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The anti-metabolite 5-fluorouracil (5-FU) is employed clinically to manage solid tumors including colorectal and breast cancer.
Intracellular metabolites of 5-FU can exert cytotoxic effects via inhibition of thymidylate synthetase, or through incorporation
into RNA and DNA, events that ultimately activate apoptosis. In this review, we cover the current data implicating DNA repair
processes in cellular responsiveness to 5-FU treatment. Evidence points to roles for base excision repair (BER) and mismatch
repair (MMR). However, mechanistic details remain unexplained, and other pathways have not been exhaustively interrogated.
Homologous recombination is of particular interest, because it resolves unrepaired DNA intermediates not properly dealt with
by BER or MMR. Furthermore, crosstalk among DNA repair pathways and S-phase checkpoint signaling has not been examined. Ongoing
efforts aim to design approaches and reagents that (i) approximate repair capacity and (ii) mediate strategic regulation of
DNA repair in order to improve the efficacy of current anticancer treatments.
Received 08 September 2008; received after revision 25 September 2008; accepted 03 October 2008 相似文献
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Serum enzyme changes during sleep deprivation 总被引:1,自引:0,他引:1
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A. G. Heppleston K. Fletcher I. Wyatt 《Cellular and molecular life sciences : CMLS》1972,28(8):938-939
Zusammenfassung Lungen alveolare Lipo-proteinose, durch Inhalation Quarzstaubes herbeigeführt, zeigt eine starke Vermehrung neutraler Lipide und Phospholipide, wobei Phosphatidylcholin und besonders Dipalmityl-Lecithin hervortreten. Eine silikotische Fibrose lässt sich nicht nachweisen. Diese ungewöhnliche Reaktion auf Quartz wird diskutiert.
Mrs.M. McDermott of the Pneumoconiosis Research Unit collaborated in the surface tension studies. 相似文献
Mrs.M. McDermott of the Pneumoconiosis Research Unit collaborated in the surface tension studies. 相似文献
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IgA nephropathy, the most common cause of glomerulonephritis, is linked to 6q22-23 总被引:22,自引:0,他引:22
Gharavi AG Yan Y Scolari F Schena FP Frasca GM Ghiggeri GM Cooper K Amoroso A Viola BF Battini G Caridi G Canova C Farhi A Subramanian V Nelson-Williams C Woodford S Julian BA Wyatt RJ Lifton RP 《Nature genetics》2000,26(3):354-357
End-stage renal disease (ESRD) is a major public health problem, affecting 1 in 1,000 individuals and with an annual death rate of 20% despite dialysis treatment. IgA nephropathy (IgAN) is the most common form of glomerulonephritis, a principal cause of ESRD worldwide; it affects up to 1.3% of the population and its pathogenesis is unknown. Kidneys of people with IgAN show deposits of IgA-containing immune complexes with proliferation of the glomerular mesangium (Fig. 1). Typical clinical features include onset before age 40 with haematuria and proteinuria (blood and protein in the urine), and episodes of gross haematuria following mucosal infections are common; 30% of patients develop progressive renal failure. Although not generally considered a hereditary disease, striking ethnic variation in prevalence and familial clustering, along with subclinical renal abnormalities among relatives of IgAN cases, have suggested a heretofore undefined genetic component. By genome-wide analysis of linkage in 30 multiplex IgAN kindreds, we demonstrate linkage of IgAN to 6q22-23 under a dominant model of transmission with incomplete penetrance, with a lod score of 5.6 and 60% of kindreds linked. These findings for the first time indicate the existence of a locus with large effect on development of IgAN and identify the chromosomal location of this disease gene. 相似文献