Plasmas: damage

In normal physiological conditions, it is inhibited by a-1-protease inhibitor of plasma. Damage to connective caused by leakage of elastases leads to damage associated with inflammatory diseases, such as pulmonary emphysema, adult respiratory distress syndrome, septic shock, cystic fibrosis, carcinogenesis, chronic bronchitis, and rheumatoid arthritis. Compounds that directly inhibit elastase or its release from human neutrophils are of enormous pharmaceutical and cosmetological interest in the development of new anti-inflammatory drugs. A possible source for elastase inhibitors are the medicinal Asteraceae and Droseraceae, particularly those used as traditional medicine in Asia. 

Ajmera, S.K., et al., 2004. Plasma damage and pore sealing increasingly coupled ULK integration challenges. Future Fab. Int. 17. Section 6. 

S1H2 is also believed to contribute to film growth when vacuum ultraviolet radiation is employed to decompose silane, thus avoiding both high temperatures and plasma damage . These conditions produce SiH, S1H2 and H atoms as primary dissociation products in unknown ratios . 

After image transfer, the patterned resist must be readily and completely removable without substrate damage. The pattern often can be stripped from the substrate with a mild organic solvent. Proprietary stripper formulations or plasma oxidation treatments are utilized when the imaging chemistry or image transfer process has iasolubilized the pattern. 

Homocysteine arises from dietary methionine. High levels of homocysteiae (hyperhomocysteinemia) are a risk factor for occlusive vascular diseases including atherosclerosis and thrombosis (81—84). In a controlled study, semm folate concentrations of <9.2 nmol/L were linked with elevated levels of plasma homocysteiae. Elevated homocysteine levels have beea associated also with ischemic stroke (9). The mechanism by which high levels of homocysteine produce vascular damage are, as of yet, aot completely uaderstood. lateractioa of homocysteiae with platelets or eadothehal cells has beea proposed as a possible mechanism. Clinically, homocysteine levels can be lowered by administration of vitamin B, vitamin B 2> foHc acid. 

Dietary deficiency in the absence of absorption defects can be effectively reversed with oral supplementation of 1 p.m of vitamin B 2 daily. If deficiency is related to a defect in vitamin absorption, daily doses of 1 pg adininistered subcutaneously or intramuscularly are effective (33). However, a single intramuscular dose of 100 pg of cobalamin once per month is adequate in patients with chronic gastric or ileal damage. Larger doses are generally rapidly cleared from the plasma into the urine and are not effective unless the patient demonstrates poor vitamin retention. 

T.D. Burchell, Radiation Damage in Carbon Materials. In Physical Processes of the Interaction of Fusion Plasmas with Solids, W.O. Hofer and J. Roth, Eds., 1996, Academic Press, pp. 341-382. 

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