Objective To investigate the change situation of serum pepsinogen (PG) and gastrin-17(G-17) levels change in gastric cancer,and on this basis diagnostic significance of combined detection of carbohydrate antigen 72-4 (CA72-4) and 13C urea breath test (13C UBT) detection in early gastric cancer.Methods The enzyme-linked immunosorbent (ELISA) method was used to detect serum PG Ⅰ,PG Ⅱ and G-17 levels in healthy people,atrophic gastritis group and gastric cancer group.Firstly the changes of above three indicators were compared;then according to PG Ⅰ and G-17,the carcinoma group was divided into the group A,B,C and D,these four groups were detected the helicobacter pylori infection status by 13C UBT.Finally the CA72-4 levels were performed the statistics by using the tumor markers detection results.Results Serum PG Ⅰ level and PG Ⅰ/PG Ⅱ ratio in the control group,atrophic gastritis group and gastric cancer group was gradually declined,the difference was statistically significant (P＜0.05);serum G-17 level in the control group,atrophic gastritis group and gastric cancer group was gradually increased,the difference among 3 groups was statistically significant (P＜0.05);in early gastric cancer rate ratio among 4 groups,which in the group B was highest,the difference was statistically significant (P＜0.05);in the comparison of positive rates of 13 C UBT and CA72-4 level in early gastric cancer among 4 group,the 13 C UBT positive rate and CA72-4 level in the group B were higher than those in the group A,C and D,the differences were statistically significant (P＜0.05).Moreover the CA72-4 level in the group B had significant difference between early gastric cancer and advanced gastric cancer (P＜0.01).Conclusion Serum PG Ⅰ reduce and G-17 increase combined with CA72-4 high level and 13C UBT positive have an important forewarning value for the diagnosis of gastric cancer.

BACKGROUND: Research on mapping the gene for benign familial infantile convulsion(BFIC) has been conducted mainly in western countries. Although three chromosome loci have been found by three research groups, up to now the gene responsible for BFIC has been neither found nor identified. Mapping the gene and studying locus heterogeneity is the first step toward cloning the disease gene.OBJECTIVE: To explore the relation between BFIC loci and the gene for BFIC in five Chinese pedigrees with BFIC. Locus heterogeneity among these pedigrees will be revealed based on the findings so as to further map the gene.DESIGN: Retrospective and observational controlled study using five Chinese pedigrees with BFIC as subjects.SETTING: Laboratory of cell biology and medical genetics in a university.PARTICIPANTS: The study was conducted in the Laboratory of Cell Biology and Medical Genetics of Zhengzhou University from July 2001 to July 2003. Five BFIC pedigrees of 70 subjects, 28 BFIC patients and 42 non-BFIC patients, from Xinxiang, Nanyang, Zhoukou, and Hebi of Henan Province,China, were involved. Inclusion criteria: Those met the epileptic seizure classification criteria issued by the International Anti-epilepsy Commissi6n[2].Exclusion criteria: The patients were excluded from the group of the affected members if any of the three examinations, namely, interictal electroencephalograms, computed-tomography scanning and magnetic-resonance imagining, was abnormal. The same exclusion criteria applied to patients who had suffered either toxicosis or cerebral damage.METHODS: To get the genotypes of these family members, such techniques as polymerase chain reaction, polyacrlamide and agarose gels electrophresis and sliver straining were used. The procedure was as follows: first, DNA was extracted from the peripheral blood of the members of five pedigrees with BFIC. Then, six short tandem repeat(STR) loci, namely, D19S245,D19S250, D16S3131, D16S3133, D2S399 and D2S2330, were used to detect genotype of each family member, followed by input of the genotypes into the computer and linkage analysis by MLINK program from LINKAGE package. Finally, the results of linkage analysis were analyzed by HOMOGM program and locus heterogeneity was obtained.MAIN OUTCOME MEASURES: Analysis results of genotype of each subject and the results of heterogeneity detection.RESULTS: One maximum two-point limit of detection (LOD) score of 2. 151 for D19S250 was obtained at recombination rate of 0. 000 under autosomal dominant model with 90% penetrance. For D16S3131, two maximum two-point LOD scores of 1. 056 and 1. 155 were obtained at recombination rate of 0. 085 under autosomal dominant model with 70% and 60% penetrance. This suggested that the gene for BFIC pedigree might be linked to D16S3131 or D19S250. At the other DNA markers, no information suggested that linkage was produced. The results of heterogeneity detection showed that there was locus heterogeneity among the BFIC pedigrees.CONCLUSION: The gene for BFIC may be linked to D16S3131 or D19S250. Heterogeneity exists in BFIC, which serves as primary information for the further study of mapping the disease gene for BFIC.

Objective To explore the relationship between NAT2 genetic polymorphism and the risk of colorectal cancer. Methods A hospital-based case-control study was conducted and polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method was used to detect its genotypes.Results The frequency of NAT2 slow genotype was 19.58% in cases with colorectal cancer compared.with increased the risk for developing colorectal cancer and their OR were 2.16(95% CI:1.31～3.54).Conclusion The results suggest that NAT2 genetic polymorphism is associated with colorectal canoer susceptibility.People with NAT2 slow genotype have higher coloreetal cancer risk.