Integrated stepped alcohol treatment for patients with HIV and at-risk alcohol use: a randomized trial.

Background: At-risk levels of alcohol use threaten the health of patients with HIV (PWH), yet evidence-based strategies to decrease alcohol use and improve HIV-related outcomes in this population are lacking. We examined the effectiveness of integrated stepped alcohol treatment (ISAT) on alcohol use and HIV outcomes among PWH and at-risk alcohol use.

Methods: In this multi-site, randomized trial conducted between January 28, 2013 through July 14, 2017, we enrolled PWH and at-risk alcohol use [defined as alcohol consumption of ≥ 14 drinks per week or ≥ 4 drinks per occasion in men ≤ 65 years old or ≥ 7 drinks per week or ≥ 3 drinks per occasion in women or men > 65 years old].

Mechanoregulation of monocyte chemoattractant protein-1 expression in rat vascular smooth muscle cells.

The authors have previously shown that arterial wall strain mediates the development of vessel wall inflammation in experimental hypertension. The current studies explore the mechanoregulation of monocyte chemoattractant protein-1 (MCP-1), a potent pro-inflammatory chemokine, by mitogen-activated protein kinases (MAPK) and oxidative stress. Rat aortic smooth muscle (RASM) cells were subjected to cyclic strain on a uniform biaxial strain device.

Angiotensin II evokes calcium-mediated signaling events in isolated dog pancreatic epithelial cells.

Introduction: Calcium-activated chloride conductance has been identified in normal pancreatic duct cells. Recent in vitro evidence suggests that angiotensin II (AngII) stimulates pancreatic secretion in both cystic fibrosis (CFPAC) and transformed pancreatic cells.

Aims: To investigate calcium-mediated stimulatory effects of AngII in both nontransformed dog pancreatic duct epithelial (DPDE) and CFPAC cells.

Mechanical deformation of the arterial wall in hypertension: a mechanism for vascular pathology.

Hypertension is an independent risk factor for atherosclerotic disease. It has been proposed that the atherogenic potential of hypertension is due to the development of a proinflammatory state within the arterial wall that is, at least in part, a result of the generation of reactive oxygen species. This article proposes that mechanical deformation of the arterial wall is a critical stimulus in this scheme.