hyperplasia/nicitín

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Leathanach 1 ó 345 torthaí

Effect of oral acetylcysteine on tobacco smoke-induced secretory cell hyperplasia.

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Logáil Isteach / Cláraigh

The present investigation explores whether N-acetylcysteine (NAC) inhibits the secretory cell hyperplasia known to occur experimentally in specific pathogen-free (SPF) bronchitic rats. The animals were divided into 4 groups: no tobacco smoke (TS), no drug, no TS but NAC (1040 mg/kg body weight), TS

Morphometric and biochemical analysis of adrenal medullary hyperplasia induced by nicotine in rats.

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Logáil Isteach / Cláraigh

The administration of nicotine (1 and 4 mg/kg/day, subcutaneously for up to 6 weeks) to male Sprague-Dawley rats first induced a time-and dose-dependent increase in catecholamine (CA) synthesis. This was followed by an increase in endogenous CA levels and in total volume and number of chromaffin

Effect of nicotine on the intimal hyperplasia after endothelial removal of the rabbit carotid artery.

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Logáil Isteach / Cláraigh

1. The present experiments were designed to investigate the effect of long-term oral nicotine (10 mg/200 ml/kg/day for 7 weeks) on the intimal hyperplasia after endothelial removal of the rabbit carotid artery. 2. The plasma concentrations of nicotine were determined to be 11.7-12.5 ng/ml during the

Factors effecting the induction of rat forestomach hyperplasia induced by Swedish oral smokeless tobacco (snus).

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Logáil Isteach / Cláraigh

Long term exposure to oral smokeless tobacco may induce lesions in the oral cavity characterized by a hyperplastic epithelium. The possible role of nicotine and the physical properties of oral tobacco for developing these lesions, as well as of dysplasia and neoplasia is unclear. Low nitrosamine

Tobacco smoking and colorectal hyperplastic and adenomatous polyps.

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Logáil Isteach / Cláraigh

Colorectal adenomas and possibly some hyperplastic polyps are precursors of colorectal cancer. Tobacco use is associated in epidemiologic studies with these polyps, although links between smoking and colorectal cancer are less consistent. To characterize the role of tobacco in early colorectal

Novel molecular targets of smokeless tobacco (khaini) in cell culture from oral hyperplasia.

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Logáil Isteach / Cláraigh

Knowledge of molecular mechanism(s) implicated in smokeless tobacco (ST) associated oral carcinogenesis is meager. In an attempt to identify genes that are modulated by ST, we recently reported establishment of an oral epithelial cell culture, AMOL III from oral hyperplasia with hyperkeratosis of a

Orally administered nicotine induces urothelial hyperplasia in rats and mice.

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Logáil Isteach / Cláraigh

Tobacco smoking is a major risk factor for multiple human cancers including urinary bladder carcinoma. Tobacco smoke is a complex mixture containing chemicals that are known carcinogens in humans and/or animals. Aromatic amines a major class of DNA-reactive carcinogens in cigarette smoke, are not

Smokeless tobacco (khaini) extracts modulate gene expression in epithelial cell culture from an oral hyperplasia.

Ní féidir ach le húsáideoirí cláraithe ailt a aistriú

Logáil Isteach / Cláraigh

Smokeless tobacco (ST) usage is a growing public health problem worldwide. Exposure to smokeless tobacco is carcinogenic to humans. The molecular mechanism(s) underlying ST associated oral carcinogenesis remain largely unknown. The major challenge is to identify the key factor(s) involved in

Inhibition by blueberries (bilberries) and extract from milk thistle of rat forestomach hyperplasia induced by oral smokeless tobacco (Swedish snus).

Ní féidir ach le húsáideoirí cláraithe ailt a aistriú

Logáil Isteach / Cláraigh

The aim of this study was to identify palatable additives which have a significant protective action against soft tissue changes in the oral cavity caused by Swedish smokeless tobacco ("snus"), and that satisfy existing legal requirements. Although the cancer risk from snus is extremely low, long

Nodular hyperplasia and increase of noradrenaline content in the adrenal medulla of nicotine-treated rats.

Ní féidir ach le húsáideoirí cláraithe ailt a aistriú

Logáil Isteach / Cláraigh

Palatal leukoplakia in a female cigaret smoker. Contribution to study of tobacco-induced epithelial hyperplasia in human beings.

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Logáil Isteach / Cláraigh

"Sebaceous glands" and "hyperplasia" tests as screening methods for tobacco tar carcinogenesis.

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Logáil Isteach / Cláraigh

Secretory cell hyperplasia and modification of intracellular glycoprotein in rat airways induced by short periods of exposure to tobacco smoke, and the effect of the antiinflammatory agent phenylmethyloxadiazole.

Ní féidir ach le húsáideoirí cláraithe ailt a aistriú

Logáil Isteach / Cláraigh

An in vitro approach to assess the toxicity of inhaled tobacco smoke components: nicotine, cadmium, formaldehyde and urethane.

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Logáil Isteach / Cláraigh

One of the first lines of defence to inhaled toxins is the barrier formed by the tracheobronchial epithelium, making this the ideal region for studying the toxicity of inhaled substances. This study utilises a highly differentiated, three-dimensional, in vitro model of human upper respiratory tract

Nicotine-induced smooth muscle cell proliferation is mediated through bFGF and TGF-beta 1.

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Logáil Isteach / Cláraigh

BACKGROUND Cigarette smoking influences and enhances the development of atherosclerosis. We investigated if nicotine, an important constituent of cigarette smoking, has a stimulatory effect on bovine smooth muscle cell proliferation in vitro through the mediation of bFGF and TGF-beta

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