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)

3-Methylindole has been shown in previous work to cause pulmonary edema and emphysema in cattle and goats. In this paper, evidence is presented to show that 3-methylindole induces structural perturbations in bovine erythrocyte membranes. The structural perturbations which were induced as a function of 3-methylindole concentration in the membranes were measured by EPR using the attachment of maleimide spin label to the sulfhydryl groups of membrane proteins and by intercalation of methyl-5- doxylstearate, methyl-12-doxylstearate, and methyl-16-doxylstearate into the lipid region. The EPR spectra of the malemide spin-labeled membrane proteins became more immobilized as the concentration of 3-methyl-indole increased. The order parameter describing the EPR spectra of methyl-5-doxylstearate decreased from 0.69 to 0.55 as the concentration of 3-methylindole increased. The acyl chains in the region of the carbon 5 position were converted to a less ordered structure. The EPR-spectra of methyl-12-doxylstearate was a superposition representing at least three tumbling rates. As the concentration of 3-methylindole increased, the major fraction of the methyl-12-doxylstearate probes experienced an increase in tumbling rate and a smaller fraction is observed a strongly immobilized state. The EPR spectra of methyl-16-doxylstearate were not perceptibly changed in the presence of 3-methylindole. The concentration dependence suggests that 3-methylindole preferentially intercalates into the ordered region of the alkyl chains sampled by the methyl-5-doxylstearate. These results confirm that 3-methylindole induced structural changes at the molecular level.
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PMID:An EPR study of structural perturbations induced by methylindole in the protein and lipid regions of erythrocyte membranes. 16 12

A patient with homozygous ZZ alpha1-antitrypsin deficiency and severe pulmonary emphysema was discovered to have a mixed hepatocellular and cholangiolar hepatic carcinoma arising in a noncirrhotic liver. Because of the increasing frequency of hepatomas in patients with alpha1-antitrypsin deficiency, it is suggested that a causal relationship may exist.
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PMID:Alpha1-antitrypsin deficiency and hepatic carcinoma. 16 82

Thioglycolate-stimulated mouse peritoneal macrophages secrete a Proteinase which degrades insoluble elastin. There is little elastase activity in cell lysates but the bulk of the enzyme accumulates extracellularly during culture in serum-free medium. The secretion of elastase is sustained for over 12 days in culture and continued secretion of elastase requires protein synthesis. Unstimulated macrophages secrete very little elastase activity but can be triggered to secrete higher levels of this enzyme by phagocytosis and intracellular storage of latex particles. The macrophages elastase is a distinctive proteinase differing from the elastases of pancreas and granulocytes and is distinct from the other secreted proteinases of macrophages, namely, collagenase and plasminogen activator. The macrophages elastase is a serine proteinase and is inhibited by di-isopropyl phosphoro-fluoridate, ovoinhibitor, EDTA, dithiothretiol, and serum. Its activity is little affected by soybean trypsin inhibitor, turkey ovomucoid and chloromethyl ketones derived from tosyl lysine, tosyl phenylalanine, and acetyltetra alanine. Hydrolysis by macrophage elastase of chromogenic ester substrates for pancreatic elastase could not be detected. Elastase secretion by stimulated macrophages exceeds that by primary and established fibroblast cell strains. It is likely that elastase secretion by macrophages plays a major role in the pathogenesis of chronic destructive pulmonary diseases such as emphysema.
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PMID:Elastase secretion by stimulated macrophages. Characterization and regulation. 16 96

Spontaneous pneumomediastinum is a relatively rare disease, the clinical signs of which may be misleading, and the physiopathology is still unknown. The authors report 7 cases collected over a period of 3 years and note the etiology, the clinical findings and the X-ray findings. The disease often affectsyoung sybjects, without any sex predominance. The initial symptom is thoracic pain and is often accompanied by dispnea. Subcutaneous emphysema only appears secondarily and may be mild. The association with pneumothorax is not rare. Among the etiological circumstances, pneumomediastinum often occurs after an effort or a respiratory infection with dyspnea. The diagnosis depends on the discovery of subcutaneous emphysema and on radiological signs in A.P. and lateral chest views. Treatment should be as conservative as possible in the usual benign forms. It should be limited to bed rest, analgesics and sedatives. In severe cases, supra-sternal drainage permits decompression of the mediastinum. The physiopathological mechanisms are discussed, but the usually accepted theory is rupture of an alveolus into the pulmonary interstitial tissue. The pressure gradient necessary for this rupture may be due to variations in alveolar or vascular pressure.
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PMID:[Spontaneous pneumomediastinum]. 17 Jun 84

A 70-year-old man with homozygous alpha1-antitrypsin deficiency (AATD) (Pi-ZZ phenotype) at tutopsy was found to have a hepatocellular carcinoma and hepatic fibrosis, pulmonary emphysema, and cor pulmonale. Characteristic cytoplasmic inclusion bodies, with identical histochemical and ultrastructural features, were detected in both normal and malignant liver cells. It is suggested that AATD may precede malignancy, since this is the eleventh case report of this association.
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PMID:Alpha1-antitrypsin deficiency--an association with hepatic malignancy. 17 81

Theoccurrence of PAS-positive, diastase-resistant, inclusion bodies in hepatocytes has been used as a marker of heterozygous (Pi MZ) alpha1-antitrypsin deficiency in order to study the frequency of lung, liver and malignant disease in a consecutive autopsy material from a well defined population. Typical PAS-positive inclusion bodies were found in the liver in 26 (3.7%) of the 700 cases studied. In these 26 subjects both liver (cirrhosis or fibrosis) and lung disease (emphysema) were significantly more prevalent (p less than 0.001) than among PAS-negative controls. The prevalence of malignant disease did not differ between the groups. The results are consistent with the concept that heterozygous (Pi MZ) alpha1-antitrypsin deficiency predisposes to both liver and lung disease but does not influence the survival rate.
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PMID:Liver, lung and malignant disease in heterozygous (Pi MZ) alpha1-antitrypsin deficiency. 17 17

The treatment procedure with 121 in-patients suffering from respiratory obstruction is described following a short review of the etiology and pathogenesis of bronchial asthma, and the consequences for treatment resulting therefrom. While patients with chronic bronchitis caused by an emphysema of the lungs were treated primarily with antibiotics, synthetic corticotrophin (Synacthen, Synacthen Depot) and/or cortisone were prescribed in the treatment of 3/4 of the cases involving asthmatics and patients with chronic asthmatoid bronchitis caused by an emphysema. In severe cases ACTH was combined with cortisone. As a result of corticotrophin's direct effect on the bronchial muscles and the mast cells, along with its stimulation of the adrenal cortex, treatment with ACTH has the advantage over the classic cortisone treatment of retaining the functional ability of the adrenal cortex and reducing the amount of cortisone needed. No ACTH-caused side effects were reported. Included are tables containing guidelines for therapy suitable in private practice.
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PMID:[Bronchial asthma. Pathogenetic assumptions - therapeutic guidelines - the significance of synthetic corticotrophin (ACTH) in its treatment (author's transl)]. 17 68

Twenty-six cases of so-called "minute pulmonary chemodectoma" are presented. The patient population showed a marked female preponderance, and there appeared to be an association of the lesion with pulmonary injury from a variety of causes including cardiac failure, chronic bronchitis and emphysema, and thromboemboli. Half the cases had multiple tumors. Microscopically, the tumors consisted of nests of cells in the interstitial tissue near small veins. Argentaffin and argyrophil stains failed to demonstrate cytoplasmic granules in any case. By electron microscopy, the nests were composed of large cells with broadly interdigitating processes connected by many well-formed desmosomes. The cytoplasm was filled with numerous 60-A filaments. The Golgi apparatus was prominent, while other organelles were sparse. No secretory granules were identified. It is concluded that the fine structure and lack of silver-positive granules are inconsistent with the morphology of previously reported paragangliomas, but that there is a resemblance at the light and electron microscopic level to meningeal arachnoed cells and the cells of meningiomas.
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PMID:So-called "minute pulmonary chemodectoma": a tumor not related to paragangliomas. 17 76

Both clinical and experimental evidence implicate proteolytic enzymes active against elastin in the pathogenesis of emphysema. Paradoxically, however, the elastin content of emphysematous human lungs at autopsy has been normal. When emphysema was produced in hamsters by a single intratracheal injection of 25 units of porcine pancreatic elastase, the elastin content of the lungs was reduced from 1.40 +/- 0.22 mg. in controls to 0.43 +/- 0.10 mg. 24 hours after injection, and histologic sections showed that many elastic fibers had disappeared. The elastin content of the lungs gradually increased, approaching normal values by 2 months after injection. The incorporation of 14C-proline into elastin was markedly elevated during the first 2 weeks after injection, decreasing nearly to normal by 2 months. The synthesis of collagen was also increased, indicated by an increase in the collagen content of the lung, an increase in the prolyl hydroxylase activity, and an increase in incorporation of labeled proline into collagen. During the period of active resynthesis of elastin, small clumps of microfibrils and elastic fibrils were visible by electron microscopy within grooves on the surface of septal connective tissue cells in the lungs. Many elastic fibers seen in histologic sections up to 4 months after injection were of abnormal configuration and disorganized.
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PMID:The induction of emphysema with elastase. II. Changes in connective tissue. 17 9

The most important primary cause of generalized pulmonary emphysema is in all probability the loss of mechanical stability of the connective tissue framework in the lung parenchyma. The complexity of the interrelations and interdependencies between the fibres and the ground substance, leads to the mapping out of a more detailed outline of the vulnerable parts in a similar framework. It is concluded that the junctions especially constitute weak spots. Glycosaminoglycans, glycoproteins and proteoglycans particularly hold a key position as cementing substances. The importance of female sex hormones in the metabolism of the ground substance is indicated. A survey is given of the possible threats to a similar system. An attempt is made to disentangle the multitude of possible pathogenetic pathways which lead to emphysematous disintegration. Perspectives of future emphysema research are discussed on the basis of these considerations. Preventive, protective, and reconstructive measures are proposed.
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PMID:The pathogenesis of pulmonary emphysema (II). 18 May 82


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