Peer Teaching in Undergraduate Medical Education: What are the Learning Outputs for the Student-Teachers? A Systematic Review.

Introduction: To achieve quality in medical education, peer teaching, understood as students taking on roles as educators for peers, is frequently used as a teaching intervention. While the benefits of peer teaching for learners and faculty are described in detail in the literature, less attention is given to the learning outputs for the student-teachers. This systematic review focuses on the learning outputs for medical undergraduates acting as student-teachers in the last decade (2012-2022).

Exercise reduces intramuscular stress and counteracts muscle weakness in mice with breast cancer.

Background: Patients with breast cancer exhibit muscle weakness, which is associated with increased mortality risk and reduced quality of life. Muscle weakness is experienced even in the absence of loss of muscle mass in breast cancer patients, indicating intrinsic muscle dysfunction. Physical activity is correlated with reduced cancer mortality and disease recurrence.

Neutrophils in chronic inflammatory diseases.

Chronic inflammation is a component of many disease conditions that affect a large group of individuals worldwide. Chronic inflammation is characterized by persistent, low-grade inflammation and is increased in the aging population. Neutrophils are normally the first responders to acute inflammation and contribute to the resolution of inflammation.

Mitochondrial NDUFA4L2 is a novel regulator of skeletal muscle mass and force.

The hypoxia-inducible nuclear-encoded mitochondrial protein NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 4-like 2 (NDUFA4L2) has been demonstrated to decrease oxidative phosphorylation and production of reactive oxygen species in neonatal cardiomyocytes, brain tissue and hypoxic domains of cancer cells. Prolonged local hypoxia can negatively affect skeletal muscle size and tissue oxidative capacity. Although skeletal muscle is a mitochondrial rich, oxygen sensitive tissue, the role of NDUFA4L2 in skeletal muscle has not previously been investigated.

Heparinoid sevuparin inhibits -induced vascular leak through neutralizing neutrophil-derived proteins.

Acute lung injury (ALI) and respiratory distress can develop as a consequence of sepsis with pathogens such as group A (GAS). In the pathogenesis of sepsis-associated ALI, endothelial barrier disruption brought on by phagocyte activation is considered a causative factor. Here, we find that sevuparin, a heparinoid with low anticoagulant activity, prevents neutrophil-induced lung plasma leakage in a murine model of systemic inflammation evoked by heat-killed GAS (hkGAS).