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Inflammation effects

Recent studies revealed that resveratrol protects from inflammation by acting at different phases of inflammation. Protection at the pro-inflammatory phase appears to be very important for reducing inflammation effectively and promptly. A recent study [Ge et al., 2006] showed that resveratrol inhibits macrophage expression of EMMPRIN by activating PPAR-y. In another similar study, Ma et al., [2006] showed a similar observation, but additionally found a role of nuclear transcription factor kB (NF-kB) in macrophage inhibition. Numerous studies confirmed that resveratrol suppresses the TNF-a... [Pg.311]

Lim, L.H., Solito, E., Russo-Marie, F., Flower, R.J., and M. Perretti, 1998, Promoting detachment of neutrophils adherent to murine postcapillary venules to control inflammation effect of lipocortin 1. Proc Natl Acad Sci USA. 24 95(24) 14535-9. [Pg.23]

Terano T, Salmon JA, Higgs GA, and Moncada S. (1986) Eicosapentaenoic acid as a modulator of inflammation Effect on prostaglandin and leukotriene synftiesis. Biocheia Pharm. 33,779-783. [Pg.290]

Hugh, T. E. 1977. Complement factors and inflammation effects of a-thrombin on components C3 and C5. In Chemistry and biology of thrombin. R. L. Lundblad, J. W. Fenton, and K. G. Mann, editors. Aim Arbor Science, Ann Arbor, Mich. 345-360. [Pg.369]

The vaccine being tested contains a small protein called P amyloid (A/ ). This protein forms abnormal deposits, or plaques , in the brains of people with Alzheimer s disease. Researchers believe that Ap deposition causes loss of mental function by killing the brain neurons. The strategy of Ap vaccination is to stimulate the immune system to clean up plaques and prevent further Afi deposits. Although preclinical and Phase I studies showed the potential of the vaccine, the Phase II clinical trial was halted because 15 of 360 patients developed severe brain inflammation. Further studies showed that the A/S did generate the desired antibody response. An acceptable vaccine may still be possible by modifying the epitope to reduce the inflammation effect. [Pg.83]

F. Antitumor and Anti-inflammation Effects through iNOS Suppression... [Pg.197]

Fujie K, Shinguh Y, Inamura N, Yasumitsu R, Okamoto M, Okuhara M Release of neutrophil elastase and its role in tissue injury in acute inflammation Effect of the elastase inhibitor, FR134043. EurJ Pharmacol 1999 374 117. [Pg.91]

Jean, T., and Bodinier, M.C. (1994) Mediators Involved in Inflammation Effects of Daflon 500 mg on Their Release, An-giology 45,554—559. [Pg.149]

Nitrogen dioxide (NO2) at levels found in healthy subjects indoors caused mild airway inflammation, effects on blood cells, and increased susceptibility of airway epithelial cells to injury from respiratory viruses (Frampton et al. 2002). [Pg.11]

Liu, X. Miyazaki, M. Flowers, M.T. Sampath, H. Zhao, M. Chu, K. Paton, C.M. Joo, D.S. Ntambi, J.M. Loss of stearoyl-CoA desaturase-1 attenuates adipocyte inflammation effects of adipocyte-derived oleate. Arterioscler. Thromb. Vase. Biol. 2010, 30, 31-38. [Pg.312]

An injection of the steroid cortisone (Section 26 14) IS often effective for reducing the pain and inflammation that comes from an injury But chronic pain and inflammation such as occurs with arthritis is better managed with an orally ad... [Pg.1083]

Transactivation. Protein synthesis is initiated or inhibited by the action of the activated GR on DNA. The use of glucocorticoids leads to antiinflammatory effects by first controlling gene expression, which subsequentiy leads to the synthesis and/or suppression of inflammation regulatory proteins. [Pg.98]

Repeated exposures of animals to high (near-lethal) concentrations of vapors result in inflammation of the respiratory tract, as weU as degenerative changes in the Hver, kidneys, and heart muscle. These effects arise at concentrations far above those causing irritation. Such effects have not been reported in humans. The low odor threshold and irritating properties of acrylates cause humans to leave a contaminated area rather than tolerate the irritation. [Pg.157]

Mild exposure to HF via inhalation can irritate the nose, throat, and respiratory system. The onset of symptoms may be delayed for several hours. Severe exposure via inhalation can cause nose and throat bums, lung inflammation, and pulmonary edema, and can also result in other systemic effects including hypocalcemia (depletion of body calcium levels), which if not promptly treated can be fatal. Permissible air concentrations are (42) OSHA PEL, 3 ppm (2.0 mg/m ) as E OSHA STEL, 6 ppm (5.2 mg/m ) as E and ACGIH TLV, 3 ppm (2.6 mg/m ) as E. Ingestion can cause severe mouth, throat, and stomach bums, and maybe fatal. Hypocalcemia is possible even if exposure consists of small amounts or dilute solutions of HE. [Pg.200]

Toxicity. Many /V-nitrosamines are toxic to animals and cells in culture (4,6—8,88). /V-Nitrosodimethy1amine [62-75-9] (NDMA) is known to be acutely toxic to the Hver in humans, and exposure can result in death (89). Liver damage, diffuse bleeding, edema, and inflammation are toxic effects observed in humans as a result of acute and subacute exposure to NDMA. These effects closely resemble those observed in animals dosed with NDMA (89,90). [Pg.109]

Theophylline s predominant mode of action appears to be bronchocHlation. However, it has also been shown that prophylactic acHriinistration of theophylline provides some protection from asthma attacks and suppresses the late-phase response (67,68). Some researchers beHeve that at therapeutic semm concentrations theophylline may inhibit the development of airway inflammation (69). There are conflicting reports on the effect of theophylline on allergen-induced bronchial hyperresponsiveness some clinical stucHes report a reduction in hyper-responsiveness, others do not (69,70). Theophylline clearly does not reverse the general bronchial hyperresponsiveness over the course of long-term therapy (71). Because of the relationship between... [Pg.440]

In 1956 selenium was identified (123) as an essential micronutrient iu nutrition. In conjunction with vitamin E, selenium is effective iu the prevention of muscular dystrophy iu animals. Sodium selenite is adrninistered to prevent exudative diathesis iu chicks, a condition iu which fluid leaks out of the tissues white muscle disease iu sheep and infertility iu ewes (see Eeed ADDITIVES). Selenium lessens the iacidence of pneumonia iu lambs and of premature, weak, and stillborn calves controls hepatosis dietetica iu pigs and decreases muscular inflammation iu horses. White muscle disease, widespread iu sheep and cattle of the selenium-deficient areas of New Zealand and the United States, is insignificant iu high selenium soil areas. The supplementation of animal feeds with selenium was approved by the U.S. EDA iu 1974 (see Eeed additives). Much of selenium s metaboHc activity results from its involvement iu the selenoproteia enzyme, glutathione peroxidase. [Pg.337]

Instillation of pure thioglycolic acid iato the eyes of a rabbit resulted iu severe pain, severe conjunctival inflammation, dense corneal opacity, and severe idtis. These effects had not improved at the end of 14 d after exposure. Washing immediately after exposure did not modify the response (23). [Pg.5]

Skin. The skin may become contaminated accidentally or, in some cases, materials may be deHberately appHed. Skin is a principal route of exposure in the industrial environment. Local effects that are produced include acute or chronic inflammation, allergic reactions, and neoplasia. The skin may also act as a significant route for the absorption of systemicaHy toxic materials. Eactors influencing the amount of material absorbed include the site of contamination, integrity of the skin, temperature, formulation of the material, and physicochemical characteristics, including charge, molecular weight, and hydrophilic and lipophilic characteristics. Determinants of percutaneous absorption and toxicity have been reviewed (32—35,42,43,46—49). [Pg.229]

The likelihood that materials will produce local effects in the respiratory tract depends on their physical and chemical properties, solubiHty, reactivity with fluid-lining layers of the respiratory tract, reactivity with local tissue components, and (in the case of particulates) the site of deposition. Depending on the nature of the material, and the conditions of the exposure, the types of local response produced include acute inflammation and damage, chronic... [Pg.229]

Eye. Adverse effects may be produced by splashes of Hquids or soflds, and by materials dispersed in the atmosphere. The eye is particularly sensitive to peripheral sensory irritants in the atmosphere. Toxic effects that may be induced include transient acute inflammation, persistent damage, and, occasionally, sensitivity reactions. ToxicologicaHy significant amounts of material may be absorbed by the periocular blood vessels in cases of splash contamination of the eye with materials of high acute toxicity (58). [Pg.230]

Primary Irritancy Studies. These studies are employed to determine the potential of materials to cause local inflammatory effects in exposed body surfaces, notably skin and eye, following acute or short-term repeated exposure. In general, the approach involves applying the test material to the surface of the skin or eye, and observing for signs of inflammation, their duration, and resolution. Reviews have been written about the conduct of primary eye irritation (58,86,87) and primary skin irritation studies (88,89). [Pg.236]


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