Objective This study was to determine the role of the Xeroderma pigmentosum group D (XPD) Asp312Asn polymorphism in predicting response to Oxaliplatin based chemotherapies and survival in patients with metastatic colorectal cancer.Methods This study enrolled a total of 106 patients treated with FOLFOX4 (n =72) or XELOX (n =34) regimen.The genotype of XPD Asp312Asn was analyzed by TaqMan probe based real-Time polymerase chain reaction (PCR).Logistic regression was used to predict the response to the treatments.Cox proportion hazards models and Kaplan-Meier method were applied to predict the survival.Results The effective rate of chemotherapy in 106 patients with colorectal cancer was 57.6％ (61/106).There was no significant difference in the distribution of G/G,G/A and A/A genotypes between the two groups (P ＞ 0.05).Multivariate survival analysis showed that the survival time of patients with A/A genotype,carcinoembryonic antigen (CEA) (＞5 ng/ml) and age (＞65 years) was relatively short,with statistical significance (P ＜ 0.05).Conclusions XPD Asp312Asn single nucleic acid polymorphism can be used as a predictor of survival in patients with metastatic colorectal cancer,but it is not associated with oxaliplatin sensitivity and needs further study.

Aim ToinvestigatetheeffectsofCa2+/calmodulin-dependent protein kinase Ⅱ inhibitor KN-93 on calcium overload-induced heart injury.Methods Thirty-twoisolatedratheartswererandomlydivided into the control group,KN-93 control group,calcium paradox group,and calcium paradox with KN-93 treat-ment group.Left ventricular pressure were recorded, and the heart function was evaluated by the left ventric-ular end-diastolic pressure (LVEDP ) and developed pressure (LVDP).Coronary flow (CF)were collect-ed,and lactate dehydrogenase (LDH)content was de-termined.Triphenyltetrazolium chloride staining was usedtomeasuretheinfarctsize.Results Compared with the control group,KN-93 at 2. 5 μmol·L-1 had no effects on coronary flow,cardiac performance and cell death at the end of perfusion in normal rats (P>0. 05 );The hearts of calcium paradox exhibited a de-crease in LVDP and CF,meanwhile an increase in LV-EDP,LDH,and infarct size of 18 ±7. 2% (P <0. 01).2. 5 μmol·L-1 KN-93 further increased the levels of LVEDP,LDH and infarct size (P<0. 01)in Ca2+paradoxical hearts,while it provoked the decline intheCFandLVDP(P<0.01).Conclusion The data demonstrates that KN-93 aggravates heart injury in calcium paradox,it also suggests that CaMKⅡ is in-volved in the Ca2+overload-induced heart injury.