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)

Pressure-volume curves and simulated single-breath nitrogen tests were performed on 32 excised left human lungs and the slope of phase III, and phase IV plus minimal volume, expressed as percent of the lung volume at a transpulmonary pressure of 30 cmH2O (closing capacity), was calculated. The lungs were graded as to the degree of emphysema and degree of peripheral airways disease. Peripheral airway dimensions were also measured. The closing capacity expressed as percent predicted in vivo was significantly correlated with the total pathological scores (P less than 0.01) and inflammation scores (P less than 0.01) as well as the transpulmonary pressures at the onset of phase IV (P less than 0.01). Correlations with the emphysema grade were not significant. The slopes of phase III were highly variable even among normal lungs and could not be shown to correlate with airways disease or emphysema.
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PMID:Single-breath nitrogen test in excised human lungs. 731 85

In the present paper, we have reviewed experimental animal studies on the effects of the two most important oxidant airborne pollutants, nitrogen dioxide and ozone, on the respiratory system. The toxic effects depend on concentration and length of exposure, and are generally similar for both oxidants, with ozone operative at lower concentrations. High doses of both oxidants cause death due to lung oedema. Exposure to sublethal levels causes functional alterations such as airflow limitation and airway hyperresponsiveness to bronchoconstrictor stimuli. These effects, which are generally reversible, are associated with epithelial injury, oedema and airway and parenchymal infiltration by inflammatory cells. Loss of cilia of airway epithelium and necrosis of type I alveolar epithelial cells are the most prominent consequences at the epithelial level. Inflammation is characterized by early neutrophilic infiltration, followed by an increased number of mononuclear cells, predominantly alveolar macrophages. After long-term exposure, whilst nitrogen dioxide causes predominantly emphysema, ozone produces mainly pulmonary fibrosis. Biochemical effects include lipid peroxidation, increased antioxidant metabolism, and alteration of enzyme activity. Nitrogen dioxide and ozone may also alter the immunological response and reduce the defence against infections, increasing the susceptibility of exposed animals to infections.
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PMID:Effect of oxidant air pollutants on the respiratory system: insights from experimental animal research. 748 4

Epidemiologic evidence suggests that cigarette smoking is a major risk factor for chronic obstructive pulmonary diseases such as chronic bronchitis and emphysema, for carcinogenesis, and for cardiovascular disease. However, the precise mechanisms of these effects are incompletely understood. The gas phase of cigarette smoke contains abundant free radicals including nitric oxide. Hence, cigarette smoke may induce some of its damaging effects by free radical mechanisms. We report that exposure of plasma, a model for respiratory tract lining fluids, to gas-phase cigarette smoke causes depletion of antioxidants, including ascorbate, urate, ubiquinol-10, and alpha-tocopherol, and a variety of carotenoids, including beta-carotene. Gas-phase cigarette smoke induced some lipid peroxidation, as measured by cholesteryl linoleate hydroperoxide (18:2OOH) formation. Ascorbate was effective in preventing 18:2OOH formation. In contrast to the low concentrations of lipid hydroperoxides measured (< 1 mumol/L), protein carbonyl formation, a measure of protein modification, increased by approximately 400 mumol/L after nine puffs of cigarette smoke. Reduced glutathione inhibited protein carbonyl formation, whereas other plasma antioxidants, including ascorbate, were ineffective. alpha, beta-Unsaturated aldehydes (acrolein and crotonaldehyde) in cigarette smoke may react with protein -SH and -NH2 groups by a Michael addition reaction that results in a protein-bound aldehyde functional group. Gas-phase cigarette smoke is capable of converting tyrosine to 3-nitrotyrosine and dityrosine, indicating free radical mechanisms of protein damage by nitrogen oxides. Aldehydes and nitrogen oxides in cigarette smoke may be significant contributors to biomolecular damage, and endogenous antioxidants can attenuate some of these adverse effects.
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PMID:Dietary antioxidants and cigarette smoke-induced biomolecular damage: a complex interaction. 749 50

Poloxalene and a mineral mixture feed supplement patented for the treatment of emphysema, polyarthritis, and other pectin related diseases were tested in two trials for their ability to prevent bloat in cattle fed fresh alfalfa. Each trial had a crossover design using three Jersey steers with rumen fistulas per group. Each trial period continued until the total number of cases of bloat reached > or = 24. Treatments were given at 0800 each day. The mineral mixture was given at 100 g/d and 190 mg/kg body weight per day in the first and second trials, respectively. Poloxalene, which was tested only in the second trial, was given at 23 mg/kg body weight per day. Each group of steers was then fed 200 kg of freshly harvested alfalfa in the vegetative to early bloom stages of growth at 0830. In the first trial, only 69% as many cases of bloat occurred on the mineral mixture as on the control treatment, but no significant difference was detected in the second trial. The potency of the alfalfa may have been higher in the second trial, when forage dry matter was lower, magnesium and soluble nitrogen were higher, and bloat occasionally occurred twice a day. Bloat did not occur when the steers were treated with poloxalene. In these trials, poloxalene was completely effective in preventing bloat, but the mineral mixture was only partially so.
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PMID:Evaluation of two supplements for the prevention of alfalfa bloat. 786 60

3-Methylindole (3-MI) is a metabolite of tryptophan that causes acute pulmonary edema and emphysema in ruminants when administered orally or intravenously. Electron paramagnetic resonance (EPR) spin-trapping techniques have been used to investigate the in vitro and in vivo formation of free radicals during 3-MI metabolism by goat lung. Utilizing C-phenyl-N-tert-butyl nitrone (PBN), a nitrogen-centered free radical has been detected from 3-MI in goat lung microsomal incubation. The EPR spectrum of the spin adduct is identical to that observed when 3-MI is irradiated with ultraviolet light. The formation of a nitrogen-centered 3-MI free radical is followed by the appearance of a carbon-centered radical in microsomal preparations. The objective of the present study is to prove that the nitrogen-centered radical generated from the 3-MI incubation system is a 3-MI radical utilizing [14C]-3 MI and the EPR-HPLC technique. The HPLC chromatogram includes three peaks that give EPR signals. These peaks are assigned to nitrogen-, oxygen- and carbon-centered radical adducts. The polarity of the three peaks follows the order: carbon-centered radical adduct > oxygen-centered radical adduct > nitrogen-centered radical adduct. The last has a polarity that is weaker than 3-MI. Only the nitrogen-centered peak and the 3-MI peak possessed radioactivity. The retention time of the nitrogen centered radical is the same as the spin adduct generated by 3-MI irradiation with ultraviolet light. These results demonstrate that the nitrogen-centered radical is a 3-MI-PBN spin adduct, and supports the hypothesis that 3-MI-induced lung damage results from activation of 3-MI to a free radical. Also, in this study the stability of the radical spin adducts and the best conditions to produce the radicals in the incubation system was investigated.
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PMID:Identification of 3-MI-derived N-centered radicals obtained from incubation of 3-MI with microsomal-NADPH system by EPR-HPLC spin trapping. 795 63

The effects of low levels of air pollution and weather conditions on the number of patients admitted to hospitals for exacerbation of chronic bronchitis or emphysema (n = 2807) was studied in Helsinki during a 3-year period, 1987-1989. The daily number of admissions via the emergency room was significantly associated with prevailing levels of sulfur dioxide (SO2) and nitrogen dioxide (NO2) in Poisson regressions controlled for weather, season, time trends, and day of the week, whereas the total number of admissions (via the emergency room and otherwise) was not significantly associated with these pollutants. The effect of SO2 was observed only among those under 65 years old; a significant peak of admissions was seen during the same day (RR, 1.31 for a 2.7-fold increase in SO2; 95% CI, 1.01-1.70; P = 0.039), and another after a 3-day lag (RR, 1.39; 95% CI, 1.05-1.86; P = 0.021). The effect of NO2 was strongest after a 6-day lag and was significant only among those over 64 years old (RR, 1.31; 95% CI, 1.03-1.66; P = 0.022). The average of mean 24-hr concentrations of NO2 was 39 micrograms/m3 (0.021 ppm) and that for SO2 was 19 micrograms/m3 (0.0067 ppm). No relationship was found between admissions and the concentrations of total suspended particulates (TSP) or ozone (O3), the temperature, or the relative humidity. However, the number of admissions among those over 64 years of age was significantly lower, irrespective of temperature, during the summer than during other seasons. The mean daily concentration of O3 was fairly low (22 micrograms/m3 or 0.011 ppm), but that of TSP was high, 76 micrograms/m3. the mean temperature was low, +4.7 degrees C. These results suggest that SO2 and NO2 concentrations lower than those given as guidelines in many countries, and lower than previously shown, may increase the incidence of symptoms in some patients with chronic bronchitis or emphysema.
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PMID:Chronic bronchitis, emphysema, and low-level air pollution in Helsinki, 1987-1989. 818 37

Nitrogen dioxide (NO2), an air pollutant produced by burning fossil fuels and a component of cigarette smoke, is thought to contribute to the pathogenesis of pulmonary diseases, such as emphysema. In order to gain information on the mechanism by which NO2 damages the lung and proteins vital to its function, as well as its reaction with proteins in general, in vitro exposures of alpha-1-proteinase inhibitor (alpha 1PI), elastin, poly-L-lysine, and poly-L-arginine were performed. The ability of alpha 1PI to inhibit its natural physiological target, human neutrophil elastase (HNE), declined with exposure to 54% of the control value at molar ratios of NO2:alpha 1PI of 400:1 and greater. Exposure of alpha 1PI to NO2 resulted in a 50% loss of immunoreactivity with either monoclonal or polyclonal antibodies in an enzyme-linked immunosorbent assay at molar ratios of NO2:alpha 1PI of 100:1 and greater. The results of parallel O-phthalaldehyde and bicinchoninic acid protein assays as well as amino acid analysis on control and NO2-exposed alpha 1PI suggested a reactivity of NO2 with lysine residues. Elastin and poly-L-lysine were labeled by reductive methylation of amino groups with [3H]HCHO prior to treatment with NO2 in aqueous solutions at physiological pH. NO2 exposure of elastin resulted in the solubilization of 84% of the associated radioactivity of which 79% was identified as [3H]methyllysine by amino acid analysis. After NO2 exposure of poly-L-[3H]lysine, gel filtration chromatography revealed that the 50,000 M(r) poly-L-[3H]lysine had been degraded to small peptides of 1-3000 M(r). Similarly, after NO2 exposure of unlabeled poly-L-arginine, gel filtration chromatography, and total peptide analysis revealed that the 47,500 M(r) peptide was also partially degraded to peptides. These results suggest that NO2 reacts with the epsilon-amino groups of Lys residues (primary amines) and with the amide nitrogen (secondary amines) of surface-exposed Lys and Arg residues in the peptide backbone to result in peptide bond cleavage. These findings are the first indication of NO2-mediated peptide degradation and provide additional data on the potential of NO2 to damage proteins vital to the function of the lung in an in vitro exposure system.
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PMID:Nitrogen dioxide reactivity with proteins: effects on activity and immunoreactivity with alpha-1-proteinase inhibitor and implications for NO2-mediated peptide degradation. 832 82

Airways represent a serial and parallel branched system, through which the alveoli are connected with the external air. They participate in the mechanical and immune defense against noxious agents, regional flow regulation to optimize the perfusion/ventilation ratio and provide lung mechanical support. Functional exploration of central airways is based on resistance measurement, flow-volume curve or spirometry, while peripheral airways influence parameters as the upstream resistance, the slope of phase III nitrogen washout and the residual volume. Bronchodynamic tests supply important information on airway reversibility and nonspecific reactivity. Anatomopathologic alterations of obstructive chronic bronchitis, pulmonary emphysema and bronchial asthma account for their specific functional and bronchodynamic alterations. There is a growing interest for bronchiolitis in the clinical, radiologic and functional field. This type of lesion, always present in COPD, asthma and interstitial disease, becomes relevant when isolated or predominant. The most useful anatomofunctional classification separates the "constrictive" forms, the cause of obstruction and hyperinflation, from "proliferative" forms where an intraluminal proliferation more or less extended to alveolar air spaces as in BOOP (bronchiolitis obliterans organizing pneumonia) results in restrictive dysfunction. Constrictive bronchiolitis obliterans represents a severe and frequent complication of lung and bone marrow transplantation. Idiopathic BOOP may occur with cough or flue-like symptoms. In other cases, constrictive and proliferative forms may have a toxic (gases or drugs), postinfective or immune etiology (rheumatoid arthritis, LES, etc). Respiratory bronchiolitis or smokers' bronchiolitis, an often asymptomatic lesion, rarely associated to an interstitial lung disease, should be considered separately. The relationships between respiratory bronchiolitis, COPD and initial centriacinar emphysema is still to be elucidated. The diagnostic combination of the more sensitive functional tests with HRCT will allow a better understanding of the natural history of the various forms of bronchiolitis.
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PMID:Airway disease: anatomopathologic patterns and functional correlations. 914 18

Gas bubble disease (GBD), a non-infectious, environmentally/physically induced trauma, is caused by an increase in the dissolved gas pressure above the ambient air pressure (supersaturation). Frequently the cause is an increased partial pressure of nitrogen-especially in spring-/groundwater. All fish species as well as amphibians and aquatic invertebrates are susceptible. Fish species and age groups are different sensitive; swim up fry is very endangered. The disease may occur in a chronic form at approximately 103% and in an acute form at above 110/115% total gas pressure (TGP). Fish, especially fry, with the chronic form die slowly without symptoms. The clinical symptoms of the acute form are disorientation, subcutaneous emphysema, embolism, exophthalmus mostly only on one side, swimming near the water surface with darkened skin, haemorrhages and high mortality. Losses increase with increased TGP. Generally, mortality in the chronic form increases by secondary infections of emphysematous tissue. As technical processes may be the cause for an increased total gas pressure, such as water pumping, heating water or mixing cold with warm water, in this context we could speak from a "technopathy". The following "therapeutic" measurement is recommended: avoid causal factors, transfer damaged fish in expanded water, turn off the cause, compensate the pressure in deeper water, if possible.
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PMID:[Gas bubble disease of fish]. 928 92

During the 1991 Gulf War, the Iraqi army set Kuwait oil wells on fire. Wells and some oil refineries were burned, resulting in Kuwait and the surrounding Gulf region being exposed to toxic gases. The oil fires reached their peak in February 1991. On March 7, the fires in some fields were still burning at peak strength. Sulfur dioxide, particulates, carbon monoxide, and nitrogen oxides were emitted into the atmosphere. All of these substances can cause adverse health effects, which vary according to concentration and duration of exposure. A survey conducted in Kuwait clinics and emergency rooms showed an increase in upper respiratory irritation consistent with environmental air sampling results, indicating occasional high levels of particulates. Patient visits related to gastrointestinal illness, heart disease, psychiatric illness, chronic bronchitis and emphysema, and bronchiectasis increased during the period following the burning of the oil wells. There was no documented evidence of an increase in visits for acute upper and lower respiratory infections or asthma. Public health workers must recognize the high priority of collecting long-term health data and developing public health systems to assess those data.
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PMID:Environmental surveys conducted in the Gulf region following the Gulf War to identify possible neurobehavioral consequences. 931 49


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