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Correlation of bronchial epidermoid metaplasia with level of tobacco consumption in heavy smokers.

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One hundred forty-four heavy-smoker (125 males, 19 females) volunteers with at least 15 packet-year of smoking experience (number of daily packets of cigarettes X number of years of smoking) underwent bronchoscopy with systematic biopsies in ten sites of the bronchial tree. No morbidity was related

Environmental tobacco smoke and progesterone alter lung inflammation and mucous metaplasia in a mouse model of allergic airway disease.

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The prevalence and severity of asthma is sexually dimorphic. Adult women have a higher incidence of asthma than men. This suggests that this disease may have a hormonal component. Progesterone has been shown to elicit an immune response similar to that seen in allergic asthma and previous studies

MAPK/AP-1 signal pathway in tobacco smoke-induced cell proliferation and squamous metaplasia in the lungs of rats.

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Overwhelming evidence has demonstrated tobacco smoke (TS) is causally associated with various types of cancers, especially lung cancer. Sustained epithelial cell hyperplasia and squamous metaplasia are considered as preneoplastic lesions during the formation of lung cancer. The cellular and

Characterisation of the proximal airway squamous metaplasia induced by chronic tobacco smoke exposure in spontaneously hypertensive rats.

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BACKGROUND Continuous exposure to tobacco smoke (TS) is a key cause of chronic obstructive pulmonary disease (COPD), a complex multifactorial disease that is difficult to model in rodents. The spontaneously hypertensive (SH) rat exhibits several COPD-associated co-morbidities such as hypertension

Interaction of tobacco smoke exposure and ovalbumin-sensitization promotes goblet cell and submucosal gland metaplasia in guinea pigs.

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Exposure to irritants such as tobacco smoke (TS) causes acute airway inflammation. Chronic exposure may cause airway remodeling contributing to enhanced airway resistance. We hypothesize that combining airway sensitization and inhalation of irritants enhances the number of mucous producing cells

Tobacco smoking and intestinal metaplasia: Systematic review and meta-analysis.

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BACKGROUND The evaluation of specific risk factors for early endpoints in the gastric carcinogenesis pathway may further contribute to the understanding of gastric cancer aetiology. OBJECTIVE To quantify the relation between smoking and intestinal metaplasia through systematic review and

A small proline-rich protein, SPRR1, is upregulated early during tobacco smoke-induced squamous metaplasia in rat nasal epithelia.

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Small proline-rich proteins, believed to be precursor proteins for the crosslinked envelope formation in cells undergoing squamous differentiation, are encoded by the SPRR genes. To further investigate the role of these proteins, the time course of increased synthesis of SPRR1 mRNA in nasal

Squamous metaplasia of the respiratory tract epithelium; an autopsy study of 214 cases. II. Relation to tobacco smoking, occupation and residence.

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Systematic review of the prevalence of gastric intestinal metaplasia and its area-level association with smoking.

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OBJECTIVE We aimed to show an area-level association between the frequency of intestinal metaplasia (IM) in Helicobacter pylori-infected patients and tobacco consumption. METHODS We systematically reviewed the literature to retrieve data on the prevalence of IM in different countries and performed

Certain aspects of the responses of laboratory rats to exposure to (a) nitrogen dioxide and (b) tobacco smoke.

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Exposure of rats to 150 ppm NO2 for 2 hours causes death from pulmonary oedema. Continuous exposure to 25 ppm for 150 days causes gross enlargement with loss of elastic recoil and proliferative and metaplastic epithelial changes in the vicinity of the terminal bronchioles. Continuous exposure to 2

Carcinogenic Helicobacter pylori in gastric pre-cancer and cancer lesions: association with tobacco-chewing.

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OBJECTIVE To investigate the low gastric cancer incidence rate relative to the highly prevalent Helicobacter pylori (H. pylori) infection; data relevant to H. pylori infection during gastric carcinogenesis in Indian patients is currently lacking. METHODS The present study examines the prevalence of

[Influence of tobacco smoking on the development of experimental pulmonary tuberculosis].

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The present investigation was designed to the study, in rabbits, of morphologic and enzymatic pulmonary alterations produced by tobacco smoke and the course of tuberculosis under these conditions. The histologic examination revealed muciparous hyperplasia and pavementing metaplasia of the bronchic

Tobacco smoke induced lung granulomas and tumors: association with pulmonary Langerhans cells.

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The density of zinc-iodide-osmium (ZIO) positive pulmonary Langerhans dendritic cells (LC) was increased about 20-fold in mice after passive exposure to tobacco smoke. This was associated with pulmonary changes consistent with the cigarette smoking-related clinical syndrome in humans, pulmonary

Is there a relationship between the presence of lung mucosa preinvasive lesions and lung cancer incidence? Influence of tobacco consumption.

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Although studied for years, the nature of the relationships between tobacco consumption, bronchial preinvasive lesions and lung cancer are still not completely elucidated. Objectives were to determine the relationship between tobacco consumption and lung mucosa preinvasive and invasive lesions and

Phenotypic modification of human airway epithelial cells in air-liquid interface culture induced by exposure to the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK).

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The nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a potent tobacco-specific carcinogen. We used an air-liquid interface epithelial cell culture system to model changes associated with NNK exposure relative to pathologies documented in human tobacco-related illnesses. Although

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