RÉSUMÉ
Objective To explore the relationship between NF-kB1-94ins/delATTG gene polymorphism and acute progressive cerebral infarction(APCD ofChinese Hart population in Qingdaodistrict Methods We detected the polymorphism of NF-κB1 -94ins/delA TTG gene in 100 patients with acute cerebral infarction (ACI group) and 99 patients with acute progressive cerebral infarction (APCI group) by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP)analysis. The changes of expression of NF-κBp65 in PBMC cellular nucleus in the 2 groups were detected by cell immunohistochemistry. Results The frequency of TT genetype and T allele in the APCI group was significantly higher than that in the ACI group (P<0.05). Analysis on the relative risk of allele frequency showed that patients with T allele had 1.622 times of risk in having APCI than patients with C allele; logistic regressive analysis indicated that NF-κB1 TT genotype was independently related to the attacking of APCI (OR=2.14, 95% CI: 2.654-8.296, P<0.05). The expressions of NF-κBp65 of PBMC cellular nucleus of TT genotypic individuals in APCI group were significantly higher than those in ACI group (P<0.05); logistic regressive analysis indicated that the expressions of NF-KBp65 in PBMC cellular nucleus of TT genotypic individuals were independently related to the attacking of APCI (OR=1.96; 95% CI: 2.267-7.691; P<0.05). Conclusion The NF-κB1 gene polymorphism might participate in the onset of APCI and T allele of NF-κB1 gene might be a genetic risk factor of getting APCI for Chinese Han populations in Qingdao district. The NF-κB1 T allele carrier might increase the happening of APCI through up regulating the expression of NF-kB1.
RÉSUMÉ
Objective: To explore the association between polymorphisms of NF-κBl and NF-κBIα and the risk of hepatitis B virus-associated heptocellular carcinoma (HCC). Methods: The genetic polymorphisms of NF-κBl and NF-κBIα were detected using restriction fragment length polymorphism-polymerase chain reaction (RFLP-PCR) in patients with the hepatitis B virus-associated HCC, patients with chronic hepatitis B and healthy controls. Multivariate Logistic regression model was used to assess the association of the age, sex, smoking history, alcohol drinking, and site of genetic polymorphisms with the susceptibility to HCC. Results: The frequency of NF-κBl (ATTG2/ATTG2) genotype was significantly higher in HCC group than in healthy controls (odd ratio [OR] = 2.21, 95% CI 1.25-3.88). Compared to the people who carried NF-κBl (ATTG1/ATTG1) and NF-κBIα (AA) genotype spontaneously, healthy controls who carried NF-κBl (ATTG2/ATTG2) and NF-κBIα (GG) genotype had an increased risk for HCC (OR=2.94, 95%, CI 1.03-8.44). Chronic hepatitis B patients who carried NF-κBl (ATTG2/ATTG2) genotype had an increased risk for HCC (OR = 2.31, 95% CI 1.22-4.38). Multivariate analysis showed increased risk in male HCC patients with chronic hepatitis B (OR = 2.01, 95% CI 1.19-3.41), in those who carried NF-κBl (ATTG2/ATTG2) genotype (OR = 2.17, 95% CI 1.23-3.85), in those who had a smoking history (OR = 1.79, 95% CI 1.04-3.07), and in those who had a drinking history (OR = 2.58, 95% CI 1.50-4.43). Conclusion: Genotype NF-κBl (ATTG2/ATTG2) is a risk factor of HCC, and it has a synergistic effect with NF-κBI(GG) genotype in contributing to hepatocarcinogenesis. Smoking and alcohol drinking are also risk factors for HCC.