Inhibition of endothelial histone deacetylase 2 shifts endothelial-mesenchymal transitions in cerebral arteriovenous malformation models.

Cerebral arteriovenous malformations (AVMs) are the most common vascular malformations worldwide and the leading cause of hemorrhagic strokes that may result in crippling neurological deficits. Here, using recently generated mouse models, we uncovered that cerebral endothelial cells (ECs) acquired mesenchymal markers and caused vascular malformations. Interestingly, we found that limiting endothelial histone deacetylase 2 (HDAC2) prevented cerebral ECs from undergoing mesenchymal differentiation and reduced cerebral AVMs.

CDK1 inhibition reduces osteogenesis in endothelial cells in vascular calcification.

Vascular calcification is a severe complication of cardiovascular diseases. Previous studies demonstrated that endothelial lineage cells transitioned into osteoblast-like cells and contributed to vascular calcification. Here, we found that inhibition of cyclin-dependent kinase (CDK) prevented endothelial lineage cells from transitioning to osteoblast-like cells and reduced vascular calcification.

Developing a User-Centered Digital Clinical Decision Support App for Evidence-Based Medication Recommendations for Type 2 Diabetes Mellitus: Prototype User Testing and Validation Study.

Background: Closing the gap between care recommended by evidence-based guidelines and care delivered in practice is an ongoing challenge across systems and delivery models. Clinical decision support systems (CDSSs) are widely deployed to augment clinicians in their complex decision-making processes. Despite published success stories, the poor usability of many CDSSs has contributed to fragmented workflows and alert fatigue.

Elevation of serum creatine phosphokinase in hospitalized patients.

Background: The clinical characteristics and outcomes of patients with significant noncardiac and cardiac serum creatine phosphokinase (CPK) elevations are not well described.

Methods: One hundred fifty-eight inpatients who had CPK elevation of >1000 IU/L were identified. One hundred thirty-seven patients whose CPK elevations could be attributed to either noncardiac or cardiac etiologies were included and analyzed for clinical characteristics, 30-day, 3-month, and 1-year all-cause mortality rates.

New onset atrial fibrillation developing in medical inpatients.

Background: The outcome of patients who develop new onset atrial fibrillation (AF) after admission to an Internal Medicine service for acute medical illnesses is unknown.

Methods: In a retrospective review, we compared patients in the study group: patients who were admitted to hospital for acute medical illnesses and subsequently developed new onset AF during hospitalization, with a control group 1: patients whose admitting diagnosis was new onset AF and a control group 2: patients who were admitted for acute medical illnesses and never developed AF. We analyzed clinical characteristics and all-cause mortality rate during the first 30 days, 6 months, and 1 year after admission.