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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Radionuclide injury to the lung has been studied in rats, hamsters, dogs, mice and baboons. Exposure of the lung to high dose levels of radionuclides produces a spectrum of progressively more severe functional and morphological changes, ranging from radiation pneumonitis and fibrosis to lung tumors. These changes are somewhat similar for different species. Their severity can be related to the absorbed radiation dose (measured in rads) produced by alpha, beta or gamma radiation emanating from various deposited radionuclides. The chemicophysical forms of radionuclides and spatial-temporal factors are also important variables. As with other forms of injury to the lung, repair attempts are highlighted by fibrosis and proliferation of pulmonary epithelium. Lung tumors are the principal late effect observed in experimental animals following pulmonary deposition of radionuclides at dose levels that do not result in early deaths from radiation pneumonitis or fibrosis. The predominant lung tumors described have been of epithelial origin and have been classified, in decreasing frequency of occurrence, as adenocarcinoma, bronchioloalveolar carcinoma, epidermoid carcinomas and combined epidermoid and adenocarcinoma. Mesothelioma and fibrosarcoma have been observed in rats, but less commonly in other species. Hemangiosarcomas were frequency observed in dogs exposed to beta-gamma emitters, and occasionally in rats exposed to alpha emitters. These morphologic changes in the lungs of experimental animals were reviewed and issues relevant to the prediction of human hazards discussed.
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PMID:Radionuclide injury to the lung. 637 95

The aim of this investigation was to develop a mathematical model of mean age, mean arsenic dietary dose, and age-specific prevalence rate for endemic chronic arsenic poisoning. Data on mean age (years), mean arsenic dietary dose (mg/kg body weight/day), and age-specific prevalence rate per 100,000 population for endemic chronic arsenic poisoning in Antofagasta Commune, northern Chile, for the 1968-1971 period, were collected. Endemic chronic arsenic poisoning means here chronic arsenical dermatosis associated with marked or sever symptoms (or signs) of chronic arsenic poisoning (chronic diarrhoea, hepatic cirrohsis, chronic bronchitis, bronchiectasis, recurrent broncho-pneumonia, cardiomegaly, systemic occlusive arterial disease, cerebral thrombosis, etc.) There was a strong positive correlation between age-specific prevalence rate per 100,000 population and mean arsenic dose (r = + 0.9593) and a negative correlation between prevalence rate and mean age (r = 0.8789). These findings show that the prevalence rate declines with the advancing age and increases with the increase of arsenic dose. A multiple linear regression model E(y) = alpha + beta X1 + gamma X2, where y represents the age-specific prevalence rate per 100,000 population, X1 the mean arsenic dose, and X2 the mean age, was fitted to the data. The estimates of the parameters (alpha, beta, and gamma) were obtained by minimizing the residual sum of squares sigma(y - alpha - beta X1 - gamma X2)2. The following multiple linear regression equation was obtained: Y = 202.161 + 8452.455 X1 - 2.394 X2. Of the total variability in the prevalence rate, 96.22 per cent was accounted for by the multiple regression.
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PMID:Mathematical model of mean age, mean arsenic dietary dose and age-specific prevalence rate from endemic chronic arsenic poisoning: a human toxicology study. 742 80

The behaviour of radionuclides after entry into the body and the radiation doses received by individual tissues depend on the chemical nature of the element, the physicochemical form of the intake, the radioactive half-life of the isotope and the type and energy of the emissions. Ingestion of radionuclides in insoluble particles will result in radiation doses being delivered to tissues of the gastrointestinal (GI) tract; other tissues will also be irradiated by nuclides with penetrating photons emissions (gamma) but doses may be largely confined to the GI tract for charged particle emissions (alpha, beta). Ingestion of more soluble forms will lead to greater absorption to blood and deposition in other tissues and therefore may result in greater doses to other tissues. Similar considerations apply to inhaled material and to the entry of radionuclides through cuts or wounds. For ingested materials, including particles, more information is needed on uptake and retention in intestinal tissues and consequent doses to sensitive cells, particularly for alpha emitters. There has been concern that the pattern of distribution of activity throughout irradiated tissues may influence the extent of damage, particularly for alpha emitters because of the localised deposition of energy and their greater relative biological effectiveness compared with beta/gamma emitters. Aggregation of activity has the potential to result in greater acute tissue damage and has been shown, for example, to result in focalised pneumonitis and fibrosis in the lung and ulceration of the skin. The main long-term effect of irradiation of tissues is the induction of malignant change, although hereditary disease may also be of concern following irradiation of the gonads. There are only limited data available to compare the effect on cancer induction of heterogeneous and homogeneous irradiation of tissues. However, the available information, for irradiation of the lung, skin or liver, indicates that in general nonuniform alpha irradiation from radioactive particles is no more hazardous, and may be less hazardous, than if the same activity is uniformly distributed.
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PMID:The assessment of doses and effects from intakes of radioactive particles. 898 26

Streptococcus pneumoniae is a major cause of community-acquired pneumonia and death from infectious diseases in industrialized countries. Lung airway and alveolar epithelial cells comprise an important barrier against airborne pathogens. Cyclooxygenase (COX)-derived prostaglandins, such as PGE(2), are considered to be important regulators of lung function. Herein, we tested the hypothesis that pneumococci induced COX-2-dependent PGE(2) production in pulmonary epithelial cells. Pneumococci-infected human pulmonary epithelial BEAS-2B cells released PGE(2). Expression of COX-2 but not COX-1 was dose and time dependently increased in S. pneumoniae-infected BEAS-2B cells as well as in lungs of mice with pneumococcal pneumonia. S. pneumoniae induced degradation of IkappaBalpha and DNA binding of NF-kappaB. A specific peptide inhibitor of the IkappaBalpha kinase complex blocked pneumococci-induced PGE(2) release and COX-2 expression. In addition, we noted activation of p38 MAPK and JNK in pneumococci-infected BEAS-2B cells. PGE(2) release and COX-2 expression were reduced by p38 MAPK inhibitor SB-202190 but not by JNK inhibitor SP-600125. We analyzed interaction of kinase pathways and NF-kappaB activation: dominant-negative mutants of p38 MAPK isoforms alpha, beta(2), gamma, and delta blocked S. pneumoniae-induced NF-kappaB activation. In addition, recruitment of NF-kappaB subunit p65/RelA and RNA polymerase II to the cox2 promoter depended on p38 MAPK but not on JNK activity. In summary, p38 MAPK- and NF-kappaB-controlled COX-2 expression and subsequent PGE(2) release by lung epithelial cells may contribute significantly to the host response in pneumococcal pneumonia.
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PMID:Streptococcus pneumoniae induced p38 MAPK- and NF-kappaB-dependent COX-2 expression in human lung epithelium. 1641 78