Does nox1 overexpression potentiate angiotensin II-induced hypertension and vascular smooth muscle hypertrophy in transgenic mice?
These data indicate that smooth muscle-specific Nox1 overexpression augments the oxidative, pressor, and hypertrophic responses to Ang II, supporting the concept that medial Nox1 participates in the development of cardiovascular pathologies.
Primary healthcare centres appear to lack the training and equipment to manage common paediatric emergencies. We recommend standardization of equipment and algorithms, training and assessment of key personnel, and critical incident reporting within primary healthcare centres.