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pulmonary fibrosis/nikotin

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Tobacco smoke-induced lung fibrosis and emphysema.

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Despite public health campaigns discouraging smoking, 1,000 American children every day become smokers, ensuring that tobacco-related health complications will be with us for decades to come. Smoking is the greatest risk factor for both chronic obstructive lung disease and interstitial lung disease.

Maternal nicotine exposure exacerbates neonatal hyperoxia-induced lung fibrosis in rats.

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BACKGROUND Maternal nicotine exposure increases lung collagen in fetal and newborn animals. Connective tissue growth factor (CTGF) plays a role in hyperoxia-induced pulmonary fibrosis. OBJECTIVE To determine whether pre- and postnatal nicotine exposure can augment CTGF expression and postnatal

CB2R agonist prevents nicotine induced lung fibrosis.

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Nicotine stimulates fibroblast proliferation while increasing inflammation and fibrosis of tissues. The cannabinoid receptor 1 (CB1R) is mainly located in the CNS, while cannabinoid receptor 2 (CB2R) is located in the immune cells within the body. CB2R regulates inflammatory processes
OBJECTIVE To determine the long-term effect of maternal nicotine intake on the lung development of the offspring in adult life, we analyzed the alveolar structure, protein expression in the adult rat offspring lungs. METHODS We determined animal body weight (BW), lung weight (LW), lung/body weight
Cigarette smoking is a devastating risk factor for cardiovascular diseases and nicotine is believed the main toxin component responsible for the toxic myocardial effects of smoking. Nonetheless, neither the precise mechanism of nicotine-induced cardiac dysfunction nor effective treatment is

Diffuse pulmonary fibrosis and blackfat-tobacco smoking in Guyana.

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[Pulmonary fibrosis caused by tobacco].

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[Combination of pulmonary fibrosis and emphysema: Is tobacco once again the protagonist?].

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[Diffuse interstitial pulmonary fibrosis in tobacco-industry workers].

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Serum angiotensin-converting enzyme and lysosomal enzymes in tobacco workers.

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The activities of angiotensin-converting enzyme (ACE) in people with extrinsic allergic alveolitis (EAA) have been both increased and decreased. These observations suggest that pulmonary macrophages or endothelial cells participate in the disease process. Exposure to molds in the tobacco industry

Distribution of emphysema and fibrosis in idiopathic pulmonary fibrosis with coexisting emphysema.

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Combined pulmonary fibrosis and emphysema (CPFE) is a syndrome that results from tobacco smoking. Emphysema and fibrosis in CPFE patients have been considered to exist separately, with emphysema in the upper lobes and interstitial pneumonia in the lower lobes. The aim of this study was

Lung bullae and pulmonary fibrosis associated with marijuana smoking.

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A 26-year-old man with a history of heavy marijuana and minimal tobacco use was found to have extensive bilateral lung bullae and interstitial fibrosis, heavily infiltrated by pigmented macrophages. These features can be associated with marijuana smoking. The differential diagnoses in this patient
The potential of chronic nicotine exposure for atrial fibrillation (AF) and atrial flutter (AFL) in hearts with and without chronic myocardial infarction (MI) remains poorly explored. MI was created in dogs by permanent occlusion of the left anterior descending coronary artery, and dogs were
Tobacco smoking causes a variety of smoking-related diseases, death, and economic damage. Despite targeted anti-smoking campaigns, tobacco-related deaths are expected to increase in Japan. We investigated the current state of non-cancerous lung diseases such as idiopathic interstitial
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