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Elevated serum gamma-glutamyl transferase (GGT) levels were found in 29% of 155 chronic alcoholics undergoing detoxification treatment. Alkaline phosphatase (AP) was increased in 16%, alanine aminotransferase--SGPT (ALT) in 12% of the patients, while 23% had elevations of either AP or ALT or both. Of the foregoing parameters, GGT was the best single indicator of liver involvement. In course of the follow-ups GGT/ALT correlation improved, but GGT/AP correlation deteriorated. In 9 patients, abstinence during follow-up was associated with progressive decrease in previously elevated serum GGT. Because of its unique sensitivity, GGT may be useful as a screening and/or monitoring aid in alcoholism. 相似文献
144.
Alexander Koshkaryev Gregory Barshtein Saul Yedgar 《Cell biochemistry and biophysics》2010,56(2-3):109-114
Red blood cell (RBC) adhesion to vessel wall endothelium is a potent catalyst of vascular occlusion and occurs in oxidative stress states such as hemoglobinopathies and cardiovascular conditions. These are often treated with vitamin E (VitE), a “classic” antioxidant. In this study, we examined the effects of VitE on RBC adhesion to vascular endothelial cells (EC), and on translocation of phosphatidylserine (PS) to RBC surface, known as a potent mediator of RBC/EC adhesion, facilitating thrombus formation. Treatment of RBC with VitE strongly induces (up to sevenfold) PS externalization and enhances (up to 20-fold) their adherence to EC. The VitE hydrophilic analogue—Trolox—does not incorporate into cell membranes. Trolox did not exhibit any of these effects, implying that the VitE effect is due to its known ability to incorporate into cell membranes. The membrane-incorporated VitE significantly reduced the level of reactive oxygen species in H2O2-treated RBC, demonstrating that VitE elevates RBC/EC adhesion despite acting as an anti-oxidant. This study demonstrates for the first time that contrary to the common view of VitE as a beneficial supplement, VitE may introduce a circulatory risk by inducing flow-disturbing RBC adherence to blood vessel wall and the pro-thrombotic PS exposure. 相似文献
145.
E. B. Burova I. S. Smirnova A. N. Shatrova I. V. Gonchar N. N. Nikolskii 《Cell and Tissue Biology》2011,5(1):9-14
Interferon gamma (IFNγ) is known to inhibit the proliferation of some transformed cell lines. Recently, we demonstrated the
transactivation of the epidermal growth factor receptor (EGFR) in response to IFNγ (Burova et al., 2007) and provided direct
evidence for the dependence of IFNγ-induced EGFR transactivation on the EGFR expression level in epithelial cells (Gonchar
et al., 2008). This study examines an antiproliferative effect of IFNγ on human epithelial cell lines—A431 and HeLa that express
high levels of EGFR, as well as HEK293 that expresses low levels of EGFR. To characterize the IFNγ-induced changes in these
cells, we studied cell growth, the cell cycle, and induction of apoptosis. The response to IFNγ differed in the compared cell
lines; cell growth was inhibited in both A431 and HeLa cells, but not in HEK293 cells, as was shown by the cell count and
MTT. The cell-cycle phases analyzed by flow cytometry were disturbed in A431 and HeLa cells in response to IFNγ. On the contrary,
in HEK293 cells, the IFNγ treatment did not alter distribution by cell cycle phases. Our results indicate that IFNγ produces
an antiproliferative effect that depends on the increased expression of EGFR in A431 and HeLa cells. Furthermore, it was demonstrated
that IFNγ induced the caspase 3 activation in A431 cells, which suggests the involvement of active caspase 3 in the IFNγ-induced
apoptosis. 相似文献
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Serological comparison of bovine T-mycoplasmas 总被引:1,自引:0,他引:1
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