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71.
Reserve effects and natural variation in coral reef communities 总被引:2,自引:0,他引:2
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V?Srinivasan GJM?Maestroni DP?Cardinali AI?Esquifino SR?Pandi?Perumal SC?MillerEmail author 《Immunity & ageing : I & A》2005,2(1):17
Aging is associated with a decline in immune function (immunosenescence), a situation known to correlate with increased incidence
of cancer, infectious and degenerative diseases. Innate, cellular and humoral immunity all exhibit increased deterioration
with age. A decrease in functional competence of individual natural killer (NK) cells is found with advancing age. Macrophages
and granulocytes show functional decline in aging as evidenced by their diminished phagocytic activity and impairment of superoxide
generation. There is also marked shift in cytokine profile as age advances, e.g., CD3+ and CD4+ cells decline in number whereas
CD8+ cells increase in elderly individuals. A decline in organ specific antibodies occurs causing reduced humoral responsiveness.
Circulating melatonin decreases with age and in recent years much interest has been focused on its immunomodulatory effect.
Melatonin stimulates the production of progenitor cells for granulocytes-macrophages. It also stimulates the production of
NK cells and CD4+ cells and inhibits CD8+ cells. The production and release of various cytokines from NK cells and T-helper
lymphocytes also are enhanced by melatonin. Melatonin presumably regulates immune function by acting on the immune-opioid
network, by affecting G protein-cAMP signal pathway and by regulating intracellular glutathione levels. Melatonin has the
potential therapeutic value to enhance immune function in aged individuals and in patients in an immunocompromised state. 相似文献
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Purification and isoelectric heterogeneity of chicken tyrosinase 总被引:1,自引:0,他引:1
Alterations in rat liver transfer RNA (tRNA) methyltransferase activities have been observed after liver damage by various chemicals or by partial hepatectomy. The qualitative and quantitative nature of these activity changes and the time course for their induction have been studied. Since homologous tRNAs are essentially fully modified in vivo, E. coli tRNAs were used as in vitro substrates for the rat liver enzymes in these studies. Each of the liver-damaging agents tested rapidly caused increases in activities of the enzyme(s) catalyzing methyl group transfer to tRNAs that have an unmodified guanine at position 26 from the 5' end of the molecule. This group of tRNAs includes E. coli tRNANfmet, tRNAAla1, tRNALeu1, or Leu2, and tRNASer3 (Group 1). In each case N2-methylguanine and N2,N2-dimethylguanine represented 90% or more of the products of these in vitro methylations. The product and substrate specificity observed are characteristic of N2-guanine methyltransferase II (S-adenosyl-L-methionine : tRNA (guanine-2)-methyltransferase, EC 2.1.1.32). In crude and partially purified preparations derived from livers of both control and treated animals this enzyme activity was not diminished significantly by exposure to 50 degrees C for min. The same liver-damaging agents induced little or no change in the activities of enzymes that catalyze methyl group transfer to various other E. coli tRNAs that do not have guanine at position 26 (Group 2). The results of mixing experiments appear to rule out the likelihood that the observed enzyme activity changes are due to stimulatory or inhibitory materials present in the enzyme preparations from control or treated animals. Thus, our experiments indicate that liver damage by each of several different methods, including surgery or administration of chemicals that are strong carcinogens, hepatotoxins, or cancer-promoting substances, all produce changes in liver tRNA methyltransferase activity that represent a selective increase in activity of N2-guanine tRNA methyltransferase II. It is proposed that the specificity of this change is not fortuitous, but is the manifestation of an as yet unidentified regulatory process. 相似文献
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