Inhibition of vascular smooth muscle cell PERK/ATF4 ER stress signaling protects against abdominal aortic aneurysms.

Abdominal aortic aneurysms (AAA) are a life-threatening cardiovascular disease for which there is a lack of effective therapy preventing aortic rupture. During AAA formation, pathological vascular remodeling is driven by vascular smooth muscle cell (VSMC) dysfunction and apoptosis, for which the mechanisms regulating loss of VSMCs within the aortic wall remain poorly defined. Using single-cell RNA-Seq of human AAA tissues, we identified increased activation of the endoplasmic reticulum stress response pathway, PERK/eIF2α/ATF4, in aortic VSMCs resulting in upregulation of an apoptotic cellular response.

Evaluating an Emergency Department Discharge Center: A Learning Organization Approach for Efficiency and Future Directions.

Introduction Our pilot Emergency Department Discharge Center (EDDC) facilitates post-discharge appointments, and screens for social determinants of health (SDoH) with a long, paper-based tool. No criteria guide which patients to refer to EDDC for appointment-making. Patients screening positive for SDoH are texted or emailed a list of community-based organizations (CBOs) to contact; the screening tool doesn't assess patients' interest or ability to contact CBOs.

Enhancing the Properties of Liquid Crystal Polymers and Elastomers with Nano Magnetic Particles.

Side-chain liquid crystal polymers have been mixed with ferromagnetic particles, and the formation of a monodomain in magnetic fields studied. At relatively low concentrations, the presence of ferroparticles substantially speeds up the rate of formation of a monodomain within the magnetic field, and, at a given concentration of ferroparticles, that rate is independent of the magnetic field's strength. In this way, the rapid formation of a monodomain is possible at magnetic field strengths far lower those required for the liquid crystal polymer alone.

The STAT3/SETDB2 axis dictates NF-κB-mediated inflammation in macrophages during wound repair.

Macrophage transition from an inflammatory to reparative phenotype after tissue injury is controlled by epigenetic enzymes that regulate inflammatory gene expression. We have previously identified that the histone methyltransferase SETDB2 in macrophages drives tissue repair by repressing NF-κB-mediated inflammation. Complementary ATAC-Seq and RNA-Seq of wound macrophages isolated from mice deficient in SETDB2 in myeloid cells revealed that SETDB2 suppresses the inflammatory gene program by inhibiting chromatin accessibility at NF-κB-dependent gene promoters.

Mesenteric Ischemia.

Mesenteric ischemia occurs when perfusion of the visceral organs fails to meet normal metabolic requirements and subsequently results in abdominal symptoms such as diffuse postprandial pain, peritonitis, food fear, and weight loss. While generally divided into acute and chronic manifestations, mesenteric ischemia is commonly misdiagnosed at initial presentation due to the significant overlap with symptoms of other abdominal pathologies. Prompt recognition and diagnosis, mesenteric revascularization, and critical care management remain the mainstay of treatment in these patients for optimal outcomes.