Advances in the etiology of chronic pancreatitis.

In the past, chronic pancreatitis has been regarded as a fairly uniform and largely untreatable disorder that most commonly affects patients who both lack gainful employment or adequate insurance coverage and have a tendency to smoke and drink. Large clinical trials suggest that this perception is not only misguided and discriminatory but also not based on facts. We forgot that the perception of chronic liver disease was similar before World War II, and just like liver cirrhosis the fibrosis and cirrhosis of the pancreas--i.

Nonapoptotic effects of tumor necrosis factor-related apoptosis-inducing ligand on interleukin-6, leukemia inhibitory factor, interleukin-8, and monocyte chemoattractant protein 1 vary between undifferentiated and decidualized human endometrial stromal cells.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), which is known to exert death-inducing as well as nonapoptotic functions, has been shown to be expressed by the early trophoblast. Here we report that TRAIL has no apoptotic effects on human endometrial stromal cells, but differentially regulates cytokines and chemokines and might therefore play a role in the modulation of the cytokine milieu at the implantation site.

Major differences in gene expression in human coronary smooth muscle cells after nebivolol or metoprolol treatment.

Objective: Vascular smooth muscle cells play a pivotal role in all stages of atherogenesis. Targeting their inflammatory and proliferative qualities might therefore inhibit the progression of atherosclerosis. This study aimed to characterize and compare the effects of the beta-receptor antagonists nebivolol and metoprolol on gene expression in human coronary artery smooth muscle cells (hcaSMC).

Influence of nebivolol and metoprolol on inflammatory mediators in human coronary endothelial or smooth muscle cells. Effects on neointima formation after balloon denudation in carotid arteries of rats treated with nebivolol.

Objective And Background: Inflammation plays a critical role in all stages of atherogenesis. Proliferating vascular smooth muscle cells (SMC) and endothelial cells (EC) enhancing the inflammatory response, both contribute to the progression of atherosclerosis. Anti-proliferative, anti-inflammatory and anti-oxidative therapy seems to be a promising therapeutic strategy.

Effects of combined endothelin and angiotensin II antagonism on growth factor-induced proliferation of vascular smooth muscle cells isolated from uremic rats.

Background: The activation of both the renin-angiotensin-aldosterone and endothelin (ET) system in uremia contributes to the development of cardiovascular disease. The combination of ET receptor antagonists and inhibitors of the angiotensin-converting enzyme (ACE) or angiotensin II type 1 (AT,) receptor could therefore inhibit atherogenesis. We studied the effects of different medications on growth-factor-induced proliferation of vascular smooth muscle cells (VSMC) isolated from uremic rats.

Endothelin-1 increases serum-glucocorticoid-regulated kinase-1 expression in smooth muscle cells.

The mechanism of salt-sensitive hypertension is not fully understood. Several studies point to a possible role of endothelin (ET)-1 in this form of hypertension. Serum-regulated and glucocorticoid-regulated kinase-1 (SGK1) mediates trafficking of the renal epithelial sodium channel.

Endothelin-1 regulates protein kinase C isoforms differently in smooth muscle cells and in cardiomyocytes.

Endothelin-1 (ET-1) is known to increase the mitotic response of different growth factors but also to different vasoactive hormones already at threshold concentrations. The aim of this study was to investigate the influence of chronic elevated ET-1 concentrations on protein kinase C (PKC) isoforms in vitro and in vivo. Smooth muscle cells were incubated with ET-1 at a concentration of 10 mol/L.

Influence of endothelin receptor antagonism on smooth muscle cell proliferation after chronic renal failure.

Uremic patients suffer from an accelerated development of atherosclerosis. In uremia the angiotensin-aldosterone-endothelin system is activated. It is not known, however, whether endothelin receptor antagonism inhibits atherosclerosis in uremia.

Influence of growth factors on the proliferation of vascular smooth muscle cells isolated from subtotally nephrectomized rats after endothelin or angiotensin II antagonism.

Background: Cardiovascular disease is the most important cause of death in patients with end-stage renal disease. In uraemia, the renin-angiotensin-aldosterone and endothelin (ET) systems are activated. It is not known whether inhibition of these systems attenuates the proliferation of isolated smooth muscle cells of uraemic rats.