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Pulmonary inflammation

Acute Pulmonary Inflammation Alkylating Agents Busulfan Cyc1ophosphamide... [Pg.171]

Bauer, A. K. Dwyer-Nield, L. D. Keil, K. Koski, K. Malkinson, A. M. Butylated hydroxytoluene (BHT) induction of pulmonary inflammation arole in tumor promotion. [Pg.351]

Lukacs NW, Prosser DM, Wiekowski M, Lira SA, Cook DN. Requirement for the chemokine receptor CCR6 in allergic pulmonary inflammation. J Exp Med 2001 194(4) 551-555. [Pg.251]

Schaller MA, Lundy SK, Huffnagle GB, Lukacs NW. CD8+ T cell contributions to allergen induced pulmonary inflammation and airway hyperreactivity. Eur J Immunol 2005 35(7) 2061-2070. [Pg.254]

McKinley L, Kim J, Bolgos GL, Siddiqui J, Remick DG. CXC chemokines modulate IgE secretion and pulmonary inflammation in a model of allergic asthma. Cytokine 2005 32(3-4) 178-185. [Pg.256]

Kagan, V.E. et al. (2010) Carbon nanotubes degraded by neutrophil myeloperoxidase induce less pulmonary inflammation. Nature Nanotechnology,... [Pg.216]

In studies conducted at the 1TRI, rats were exposed to 3.5 and 10 mg particles/m air of either F.lftex 12 carbon black or diesel exhaust. These exposures were 7 h/day, 5 days/wk for 12 wk (Wolff et al. Inhal. Toxicol., in press Bond et al. In Assessment of Inhalation Hazards Integration and Extrapolation Using Diverse Data. 1989, in press). Dosimetry (mg particles/g lung), microdosimetry (DNA adducts), pulmonary inflammation, and histopathology of the lungs of... [Pg.59]

The low concentration group appeared normal at 1000 gg/L, pulmonary inflammation and liver necrosis at high concentration, all had nonspecific inflammation of brain, heart, lung, liver, and kidney... [Pg.762]

Ernst, M. et al. Constitutive activation of the SRC family kinase Hck results in spontaneous pulmonary inflammation and an enhanced innate immune response. J. Exp. Med. 196, 589, 2002. [Pg.303]

A number of studies of the toxicity of zinc oxide/hexachloroethane smoke have been conducted (Brown et al. 1990 Karlsson et al. 1986 Marrs et al. 1983). These studies demonstrate that smoke exposure results in pulmonary inflammation and irritation. When male Porton Wistar rats were exposed to hexachloroethane/zinc oxide smoke for 60 minutes, the lungs showed pulmonary edema, alveolitis, and areas of macrophage infiltration 3 days later. At 14 days, there was interstitial fibrosis and macrophage infiltration. At 28 days, increased fibrosis and macrophage infiltration were noted. However, these same symptoms occurred when the animals inhaled zinc chloride there was no apparent synergism between the zinc chloride and residual hexachloroethane (Brown et al. 1990 Richard et al. 1989). This is consistent with the fact that smoke contains little hexachloroethane and the observation that acute exposure to 260 ppm hexachloroethane had no effects on the lungs of rats (Weeks et al. 1979). [Pg.98]

Ernst H, Rittinghausen S, Bartsch W, Creutzenberg O, Dasenbrock C, Gorlitz BD, Hecht M, Kairies U, Muhle H, Muller M, Heinrich U, Pott F (2002) Pulmonary inflammation in rats after intratracheal instillation of quartz, amorphousSiO(2),carbon black, and coal dust and the influence of poly-2-vinylpyridine-N-oxide (PVNO). Experimental and Toxicologic Pathology 54 109-126. [Pg.260]

Audi SH, Roerig DL, Ahlf SB, Lin W, Dawson CA (1999) Pulmonary inflammation alters the lung disposition of lipophilic amine indicators. J Appl Physiol 87 1831-1842. [Pg.155]

Makela MJ, Kanehiro A, Borish L, Dakhama A, Loader J, Joetham A, et al IL-10 is necessary for the expression of airway hyperresponsiveness but not pulmonary inflammation after allergic sensitization. Proc Natl Acad Sci USA 2000 97 6007-6012. [Pg.176]

In male rats the LC50 was 7 500 ppm for a single 8-hour exposure there was prostration followed by convulsive seizures at autopsy there was pulmonary hemorrhage. Rats exposed 6 hours/day, 5 days/week for 4 weeks to concentrations greater than 600 ppm had respiratory and ocular irritation and anemia. In another study rats repeatedly exposed to 665 ppm for 7 hours daily developed pulmonary inflammation, and there were minor changes in the liver and kidneys in some animals. ... [Pg.19]

Rats exposed for 7 hours/day for 50 days to about 10 ppm showed no overt signs of toxicity and no deaths, although a few animals, when euthanized, had mild pulmonary inflammation and nonspecific cellular changes in the liver. Exposure to 5 and 12 ppm PGE 30 hours/week for 13 weeks caused hair loss in rats attributed to direct irritation of the skin rather than to systemic toxicity. ... [Pg.573]

Dambach, et al. A murine model of cigarette smoke-induced pulmonary inflammation using intranasally administered smoke-conditioned medium. Exp Lung Res 2002 28(6) 435-455. [Pg.341]

Alkali antacids are very effective at neutralising acid rapidly, but as described above, particulate antacids—especially aluminium salts, can cause pulmonary inflammation, and are no longer widely used. Non-particulate antacids, sodium citrate or bicarbonate, have not been shown to cause damage, and are used in conjunction with H2 blockers. They will neutralise acid already in the stomach, although pocketing of the stomach contents may prevent mixing with and neutralisation of all the contents. [Pg.187]

Upregulation associated with allergic pulmonary inflammation... [Pg.14]

Mediators of Pulmonary Inflammation, edited by M. A. Bray and W. H. Anderson... [Pg.596]

However, the exceptional size-specific behavior of nanomaterials in combination with their relatively large surface-to-volume ratio might result in potential risk for human health and the environment [26-28]. For example, fullerene (C60) particles suspended in water are characterized by antibacterial activity against Escherichia coli and Bacillus subtilis [29] and by cytotoxicity to human cell lines [30]. Single- and multiwalled carbon nanotubes (CWCNTs and MWCNTs) are toxic to human cells as well [31, 32]. Nano-sized silicon oxide (Si02), anatase (Ti02), and zinc oxide (ZnO) can induce pulmonary inflammation in rodents and humans [33-35],... [Pg.207]

Stockley RA, Shaw J, Whitfield AG, Whitehead TP, Clarke CA, Burnett D, Effect of cigarette smoking, pulmonary inflammation, and lung disease on concentrations of carcinoembryonic antigen in serum and secretions, Thorac., 41 17-24, 1986. [Pg.536]

Cox G, Crossley J, Xing Z. Macrophage engulfment of apoptotic neutrophils contributes to the resolution of acute pulmonary inflammation in vivo. Am J Respir Cell Mol Biol 1995 12 232-237. [Pg.41]


See other pages where Pulmonary inflammation is mentioned: [Pg.121]    [Pg.405]    [Pg.306]    [Pg.186]    [Pg.576]    [Pg.768]    [Pg.196]    [Pg.313]    [Pg.321]    [Pg.73]    [Pg.762]    [Pg.768]    [Pg.68]    [Pg.32]    [Pg.58]    [Pg.97]    [Pg.130]    [Pg.14]    [Pg.221]    [Pg.221]    [Pg.241]    [Pg.255]    [Pg.355]    [Pg.465]    [Pg.46]    [Pg.39]    [Pg.222]   
See also in sourсe #XX -- [ Pg.31 , Pg.71 ]

See also in sourсe #XX -- [ Pg.577 , Pg.580 , Pg.581 , Pg.583 , Pg.643 ]




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