Risk Factors for Adverse Pregnancy Outcomes among Zhuang Ethnic Pregnant Women: A Cohort Study in Guangxi, China.

Risk factors for adverse pregnancy outcomes among Zhuang ethnic pregnant women are unclear. This study analyzed the incidence and risk factors related to preterm birth (PB), low birth weight (LBW) and macrosomia in Zhuang population. We conducted a prospective cohort study of 9965 Zhuang pregnancy women in Guangxi, China. Information on mothers and newborns was obtained by using questionnaires and referring to medical records. Multivariate logistic regression analyses were used to evaluate the association between related factors and adverse pregnancy outcomes. Our results showed that the incidence of PB, LBW and macrosomia in Zhuang people was 5.55%, 5.64% and 2.19%, respectively. Maternal age ≥36 years (OR=2.22, 95% CI: 1.51-3.27) was related to a higher incidence of PB. Those with pre-pregnancy body mass index (BMI) <18.5 kg/m2 (OR=1.91, 95% CI: 1.45-2.51), and had a female fetus (OR=1.74, 95% CI: 1.36-2.23) were more likely to have LBW infants. Maternal age between 31 and 35 years (OR=1.76, 95% CI: 1.03-2.99) and pre-pregnancy overweight or obesity (OR=1.79, 95% CI: 1.15-2.80) were associated with a higher risk of macrosomia. The protective factors of macrosomia were maternal pre-pregnancy BMI <18.5 kg/m2 (OR=0.30, 95% CI: 0.15-0.60) and female fetus (OR=0.41, 95% CI: 0.28-0.59). Our study provided a reference for maternal and childcare administration among Zhuang population.

Genetic variants of cell cycle pathway genes predict disease-free survival of hepatocellular carcinoma.

Disruption of the cell cycle pathway has previously been related to development of human cancers. However, associations between genetic variants of cell cycle pathway genes and prognosis of hepatocellular carcinoma (HCC) remain largely unknown. In this study, we evaluated the associations between 24 potential functional single nucleotide polymorphisms (SNPs) of 16 main cell cycle pathway genes and disease-free survival (DFS) of 271 HCC patients who had undergone radical surgery resection. We identified two SNPs, i.e., SMAD3 rs11556090 A>G and RBL2 rs3929G>C, that were independently predictive of DFS in an additive genetic model with false-positive report probability (FPRP) <0.2. The SMAD3 rs11556090G allele was associated with a poorer DFS, compared with the A allele [hazard ratio (HR) = 1.46, 95% confidential interval (95% CI) = 1.13-1.89, P = 0.004]; while the RBL2 rs3929 C allele was associated with a superior DFS, compared with the G allele (HR = 0.74, 95% CI = 0.57-0.96, P = 0.023). Additionally, patients with an increasing number of unfavorable genotypes (NUGs) of these loci had a significant shorter DFS (Ptrend  = 0.0001). Further analysis using receiver operating characteristic (ROC) curves showed that the model including the NUGs and known prognostic clinical variables demonstrated a significant improvement in predicting the 1-year DFS (P = 0.011). Moreover, the RBL2 rs3929 C allele was significantly associated with increased mRNA expression levels of RBL2 in liver tissue (P = 1.8 × 10-7 ) and the whole blood (P = 3.9 × 10-14 ). Our data demonstrated an independent or a joint effect of SMAD3 rs11556090 and RBL2 rs3929 in the cell cycle pathway on DFS of HCC, which need to be validated by large cohort and biological studies.

Combined effects of six cytokine gene polymorphisms and SNP-SNP interactions on hepatocellular carcinoma risk in Southern Guangxi, China.

Cytokine gene single nucleotide polymorphisms (SNPs) are involved in the genesis and progression of hepatocellular carcinoma (HCC). We hypothesized that combined effects of cytokine gene SNPs and SNP-SNP interactions are associated with HCC risk. Six SNPs in cytokine genes (IL-2, IFN-γ, IL-1ß, IL-6, and IL-10) were genotyped in a study of 720 Chinese HCC cases and 784 cancer-free controls. Although none of these SNPs individually had a significant effect on the risk of HCC, we found that the combined effects of these six SNPs may contribute to HCC risk (OR=1.821, 95% CI=1.078-3.075). This risk was pronounced among smokers, drinkers, and hepatitis B virus carriers. A SNP-SNP interaction between IL-2-330 and IFN-γ-1615 was associated with an increased HCC risk (OR=1.078, 95% CI=1.022-1.136). In conclusion, combined effects of SNPs and SNP-SNP interactions in cytokine genes may contribute to HCC risk.

Assessment of the platelet parameters and serum butyrylcholinesterase activity in type 1 diabetes patients with ketoacidosis.

The potential roles of serum butyrylcholinesterase (BChE) activity and platelet indices in type 1 diabetes (T1D) remain uncertain. We aimed to investigate the correlation among the platelet indices, serum BChE activity, and diabetic ketoacidosis (DKA). Sixty-one T1D patients, 29 patients with DKA, and 30 age- and sex-matched controls were enrolled. Mean platelet volume (MPV), platelet distribution width (PDW), and serum BChE activity were measured and evaluated at admission and after the treatment. The serum BChE activity was significantly lower in patients with DKA at admission to the hospital compared with non-DKA and control subjects; however, plasma glucose level, HbA1c level, MPV and PDW were significantly higher. Serum BChE activity, variables related to glycemic control, and platelet parameters were higher in non-DKA patients than in controls. Serum BChE activity was correlated with the serum HCO3 level (r = 0.375, p < 0.05) and plasma glucose level (r = -0.387, p < 0.05). Receiver operating characteristic curve analyses showed no difference between serum BChE activity and the platelet parameters with respect to the ability to reflect DKA. Logistic regression showed that increased PDW can act as a risk marker for the presence of DKA. Serum BChE activity and the platelet parameters returned to normal along with the plasma glucose levels when metabolic acidosis was well controlled. Serum BChE activity and the platelet parameters were significantly correlated with DKA. Measurement of PDW can provide complementary information and a risk biomarker reflecting the presence of DKA.

[Relationship between hepatocellular carcinoma and the interaction between NQO1 polymorphisms and environmental factors].

OBJECTIVE: To study the relationship between hepatocellular carcinoma (HCC) and the interaction of polymorphisms in the NAD(P)H:quinone oxidoreductase (NQO1) gene with environmental factors using a hospital-based case-control study. FMETHODS: our-hundred newly diagnosed HCC cases and 400 healthy individuals (non-tumor controls) were enrolled in the study. Demographic information and medical history was obtained by questionnaire. TaqMan minor groove binder real-time PCR was carried out to detect the NQO1 C609T genotype using blood-derived DNA from all study participants. Unconditional logistic regression analysis was carried out to estimate the odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: The frequencies of NQO1 609 CC, CT and TT genotypes were 23.75%, 50.25% and 28.00% in the HCC group, and 37.55%, 43.75% and 18.25% in the control group. The differences between the HCC and control group reached statistical significance (all P less than 0.05). The ORs of NQO1 609 CT and TT genotypes were significantly higher compared to the CC genotype; the adjusted OR(95% CI) of CT was 2.106(1.137-3.110) and of TT was 2.564(1.357-4.744). Individuals carrying the NQO1 609 T allelic gene had a significantly higher risk of HCC than those carrying the C allelic gene; the adjusted OR(95% CI) was 1.86(1.235-2.980). Interactions were found between hepatitis B virus infection with hepatitis B surface antigen (HBsAg)-positivity and NQO1 gene polymorphisms (adjusted OR: 2.431) and history of cancer (adjusted OR: 8.3592). CONCLUSION: The NQO1 C609T genotype is associated with increased risk of HCC. Interactions between HBsAg-positive infection, history of cancer, and NQO1 gene polymorphisms may contribute to HCC.

[Relationship between IL6 -572G/C polymorphism and hepatocellular carcinoma in men].

To study the relationship between the interleukin (IL)6 -572G/C polymorphism and risk of hepatocellular carcinoma (HCC) in men.A hospital-based case-control study was conducted with 500 male HCC patients without tumor history in other organs and 590 healthy male controls without history of tumors or chronic diseases. All HCC cases were diagnosed by histopathology. The controls were recruited from the Department of Orthopedic Trauma and Ophthalmology at the same hospital. The IL-6 promoter -572G/C polymorphism and its genotype variants were detected by real-time fluorescence quantitative PCR. The Chi-squared test and unconditional logistic regression analyses were applied to determine the risk of HCC among men carrying the different genotype variants.The frequencies of alleles and distribution of genotypes in the -572G/C loci were not significantly different between the HCC cases and controls (P more than 0.05). The Chi-squared test indicated that the polymorphisms of the loci were not associated with HCC in our male population. However, after adjusting by multivariate logistic regression, the odds ratio (OR) of HCC for the G allele (CG + GG genotypes) carriers was 1.31 (95% confidence interval (CI): 1.00 - 1.71) compared with the CC genotype. Among the male HBV carriers, the CG genotype increased HCC risk significantly (OR = 1.60, 95% CI: 1.14 - 2.24) compared with the CC genotype. A trend test indicated that HCC risk was significantly increased with the numbers of G alleles (P trend less than 0.05). Breslow-Day tests of homogeneity of the ORs indicated an interaction between hepatitis B virus (HBV) infection and polymorphisms of IL-6 (P less than 0.05). The synthetic odds ratio (OReg) of HBV infection and harboring a G allele was 5.95 (95% CI: 3.99-8.87), which represented a super multiplication interaction.Polymorphism of the IL-6 promoter -572 loci may be associated with HCC occurrence in men. Moreover, there is a super multiplication interaction for HCC risk between HBV infection and harboring the IL-6 G allele.

[Correlation between polymorphism of sex hormone binding globulin and occurrence of hepatocellular carcinoma].

OBJECTIVE: This study aims to investigate the correlation between polymorphism of sex hormone-binding globulin (SHBG) Asp327Asn (rs6259) locus and occurrence of hepatocellular carcinoma (HCC). METHODS: 621 cases with HCC and 621 cancer-free controls from two hospitals of Guangxi were recruited from January, 2007 to June, 2010. Single nucleotide polymorphisms (SNP) of SHBG Asp327Asn were detected by ABI7500 Fast Real-Time fluorescence quantitative PCR. Multivariate unconditional logistic regression was applied to analyze risk of HCC among different genotypes carriers and their interaction with the exposure factors. The Kaplan-Meier survival analysis was used to detect the relationship between onset age of HCC and genotypes. RESULTS: The frequencies of Asp/Asp, Asp/Asn and Asn/Asn genotype in case group were 86.31% (536/621), 12.40% (77/621) and 1.29% (8/621), respectively; while those in control group were 81.00% (503/621), 17.39% (108/621) and 1.61% (10/621), respectively. Significant difference in the genotype frequencies distribution was found between case and control groups (χ2=6.465, P<0.05). Compared with those harboring Asp/Asp genotype, multivariate logistic regression analysis revealed that the HCC risk of Asn/Asn+Asp/Asn genotype carriers was significantly decreased (adjusted OR=0.63, 95%CI: 0.40-0.98). Interaction analysis showed that there was interaction between the polymorphisms and two exposure factors, drinking (adjusted OR=3.45, 95%CI: 1.74-6.83) and HBV infection (adjusted OR=40.77, 95%CI: 21.60-76.97). Among those male patients with history of drinking, survival analysis indicated that the mean age of onset of individuals harboring Asp/Asp genotypes ((47.99±0.75) years-old) was 6 years earlier than those with Asn/Asn or Asp/Asn genotypes ((53.68±2.07) years-old) (χ2=6.91, P<0.01). CONCLUSION: Polymorphism of SHBG (Asp327Asn) may be associated with both the risk of HCC occurrence and onset age of HCC.

TNF-α -863 polymorphisms and the risk of hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is a common type of highly malignant tumor. Guangxi is an area of China characterized by a high incidence of HCC. Previous epidemiological studies have found that chronic infection with hepatitis B virus (HBV) is one of the major etiological risk factors for HCC in China. With the increased understanding of the host immune response against HBV and the pathogenesis of the virus, at present, greater attention is being given to the immune response of cytokine genes, as polymorphisms may have a major impact on the course and outcome of HBV infection. In the present study, we genotyped tumor necrosis factor-α (TNF-α) rs1800629 (-308G/A), rs1800630 (-863C/A); interleukin-1B rs1143627 (-31T/C); and transforming growth factor ß1 (TGF-ß1) rs1800469 (-509C/T) in a hospital-based study of 772 HCC cases and 852 cancer-free controls. The distribution of the frequency of TNF-α rs1800630 sites of CC, CA, AA were 65.67, 27.46 and 6.87% in the case group, respectively, as compared with 67.02, 29.58 and 3.40% in the controls, all with a statistical significance (P<0.05). The logistic regression analysis revealed that the variant rs1800630 AA genotypes were associated with a significantly increasing risk of HCC (OR=2.058, 95% CI 1.289-3.287), compared with the wild-type rs1800630 CC. Further stratified analyses showed that after stratification for history of alcohol drinking, in a subgroup of individuals without a history of drinking, the HCC risk in the group with the TNF-α rs1800630 A allele was 1.839 times higher than that in the group with TNF-α rs1800630 C (P<0.010). These findings suggest that TNF-α rs1800630 may contribute to the risk of HCC, however, these data require further validation.

[Study on the relationship between single-nucleotide polymorphisms in IL-6, IL-10 genes and HBV-related hepatocellular carcinoma].

OBJECTIVE: To investigate the association between single nucleotide polymorphisms (SNPs) in cytokine IL-6, IL-10 genes and HBV-related hepatocellular carcinoma (HCC). METHODS: A hospital-based case-control study was conducted in 381 cases with HBV-related HCC, 340 HBsAg carriers and 359 non-tumor controls. Genotypes of -572 site of IL-6 gene and -819, -592 sites of IL-10 gene were determined by real-time polymorphism chain reaction. Unconditional logistic regression was used to estimate the odds ratios (ORs) and 95 confidence intervals (CIs). RESULTS: For the G/C alleles of -572 loci on IL-6 gene, there were significant differences between the three groups (P < 0.05). Compared with CC genotype, GG genotype increased the risk of HBV infection (OR = 2.171, 95%CI: 1.068 - 4.415), but did not seem to be associated with HCC. For the alleles of -819 and -592 site of IL-10 gene, there were significant differences between the three groups (P < 0.05). Compared with CC genotype, TT genotype increased the risks of both HCC (OR = 2.791, 95%CI: 1.326 - 5.874), and HCC in HBsAg carriers (OR = 3.522, 95%CI: 1.707 - 7.266). When compared with CC genotype on -592 site, the AA genotype reduced the risk of both HCC (OR = 0.389, 95%CI: 0.173 - 0.875), and HCC in HBsAg carriers (OR = 0.336, 95%CI: 0.154 - 0.734). CONCLUSION: The SNPs in -572 site of IL-6 gene might be associated with the risk of HBV infection. The SNPs in -819 site of IL-10 gene increased the risk of HCC, but -592 site of IL-10 gene decreased the risk of HCC.

[On-site assessment on the definition and classification of suspected cases in the manual of WHO Japanese Encephalitis Surveillance Standards].

OBJECTIVE: To assess the new edition of WHO Japanese Encephalitis (JE) Surveillance Standards (WHO Standards) based on syndrome surveillance data and to provide field evidence regarding the standards. METHODS: Based on syndrome surveillance data, acute encephalitis syndrome (AES) case was categorized, according to the WHO Standards. A cohort study was applied to estimate the AES definition set in the Standard and relative risk was computed to estimate the existence and intensity of statistical correlation between AES and JE cases. Percentage of attributable risk was counted to describe the coverage of AES for JE cases in the studied population. Sensitivity, specificity, Youden index and positive predictive value of AES components were calculated for the purpose of identifying the clinical values under the screening program. RESULTS: 1424 suspected cases were evaluated in the surveillance program and 1396 cases with ELISA result, of which 109 positive cases were detected. According to the "standardized" classification, a total of 706 cases in line with AES case definition, were categorized into 83 cases of JE, 425 cases of AES unknown and 198 cases of AES other agent. In the cohort study, a relative risk of 4.62 (95%CI: 2.80 - 7.63) and the percentage of attributable risk as 78.35% (95%CI: 64.25% - 86.89%) were observed. CONCLUSION: The AES definition for JE was significantly effecting on the screening programs and a strong correlation strength was observed in the study. AES syndrome could cover most of the JE cases. "Convulsions", with appreciative screening value, was recommended to be involved into the new version of the WHO Standards.

[Association of XPC and XPG polymorphisms with the risk of hepatocellular carcinoma].

OBJECTIVE: To investigate whether the polymorphism of DNA repair genes XPC (Ala499Val and Lys939Gln) and XPG (His1104Asp) is associated with the susceptibility to hepatocellular carcinoma (HCC). METHODS: A hospital-based case-control study was conducted in 500 cases with HCC and 507 controls. Genotypes of XPC and XPG were determined by real-time polymerase chain reaction with the TaqMan MGB probe. RESULTS: Compared to the CC genotype, the CT genotype and the TT genotype of XPC Ala499Val were not associated with the susceptibility to HCC (adjusted OR = 1.34, 95% CI: 0.85-2.12; adjusted OR = 1.30, 95% CI: 0.68-2.51, respectively). Compared to the AA genotype, the AC genotype and the CC genotype of Lys939Gln were not associated with the susceptibility to HCC (adjusted OR = 1.20, 95% CI: 0.78-1.85; adjusted OR = 1.81, 95% CI: 0.88-3.73, respectively). Compared to the CC genotype, the CG genotype and the GG genotype of XPG His1104Asp were not associated with the susceptibility to HCC (adjusted OR = 0.85, 95% CI: 0.56-1.27; adjusted OR = 1.12, 95% CI: 0.67-1.87, respectively) However, the stratified analysis revealed that the females with the AC+CC genotype of XPC Lys939Gln had increased risk of HCC compared to those with AA genotype (OR = 2.17, 95% CI: 1.01-4.64). CONCLUSION: Our results suggest that XPC and XPG polymorphisms do not independently affect on the susceptibility to HCC, but the joint effect of C allele of XPC Lys939Gln and female may modify the risk of HCC.

[Study on the relationship between hepatocellular carcinoma and the interaction between polymorphisms in DNA repair gene XPD and environmental factors].

OBJECTIVE: To study the relationship between hepatocellular carcinoma and the interaction of polymorphisms in DNA repair gene XPD with environmental factors. METHODS: A hospital-based case-control study on hepatocellular carcinoma was conducted. All the hepatocellular carcinoma cases (n=300) were newly diagnosed and controls (n=312) were diagnosed with non-tumor cases. XPD genotype (Lys751 Gln and Asp312 Asn) from blood derived DNA was determined using TaqMan MGB Real-time PCR. Unconditional logistic regression was used to estimate the odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: For XPD condon 751 genotypes, there was no significant difference between frequencies of the AC or CC among patients and controls (P>0.05) (referent AA). The frequency of XPD312A allelic gene was higher in cases than that in controls and was associated with an increased risk (adjusted OR=2.62, 95% CI: 1.626-4.222) for hepatocellular carcinoma when compared with GG genotype. Interactions were found between infection of HBsAg and XPD312 (OR=7.348), as well as between smoking and non-wild type gene of XPD751 (OR=4.291) and XPD312 (OR=5.341). CONCLUSION: DNA repair XPD312A allelic gene might increase the risk of Hepatocellular carcinoma. Interactions between HBsAg infection, smoking and XPD were observed in Hepatocellular carcinoma.

In vitro toxicity of surface water disinfected by different sequential treatments.

The in vitro toxicity of extracts of Hanjiang water disinfected by different sequential treatments was evaluated. Hanjiang water was disinfected using ozone, chloride dioxide or chlorine as the primary disinfectant followed by chlorine as the secondary disinfectant. HepG(2) cells were exposed to extracts corresponding to concentrations of 0.2, 1, 5, 25 and 125 mL water/mL medium. Compared with control, HepG(2) cells exposed to extracts of raw water and all disinfected water for 24h increased oxidative stress level, DNA damage and micronuclei frequency, and decreased cell viability. Water disinfected by Cl(2)+Cl(2) had the highest DNA double-strand breaks. All disinfected water and raw water increased micronuclei frequency via clastogenic and aneugenic effects. Oxidative stress induced DNA strand breaks and micronuclei frequency and therefore reduced cell viability either in disinfected water or raw water. Compared with raw water, water after disinfection increased DNA strand breaks, decreased cell viability and changed oxidative stress potential. Compared with chlorination, sequential treatment using O(3) or ClO(2) as primary disinfectant followed by chlorine disinfection reduced chlorinated by-products, DNA double-strand breaks and cell viability, but did not decrease micronuclei frequency and other DNA damage such as DNA single-strand break, alkali liable sites and incomplete excision sites. Sequential treatments did not significantly reduce in vivo toxicity of disinfected Hanjiang water.

[Study on the incidence of beta-Thalassemia and genotypes among children under 7 year-olds in Nanning, Liuzhou and Baise areas, Guangxi province].

OBJECTIVE: To conduct research of beta-Thalassemia incidence and genotypes on children below 7 years of age in Nanning, Liuzhou and Baise areas, Guangxi province. METHODS: A total of 2261 children aged below 7 in Nanning, Liuzhou and Baise areas were studied. Venous blood was detected by routine blood test, hemoglobin analysis and beta-Thalassemia genotyping. RESULTS: Among 2261 samples, 125 showed high level of HbA2 and were diagnosed as beta-Thalassemia (5.53%). Genotypes of the patients were classified as: 59 cases with beta-globin gene condon (CD) 41-42 mutation, 33 cases CD17 mutation, 18 cases with TA TA box nt-28 mutation, 7 with IVS-II-654 mutation, 3 with CD43 mutation, 3 with HbE mutation, one with CD71-72 and TATA box nt-29 mutation, respectively. The genotyping frequencies of beta-Thalassemia were as follows: 47.20% for CD41-42 mutation, 26.40% for CD17 mutation, 14.40% for TATAbox nt-28 mutation, 5.60% for IVS-II-654 mutation, 2.40% for CD43 mutation, 2.40% for HbE mutation, 0.80% for CD71-72 mutation and TATAbox nt-29 mutation respectively. CONCLUSION: This study on children in the area with high incidence of beta-Thalassemia reflected the incidence and characteristics of genotypes in this area. Our data also provided evidence for the development of a program on genetic counseling and prevention for thalassemia.

[Etiologic fraction and interaction of risk factors for primary hepatic carcinoma in Guangxi, China].

OBJECTIVE: To explore etiologic fraction (EF) and interaction of hepatitis B virus (HBV) infection and other risk factors for primary hepatocellular carcinoma (PHC) in Guangxi, China. METHODS: A hospital-based case-control study including 500 PHC patients and 500 nontumorous patients was carried out in Guangxi. EF and interactions of HBV infection and other risk factors for PHC were analyzed by crossover analysis and nonconditional multiple logistic regression. RESULTS: HBV infection, family history of PHC, diabetes mellitus, eating raw fish, heavy alcohol consumption, frequently used drug, low income, mental oppression and blood type B all were risk factors for PHC. With EFs of 0.725, 0.186, 0.119, 0.486, 0.385, 0.438, 0.277, 0.607, 0.299, respectively and with etiologic fractions attributable to interaction [EF(A xB)] of 0.736, 0.643, 0.849, 0.551, 0.592, 0.618, 0.902, 0.577; and indices of interaction of 0.743, 0.651, 0.853, 0.560, 0.600, 0.626, 0.907, 0.586, respectively. CONCLUSION: Main risk factors for PHC might include HBV infection, family history of PHC, diabetes mellitus, eating raw fish, heavy alcohol consumption, frequently used drug, low income, mental oppression and blood type B. HBV infection with other risk factors might exert synergistic action on developing PHC and increase the risk of PHC.

[Synergistic effect of HBV infection, alcohol and raw fish consumption on oncogenisis of primary hepatic carcinoma].

OBJECTIVE: To study the correlation of eating raw fish with primary hepatic carcinoma (PHC), and to investigate the synergistic effect of HBV infection, alcohol consumption and eating raw fish on the oncogenesis of PHC. METHODS: A hospital-based case-control study was conducted among 500 PHC patients and 500 non-cancerous patients in order to compare the history of eating raw fish. The synergistic pathogenetic action of eating raw fish, HBV infection and alcohol consumption on carcinogenesis of PHC was analyzed by crossover analysis and multiple logistic regression. RESULTS: The rates of eating raw fish in the past between the case (54.8%) and the control group (8.4%) were significantly different (P < 0.001). OR value of suffering PHC in the patients who ate raw fish in the past was 13.6 (95% CI: 9.1-19.5) when compared with the non-cancerous patient. HBV infection, alcohol consumption and eating raw fish showed an interactive effect on the development of PHC, with a relative excessive risk of interaction(RERI) of 195.3 and 17.8; attributable proportion of interaction (API) of 0.8630 and 0.5251; and synergy index (S) of 7.5 and 2.8, respectively. CONCLUSION: A history of eating raw fish may be an important risk factor for suffering primary hepatic carcinoma. HBV infection, alcohol consumption and eating raw fish may have a synergistic effect on the developing of primary hepatic carcinoma.

[Evaluation of the risk of clonorchiasis inducing primary hepatocellular carcinoma].

OBJECTIVE: To explore the relationship between clonorchiasis and primary hepatocellular carcinoma (HCC) and analyze the synergistic actions of HBV infection, alcohol consumption and clonorchiasis on HCC development. METHODS: This hospital-based case-control study was conducted among 444 HCC patients (cases) and 500 non tumor patients (controls) to compare the prevalence of clonorchiasis in the cases and the controls. The risk of clonorchiasis and the synergistic actions between HBV infection, alcohol consumption and clonorchiasis on HCC development were analyzed by crossover analysis and multiple logistic regression. RESULTS: The prevalence of clonorchiasis in the cases (16.44%) was much higher than that of the controls (2.40%) (X2 = 56.58, P less than 0.01). In the case group, the OR value of those with clonorchiasis was 8.00 (95% CI: 4.34-14.92). The OR value was 4.82 (95% CI: 2.32-10.26) for the subjects whose clonorchiasis was diagnosed less than 10 years before their diagnosis of HCC, and was 17.54 (95% CI: 5.47-57.18) for those whose HCC was diagnosed more than 10 years ago. HBV infection, alcohol consumption and clonorchiasis showed an additive interaction in the development of HCC, with a relative excess risk of interaction of 110.43 and 18.23; attributable proportion of interaction of 0.80 and 0.63; synergy index of 5.18 and 2.84, respectively. CONCLUSION: Clonorchiasis could be an important risk factor for HCC. When the course of clonorchiasis is prolonged, the risk of HCC could increase. HBV infection, alcohol consumption and clonorchiasis might have synergistic actions on the development of HCC.

[A case-control study on congenital heart diseases with methylenetetrahydrofolate reductase gene, cystathionine beta-synthase gene, and environmental factors].

OBJECTIVE: To explore congenital heart diseases (CHD) in their offsprings in association with parental methylenetetrahydrofolate reductase (MTHFR) gene C677T, cystathionine beta-synthase (CBS) gene T833C, and environmental factors. METHODS: A 1:1 case-control study was carried out to investigate 115 pairs of case and controlled children and their parents, and the parents' MTHFR gene 677 C-->T mutation and CBS gene 833 T-->C mutation were also identified. The possible risk factors were analysed by simple and multiple factors logistic regression methods. RESULTS: Results revealed that 5 factors were related to the occurrence of CHD in the offsprings: maternal exposures to pesticides in the early stage of pregnancy (OR = 8.62), suffering from diseases during pregnancy (OR = 2.069), catching cold in the early stage of pregnancy (OR = 4.125), under depressed or nervous condition during pregnancy (OR = 4.653), maternal MTHFR 677TT genotype (OR = 3.872). CONCLUSION: These results suggested that maternal MTHFR 677TT genotype was one of the risks to the occurrence of CHD in offspring but parents' CBS gene 833 T-->C mutation did not get involved in CHD. In addition, the occurrence of CHD was related to maternal exposures to pesticides, catching a cold, suffering from diseases, depressed or under nervous condition in the early stage of pregnancy or during pregnancy.

[A case-control study on the risk factor of perinatals' congenital malformations in seven cities of Guangxi].

OBJECTIVE: To investigate the possible risk factors of congenital malformations in cities of Guangxi. METHODS: A case-control study was carried out on 281 cases of congenital malformations and 730 controls. Analysis of simple factor and multiple factors unconditional logistic regression were done. RESULTS: The analysis of simple factor and multiple factors showed that main risk factors of congenital malformations as multiple pregnancies (OR = 2.6), pregnancy complications (OR = 3.2), exposure to chemical substances before or during pregnancy (OR = 3.0), taking sedatives (OR = 10.2), hormone drug (OR = 9.4) or Chinese herbal medicines (OR = 2.5) during the early stage of pregnancy, mothers' blood type as AB (OR = 3.5) or A (OR = 2.2), mothers' emotion being nervous and melancholy (OR = 2.6), mothers' occupation being workers (OR = 3.8) or peasants (OR = 3.0), fathers' exposure to noise (OR = 5.7) or suffering from chronic diseases (OR = 2.8). CONCLUSIONS: Some risk factors were identified as having important effect on perinatal congenital malformations, including taking sedatives, hormone drug or Chinese herbal medicines during the early stage of pregnancy, mothers' emotion being nervous and melancholy, multiple pregnancies, pregnancy complications, exposure to chemical substances before or during pregnancies, mothers' blood type as AB or A, mothers' occupation being workers or peasants, fathers' exposure to noise or suffering from chronic diseases.