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MeSH Review

Cold Ischemia

 
 
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Disease relevance of Cold Ischemia

 

High impact information on Cold Ischemia

 

Chemical compound and disease context of Cold Ischemia

 

Biological context of Cold Ischemia

 

Anatomical context of Cold Ischemia

 

Associations of Cold Ischemia with chemical compounds

  • This endogenous protective mechanism is capable of blocking xanthine/XOD generation in liver grafts during cold ischemia [26].
  • The addition of U74006F to University of Wisconsin preservation solution significantly prolonged endothelial cell viability after 48 and 72 hr of cold ischemia and reoxygenation (p < 0.01) [27].
  • The following experimental groups were studied: I, cold ischemia; I+X, effect of xanthine; I+T, effect of adenosine (blocking its receptor by theophylline); I+A, effect of excess adenosine; I+T+X, effect of xanthine alone, and I+T+ spermine NONOate (NONOs), I+A+NONOs, I+X+NONOs, role of NO [28].
  • The study objective was to assess hepatic utilization of exogenous adenosine or adenine to enhance ATP recovery in rat liver after cold ischemia [29].
  • In a multivariate regression model, donor age and recipient creatinine were observed to be significant covariates in both groups, while donor race, cold ischemia time (CIT), female to male transplants, and recipient albumin were independent predictors of survival of HCV- recipients [30].
 

Gene context of Cold Ischemia

  • Interleukin-10 plasma levels did not correlate either with cold ischemia time or with the occurrence of rejection episodes [31].
  • CINC mRNA also increased as cold-ischemia time was prolonged [32].
  • The W/D ratio and myeloperoxidase decreased in both 24- and 48-hour groups, with TGF-beta1-active compared with CAT, and 18-hour cold ischemia groups (W/D, p < 0.02 and p < 0.004, respectively; myeloperoxidase, p < 0.05 and p < 0.01, respectively) [33].
  • Multiple regression revealed a significant correlation between cold ischemia time and posttransplant urinary FBPase excretion (multiple R = 0.65, p < 0.001) [34].
  • In renal grafts with pretransplantation cold ischemia and subsequent ischemia-reperfusion injury, overactivation of PARP-1 may lead to a higher index of acute tubular necrosis, a delay in total recovery of the function of the transplanted organ, and an early progression to chronic graft nephropathy [35].
 

Analytical, diagnostic and therapeutic context of Cold Ischemia

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