Identification of emergency department patients for referral to rapid-access addiction services.

Objectives: Substance-related emergency department (ED) visits are rapidly increasing. Despite this finding, many EDs do not have access to on-site addiction services. This study characterized substance-related ED presentations and assessed the ED health care team's perceived need for an on-site rapid-access addiction clinic for direct patient referral from the ED.

Interventions to Improve Emergency Department-Related Transitions in Care for Adult Patients With Atrial Fibrillation and Flutter.

Background: Patients presenting to emergency departments (EDs) with acute atrial fibrillation or flutter undergo numerous transitions in care (TiC), including changes in their provider, level of care, and location. During transitions, gaps in communications and care may lead to poor outcomes.

Objective: We sought to examine the effectiveness of ED-based interventions to improve length of stay, return to normal sinus rhythm, and hospitalization, among other critical patient TiC outcomes.

Treatment of obesity and diabetes in mice by transplant of gut cells engineered to produce leptin.

Leptin injections evoke weight loss by causing a reduction in food consumption and an increase in energy expenditure. Also, the administration of leptin lowers blood glucose levels in some rodent models of diabetes and in humans with lipodystrophy. We explored the therapeutic potential of delivering leptin to obese, diabetic ob/ob mice and to mice fed on a high-fat diet (HFD), by transplanting gut-derived cells engineered to produce leptin, under the regulation of an inducing agent, mifepristone.

Inhibition of preproinsulin gene expression by leptin induction of suppressor of cytokine signaling 3 in pancreatic beta-cells.

Leptin inhibits insulin secretion and preproinsulin gene expression in pancreatic beta-cells, but signal transduction pathways and molecular mechanisms underlying this effect are poorly characterized. In this study, we analyzed leptin-mediated signal transduction and preproinsulin gene regulation at the molecular level in pancreatic beta-cells. Leptin stimulation led to janus kinase (JAK)2-dependent phosphorylation and nuclear translocation of the transcription factors signal transducer and activator of transcription (STAT)3 and STAT5b in INS-1 beta-cells.

Leptin increases hepatic insulin sensitivity and protein tyrosine phosphatase 1B expression.

Leptin has been shown to improve insulin sensitivity and glucose metabolism in obese diabetic ob/ob mice, yet the mechanisms remain poorly defined. We found that 2 d of leptin treatment improved fasting but not postprandial glucose homeostasis, suggesting enhanced hepatic insulin sensitivity. Consistent with this hypothesis, leptin improved in vivo insulin receptor (IR) activation in liver, but not in skeletal muscle or fat.