Quantitative and Qualitative Analysis on Sex and Gender in Preparatory Material for National Medical Examination in Germany and the United States

Background: Sex- and gender-based medicine (SGBM) should be a mandatory part of medical education. We compared the quantity and quality of sex- and gender-related content of e-learning materials commonly used by German and American medical students while preparing for national medical examinations. Methods: Quantitative, line-by-line analysis of the preparatory materials AMBOSS 2017 and USMLE Step 1 Lecture Notes (2017) by KAPLAN MEDICAL was performed between April and October 2017. Subjects were allocated to one of the three main fields: clinical subjects, behavioral and social science, and pharmacology. Qualitative analysis comprised binary categorization into sex- and gender-based aspects and qualification with respect to the presence of a pathophysiological explanation for the sex or gender difference. Results: In relation to the total content of AMBOSS and KAPLAN, the sex- and gender-based share of the clinical subjects content was 26.8% (±8.2) in AMBOSS and 21.1% (±10.2) in KAPLAN. The number of sex- and gender-based aspects in the behavioral and social science learning material differed significantly for AMBOSS and KAPLAN (4.4% ± 3.1% vs 10.7% ± 7.5%; P = .044). Most of the sex- and gender-related content covered sex differences. Most learning cards and texts did not include a detailed pathophysiological explanation for sex- or gender-based aspects. The knowledge provided in the preparatory documents represents only a small part of facts that are already known about sex and gender differences. Conclusions: The preparatory materials focused almost exclusively on biological sex differences and the sociocultural dimension in particular is underrepresented. A lot more evidence-based facts are known and should be integrated into the materials to reflect the importance of SGBM as an integral component of patient-centered medicine

Chronic Naltrexone Therapy Is Associated with Improved Cardiac Function in Volume Overloaded Rats

Purpose: Myocardial opioid receptors were demonstrated in animals and humans and seem to colocalize with membranous and sarcolemmal calcium channels of the excitation-contraction coupling in the left ventricle (LV). Therefore, this study investigated whether blockade of the cardiac opioid system by naltrexone would affect cardiac function and neurohumoral parameters in Wistar rats with volume overload-induced heart failure. Methods: Volume overload in Wistar rats was induced by an aortocaval fistula (ACF). Left ventricular cardiac opioid receptors were identified by immunohistochemistry and their messenger ribonucleic acid (mRNA) as well as their endogenous ligand mRNA quantified by real-time polymerase chain reaction (RT-PCR). Following continuous delivery of either the opioid receptor antagonist naltrexone or vehicle via minipumps (n = 5 rats each), hemodynamic and humoral parameters were assessed 28 days after ACF induction. Sham-operated animals served as controls. Results: In ACF rats mu-, delta-, and kappa-opioid receptors colocalized with voltage-gated L-type Ca2+ channels in left ventricular cardiomyocytes. Chronic naltrexone treatment of ACF rats reduced central venous pressure (CVP) and left ventricular end-diastolic pressure (LVEDP), and improved systolic and diastolic left ventricular functions. Concomitantly, rat brain natriuretic peptide (rBNP-45) and angiotensin-2 plasma concentrations which were elevated during ACF were significantly diminished following naltrexone treatment. In parallel, chronic naltrexone significantly reduced mu-, delta-, and kappa-opioid receptor mRNA, while it increased the endogenous opioid peptide mRNA compared to controls. Conclusion: Opioid receptor blockade by naltrexone leads to improved LV function and decreases in rBNP-45 and angiotensin-2 plasma levels. In parallel, naltrexone resulted in opioid receptor mRNA downregulation and an elevated intrinsic tone of endogenous opioid peptides possibly reflecting a potentially cardiodepressant effect of the cardiac opioid system during volume overload