BackgroundCritical appraisal is an important skill for clinicians of the future which medical students often have limited opportunities to develop. This study aimed to evaluate whether a national journal club session could improve medical students’ confidence with critical appraisal.Methods98 medical students attended a critical appraisal lecture and supervised journal article discussions. Junior doctor mentors supported students to submit discussion points as a letter-to-the-editor. An online cross-sectional survey was administered before and after the conference.Results74 students responded, reporting increased confidence with critically appraising research articles (median score 2 vs 4, p<0.01) and increased understanding of why critical appraisal was important to their careers (median score 3 vs 5, p<0.01).DiscussionThis is the first study to demonstrate that a single national journal club session can significantly improve UK medical students’ confidence with the critical appraisal process. These opportunities are valued by medical students.
Objectives:Approximately 35% of colorectal cancer (CRC) risk is attributable to heritable factors known hereditary syndromes, accounting for 6%. The remainder may be due to lower penetrance polymorphisms particularly of DNA repair genes. DNA repair pathways, including base excision repair (BER), nucleotide excision repair (NER), mismatch repair (MMR), direct reversal repair (DRR), and double-strand break repair are complex, evolutionarily conserved, and critical in carcinogenesis. Germline mutations in these genes are associated with high-penetrance CRC syndromes such as Lynch syndrome. However, the association of low-penetrance polymorphisms of DNA repair genes with CRC risk remains unclear.Methods:A systematic literature review of PubMed, Embase, and HuGENet databases was conducted. Pre-specified criteria determined study inclusion/exclusion. Per-allele, pooled odds ratios disclosed the risk attributed to each variant. Heterogeneity was investigated by subgroup analyses for ethnicity and tumor location; funnel plots and Egger’s test assessed publication bias.Results:Sixty-one polymorphisms in 26 different DNA repair genes were identified. Meta-analyses for 22 polymorphisms in 17 genes revealed that six polymorphisms were significantly associated with CRC risk within BER (APE1, PARP1), NER (ERCC5, XPC), double-strand break (RAD18), and DRR (MGMT), but none within MMR. Subgroup analyses revealed significant association of OGG1 rs1052133 with rectal cancer risk. Egger’s test revealed no publication bias.Conclusions:Low-penetrance polymorphisms in DNA repair genes alter susceptibility to CRC. Future studies should therefore analyze whole-genome polymorphisms and any synergistic effects on CRC risk.Translational impact:This knowledge may enhance CRC risk assessment and facilitate a more personalized approach to cancer prevention.
BackgroundAortic stenosis is the most common age-related valvular pathology. Patients with aortic stenosis and myocardial fibrosis have worse outcome but the underlying mechanism is unclear. Lipoprotein(a) is associated with adverse cardiovascular risk and is elevated in patients with aortic stenosis. Although mechanistic pathways could link Lipoprotein(a) with myocardial fibrosis, whether the two are related has not been previously explored. In this study, we investigated whether elevated Lipoprotein(a) was associated with the presence of myocardial replacement fibrosis.MethodsA total of 110 patients with mild, moderate and severe aortic stenosis were assessed by late gadolinium enhancement (LGE) cardiovascular magnetic resonance to identify fibrosis. Mann Whitney U tests were used to assess for evidence of an association between Lp(a) and the presence or absence of myocardial fibrosis and aortic stenosis severity and compared to controls. Univariable and multivariable linear regression analysis were undertaken to identify possible predictors of Lp(a).ResultsThirty-six patients (32.7%) had no LGE enhancement, 38 (34.6%) had midwall enhancement suggestive of midwall fibrosis and 36 (32.7%) patients had subendocardial myocardial fibrosis, typical of infarction. The aortic stenosis patients had higher Lp(a) values than controls, however, there was no significant difference between the Lp(a) level in mild, moderate or severe aortic stenosis. No association was observed between midwall or infarction pattern fibrosis and Lipoprotein(a), in the mild/moderate stenosis (p = 0.91) or severe stenosis patients (p = 0.42).ConclusionThere is no evidence to suggest that higher Lipoprotein(a) leads to increased myocardial midwall or infarction pattern fibrosis in patients with aortic stenosis.
Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia seen in clinical practice with prevalence in excess of 33 million worldwide. Although often asymptomatic and until recently considered a “benign” arrhythmia, it is now appreciated that thromboembolism resulting from AF results in significant morbidity and mortality predominantly due to stroke. Although an arrhythmia more commonly affecting the elderly, AF can also occur in the young. This review focuses on the impact of AF in the younger population and discusses the dilemmas of managing younger patients with AF.
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