Extract of Ground Beetle was found to affect rat rheology. when given orally to rats for 10 consecutive days, it resulted in the lowering of packed corpuscular volume, high and low whole blood shear viscosity, RBC aggregation and rigidity indices and sedimentation rate,but the constant of SR equation was raised and without effect on Plasma viscosity and fibrinogen content. These results suggested that the effect of ground beetle extract is by way of its action on RBC

Objective To explore the role of genetic factors in development of esophageal cancer by studying the association of XRCC1,P53 and COX-2 genetic polymorphisms with susceptibility of esophageal cancer in Hakka population. Methods A case-control study was performed with molecular epidemiological methods. A total of 122 patients with esophageal cancer(esophageal cancer group)and 123 healthy people(control group) were randomly selected from Hakka people in Meizhou area. The genotypes and alleles of XRCC1 rs25487,P53 rs1042522,and COX-2 rs689466 in both groups were detected,and the distribution characteristics were analyzed. Results The polymorphisms of XRCC1 rs25487(A/G),P53 rs1042522(C/G)and COX-2 rs689466(A/G)were found in Hakkan people in Meizhou area ,but there were no significant differences in the genotype and allele fre-quencies between the two groups. And after such as sex,age,stratified analysis showed also no significant results. Conclusions The study shows that the genetic polymorphisms of XRCC1 gene rs25487,P53 gene rs1042522 and COX-2 gene rs689466 are possibly not related with the susceptibility of esophageal cancer in Hakka population in Meizhou area.

BACKGROUNDHerpes simplex virus thymidine kinase phosphorylates ganciclovir to ganciclovir monophosphate, which is then converted to ganciclovir triphosphate by endogenous cellular nucleoside kinases. The ganciclovir triphosphate acts as a DNA chain terminator due to the lack of a functional 3'-OH group and terminates the process of DNA replication, hence leading to cell apoptosis. At present, HSVtk gene usually acts as suicide gene to kill tumor cells. The aim of this study was to investigate the selective cytotoxicity of the herpes simplex virus thymidine kinase/ganciclovir (HSVtK/GCV) suicide gene system controlled by the a-fetoprotein (AFP) promoter on hepatocellular carcinoma (HCC) cells in vitro.

METHODSpAFP-HSVtk-IRES2-EGFP recombinant plasmid vectors driven by the AFP promoter were constructed. HL-7702 liver cells, HUH-7 HCC, and HepG2 HCC were transfected with the recombinant plasmids. HSVtK gene expression was detected using Western blotting analysis. HepG2 cells line stably expressing HSVtk gene was selected by G418 reagent. The cytotoxicity of HSVtK/GCV suicide gene system on hepatoma cells was measured by CCK-8 reagents when different doses of ganciclovir were added.

RESULTSPlasmid pAFP-TK-IRES2-EGFP-expressed HSVtk gene was constructed successfully. HSVtk gene expression level was significantly higher in AFP-positive hepatoma cells than in AFP-negative liver cells. After G418 selection, a HepG2 cells line stably expressing HSVtk gene was acquired. With the increase of the dose of ganciclovir the optical density at 450 nm of HepG2 cells stably expressing HSVtk gene gradually decreased (P < 0.05).

CONCLUSIONThe HSVtK gene-specific expression in hepatoma cells as well as the cytotoxicity of the suicide gene system in HepG2 cells provided the basis for the targeted gene therapy of HCC.

Apoptosis ; drug effects ; genetics ; Carcinoma, Hepatocellular ; genetics ; Cell Line, Tumor ; Fetal Proteins ; genetics ; Ganciclovir ; analogs & derivatives ; pharmacology ; Hep G2 Cells ; Humans ; Liver Neoplasms ; genetics ; Promoter Regions, Genetic ; genetics ; Transfection