members of the Tutorial Education Program at the Federal University of Santa Maria. METHODS: Through teaching, research, and extension activities, which are the structuring pillars of Brazilian universities, PET enables the improvement of education and pedagogical projects in higher education courses. RESULTS: With regard to teaching and the search for knowledge construction, the group has been conducting six projects focused on dental students, in the form of lectures and workshops, as well as innovated the teaching-learning process through the preparation of video classes and the monitoring of freshmen students. Regarding the production of new knowledge through research, three projects focused on dental trauma, xerostomia, and the impact of COVID-19 on the teaching of dental students. As an exchange between community and university, in the extension pillar, the group participates in three projects aimed at blood donation, divulgation of the university, and the elderly public. During the 2020 pandemic, the group made adaptations and created new actions. CONCLUSION: Therefore, the activities planned and performed by the Tutorial Education Program have developed its members' skills and contributed to improvements in the quality of Brazilian higher education.

The Pathogenesis of COVID-19 Myocardial Injury: An Immunohistochemical Study of Postmortem Biopsies.

Rationale: Myocardial injury associates significantly and independently with mortality in COVID-19 patients. However, the pathogenesis of myocardial injury in COVID-19 remains unclear, and cardiac involvement by SARS-CoV-2 presents a major challenge worldwide. Objective: This histological and immunohistochemical study sought to clarify the pathogenesis and propose a mechanism with pathways involved in COVID-19 myocardial injury. Methods and Results: Postmortem minimally invasive autopsies were performed in six patients who died from COVID-19, and the myocardium samples were compared to a control group (n=11). Histological analysis was performed using hematoxylin-eosin and toluidine blue staining. Immunohistochemical (IHC) staining was performed using monoclonal antibodies against targets: caspase-1, caspase-9, gasdermin-d, ICAM-1, IL-1ß, IL-4, IL-6, CD163, TNF-α, TGF-ß, MMP-9, type 1 and type 3 collagen. The samples were also assessed for apoptotic cells by TUNEL. Histological analysis showed severe pericardiocyte interstitial edema and higher mast cells counts per high-power field in all COVID-19 myocardium samples. The IHC analysis showed increased expression of caspase-1, ICAM-1, IL-1ß, IL-6, MMP-9, TNF-α, and other markers in the hearts of COVID-19 patients. Expression of caspase-9 did not differ from the controls, while gasdermin-d expression was less. The TUNEL assay was positive in all the COVID-19 samples supporting endothelial apoptosis. Conclusions: The pathogenesis of COVID-19 myocardial injury does not seem to relate to primary myocardiocyte involvement but to local inflammation with associated interstitial edema. We found heightened TGF-ß and interstitial collagen expression in COVID-affected hearts, a potential harbinger of chronic myocardial fibrosis. These results suggest a need for continued clinical surveillance of patients for myocardial dysfunction and arrythmias after recovery from the acute phase of COVID-19.

The effect of ivabradine therapy on heart failure patients with reduced ejection fraction: a systematic review and meta-analysis.

Background Ivabradine is currently indicated to lower heart rate in Heart Failure with Reduced Ejection Fraction (HFrEF) patients. However its effect apart from beta-blockers is not clear. Aim of the review To study the additional effect of ivabradine, apart from the effect of beta-blockers, on cardiovascular death, all-cause mortality, hospitalization due to HF and heart rate in HFrEF population. Method Electronic searches were conducted up to June 2016 to include randomized controlled trials where ivabradine was compared to a control group. Relative risks RRs and their 95% confidence intervals (CI 95%) were pooled and the random and fixed effect were used to summarize the results according to heterogeneity levels. Heterogeneity among studies was measured by the I-squared statistic Results Of 1790 studies, seven met the inclusion criteria for the systematic review and meta-analysis. The population consisted of 17,747 patients. Risk of bias was generally high for beta-blocker doses lower than recommended. Interventions lasted 1.5-22.9 months and pooled relative risks RR (95%) for all-cause mortality, cardiovascular death and hospitalization for HF were 0.98 (0.90-1.06); 0.99 (0.91-1.08); and 0.87 (0.68-1.12) respectively. Heart rate (CI 95%) decreased by 8.7 (6.37-11.03) beats per minute with ivabradine compared to the control group. Subgroup analysis by beta-blocker dose showed that for patients on recommended treatment (at least 50% of the beta-blocker target dose), heart rate (CI 95%) decreased by 4.70 (3.67-5.73), whereas for patients not on recommended treatment or with unreported dose, heart rate decreased by 8.60 (8.13-9.08). Conclusion Ivabradine significantly reduced heart rate and its additional effect on heart rate appears to be inversely correlated with the dose of beta-blocker. It showed no significant effect for all-cause mortality, cardiovascular death and hospitalization due to HF. Unreported beta-blocker doses and beta-blocker doses lower than recommended limited the conclusions.

High levels of cellular prion protein improve astrocyte development.

Prion protein (PrP(C)) has neuroprotective functions and herein we demonstrate that astrocytes from PrP(C)-over-expressing mice are more resistant to induced cell death than wild-type astrocytes. The Stress-Inducible-Protein 1 (STI1), a PrP(C) ligand, prevents cell death in both wild-type and PrP(C)-over-expressing astrocytes through the activation of protein-kinase-A. Cultured embryonic astrocytes and brain extracts from PrP(C)-over-expressing mice show higher glial fibrillary acidic protein expression and reduced vimentin and nestin levels when compared to wild-type astrocytes, suggesting faster astrocyte maturation in the former mice. Our data indicate that PrP(C) levels modulate astrocyte development, and that PrP(C)-STI1 interaction contributes to protect against astrocyte death.