Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To gain further insight into the pathogenesis of the adult respiratory distress syndrome (ARDS), we studied possible relationships among the activation status of circulating polymorphonuclear neutrophils (PMN), cytokine levels, and the severity of lung injury in 31 patients: 15 with ARDS, nine with severe pneumonia uncomplicated by ARDS, and seven mechanically ventilated with neither ARDS nor pneumonia. Nine healthy subjects served as controls. Using flow cytometry, we identified a subpopulation of PMN with an increased capacity to generate hydrogen peroxide after stimulation ex vivo in all three patient groups; significantly higher values were found in those with ARDS. The PMN stimulation index, a reflection of the degree of hyperresponsiveness, correlated with elevated levels of tumor necrosis factor-alpha (TNF alpha) in plasma, and both spontaneous and lipopolysaccharide-induced TNF alpha production by cultured monocytes. These biologic expressions of PMN activation and cytokine generation both correlated with indices of the severity of lung injury, but not with the overall clinical severity. In contrast, IL-6 and IL-1 beta showed little or no relationship with either the degree of lung injury or PMN hyperresponsiveness. We conclude that TNF-alpha-primed PMN may play a major role in the pathogenesis of ARDS-associated lung injury.
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PMID:Subpopulation of hyperresponsive polymorphonuclear neutrophils in patients with adult respiratory distress syndrome. Role of cytokine production. 141 30

Altogether 101 children under one year of age with infectious toxicosis due to acute pneumonia were examined for the clinical, roentgenomorphological and biochemical aspects of the given condition. The clinical aspects were delineated on the basis of the universal status covered by the formalized case report. The biochemical processes were analyzed according to the content of peroxidation products of membrane lipids, the concentration of hydrogen peroxide, phospholipase activity, antioxidant and antiperoxide defence of the blood as well as according to the physical constants of red blood cell membranes. A direct relationship was discovered between the clinical picture (the degree of toxicosis) and membranopathological processes. The data obtained make it possible to conceive the model of infectious toxicosis as a membranopathological one, induced by the syndrome of the deficiency of antioxidant and antiperoxide enzymes.
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PMID:[Clinico-pathogenetic aspects of infectious toxicosis in infants caused by acute pneumonia]. 194 52

A 60-year-old laboratory technician developed pulmonary infiltrates consistent with chemical pneumonitis following accidental exposure to a mixture of hydrogen bromide and phosphorus tribromide. A protracted clinical course ensued consistent with bronchiolitis obliterans. These problems may have been avoided if the potential for subsequent damage had been realized at the time of the initial exposure. Health personnel must be aware of the potentially delayed effects of accidental exposures to respiratory irritants.
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PMID:Chemical pneumonitis due to exposure to bromine compounds. 338 40

Humans with bacterial sepsis are predisposed to acute lung injury with respiratory failure and have an increased risk of pulmonary infection. Because the alveolar macrophage is the resident phagocyte in the lung and a defect in antimicrobial activity could predispose to infection, we assessed the functional integrity of these cells in vitro in a canine model of Escherichia coli endotoxin-induced lung injury with respiratory failure. Dogs were given 2 or 20 mg/kg of E. coli endotoxin 055:B5, and alveolar macrophages from pulmonary lavage were compared with those from control dogs. The physiologic criteria for the adult respiratory distress syndrome and pathologic confirmation of acute lung injury were produced in all endotoxin-treated animals. The production of acute lung injury with respiratory failure by E. coli endotoxin was associated with several alterations in alveolar macrophage function. Adherence was significantly reduced for cells from the endotoxin groups. The alveolar macrophages from endotoxin-treated animals differed from those from control animals, with significantly greater production of hydrogen peroxide, significantly greater peaks in chemiluminescence, significantly reduced phagocytosis of Staphylococcus aureus and E. coli at all times, and a diminished ability to kill cell-associated S. aureus and E. coli over time. These derangements could play a role in the therapeutic failures of pneumonia, an increased risk for nosocomial pneumonias, or the propagation of acute lung injury with respiratory failure.
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PMID:Alveolar macrophage function in a canine model of endotoxin-induced lung injury. 353 87

The intravenous administration of hydrogen peroxide has been reported to benefit patients with pneumonia and to reduce Plasmodium parasitemia in experimentally infected mice. We assessed the antibacterial activity of intravenously infused hydrogen peroxide against hydrogen peroxide-susceptible Escherichia coli (MBC of hydrogen peroxide, 0.23 mM) in experimentally infected rabbits. No decrease in the level of bacteremia was detected at the maximum intravenous infusion rate of hydrogen peroxide physiologically tolerated by the rabbits (2.0 mumol/h). Moreover, the addition ex vivo of greater amounts of hydrogen peroxide to human or murine blood containing E. coli resulted in no detectable antibacterial action. In contrast, ethyl hydrogen peroxide, which is not affected by catalase, was bactericidal when added ex vivo to human blood containing E. coli. These results suggest that extracellular hydrogen peroxide, whether of exogenous or endogenous origin, does not have antibacterial activity in the blood of animals having even low levels of catalase.
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PMID:Lack of antibacterial activity after intravenous hydrogen peroxide infusion in experimental Escherichia coli sepsis. 388 40

Dimethyl hydrogen phosphite (DMHP), an intermediate in the production of insecticides or herbicides, was administered by p.o. gavage for 2 yr to male Fischer 344/N rats and male and female B6C3F1 mice at doses of 0, 100, or 200 mg/kg and to female Fischer 344/N rats at doses of 0, 50 or 100 mg/kg. Dose related toxicity was seen in the lungs of treated male and female rats. The lung lesions were most prevalent in the high dose male rat group which received a dose twice that given to the high dose female rats. Lung lesions included alveolar epithelial hyperplasia, chemically related pneumonia, alveolar-bronchiolar adenoma, alveolar-bronchiolar carcinoma, and squamous cell carcinoma. DMHP also caused neoplastic and nonneoplastic lesions of the forestomach in male rats; a similar but less pronounced effect was observed in female rats. Nonneoplastic lesions associated with administration of DMHP included mineralization of the cerebellum in male rat and focal calcification of the testis in male mice. Under the conditions of this study, there was clear evidence for carcinogenicity for male rats, equivocal evidence for carcinogenicity in female rats, and no evidence for carcinogenicity in either male or female mice. DMHP caused the highest incidence of lung tumors in the male rat of all chemicals studied to date in the National Cancer Institute-National Toxicology Program Carcinogenesis Testing Program.
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PMID:Lung neoplasms in rodents after chronic administration of dimethyl hydrogen phosphite. 394 Jan 95

Mycoplasma pulmonis, an etiological agent of murine pneumonia, produced about 0.065 mumoles of hydrogen peroxide (H(2)O(2)) per hr per 10(10) colony-forming units. When glucose was present at a concentration of 0.01 m, H(2)O(2) production was increased by 50%. To determine if H(2)O(2) production by M. pulmonis could be correlated with virulence, normal, acatalasemic, and acatalatic mice were infected with the organism. Three days after infection with M. pulmonis significantly more acatalatic mice had pneumonia than did normal or acatalasemic mice. The pneumonia in acatalatic mice was also more severe than in the other two groups. Five days after infection, pneumonia in the acatalatic mice was resolved, whereas normal mice were severely affected. The presence of pneumonia and the severity were correlated with the recovery of M. pulmonis from the lesions. In vitro studies of the effect of catalase on M. pulmonis showed that exogenously supplied catalase stimulated the growth of M. pulmonis at 37 C and prolonged its survival at 25 C. Hemolysis of sheep blood, guinea pig blood, rabbit blood, and normal and acatalasemic mouse blood by M. pulmonis was inversely related to the catalase activity of the erythrocytes. These findings suggest that H(2)O(2) secretion contributes to the virulence of M. pulmonis and to the death of the microorganism in the absence of host catalase.
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PMID:Relationship of hydrogen peroxide production by Mycoplasma pulmonis to virulence for catalase-deficient mice. 578 95

In rabbits with pneumonia induced by introduction of a foreign body to the trachea, a correlation was found between the morphological features of pneumonia (the degree and spreading of alterative-exudative and proliferative processes) and lipid peroxidation in the blood (the concentration of diene conjugates in plasma lipids, catalase activity, the intensity of hydrogen-peroxide-stimulated chemiluminescence of plasma and erythrocytes).
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PMID:[Lipid peroxidation in the blood in pneumonia]. 637 92

Four field trials were carried out to evaluate the effect of feeding tiamulin hydrogen fumarate at 20 and 30 ppm to fattening pigs over an eight week period, on farms with histories of severe, complicated, enzootic pneumonia problems. These farms had a prevalence of pigs with pneumonic lesions from 81 to 94 per cent and a range between individual batches of 69 to 96 per cent. The results of the first three trials showed that tiamulin at 30 ppm significantly improved the weight gains and feed conversion efficiency of pigs, in comparison with controls and was superior to the groups fed 20 ppm tiamulin. A further trial with tiamulin at 30 ppm and controls only, confirmed the original findings. The overall average results showed that tiamulin improved average daily gain by 33 g (4.7 per cent) and feed conversion efficiency by 0.138 (4.7 per cent). This effect did not appear to result from a reduction in the total extent of pneumonic lesions and the possible reasons for this are discussed, but in the fourth trial the number of pigs requiring parenteral treatment was noticeably reduced.
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PMID:Tiamulin feed premix in the improvement of growth performance of pigs in herds severely affected with enzootic pneumonia. 637 5

The inhibition of Pneumocystis carinii dihydrofolate reductase (DHFR) continues to be the major treatment strategy for P. carinii pneumonia (PCP). The design of new anti-pneumocystis agents would be significantly enhanced by the availability of a 3D model of the methotrexate (MTX) binding site of the P. carinii DHFR. However, an X-ray crystal structure of the P. carinii DHFR is not yet available. Alignment of the amino acid sequences of P. carinii and Lactobacillus casei DHFRs indicates that the two proteins show approximately 80% homology among MTX binding-site residues. This high level of homology suggests that the L. casei DHFR MTX binding-site structure could serve as a structural template in developing a model of the P. carinii DHFR MTX binding site. Therefore, the X-ray crystal structure of L. casei DHFR was used to develop a 3D model of the methotrexate binding site of P. carinii DHFR. The molecular modeling and dynamics software QUANTA/CHARMm was used. Amino acid residue mutations and deletions were performed using QUANTA and macromolecular minimizations were achieved with CHARMm. The MTX binding-site residues of L. casei DHFR were mutated to the corresponding residues of the P. carinii DHFR sequence. The resulting structure was extensively minimized. The resulting P. carinii MTX binding-site model showed significant differences in hydrogen-bonding patterns from the L. casei MTX binding site. Also, the P. carinii site is more hydrophobic than the corresponding L. casei site. Analysis of atom-to-atom close contacts between methotrexate and protein binding-site residues indicates that the P. carinii MTX binding-site complex is primarily stabilized by hydrophobic interactions, while the L. casei complex is mostly stabilized by electrostatic interactions. The model is consistent with the observed increased sensitivity of P. carinii DHFR to lipid-soluble inhibitors and provides a rational basis for the design of new anti-pneumocystis agents.
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PMID:A molecular model of the folate binding site of Pneumocystis carinii dihydrofolate reductase. 806 29


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