Enhanced Recovery After Surgery Is Associated With Improved Outcomes and Reduced Racial and Ethnic Disparities After Isolated Coronary Artery Bypass Surgery: A Retrospective Analysis With Propensity-Score Matching.

Objectives: To evaluate whether enhanced recovery after surgery (ERAS) protocol implementation was associated with improved outcomes and decreased racial and ethnic outcome disparities after isolated coronary artery bypass graft (CABG) surgery.

Design: A retrospective analysis of an institutional CABG database with propensity-score matching.

Setting: At a single tertiary care teaching hospital.

Multiple Drug Treatments That Increase cAMP Signaling Restore Long-Term Memory and Aberrant Signaling in Fragile X Syndrome Models.

Fragile X is the most common monogenic disorder associated with intellectual disability (ID) and autism spectrum disorders (ASD). Additionally, many patients are afflicted with executive dysfunction, ADHD, seizure disorder and sleep disturbances. Fragile X is caused by loss of FMRP expression, which is encoded by the FMR1 gene.

Trends in the Management of Patients With Left Ventricular Assist Devices Presenting for Noncardiac Surgery: A 10-Year Institutional Experience.

In our institution, the vast majority of patients presenting for noncardiac surgery (NCS) while supported by a left ventricular assist device (LVAD) are now cared for by noncardiac-trained anesthesiologists as the result of a decade of educational intervention to effect this transition. This represents a significant departure from the published experiences of other institutions. With institutional review board approval, we queried the database of our anesthesia record keeping system (CompuRecord) to determine various aspects of the perioperative management of these patients from July 1, 2003, through June 30, 2013, during which time 271 NCS procedures were performed on adult patients supported by LVADs.

PDE-4 inhibition rescues aberrant synaptic plasticity in Drosophila and mouse models of fragile X syndrome.

Fragile X syndrome (FXS) is the leading cause of both intellectual disability and autism resulting from a single gene mutation. Previously, we characterized cognitive impairments and brain structural defects in a Drosophila model of FXS and demonstrated that these impairments were rescued by treatment with metabotropic glutamate receptor (mGluR) antagonists or lithium. A well-documented biochemical defect observed in fly and mouse FXS models and FXS patients is low cAMP levels.

Lysine auxotrophy combined with deletion of the SecA2 gene results in a safe and highly immunogenic candidate live attenuated vaccine for tuberculosis.

Tuberculosis (TB) caused by Mycobacterium tuberculosis remains a major global health problem, despite the widespread use of the M. bovis Bacille Calmette-Guerin (BCG) vaccine and the availability of drug therapies. In recent years, the high incidence of coinfection of M.

Caveolin-1 expression determines the route of neutrophil extravasation through skin microvasculature.

Interleukin-8 plays a key role in the acute inflammatory response by mediating recruitment of neutrophils through vessel walls into affected tissues. During this process, molecular signals guide circulating blood neutrophils to target specific vessels for extravasation and to migrate through such vessels via particular routes. Our results show that levels of endothelial caveolin-1, the protein responsible for the induction of the membrane domains known as caveolae, are critical to each of these processes.

Enhanced priming of adaptive immunity by a proapoptotic mutant of Mycobacterium tuberculosis.

The inhibition of apoptosis of infected host cells is a well-known but poorly understood function of pathogenic mycobacteria. We show that inactivation of the secA2 gene in Mycobacterium tuberculosis, which encodes a component of a virulence-associated protein secretion system, enhanced the apoptosis of infected macrophages by diminishing secretion of mycobacterial superoxide dismutase. Deletion of secA2 markedly increased priming of antigen-specific CD8(+) T cells in vivo, and vaccination of mice and guinea pigs with a secA2 mutant significantly increased resistance to M.