beta aminopropionitrile/necrosis

We have developed a model of aortic smooth muscle necrosis in adult Sprague Dawley rats by feeding them two vascular toxins (allylamine HCl, or AA, and beta-aminopropionitrile, or betaAPN) in concert for 10 days. Either toxin given alone does not cause aortic lesions. In order to shed light on the

Allylamine (AA; 3-aminopropene) and beta-aminopropionitrile (betaAPN) combined treatment (AA + betaAPN) results in myocardial protection from AA-induced subendocardial necrosis and a rapid and extensive aortic medial smooth muscle injury in rats. To determine the mechanisms of AA + betaAPN-induced

Toxic cardiovascular effects of allylamine and beta-aminopropionitrile were studied in adult male Sprague-Dawley rats given allylamine alone (AA), 100 mg/kg/day, beta-aminopropionitrile alone (beta APN), 1 g/kg/day, or both chemicals (AA + beta APN) by gavage. Rats were given a total of 10 doses in

In the present study we describe changes in aorta at the protein level associated with allylamine (AA) and beta-aminopropionitrile (beta APN) induced vascular toxicity in a rat model. This model represents a remarkable synergistic, necrotizing toxic effect of these combined toxins, and our rationale

The endothelium of the thoracic aorta of Wistar rats intoxicated with Beta-Aminopropionitrile (BAPN) for 9 weeks was studied. The animals were sacrificed at intervals, from the first to the 9th week of the treatment and 1, 2 and 3 months after the end of the treatment. Changes in the endothelial

Administration of an antifibrotic agent as an adjunct to antihelmintic treatment with the objective of morbidity reduction was investigated in the murine schistosomiasis mansoni model. Antifibrotic, beta-aminopropionitrile treatment has a profound effect on the cellular matrix composition of the

Mice infected with Schistosoma mansoni treated with beta-aminopropionitrile (BAPN), an antifibrotic agent, and the antischistosomal drug praziquantel (PZQ) were resistant to challenge for up to 5 weeks post-treatment. The combined treatment resulted in profound changes to the liver granuloma cell

The cross-sectional structure of the vasculature is comparatively simple, comprising three layers--the intima, adjacent to the lumen, the media, and the adventitia. Notwithstanding this simplicity, the vessels are host to a variety of reactions to injury. Two cell types, endothelial cells of the

BACKGROUND Hypertrophic scarring and skin graft contracture are major causes of morbidity after burn injuries. A prominent feature is excessive fibroplasia with accumulation of increased fibrillar collagen relative to normal scar tissue. The application of split-thickness skin grafts or cultured

Allylamine (AA) and beta-aminopropionitrile (beta APN) are well known vascular toxins with a demonstrated synergistic toxic effect, i.e. given together they cause extensive smooth muscle cell necrosis of the aortic media. In this study, we investigated the possibility that the enzymes involved in

A simple procedure was developed for the estimation of bile acid taurine conjugates in fowl plasma. Laying hens fed a diet containing rapeseed meal (RSM) (400 g kg-1) for 12 weeks had higher bile acid levels (154 mumol litre-1) than hens fed a control soyabean diet (116 mumol litre-1) (P less than

The occurrence of liver haemorrhages was compared when diets containing 30 or 40 per cent rapeseed meal (RSM) or 30 per cent soybean meal (SBM), with and without experimental additives, were fed to in-lay hens of a commercial egg-producing strain for 12 weeks. The incidence of haemorrhages was

BACKGROUND The optimal medical management to delay the progression of aortic aneurysms has not been fully clarified, and the only standard treatment at present is antihypertensive therapy. Previous studies have shown beneficial effects of selective mineralocorticoid receptor (MR) antagonists on

BACKGROUND Although systemic hypertension is closely associated with aortic aneurysm (AA) formation, there are many patients with AA without hypertension. In these patients, an inflammation-mediated progression of aneurysmal disease is likely responsible for AA growth and eventual rupture.