A Feed-Forward Mechanism Involving the NOX Complex and RyR-Mediated Ca2+ Release During Axonal Specification.

Unlabelled: Physiological levels of ROS support neurite outgrowth and axonal specification, but the mechanisms by which ROS are able to shape neurons remain unknown. Ca, a broad intracellular second messenger, promotes both Rac1 activation and neurite extension. Ca release from the endoplasmic reticulum, mediated by both the IP3R1 and ryanodine receptor (RyR) channels, requires physiological ROS levels that are mainly sustained by the NADPH oxidase (NOX) complex.

Contribution of NADPH oxidase to the establishment of hippocampal neuronal polarity in culture.

Reactive oxygen species (ROS) produced by the NADPH oxidase (NOX) complex play important physiological and pathological roles in neurotransmission and neurodegeneration, respectively. However, the contribution of ROS to the molecular mechanisms involved in neuronal polarity and axon elongation is not well understood. In this work, we found that loss of NOX complex function altered neuronal polarization and decreased axonal length by a mechanism that involves actin cytoskeleton dynamics.

Muscarinic antibodies and heart rate responses to dynamic exercise and to the Valsalva maneuver in chronic chagasic patients.

We have studied the cardiac chronotropic responses to the Valsalva maneuver and to dynamic exercise of twenty chronic chagasic patients with normal left ventricular function and no segmental wall abnormalities by two-dimensional echocardiogram. The absolute increase in heart rate of the patients (Δ = 21.5 ± 10 bpm, M±SD) during the maneuver was significantly diminished when compared to controls (Δ = 31.

Exogenous subclinical hyperthyroidism: effect on the cardiovascular system.

Objective: To evaluate the effects of exogenous subclinical hyperthyroidism on left ventricular structure and function.

Material And Method: Twenty-three patients of both sexes, aged 27 to 70 years, with a diagnosis of exogenous subclinical hyperthyroidism (serum thyroid-stimulating hormone [TSH] ≤ 0.4mU/ml and normal free thyroxine [FT4]) were evaluated.

Mechanisms of neurohormonal activation in chronic congestive heart failure: pathophysiology and therapeutic implications.

Patients with chronic congestive heart failure have a sequential and incessant activation of those neurohormonal systems, which control body fluids, cardiac output and systemic blood pressure. Neurohormonal activation is initially selective and regional. Generalized activation is a late event in the natural history of congestive heart failure.