Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intraruminal doses of L-tryptophan cause acute pulmonary edema and emphysema in cattle. The D and L isomers of tryptophan and 22 related indolic compounds were incubated with ruminal microorganisms in vitro. Incubation of L-[U-benzene ring-(14)C]tryptophan with ruminal microorganisms for 24 h resulted in 39% of the added radioactivity being incorporated into skatole, 7% into indole, and 4% into indoleacetate (IAA). D-Tryptophan was not degraded to any of these metabolites. The major pathway of skatole formation from L-tryptophan appeared to be by the decarboxylation of IAA. Incubation of [2-(14)C]IAA with ruminal microorganisms for 24 h resulted in 38% incorporation into skatole. L-[5-Hydroxy]tryptophan was degraded to 5-hydroxyskatole and 5-hydroxyindole, whereas 5-hydroxyindoleacetate was degraded to only 5-hydroxyskatole. Incubation of indolepyruvate, indolelactate, and indolealdehyde with ruminal microorganisms resulted in the formation of both skatole and indole. Under similar conditions, indoleacetaldehyde was converted to IAA and tryptophol. The addition of increasing concentrations of glucose (0 to 110 mM) reduced the formation of both skatole and indole from L-tryptophan and resulted in the accumulation of IAA. Antibiotics reduced the degradation of L-tryptophan to skatole and indole, with kanamycin and neomycin particularly effective in reducing the decarboxylation of IAA to skatole.
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PMID:Dissimilation of tryptophan and related indolic compounds by ruminal microorganisms in vitro. 454 42

Glycosaminoglycans are constituents of proteoglycans, which are integral components of lung connective tissue. Glycosaminoglycans not only provide structural support to organs, but also influence extracellular matrix assembly, cell adhesion, and cell proliferation. Changes in the metabolism of glycosaminoglycans have been noted in several pulmonary diseases, for example, pulmonary fibrosis and emphysema. We studied quantitative and qualitative changes of glycosaminoglycans in the lungs of rats exposed to a range of ozone levels (0, 0.12, 0.5, 1.0 parts per million) for 20 months. Glycosaminoglycans were isolated from dry-defatted lung tissues through successive digestions by pronase, papain, and 2 M sodium hydroxide. The glycosaminoglycans then were fractionated into individual components using high-performance liquid chromatography. The concentration of total glycosaminoglycans in the tissues varied from 1.5 to 4.2 micrograms of uronate/mg of dry-defatted tissue. Although wide variations in total glycosaminoglycan concentrations exist among individual animals within each exposure group, regression analyses of data indicate a monotonic and statistically significant decrease of total glycosaminoglycans after ozone exposure (p = 0.02). Among individual glycosaminoglycans, hyaluronan, chondroitin 4-sulfate, and chondroitin 6-sulfate levels decreased significantly (p < 0.001, p < 0.05, and p < 0.01, respectively) in animals exposed to ozone when compared with control animals. Heparan sulfate concentration exhibited a significant (p < 0.05) trend toward increase with increasing doses of ozone, but the difference in heparan sulfate concentration between ozone-exposed animals and control animals was not significant. Gel filtration studies of glycosaminoglycans in pooled samples indicated that the molecular size of hyaluronan in animals exposed to ozone was lower than it was in control animals. We noted differences in heparan sulfate's chemical properties and affinity to antithrombin III in ozone-exposed animals and control animals. Although these studies do not provide the mechanism responsible for the observed changes in the lung glycosaminoglycans in ozone-exposed animals, the observations indicate that inhalation of ozone for 20 months affects normal cellular metabolism of proteoglycans, which may contribute to the functional impairment of the lung.
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PMID:Consequences of prolonged inhalation of ozone on F344/N rats: collaborative studies. Part III: Effects on complex carbohydrates of lung connective tissue. 781 21

Thirty-five subjects were divided into 4 groups; the first group was composed of 8 healthy nonsmoking subjects; the second group included 8 healthy smokers; the third group included 12 nonsmoking patients suffering from chronic obstructive pulmonary emphysema; the fourth group was composed of 7 smokers with chronic obstructive pulmonary emphysema. N,N,N'-trimethyl-N'2-Hydroxy-3-Methyl-5-iodobenzyl-1,3-propanediamine iodine-131(HIPDM) was rapidly injected into the antecubital vein. The influence of 131I-HIPDM by lung clearance was analysed thought imaging of lung and ratio of prolongation of 131I-HIPDM in the lung. Prolongation of 131I-HIPDM in the lung was shown in the smokers with chronic obstructive pulmonary emphysema in 60 minutes, and the healthy smokers, smokers with chronic obstructive pulmonary emphysema in the 24 hours after the injection of 131I-HIPDM. Smoking is an important factor of disturbance of lung clearance.
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PMID:Prolonged lung retention of 131I-HIPDM in smokers. 787 26

The relationship between elastin degradation and emphysema is well known. Recent evidence suggests that a complex process of pulmonary remodeling occurs within the emphysematous lung. The aim of this study was to assess the extent of extracellular matrix remodeling in emphysema by ultrastructural examination of elastin and collagen templates in an animal model of emphysema and in human emphysematous lungs. Emphysema was induced in rats by the intratracheal administration of porcine pancreatic elastase. Human lung samples were obtained at surgical resection for lung carcinoma. Emphysema was confirmed morphometrically and quantitated using the mean linear intercept. Matching sections were treated with sodium hydroxide and formic acid to expose collagen and elastin templates, respectively. Scanning electron microscopy with stereo-pair imaging allowed three-dimensional visualization of the exposed templates. In emphysematous lungs from both sources, sheets of elastin were disrupted and perforated with multiple fenestrations. In elastase-induced emphysema, this disintegration was accompanied by a marked increase in thickness of collagen fibrils, which contrasted with the fine fibrillar network of control lungs. Similarly, a pattern of thickened fibrils and disorganized deposition of collagen was observed in human lungs. In conclusion, these findings support the novel concept of increased collagen deposition and aberrant collagen remodeling in the pathogenesis of emphysema.
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PMID:Elastin and collagen remodeling in emphysema. A scanning electron microscopy study. 886 87