In pressurized RMA, Y-27632 and H-1152 depressed pressure-induced calcium responses and abolished see more myogenic contraction. These results stress the important differences in calcium signaling between conductance and resistance arteries. Copyright (C) 2012 S. Karger AG, Basel”
“Objective: To investigate the effect
of laughter and mental stress on arterial stiffness and central hemodynamics. Arterial stiffness and wave reflections are independent predictors of cardiovascular risk. Chronic psychological stress is an independent risk factor for cardiovascular events, whereas acute stress deteriorates vascular function. Methods: Eighteen healthy individuals were studied’ on three occasions, according to a randomized, single-blind, crossover, sham procedure-controlled design. The effects of viewing a 30-minute segment of two films inducing laughter or stress were assessed. Carotid-femoral pulse wave velocity was used as an index of arterial
stiffness; augmentation index was used as a measure of wave reflections. Results: Laughter decreased pulse wave velocity (by 0.30 m/sec, p = .01), and augmentation index (by 2.72%, p = .05). Conversely, stress increased pulse wave velocity (by 0.29 m/sec, p = .05) and augmentation index (by 5.1%, p = .005). Laughter decreased cortisol levels by 1.67 mu g/dl (p = .02), soluble P-selectin by 26 ng/ml (p = .02) and marginally von Willebrand factor (by 2.4%, p = .07) and increased total oxidative status (by 61 mu mol/L, p < .001). Stress decreased interleukin-6 (by 0.11 pg/ml, p = .04) and increased total oxidative status (by 44 mu mol/L, p = .007).
Akt inhibitor Soluble CD40 ligand and fibrinogen PI-1840 remained unchanged. Conclusions: Positive (laughter) and negative (stress) behavioral interventions have divergent acute effects on arterial stiffness and wave reflections. These findings have important clinical implications extending the spectrum of lifestyle modifications that can ameliorate arterial function.”
“Type 1 diabetes mellitus (T1DM) is a chronic disease resulting from destruction of insulin-producing pancreatic beta cells. Genetic and environmental factors contribute to T1DM onset. Use of high-throughput DNA sequencing has allowed geneticists to perform genome-wide association studies (GWAS) to identify novel gene loci associated with T1DM. Interestingly, >50% of these genes encode products that are expressed in beta cells. These studies, coupled with emerging molecular evidence that beta cells are impaired by gain-of-function or loss-of-function of these loci, suggest an active role for the beta cell in eliciting its own demise. Although immune dysregulation plays a vital role in T1DM pathogenesis, understanding the mechanisms contributing to beta cell failure may lead to new strategies to preserve or improve beta cell function in patients with T1DM.”
“We examined behavioral features of isochronous repetitive movements in two macaques.