Optimizing perioperative Crohn's disease management: role of coordinated medical and surgical care.

Aim: To investigate rates of re-establishing gastroenterology care, colonoscopy, and/or initiating medical therapy after Crohn's disease (CD) surgery at a tertiary care referral center.

Methods: CD patients having small bowel or ileocolonic resections with a primary anastomosis between 2009-2012 were identified from a tertiary academic referral center. CD-specific features, medications, and surgical outcomes were abstracted from the medical record.

Implementation of surgical quality improvement: auditing tool for surgical site infection prevention practices.

Background: Surgical site infections are a potentially preventable patient harm. Emerging evidence suggests that the implementation of evidence-based process measures for infection reduction is highly variable.

Objective: The purpose of this work was to develop an auditing tool to assess compliance with infection-related process measures and establish a system for identifying and addressing defects in measure implementation.

Measuring briefing and checklist compliance in surgery: a tool for quality improvement.

Operating room briefings improve patient outcomes; however, implementation and methods to measure are lacking. A briefing audit tool was developed with 4 domains: briefing logistics, briefing basics, specific briefing content, and briefing participation. The tool evaluated preoperative briefings across surgical services at an academic medical center.

Hospital readmission by method of data collection.

Background: Hospital readmissions are increasingly used to pay hospitals differently. We hypothesized that readmission rates, readmissions related to index admission, and potentially unnecessary readmissions vary by data collection method for surgical patients.

Study Design: Using 3 different data collection methods, we compared 30-day unplanned readmission rates and potentially unnecessary readmissions among colorectal surgery patients at a single institution between July 2009 and November 2011.

Implementation of a surgical comprehensive unit-based safety program to reduce surgical site infections.

Background: Surgical site infections (SSI) are a common and costly problem, prolonging hospitalization and increasing readmission. Adherence to well-known infection control process measures has not been associated with substantial reductions in SSI. To date, the global burden of preventable SSI continues to result in patient harm and increased health care costs on a broad scale.

Insulin acts at different CNS sites to decrease acute sucrose intake and sucrose self-administration in rats.

Findings from our laboratory and others have demonstrated that the hormone insulin has chronic effects within the CNS to regulate energy homeostasis and to decrease brain reward function. In this study, we compared the acute action of insulin to decrease intake of a palatable food in two different behavioral tasks-progressive ratios sucrose self-administration and micro opioid-stimulated sucrose feeding-when administered into several insulin-receptive sites of the CNS. We tested insulin efficacy within the medial hypothalamic arcuate (ARC) and paraventricular (PVN) nuclei, the nucleus accumbens, and the ventral tegmental area.

Deconstructing the vanilla milkshake: the dominant effect of sucrose on self-administration of nutrient-flavor mixtures.

Rats and humans avidly consume flavored foods that contain sucrose and fat, presumably due to their rewarding qualities. In this study, we hypothesized that the complex mixture of corn oil, sucrose, and flavor is more reinforcing than any of these components alone. We observed a concentration-dependent increase in reinforcers of sucrose solutions received (0%, 3%, 6.

Intraventricular insulin and leptin decrease sucrose self-administration in rats.

Data from our laboratory and others have demonstrated an effect of the candidate adiposity signals insulin and leptin to decrease brain reward function, as assessed by lateral hypothalamic self-stimulation and food-conditioned place preference. In this study, we evaluated the effect of centrally administrated insulin or leptin to acutely decrease motivated performance for 5% sucrose, i.e.

Inactivation of the DMH selectively inhibits the ACTH and corticosterone responses to hypoglycemia.

We have previously reported that repeated bouts of insulin-induced hypoglycemia (IIH) in the rat result in blunted activation of the paraventricular, arcuate, and dorsomedial hypothalamic (DMH) nuclei. Because DMH activation has been implicated in the sympathoadrenal and hypothalamic-pituitary-adrenal (HPA) responses to stressors, we hypothesized that its blunted activation may play a role in the impaired counterregulatory response that is also observed with repeated bouts of IIH. In the present study, we evaluated the role of normal DMH activation in the counterregulatory response to a single bout of IIH.

Expression of simian immunodeficiency virus (SIV) nef in astrocytes during acute and terminal infection and requirement of nef for optimal replication of neurovirulent SIV in vitro.

As the most numerous cells in the brain, astrocytes play a critical role in maintaining central nervous system homeostasis, and therefore, infection of astrocytes by human immunodeficiency virus (HIV) or simian immunodeficiency virus (SIV) in vivo could have important consequences for the development of HIV encephalitis. In this study, we establish that astrocytes are infected in macaques during acute SIV infection (10 days postinoculation) and during terminal infection when there is evidence of SIV-induced encephalitis. Additionally, with primary adult rhesus macaque astrocytes in vitro, we demonstrate that the macrophage-tropic, neurovirulent viruses SIV/17E-Br and SIV/17E-Fr replicate efficiently in astrocytes, while the lymphocyte-tropic, nonneurovirulent virus SIV(mac)239 open-nef does not establish productive infection.

Inactivation of the PVN during hypoglycemia partially simulates hypoglycemia-associated autonomic failure.

The anatomic connections of the paraventricular nucleus of the hypothalamus (PVN) are such that it is ideally situated to modulate and/or control autonomic responses to a variety of stressors, including hypoglycemia. In our experimental model of hypoglycemia-associated autonomic failure (HAAF), a syndrome in which the counterregulatory response to hypoglycemia is partially compromised via unknown mechanisms, activation of the PVN is blunted (15). We hypothesized that this blunted PVN activation during HAAF may be sufficient to cause the impaired counterregulatory response.