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)

Human neutrophilic polymorphonuclear leukocyte (PMN) elastase was purified by affinity chromatography to greater than 95% homogeneity as judged by disc-gel electrophoresis. Dog lung elastin was prepared from alveolar-enriched tissue by prior extraction of soluble and collagenous lung proteins with 0.1 M NaOH at 98 degrees C. Digestion of the remaining insoluble residue by the purified PMN enzyme was monitored by Lowry assay of acid-soluble peptides released. The PMN enzyme possessed 60% of the digestive activity of crystallized porcine pancreatic elastase (weight:weight comparison) when tested in vitro against this substrate in phosphate-NaCl buffer at pH 7.5. Whole tissue studies were then performed in lungs of laboratory animals. One-ml samples containing purified PMN elastase were instilled into lavaged and saline-perfused isolated dog lung at the level of the sixth to seventh generation bronchus. Treatment with 384 mug of the PMN enzyme produced anatomic emphysema after a 90-min incubation at room temperature, which was comparable to that produced by 100 mug of porcine pancreatic elastase. Frozen sections of treated and control lungs were examined for the presence of PMN elastase by the indirect immunoperoxidase method using a monospecific rabbit antiserum against PMN elastase as the primary stain. Light microscopy revealed elastase bound to connective tissue in the treated lungs, in close proximity to aldehyde-fuchsin-counterstained elastic fibers. A similar experiment was tn of enzyme solutions containing 1;0 mg of elastase per ml produced discrete lesions within 90 min, as before. Light microscopic studies in conjunction with the indirect immunoperoxidase staining method again demonstrated elastase in association with connective tissue elements in the lesion area. In addition, part of the instilled protease could be demonstrated within alveolar macrophages. Electron microscopy combined with immunoperoxidase staining revealed direct attachment of th einstilled enzyme to elastic fibers within alveolar septa. In enzyme-treated tissue, some septa showed severe depletion of intercellular structures with the exception of colalgen, which was generally preserved. These results show that human leukocyte elastase penetrated dog alveolar septal connective tissue after airway instillation and that the enzyme attaches to elastic fibers, inducing histologic changes comparable to thos seen in human emphysema.
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PMID:Experimental emphysema induced with purified human neutrophil elastase: tissue localization of the instilled protease. 84 56

Twelve Nubian goats were given single or repeated oral dosages of mercuric chloride at 10, 20 and 40 mg/kg and died or were killed in extremis at various times after dosing (18 hours-18 days). The main signs of poisoning were anorexia, frothing at the mouth, respiratory distress, epistaxis, bloat, diarrhoea, abnormal posture and recumbency. An increase in the activity of GOT and in the concentrations of urea and inorganic phosphate and a decrease in total protein and calcium concentrations in the serum were detected. The main lesions were dilatation and necrosis of the proximal convoluted tubules, shrinkage and disappearance of the glomerular tufts, varying amounts of acidophilic homogenous material in the lumens of the affected tubules of the kidney, enteritis, hepatocellular degeneration and/or necrosis and pulmonary congestion, haemorrhage, oedema and emphysema. The changes in the red blood cells indicated anaemia.
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PMID:Susceptibility of Nubian goats to mercury poisoning in the Sudan. 181 53

The effects of gender on mortality and morbidity of all neonates weighing less than 1500 g admitted to King's College Hospital Neonatal Intensive Care Unit during 1980-82 (n = 271) were examined. Very low birthweight boys had a significantly higher mortality and more postnatal complications than girls. The higher incidence of respiratory distress syndrome and pulmonary interstitial emphysema in boys was associated with increased mortality in the first year. Surviving boys had significantly more problems, including lower Apgar scores at five minutes, more frequent apnoeic attacks and bradycardic episodes, transient tachypnoea, neonatal anaemia, and lower blood calcium and phosphate concentrations. Surviving children were followed up at 1 and 2 years of age. Development of boys at 1 year was significantly delayed compared with girls in all fields save locomotor. Although at 2 years some of the differences had diminished, those in language and personal social skills were more pronounced. More than twice as many boys as girls had major neurodevelopmental disorders.
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PMID:Prognosis of the very low birthweight baby in relation to gender. 242 52

Lung transplantation is the last treatment for terminal respiratory failure due to irreversible pulmonary disease such as fibrosis and emphysema. In this paper we reported the results of our studies on three major problems for conducting clinical lung transplantation sefely, including lung preservation, early diagnosis of lung allograft rejection and bronchial anastomotic healing. We have developed a method for 48- and 96-hour lung preservation. Under simple hypothermic preservation using phosphate buffered solution resembling extracellular fluid, 48-hour storage of the lung becomes possible. Immunologic monitoring is feasible for early detection of postoperative rejection of the lung transplant. In this study subset and spontaneous blastogenesis of lymphocyte obtained from bronchoalveolar lavage fluid were measured in orthotopic rat lung allotransplantation. Lung allograft rejection is closely connected with wound healing of the bronchial anastomosis in lung transplantation. It seems that clinical applications of single and double lung transplantation is now possible for patients with terminal respiratory disease in our country.
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PMID:[Lung transplantation as a treatment method in terminal respiratory failure]. 279 44

Phosphate ore mining and processing operations are associated with dusty conditions and potential exposure to gamma radiation and radon daughter products. Although most current measurements are within Occupational Safety and Health Administration (OSHA) guidelines, no measurements exist for the era preceding modern standards of industrial hygiene and workplace ventilation. All workers employed by the participating phosphate company between 1950 and 1979 were ascertained, and 3451 males employed for approximately 6 months or more comprise the study population. Statistically significant elevations in lung cancer (standardized mortality ratio = 1.62) and emphysema were observed in white but not in black workers, in relation to U.S. rates. Among workers for whom 20 years had elapsed since first employment, there was a dose-response trend of increasing lung cancer risk with increasing duration of employment (standardized mortality ratio = 2.48 with 20 years of employment). There was no evidence of excess lung cancer risk among employees hired after 1960. Multivariate analyses and internal comparisons of risk by job type are consistent with a hypothesis of occupationally related lung cancer, but small numbers prevent firm conclusions.
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PMID:Cancer morbidity and mortality in phosphate workers. 319

A retrospective cohort mortality study was conducted on 17,601 white and 4,722 nonwhite male workers in the Florida phosphate mining and chemical processing industry. Concerns about potential risks from naturally-occurring sources of ionizing radiation and anecdotal reports of lung cancer among workers prompted this investigation. Historical follow-up was conducted for the years 1949 to 1978. In comparison with U.S. rates, small excess of mortality rates of lung cancer were observed for white (standardized mortality ratio [SMR] equals 1.22) and nonwhite workers (SMR = 1.24); however, these excesses disappeared when contrasts were made with prevailing rates in Florida. Emphysema mortality was also slightly elevated in comparison with U.S. rates; the SMRs were 1.48 and 1.73 for white and nonwhite workers, respectively. Neither disease was related to overall length of employment. Detailed analyses of mortality in relation to work assignments are presented in the companion article.
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PMID:Mortality among workers in the Florida phosphate industry. I. Industry-wide cause-specific mortality patterns. 408 54

Small excesses of lung cancer and emphysema mortality had been detected among an historical cohort of 17,601 white and 4,722 nonwhite Florida phosphate industry workers. Internal mortality rate comparisons were made between worker subcohorts classified according to length of employment in 16 work areas and according to employment duration in jobs grouped by potential exposures to 10 agents, including alpha radiation. The only consistent associations seen were increased lung cancer mortality rates among long-term workers in plant-wide services and skilled crafts jobs. There was no evidence to support causal associations with exposures characteristic of the phosphate industry.
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PMID:Mortality among workers in the Florida phosphate industry. II. Cause-specific mortality relationships with work areas and exposures. 408 55

Chronic toxicity of indium arsenide (InAs) and indium phosphide (InP) was studied in male Syrian golden hamsters which received InAs or InP particles containing a total dose of 7.5 mg of arsenic or phosphorus by intratracheal instillations once a week for 15 weeks. As a control, hamsters were treated with the vehicle, phosphate buffer solution. During their total life span, the cumulative body weight gain of hamsters in the InAs group was suppressed significantly compared with that in the control group, but not in the InP group when compared with that in the control group. Concerning the histopathological findings of the lung, the incidence rates of proteinosis-like lesions, alveolar or bronchiolar cell hyperplasia, pneumonia, emphysema and metaplastic ossification observed in the InAs or InP group were significantly higher than those observed in the control group. From these results, it would seem that InAs and InP produced severe damage to the lungs of hamsters.
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PMID:Chronic toxicity of indium arsenide and indium phosphide to the lungs of hamsters. 869 Mar 34

Terbutaline sulphate (TBS) is widely used in the treatment of bronchial asthma, chronic bronchitis and emphysema. Because of its short biological half life and dosing schedule, a long acting TBS formulation is required to improve patient compliance. The objective of this study was to develop a TBS containing biodegradable microsphere formulation. Poly(D,L-lactide-co-glycolide) (PLGA) and poly(L-lactic acid) (L-PLA) were chosen as matrix materials. A solvent evaporation method was used for preparation of microspheres. Surface morphology, particle size distribution and encapsulation efficiency were investigated. In vitro release studies were performed in pH 7.4 phosphate buffer. In vitro distribution of microspheres were studied in the Swiss albino male mice. All microspheres were spherical in shape and had a porous surface with mean diameters of 9-21 microm. The encapsulation efficiency was influenced by the polymer type, but not the molecular weight. About 90% of the initial amount was trapped in PLGA microspheres, and the remainder was on the surface. In the case of L-PLA, 50% of the total drug was associated with the surface of microspheres. The In vitro release pattern was biphasic characterized by an initial burst phase followed by a slower phase. The L-PLA microspheres released approximately 92% of the initial payload in 72 h. On the other hand, TBS release was increased with an increase in the molecular weight of PLGA. Biodistribution of L-PLA microspheres was characterized by an initially high uptake (35%) by the lungs. All these results suggest that L-PLA and PLGA microspheres have the potential to be used for passive lung targeting.
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PMID:Formulation and in vitro/in vivo evaluation of terbutaline sulphate incorporated in PLGA (25/75) and L-PLA microspheres. 1255 79

In a dairy herd of 21 cows which were on pasture during the day at the end of May 2002, four eight years old cows were suddenly inappetent and showed severe diarrhoea consisting of black discolorate feces. A few days after the onset of the disease, three affected cows exhibited neurological disorders. These cows were admitted to the IInd Medical Clinic of the University for Veterinary Medicine in Vienna. Following clinical signs were observed: circulatory weakness, anorexia, atony of the rumen, diarrhoea and in accordance with acute lead poisoning typical signs of the central nervous system. One cow died and the other two animals were euthanized. Results of blood testing were anaemia, basophil spotting of erythrocytes, increase of liver enzymes and CK, hypocalcaemia, decrease of potassium and phosphate. The cerebrospinal fluid of two cows showed increased CK-, LDH- and AST-values. The lead contents of whole blood samples were between 0.486 and 0.928 mg/kg, of liver samples 13.3 to 114.4 mg/kg, of kidney samples 172.2 to 448 mg/kg and of rumen content 59 mg/kg fresh matter. At necropsy, enteritis, liver fluke disease and severe interstitial and alveolar pulmonary emphysema were found. Pathohistologically typical ischaemic necrosis of neurons predominantly at the tips of the gyri, disseminated petechial hemorrhages and moderate diffuse neovascularisation, but no acid-fast intranucleolar inclusion bodies in the renal tubules were observed. As causative agent of the acute lead poisoning a residue on combustion, taken up by the cows on the pasture, was confirmed. The ash residue was formed by combustion of three tires which contained 450 g heavy weights of 96.5% lead for wheel balance. The lead content of the ash residue was between 2.9 and 28 g/kg dry matter.
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PMID:[Acute lead poisoning in cows due to feeding of lead contaminated ash residue]. 1496 24


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