AIM:Toinvestigatetheinteractionofpolymorphismsofintercellularadhesionmolecule-1(ICAM-1) gene K469E and monocyte chemoattractant protein-1 (MCP-1) gene -2518A/G in the invasion and metastasis of gas-tric carcinoma .METHODS:Based on TNM classification , 4 500 patients with confirmed gastric carcinoma from the First Affiliated Hospital of Xinxiang Medical University in China from December 2009 to November 2014 were divided into stageⅠ group, stageⅡgroup, stageⅢgroup, stageⅣgroup, and stage 0 group, with 900 cases in each group.No significant difference among the 5 groups in age, gender, ethnicity, birthplace and living habit was observed .The genetic polymor-phisms of ICAM-1 gene K469E and MCP-1 gene -2518A/G were analyzed by the technique of polymorphism-polymerase chain reaction ( PCR) in peripheral blood leukocytes of above-mentioned cases .RESULTS:Statistical tests showed signi-ficant differences in the frequencies of K469E (EE) and -2518A/G (GG) among each group (P<0.01).The risk of the invasion and metastasis of gastric carcinoma significantly increased in subjects with K 469E ( EE) genotype and in those with -2518A/G (GG) genotype.Combined analysis of the polymorphisms showed that distribution frequency of K 469E (EE)/-2518A/G ( GG) in stage Ⅰ group, stage Ⅱ group, stage Ⅲ group, stage Ⅳ group and stage 0 group was 39.22%, 53.22%, 59.22, 65.44%and 12.11%, respectively (P<0.01).The people who carried with K469E (EE)/-2518A/G ( GG) had a high risk of the invasion and metastasis of gastric carcinoma , and statistical analysis suggested a positive interaction in a super-multiplicative model between K469E (EE) and -2518A/G (GG) in increasing the risk of the invasion and metastasis of gastric carcinoma .CONCLUSION: ICAM-1 gene K469E ( EE) and MCP-1 gene-2518A/G ( GG) are the risk factors in the invasion and metastasis of gastric carcinoma , and significant interactions be-tween genetic polymorphisms of K 469E and -2518A/G added the risk of the invasion and metastasis of gastric carcinoma .

AIM:To investigate the interaction of polymorphisms of resistin gene promoter -420C/G, cyto-chromes P4501A1-MspI and cigarette smoking in nonalcoholic fatty liver disease (NAFLD).METHODS: The genetic polymorphisms in resistin gene promoter -420C/G and CYP1A1-MspI were analyzed by the technique of polymerase chain reaction ( PCR) in peripheral blood leukocytes of 900 NAFLD cases and 900 healthy persons.RESULTS:The frequencies of -420C/G (GG) and CYP1A1-MspI (m2/m2) were 49.75%and 50.08%in NAFLD cases and 24.00%and 24.25%in healthy controls, respectively.Statistical tests showed a significant difference in the frequencies between the 2 groups ( P<0.01).The risk of NAFLD with -420C/G (GG) was significantly higher than that of controls.Individuals who carried with CYP1A1-MspI (m2/m2) had a high risk of NAFLD.Combined analysis of the polymorphisms showed that the per-centages of -420C/G (GG)/CYP1A1-MspI (m2/m2) in NAFLD and control groups were 39.83% and 12.83%, re-spectively (P<0.01).The people who carried with -420C/G (GG)/CYP1A1-MspI(m2/m2) had a high risk in NAFLD group.The cigarette smoking rate in NAFLD group was signi-ficantly higher than that in control group ( P<0.01) , and the statistic analysis suggested an interaction between cigarette smoking and -420C/G (GG) and CYP1A1-MspI (m2/m2), which increased the risk of NAFLD.CONCLUSION: -420C/G (GG), CYP1A1-MspI (m2/m2) and cigarette smoking are the risk factors in NAFLD.The interactions between genetic polymorphisms in -420C/G, CYP1A1-MspI ( m2/m2) and cigarette smoking increase the risk of NAFLD.

ABSTRACT:Objective To explore the expressions of Toll-like receptor4/NF-κB and PI3K/AKT/NF-κB signa-ling pathways in rat ulcerative colitis (UC)induced by the combined enema of trinitrobenzene sulphonic acid and ethano and the interventional effect of electroacupuncture on them.Methods Totally 240 male Wistar rats were randomly divided into 6 groups:normal control group,model control group,electroacupuncture group,TLR4mAb group,LY294002 group,and TLR4mAb combined with LY294002 (T&L)group.The combined enema of trinitro-benzene sulphonic acid (TNB)and ethanol was intrarectally administered for 4 weeks to induce UC.At the same time of modeling ,Zusanli point was electro-acupunctured in electroacupuncture group while intraperitoneal injec-tion of TLR4mAb and LY294002 was given respectively to the corresponding group.Each rat was treated with the above-mentioned TLR4mAb injection and LY294002 injection in T&L group for 4 weeks.The disease activity index (DAI)of all the rats was evaluated daily.The rats were killed after 4 weeks.The colonic mucosa damage index (CMDI)and tissue damage index (TDI)were evaluated by a pathologic grading system.The expressions of P-Akt and active NF-κB protein in the colon mucosa were determined by Western blotting.TLR4 mRNA,PI3K mRNA, AKT mRNA,NF-κB mRNA,TNF-αmRNA and IL-1βmRNA expressions were measured with RT-PCR.Results Compared with those in normal control group,TLR4 mRNA,PI3K mRNA,P-AKT,active NF-κB,TNF-αmRNA and IL-1βmRNA expressions as well as DAI,CMDI and TDI were all increased obviously in model control group (P <0.01).Compared with those in model control group,TLR4mRNA expression was decreased obviously in TLR4mRNA group (P <0.01),the expressions of PI3KmRNA and P-AKT were decreased obviously in LY294002 group (P <0.01 ).Not only TLR4mRNA expression but also PI3KmRNA and P-AKT expressions were decreased significantly in electroacupuncture group and T&L group (P <0.01 ).Corresponding to the above-mentioned chan-ges,active NF-κB,TNF-αmRNA and IL-1βmRNA expressions as well as DAI,CMDI and TDI were decreased obvi-ously in all the treated groups compared with those in model control group (P <0.05 or P <0.01),but the six inde-xes were better in electroacupuncture group and T&L group than in TLR4mAb group and LY294002 group (P <0.05).There were obvious positive correlations of active NF-κB with TNF-αmRNA and IL-1β mRNA expressions (r 1 =0.579,P <0.05;r 2 =0.561,P <0.05).Conclusion Electroacupuncture can significantly decrease NF-κB activity and TNF-αmRNA and IL-1β mRNA expressions in UC rats,thus alleviating the severity of UC,which is closely correlated to its blocking both TLR4/NF-κB and PI3K/AKT/NF-κB signaling pathways.

Functional constipation is one of the most common gastrointestinal diseases. Currently, there is no effective Western medical therapy for functional constipation and it significantly impacts the quality of life of the patients. Integrated traditional Chinese and Western medicine therapies were reported to have better therapeutic effects than routine Western medicine therapies.

Objective To explore the expression of CTGFmRNA and MDA in rats with alcoholic hepatic fibrosis and intervention of Huangqi injection on them.Methods 45 male SD rats were randomly divided into three groups:a normal group,a model group,and a Huangqi injection group.Alcohol was intragastricly administrated for 16 weeks to induce the model of hepatic fibrosis.At the same time of modeling,The Huangqi injection was injected into tail vein of rats in the Huangqi injection group.The rats were killed after 16 weeks.The histomorphylogic structure of the liver tissues were observed under optical microscope;The levels of MDA in liver tissue were determined by radioimmunoassay,and the expressions of connective tissue growth factor(CTGF)mRNA were measured by reverse transcriptase-polymerase chain reaction(RT-PCR).Results Compared with the model group.the destructions and proliferations of collagen fibers were lightened,fiber cords were loosened and narrowed swelling of liver cells and degeneration were alleviated,infiltrating cells got decreased(P＜0.01)in the treated groups;Compared with the model group,the collagen area,the MDA and CTGFmRNA expression in liver tissue were decreased obviously in Huangqi injection group(P＜0.01).The expression level of MDA and CTGFmRNA was positively correlated with collagen area(R_1=0.571,P＜0.05;R_2=0.558,P＜0.05).Conclusion Huangqi injection can protect liver from chronic damage in rats and obviously decrease hepatic fibrosis,which is closely correlated to its inhibiting the expression of CTGFmRNA in liver tissues and anti-lipid peroxidation.

OBJECTIVETo investigate the correlation between drinking behavior and polymorphism combination of extracellular superoxide dismutase (EC-SOD) and aldehyde dehydrogenase 2 (ALDH2) genes and oral squamous cell carcinoma.

METHODSThe genetic polymorphisms of EC-SOD and ALDH2 were analyzed by polymorphism-polymerase chain reaction technique in peripheral blood leukocytes of 750 oral squamous cell carcinoma cases and 750 non-cancer controls.

RESULTSThe frequencies of EC-SOD (C/G) and ALDH2 variant genotypes were 38.27% and 69.47% in oral squamous cell carcinoma cases and 21.07% and 44.40% in healthy controls, respectively. Statistical tests showed significant difference in the frequencies between the two groups (P < 0.01). The risk of oral squamous cell carcinoma with EC-SOD (C/G) was significantly higher than that of controls (OR = 2.32). Individuals carrying ALDH2 variant genotypes had high risk of oral squamous cell carcinoma (OR = 2.85). Combined analysis of the polymorphisms showed that percentages of EC-SOD (C/G)/ALDH2 variant genotypes in oral squamous cell carcinoma and control groups were 30.67% and 6.80%, respectively (P < 0.01). Individuals carrying EC-SOD (C/G)/ALDH2 variant genotypes had high risk of oral squamous cell carcinoma (OR = 8.13). The drinking rate of the case group was significantly higher than that in the control group (OR = 2.70). Statistical analysis suggested an interaction between drinking and EC-SOD (C/G) and ALDH2 variant genotypes, which increase risk of oral squamous cell carcinoma (OR = 25.00).

CONCLUSIONEC-SOD (C/G) and ALDH2 variant genotypes and drinking are the risk factors in oral squamous cell carcinoma, which could carry out a coordinated attack of oral squamous cell carcinoma.

Aldehyde Dehydrogenase ; Carcinoma, Squamous Cell ; Drinking ; Genotype ; Humans ; Male ; Middle Aged ; Mouth Neoplasms ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Risk Factors ; Superoxide Dismutase

Objective To explore the therapeutic effect of Fuzbeng-Liqi mixture on hepatitis resulted from anti-tuberculosis drugs.Methods 100 inpatients of hepatitis resulted from anti-tuberculosis drugs during January 2005 to December 2007 were randomly sorted out into a treatment group and a control group.The treatment group was treated with Fuzbeng-Liqi mixture,and the control group was treated with routine drugs.The effect was analyzed by 2/2 test.Results The therapeutic effect of the treatment group markedly excelled than the control group in terms of symptoms improvement such as nausea or vomit,tiredness,icterus,bepatalgia,or augment of liver.Conclusion Fuzbeng-Liqi mixture was not only able to ameliorate the clinical manifestations of drug-induced hepatitis,but also improve hepatic function.

Objective To investigate the correlation between the combination of smoking with CYP2E1-RsaⅠ and GSTT1 genes polymorphisms and pancreatic cancer. Methods The genetic polymorphisms of CYP2E1-RsaⅠ and GSTT1 were analyzed by polymorphism-polymerase chain reaction (PCR) technique in peripheral blood leukocytes of 150 pancreatic cancer cases and 150 non-cancer controls. Results The frequency of CYP2E1-RsaⅠ(c1/c1) and GSTT1(-) was 38.7% and 69.3% in pancreatic cancer cases and 20.7% and 44.7% in healthy controls, respectively. Statistical tests showed significant differences in the frequencies between the two groups (χ~2=15.75, P<0.01; χ~2=18.62, P<0.01). The risk of pancreatic cancer patients with CYP2E1-RsaⅠ(c1/c1) was significantly higher than that of controls (OR=3.19, 95% CI=2.53-4.26). The individuals who carried with GSTT1(-) had a higher risk of pancreatic cancer (OR=2.85, 95% CI=1.92-4.64). Combined analysis of the polymorphisms showed that the percentage of CYP2E1-RsaⅠ(c1/c1)/GSTT1(-) in pancreatic cancer and control groups was 30.7% and 6.7%, respectively (χ~2= 42.39, P<0.01). People who carried with CYP2E1-RsaⅠ(c1/c1)/GSTT1(-) had a higher risk of pancreatic cancer (OR=16.63, 95% CI=8.94-22.01). The smoking ratewas significantly higher in the case group than in the control group (OR=2.74, 95% CI=1.32-4.58, P<0.01), and statistical analysis suggested an interaction between smoking and CYP2E1-RsaⅠ(c1/c1) or GSTT1(-) genotypes polymorphisms which increased the risk of pancreatic cancer (OR=8.84, 95% CI=5. 51-11.62; OR=20.40, 95% CI=4.98-29.53). Conclusion CYP2E1-RsaⅠ(c1/c1) and GSTT1(-) are the risk factors in pancreatic cancer. Smoking is also related to the susceptibility to pancreatic cancer. There may be a synergetic interaction among CYP2E1-RsaⅠ(c1/c1) and GSTT1(-) and smoking on the elevated susceptibility of pancreatic cancer.

Objective To investigate the correlation between the combination of smoking with CYP2E1-RsaⅠ and GSTT1 genes polymorphisms and pancreatic cancer.Methods The genetic polymorphisms of CYP2E1-RsaⅠ and GSTT1 were analyzed by polymorphism-polymerase chain reaction(PCR) technique in peripheral blood leukocytes of 150 pancreatic cancer cases and 150 non-cancer controls.Results The frequency of CYP2E1-RsaⅠ(c1/c1) and GSTT1(-) was 38.7% and 69.3% in pancreatic cancer cases and 20.7% and 44.7% in healthy controls,respectively.Statistical tests showed significant differences in the frequencies between the two groups(?2=15.75,P

ABSTRACT:Objective To investigate the interaction of polymorphisms of TNF-αgene promoter-308G/A and PPAR-γ2 gene-C34G with acute pancreatitis (AP)and its severity degree.Methods Totally 150 mild acute pancreatitis(MAP),150 moderately severe acute pancreatitis(MSAP)and 150 severe acute pancreatitis(SAP)cases were selected for this study,and 450 healthy persons as control group.The genetic polymorphisms of TNF-αgene promoter-308G/A and PPAR-γ2 gene-C34G were analyzed by the technique of PCR in peripheral blood leukocytes of above-mentioned cases and the results were verified by direct DNA sequencing method.Results The frequencies of -308G/A(GA),-308G/A(AA),-C34G(CG)and-C34G(GG)were 24.00%,26.67%,24.00% and 26.00% in MAP group,34.67%,36.67%,34.00% and 36.67% in MSAP group,42.00%,46.00%,43.33% and 46.00% in SAP group,and 14.44%,14.22%,12.89% and 14.67% in control group,respectively.Statistical tests showed significant difference in the frequencies among each group (all P<0 .0 1 ).The risk of AP significantly increased in subjects with-308G/A(GA),genotype (ORMAP=2.677 6,ORMSAP=6.625 0,ORSAP=21.514 7),in those with-308G/A(AA)genotype (ORMAP=2.570 0,ORMSAP=6.401 8,ORSAP=18.903 4),in those with-C34G(CG) genotype (ORMAP=2.668 4,ORMSAP=6.776 9,ORSAP=22.207 2),and in those with-C34G(GG)genotype (ORMAP=2.633 8,ORMSAP=6.472 5,ORSAP=21.570 2).Combined analysis of the polymorphisms showed that percentage of-308G/A(AA)/-C34G(GG)in MAP,MSAP,SAP and control groups was 7.33%,13.33%,20.67% and 2.00%,respectively,and statistical tests showed significant difference in the frequency among each group (all P<0.01).The people who carried-308G/A(AA)/-C34G(GG)had a high risk of AP (ORMAP=7.284 2,ORMSAP=41.296 1,ORSAP=363.973 6),and statistical analysis suggested a positive interaction between-308G/A(AA)and-C34G(GG)in increasing the risk of AP (γ2MAP=2.114 2,γ4MAP=2.080 0,γ2MSAP=2.108 7,γ4MSAP=2.050 6,γ2SAP=2.138 8,γ4SAP=2.000 1).Likewise,there were also positive interactions in the pathogenesis of AP between-308G/A(GA)and-C34G(GG),-308G/A(GA)and-C34G(CG),-308G/A(AA)and-C34G(CG)(All γ>1). Conclusion These carriers of-308G/A(GA),-308G/A(AA),-C34G(CG)and-C34G(GG)genotypes may have a high risk of developing AP,and significant interactions between genetic polymorphisms of-308G/A and-C34G add the risk of the occurrence and development of AP.