AIM: To study the relationship among peroxisome proliferator-activated receptor-gamma2(PPAR ?2) gene Pro12Ala polymorphism,Helicobacter pylori(H.pylori) infection,and gastric cancer in China.METHODS: 104 consecutive patients with gastric cancer and 104 age-and sex-matched controls from Guangdong Province of southern China were examined.PPAR?2 Pro12Ala polymorphism was analyzed by PCR-restriction fragment length polymorphism method(PCR-RFLP).H.pylori status of subjects was determined by enzyme-linked immunosorbent assay(ELISA) for anti-H.pylori IgG.RESULTS: The prevalence of H.pylori infection was significantly higher in gastric cancer patients than that in control(81.7% vs 59.6%,2=12.27,P

Objective To estimate the critical value notification of emergency specimens in general laboratory whether a-chieved the desired goals,and to apply quality improvement measures to achieve quality improvement purposes.Methods Critical values of emergency specimens in general laboratory were monitored and collected in 2014.Statistical analysis was done for non-notification rates and sources of the critical values,and quality improvement began in July,2014 by training, continuing education and amonthly bulletin of notification data of critical values.Results Total number of Critical values of emergency specimens in general laboratory in 2014 was 2 648 and 1 950 of them had been reported by telephone.Total notifi-cation rate was 61.4% in the first 6 months,and was 81.4% from July to December.At last,Critical value notification rates increased to 97.72% in December.Conclusion Strengthening the management of critical value notification can help impro-ving the quality of laboratory service,as well as enhancing stuff responsibility and awareness of service for clinic.

AIM: To study the relationship between MIF gene -173 locus polymorphism, helicobacter pylori (Hp) infection, and gastric cancer in high prevalent (Shanxi) and low prevalent (Guangdong) regions in China. METHODS: Genomic DNA was extracted from peripheral blood of 104 healthy controls, 104 gastric patients from Guangdong and 102 healthy volunteers, and 102 gastric cancer patients from Shanxi. Polymorphism of MIF-173 locus was analyzed by polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP). RESULTS: In high prevalence region, the number of patients who carrying with MIF -173 C/C is much higher than those of healthy controls (28.8% vs 15.4%, ?~2=5.47, P0.05). CONCLUSION: The C genotype of MIF -173 locus may be associated with the risk of gastric cancer in China.

Objective To investigate the modulation of ET-3 on the nuclear factor (NF)-κB/Bfl-1 antiapoptotic pathway in a malignant melanoma cell line A375. Methods Flow cytometry was performed to detect the apoptosis in cultured A375 cells after treatment with ET-3 of 100 nmol/L for 24 hours. ET-3 of various concentrations (0, 1, 10, 100 nmol/L) was used to treat some A375 cells with or without the pretreatment with the ETRB antagonist BQ788; after another 24-hour culture, RT-PCR and Western blot were conducted to examine the mRNA expression of Bfl-1 and protein expressions of Bfl-1 and ETRB, respectively. Results The 24-hour treatment with ET-3 of 100 nmol/L significantly reduced the apoptosis rate of A375 cells (F = 10.68, P ＜0.05). The mRNA and protein expressions of Bfl-1 were up-regulated by ET-3 in a concentration dependent manner (both P ＜ 0.01 ), while BQ788 significantly blocked the ET-3-induced up-regulation (F = 420.38,229.49, both P ＜ 0.01 ). The protein expression of pNF-κB in A375 cells was also enhanced by ET-3 of different concentrations (all P ＜ 0.05), but the enhancement was suppressed by BQ788, and there was a significant difference in the protein expression of pNF-κB between cells treated with ET-3 of 100 nmol/L and those treated with the combination of ET-3 of 100 nmol/L and BQ788 (F = 255.46, P ＜ 0.01 ). Conclusion ET-3/ETRB inhibits the apoptosis in A375 cells likely by activating the NF-κB/Bfl-1 anti-apoptotic pathway.

[Objective] To explore the role of endothelin-3 (ET-3) on epithelial-to-mesenchymal transition in a malignant melanoma cell line A375.[Methods] A375 cells were cultured in vitro and classified into 3 groups to be treated with ET-3 at 100 nmol/L (ET-3 group),co-cultured with ET-3 at 100 nmol/L and endothelin receptor B (ETRB) antagonist BQ788 at 100 μmo1/L (ETRB antagonist group),or to remain untreated (blank control group).After additional 24-hour culture,Transwell chamber assay was used to detect the invasive capability of A375 cells,real time-PCR to measure the mRNA expressions of Twist and Slug,and Western blot to determine the protein expression of E-cadherin,vimentin,Twist and Slug.The changes in the morphology of A375 cells were observed.Data were assessed by analysis of variance and Scheffe's method.[Results] In the Transwell assay,the number of A431 cells permeating through the basement membrane was 4.200 ± 0.837,9.400 ± 0.548 and 3.400 ± 0.894 respectively in the blank control group,ET-3 group and ETRB antagonist group (F =88.44,P ＜ 0.01 ),suggesting that ET-3 could promote the metastasis of A375 ceils,while BQ788 could block the promotive effect of ET-3.The epithelial-to-mesenehymal transition was obvious in cells treated with ET-3 alone,but was inapparent in cells treated with ET-3 and BQ788.The ET-3 at 100 nmol/Lsignificantly decreased the protein expression of E-cadhefin from 0.33 ± 0.002 (blank control group) to 0.28 ±0.007,but increased that of vimentin from 0.83 ± 0.014 (blank control group) to 1.16 ± 0.003,while BQ788upregulated the E-cadherin expression to 0.42 ± 0.008 and downregulated the vimentin expression to 0.75 ±0.030,and significant differences were observed in the E-cadherin expression and vimentin expression among the ET-3 group,ETRB antagonist group and blank control group (F =329.98,262.94,respectively,both P ＜ 0.01 ).A significant increase was observed in the mRNA and protein expression of Slug (F=376.94,288.87,both P＜ 0.01 )and Twist (F=215.62,156.96,P＜ 0.01 and 0.05) in A375 cells after treatment with ET-3.[Conclusion] ET3/ETRB axis may promote the epithelial-to-mesenchymal transition in A375 cells likely by regulating the expression of E-cadherin,vimentin and two important transcription factors Twist and Slug.