AIM To compare the performance of 3 published delayed graftfunction(DGF) calculators that compute the theoretical risk of DGF for each *** This single-center,retrospective study included 247 consecutive kidney transpl...
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AIM To compare the performance of 3 published delayed graftfunction(DGF) calculators that compute the theoretical risk of DGF for each *** This single-center,retrospective study included 247 consecutive kidney transplants from a deceased *** kidney transplantations were performed at our institution between January 2003 and December *** compared the occurrence of observed DGF in our cohort with the predicted DGF according to three different published calculators. The accuracy of the calculators was evaluated by means of the c-index(receiver operating characteristic curve).RESULTS DGF occurred in 15.3% of the transplants under *** c index of the Irish calculator provided an area under the curve(AUC) of 0.69 indicating an acceptable level of prediction,in contrast to the poor performance of the Jeldres nomogram(AUC = 0.54) and the Chapal nomogram(AUC = 0.51). With the Irish algorithm the predicted DGF risk and the observed DGF probabilities were close. The mean calculated DGF risk was significantly different between DGF-positive and DGF-negative subjects(P < 0.0001). However,at the level of the individual patient the calculated risk of DGF overlapped very widely with ranges from 10% to 51% for recipients with DGF and from 4% to 56% for those without *** sensitivity,specificity and positive predictive value of a calculated DGF risk ≥ 30% with the Irish nomogram were 32%,91% and 38%. CONCLUSION Predictive models for DGF after kidney transplantation are performant in the population in which they were derived,but less so in external validations.
AIM:To gain molecular insights into the action of the histone deacetylase inhibitor(HDACI) trichostatin-A(TSA) in pancreatic cancer(PC) ***:Three PC cell lines,BxPC-3,AsPC-1 and CAPAN-1,were treated with various conce...
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AIM:To gain molecular insights into the action of the histone deacetylase inhibitor(HDACI) trichostatin-A(TSA) in pancreatic cancer(PC) ***:Three PC cell lines,BxPC-3,AsPC-1 and CAPAN-1,were treated with various concentrations of TSA for def ined periods of *** synthesis was assessed by measuring the incorporation of 5-bromo-2'*** expression at the level of mRNA was quantif ied by real-time polymerase chain *** and phosphorylation of proteins was monitored by immunoblotting,applying an infrared imaging *** study the role of p38 MAP kinase,the specif ic enzyme inhibitor SB202190 and an inactive control substance,SB202474,were ***:TSA most eff iciently inhibited BrdU incorporation in BxPC-3 cells,while CAPAN-1 cells displayed the lowest and AsPC-1 cells an intermediate *** biological response of the cell lines correlated with the increase of histone H3 acetylation after TSA *** BxPC-3 cells(which are wild-type for KRAS),TSA strongly inhibited phosphorylation of ERK 1/2 and *** contrast,activities of ERK and AKT in AsPC-1 and CAPAN-1 cells(both expressing oncogenic KRAS) were not or were only modestly affected by TSA *** all three cell lines,but most pronounced in BxPC-3 cells,TSA exposure induced an activation of the MAP kinase *** of p38 by SB202190 slightly but signif icantly diminished the antiproliferative effect of TSA in BxPC-3 ***,only BxPC-3 cells responded to TSA treatment by a signif icant increase of the mRNA levels of bax,a pro-apoptotic member of the BCL gene ***,in BxPC-3 and AsPC-1 cells,but not in the cell line CAPAN-1,signif icantly higher levels of the cell cycle inhibitor protein p21Waf1 were observed after TSA ***:The biological effect of TSA in PC cells correlates with the increase of acetyl-H3,p21Waf1,phospho-p38 and bax levels,and the decrease of phosphoERK 1/2 and phospho-AKT.
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