Initial Assessment of a Regional Military-Civilian Partnership on Trauma Surgery Skills Sustainment.

Introduction: Trauma surgery skills sustainment and maintenance of combat readiness present a major problem for military general surgeons. The Military Health System (MHS) utilizes the knowledge, skills, and abilities (KSA) threshold score of 14,000 as a measure of annual deployment readiness. Only 9% of military surgeons meet this threshold.

Increasing medical student exposure to musculoskeletal medicine: the initial impact of the Orthopaedic Surgery and Sports Medicine Interest Group.

Purpose: To investigate the impact of the Orthopaedic Surgery and Sports Medicine Interest Group (OSSMIG) on medical student interest and confidence in core musculoskeletal (MSK) concepts through supplemental education and experiences at a single tertiary, academic institution.

Methods: Medical student OSSMIG members at various levels of training were anonymously surveyed at the beginning and end of the 2014-2015 academic year.

Results: Eighteen (N=18) medical student interest group members completed the survey.

CYR61 (CCN1) overexpression induces lung injury in mice.

Cysteine-rich protein-61 (CYR61), also known as connective tissue growth factor, CYR61, and nephroblastoma overexpressed gene 1 (CCN1), is a heparin-binding protein member of the CCN family of matricellular proteins. Gene expression profiles showed that Cyr61 is upregulated in human acute lung injury (ALI), but its functional role is unclear. We hypothesized that CYR61 contributes to ALI in mice.

Fas-deficient mice have impaired alveolar neutrophil recruitment and decreased expression of anti-KC autoantibody:KC complexes in a model of acute lung injury.

Background: Exposure to mechanical ventilation enhances lung injury in response to various stimuli, such as bacterial endotoxin (LPS). The Fas/FasL system is a receptor ligand system that has dual pro-apoptotic and pro-inflammatory functions and has been implicated in the pathogenesis of lung injury. In this study we test the hypothesis that a functioning Fas/FasL system is required for the development of lung injury in mechanically ventilated mice.

A role for prolyl 3-hydroxylase 2 in post-translational modification of fibril-forming collagens.

The fibrillar collagen types I, II, and V/XI have recently been shown to have partially 3-hydroxylated proline (3Hyp) residues at sites other than the established primary Pro-986 site in the collagen triple helical domain. These sites showed tissue specificity in degree of hydroxylation and a pattern of D-periodic spacing. This suggested a contributory role in fibril supramolecular assembly.

Evidence that angiogenesis lags behind neuron and astrocyte growth in experience-dependent plasticity.

Bill Greenough's work on the cell biology of information storage suggests that we cannot understand the mechanism of long-term memory without understanding the series of cellular transactions that drive coordinated structural changes in neurons, glia, and blood vessels. Here, we show that after 4 days of differential housing, neuropil of EC cortex has expanded significantly, but the vasculature has not, resulting in a dilution of the blood supply. Significant growth of neurons and astrocytes has been reported within this time period, suggesting expression of synaptic plasticity might involve temporally coordinated genomic responses by both neurons and glia.

Fas activation in alveolar epithelial cells induces KC (CXCL1) release by a MyD88-dependent mechanism.

Activation of the Fas/Fas ligand (FasL) system is associated with activation of apoptotic and proinflammatory pathways that lead to the development of acute lung injury. Previous studies in chimeric mice and macrophage-depleted mice suggested that the main effector cell in Fas-mediated lung injury is not a myeloid cell, but likely an epithelial cell. The goal of this study was to determine whether epithelial cells release proinflammatory cytokines after Fas activation, and to identify the relevant pathways.

Mechanical ventilation enhances lung inflammation and caspase activity in a model of mouse pneumovirus infection.

Severe infection with respiratory syncytial virus (RSV) in children can progress to respiratory distress and acute lung injury (ALI). Accumulating evidence suggests that mechanical ventilation (MV) is an important cofactor in the development of ALI by modulating the host immune responses to bacteria. This study investigates whether MV enhances the host response to pneumonia virus of mice (PVM), a mouse pneumovirus that has been used as a model for RSV infection in humans.