UK Foot and Ankle Thromboembolism (UK-FATE).

Aims: Venous thromboembolism (VTE) is a potential complication of foot and ankle surgery. There is a lack of agreement on contributing risk factors and chemical prophylaxis requirements. The primary outcome of this study was to analyze the 90-day incidence of symptomatic VTE and VTE-related mortality in patients undergoing foot and ankle surgery and Achilles tendon (TA) rupture.

Exposure to Stress Alters Cardiac Gene Expression and Exacerbates Myocardial Ischemic Injury in the Female Murine Heart.

Mental stress is a risk factor for myocardial infarction in women. The central hypothesis of this study is that restraint stress induces sex-specific changes in gene expression in the heart, which leads to an intensified response to ischemia/reperfusion injury due to the development of a pro-oxidative environment in female hearts. We challenged male and female C57BL/6 mice in a restraint stress model to mimic the effects of mental stress.

TNBC Therapeutics Based on Combination of Fusarochromanone with EGFR Inhibitors.

Fusarochromanone is an experimental drug with unique and potent anti-cancer activity. Current cancer therapies often incorporate a combination of drugs to increase efficacy and decrease the development of drug resistance. In this study, we used drug combinations and cellular phenotypic screens to address important questions about FC101's mode of action and its potential therapeutic synergies in triple negative breast cancer (TNBC).

Glucocorticoid Inhibition of Estrogen Regulation of the Serotonin Receptor 2B in Cardiomyocytes Exacerbates Cell Death in Hypoxia/Reoxygenation Injury.

Background Stress has emerged as an important risk factor for heart disease in women. Stress levels have been shown to correlate with delayed recovery and increased mortality after a myocardial infarction. Therefore, we sought to investigate if the observed sex-specific effects of stress in myocardial infarction may be partly attributed to genomic interactions between the female sex hormones, estrogen (E2), and the primary stress hormones glucocorticoids.

Deletion of the Cardiomyocyte Glucocorticoid Receptor Leads to Sexually Dimorphic Changes in Cardiac Gene Expression and Progression to Heart Failure.

Background The contribution of glucocorticoids to sexual dimorphism in the heart is essentially unknown. Therefore, we sought to determine the sexually dimorphic actions of glucocorticoid signaling in cardiac function and gene expression. To accomplish this goal, we conducted studies on mice lacking glucocorticoid receptors (GR) in cardiomyocytes (cardioGRKO mouse model).

Predictors of satisfaction and quality of life following post-mastectomy breast reconstruction.

Objective: Breast reconstruction is associated with multiple psychological benefits. However, few studies have identified clinical and psychological factors associated with improved satisfaction and quality of life. This study examined factors, which predict satisfaction with breast appearance, outcome satisfaction and quality of life following post-mastectomy breast reconstruction.

Influence of fullerene (C60) on soil bacterial communities: aqueous aggregate size and solvent co-introduction effects.

Fullerene C60 nanoparticles are being used in broad range of applications. It is important to assess their potential impacts in the environment. We evaluated the effects of C60 introduced as aqueous suspensions of nC60 aggregates of different particle size or via organic solvents on soils with different organic matter contents in this study.

Retrofitting LID Practices into Existing Neighborhoods: Is It Worth It?

Low-impact development (LID) practices are gaining popularity as an approach to manage stormwater close to the source. LID practices reduce infrastructure requirements and help maintain hydrologic processes similar to predevelopment conditions. Studies have shown LID practices to be effective in reducing runoff and improving water quality.

Myofibrillar myopathy caused by a mutation in the motor domain of mouse MyHC IIb.

Ariel is a mouse mutant that suffers from skeletal muscle myofibrillar degeneration due to the rapid accumulation of large intracellular protein aggregates. This fulminant disease is caused by an ENU-induced recessive mutation resulting in an L342Q change within the motor domain of the skeletal muscle myosin protein MYH4 (MyHC IIb). Although normal at birth, homozygous mice develop hindlimb paralysis from Day 13, consistent with the timing of the switch from developmental to adult myosin isoforms in mice.