Objective To investigate the relationship between preoperative prognostic nutritional index(PNI) and prognosis in elderly patients with gastric cancer.Methods The clinical data of 62 patients over age 65 with gastric cancer who underwent radical gastrectomy for gastric cancer were retrospectively analyzed.PNI values were calculated and the relationship between PNI and untoward reactions and prognosis were discussed.Results PNI value is closely related with patient age(t=5.576,P<0.001),tumor size(x2=4.846,P=0.033),lymphatic metastasis(x2=13.742,P<0.001),preoperative CEA level(t=5.226,P<0.001).Among the 62 patients,12 cases with high-PNI had recurrence and 5 patients died during the follow-up period, while 11 case in low-PNI had a recurrence and 7 patients died.The recurrent rate(x2=4.055,P=0.044) and mortality rate(x2=4.630,P=0.043) of the high-PNI group were significantly lower than the low-PNI group.Conclusion PNI is a simple and useful marker for predicting the long-term outcomes of elderly gastric cancer patients, which should be included in the routine assessment of gastric cancer patients.

Objective　To compare the irradiation-protective and inter-synergestic effects of E838,WR-2721, Rubia cordifolia, cystamin e hydrochloride and ethinyl estradiol on radiation and combined radiation-burn injury. Methods　Above-mentioned drugs were given to the mice i ntraperitoneally, or intragastrcally, then, the mortality and the average surviv al d for 30 d were observed before and after the administration of the drug s. Results　①When drugs were before injury , the survival rate and the average survival d of the radiation and combined radiation-burn injured mice were increased obviously with the best effect in E838 and WR-2721. ②When drugs were given after injury, E838 and R. cordifolia also kept the effect. ③Combined appling WR-2721（pre) and E838（post）displayed a significant syner gistic reaction. Conclusion　E838 and WR-2721 are more e ffective than the others in the prevention of radiation.

Objective To investigate the role of nucleotide-binding oligomerization domain 2(NOD2)modified by palmitoyltransferase(ZDHHC5)in brain injury after cardiopulmonary resuscitation(CPR)in mice.Methods Twenty-four male C57BL/6J mice were divided into the blank group,the control group,the ZDHHC5-si group and the NOD2-si group,with 6 mice in each group.Except for the blank group without any treatment,CPR modeling was performed in the other three groups.At 24 h before CPR,mice in the ZDHHC5-si group and the NOD2-si group were injected with ZDHHC5 siRNA and NOD2 siRNA via tail vein,respectively.The modified neurological deficit scale(mNSS)was used to evaluate the neurological function at 24 h,48 h and 72 h in each group.Blood samples and brain tissue were collected 72 h after modeling.Real-time fluorescent quantitative PCR(qPCR)was used to detect ZDHHC5 and NOD2 in brain tissue.The protein expression levels of IL-1β,TNF-α and IL-6 in plasma were detected by enzyme-linked immunosorbent assay(ELISA).Colorimetric method and thiobarbituric acid(TBA)method were used to detect protein expression levels of MDA and MPO in brain tissue,respectively.Western blot assay was used to detect expression levels of Cleaved Caspase-3,ZDHHC5 and NOD2 in brain tissue.HE pathological sections of brain tissue were observed under light microscope.The pathological sections of brain tissue were observed by TUNEL under fluorescence microscope.Results Compared with the blank group,the mNSS score,the expression levels of IL-1β,TNF-α,IL-6,MDA and MPO,and the protein expression levels of Cleaved Caspase-3,ZDHHC5 and NOD2 were significantly increased(P＜0.05),and brain tissue damage and cell apoptosis were aggravated in the other three groups.Compared with the control group,the above indicators were significantly decreased in the ZDHHC5-si group and the NOD2-si group(P＜0.05),and brain tissue damage and cell apoptosis were significantly attenuated.Compared with the NOD2-si group,the above parameters were significantly decreased(P＜0.05),and brain tissue damage and cell apoptosis were further attenuated in the ZDHHC5-si group.Conclusion In the mouse CPR model,NOD2 can produce palmitoylated NOD2 after regulated by ZDHHC5,which further promotes the release of inflammatory factors and causes neuronal apoptosis,ultimately damaging brain tissue and affecting neurological function.