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AGE formation

Formations from all geologic periods have been used for deep-well injection, but Paleozoic rocks are used for most injection zones (53%), followed by Tertiary-age formations (39%). Older Paleozoic rocks have been more frequently used for injection primarily because they tend to be more deeply buried. However, the more recent Tertiary-age Gulf Coast sediments are also very thick, and most injection in rocks of this age takes place there. [Pg.811]

Cantero, A. V., Portero-Otin, M., Ayala, V., Auge, N., Sanson, M., Elbaz, M., Thiers, J. C., Pamplona, R., Salvayre, R., and Negre-Salvayre, A. (2007). Methylglyoxal induces advanced glycation end product (ages) formation and dysfunction of PDGF receptor-beta Implications for diabetic atherosclerosis. FASEB J. 21,3096-3106. [Pg.136]

As introduced in Section 1.7.3 and Figure 1-20, because of diffusive loss of Ar, the "age" obtained from the K-Ar system is not necessarily the real age (formation age or peak temperature age), but is an apparent age (fa) as defined by Equation 1-114 ... [Pg.268]

AGE formation is related to hyperglycaemia in diabetes, but not in uraemia, because AGE levels do not differ between diabetic and nondiabetic haemodialysis patients, which is a mystery.435 Pentosidine and CML were elevated in uraemic plasma and then-levels were not correlated with fructoselysine levels. The addition of aminoguanidine and OPB-9195 lowered the yield of AGEs in both uraemic and control plasma. Carbonyl stress was therefore thought to be a contributory factor in uraemia. [Pg.122]

Pyridoxamine (PM) inhibits in vitro AGE formation from Amadori adducts on proteins, as well as advanced lipoxidation endproducts (ALEs). Baynes597 has now reported that PM inhibits the increase in AGE/ALEs in the skin collagen of strepto-zotocin-induced diabetic Sprague-Dawley rats and Zucker obese, nondiabetic rats. Inhibition of AGE/ALE formation was accompanied by lower increases in... [Pg.165]

Inhibition of the formation of CML and pentosidine from various AGE precursors and BSA was more efficient with OPB-9195 than with AG.601 OPB-9195 also inhibited the formation of two ALEs (malondialdehyde-lysine and 4-hydroxynonenal-protein adduct) with an efficiency similar to that of AG. In glucose-based peritoneal dialysis fluid, OPB-9195 inhibited AGE formation, probably by trapping reactive carbonyls, such as GO, MGO, and 3-deoxyglucosone. [Pg.166]

D. J. Millar, P. J. Thomalley, C. Holmes, and A. Dawnay, In vitro kinetics of AGE formation with PD fluid resembles that of glucose degradation products rather than glucose, in G, 2002, 475 177. [Pg.196]

R. Wada, Y. Nishizawa, N. Yagihashi, M. Takeuchi, Y. Ishikawa, K. Yasumura, M. Nakano, and S. Yagihashi, Inhibition of the development of experimental diabetic neurophathy by suppression of AGE formation with a new antiglycation agent, in G, 2002, 101-105. [Pg.204]

Figure 1.11 Illustration of advanced glycation end-product (AGE) formation. Figure 1.11 Illustration of advanced glycation end-product (AGE) formation.
Effects of Tea and Its Polyphenols on Diabetes-Related Complications and AGE Formation... [Pg.249]


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See also in sourсe #XX -- [ Pg.246 ]




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