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What is known and objectives Tacrolimus ( TAC) is widely used as part of immunosuppressive regimens. There is great interindividual variation on the disposition of TAC. The aim of this study was to develop a population pharmacokinetic ( PPK) model for Chinese liver transplant patients and evaluate genetic polymorphism and other possible factors on the PK parameters. The exposure of TAC is to be estimated through Bayesian modelling. Methods A total of 47 sets of rich-time PK and 1234 conventional therapeutic drug monitoring ( TDM) data were collected from 125 Chinese liver transplant patients. The pathophysiological data of these patients were recorded. CYP3A5*3 and ABCB1 genotypes were determined for each patient. The PPK model for TAC was established by nonlinear mixed-effects modelling ( nonmem). The impact of pathophysiology and genotype on PPK parameters was evaluated. Bayesian estimators for the area under concentration-time curve ( AUC) of TAC were validated. Results A two-compartment model with lag time was found to be the most suitable model for the pooled full PK and TDM data for Chinese liver transplant patients. The CL/F, V2/F, Q/F, V3/F, Ka and lag time were 17.4±0.81 L/h, 165±44.1 L, 54.9±25.8L/h, 594±87.5 L, 0.51±0.095 L/h and 1.57±0.34 h. Post-operative day ( POD), creatinine clearance ( CLcr) and ABCB1 C3435T genotypes were found to have significant influences on CL/F ( P<.01). ABCB1 C3435T genotypes showed a significant correlation with V2/F ( P<.01). C0-C2 and C0-C2-C4 were shown to be suitable for the estimation of AUC in Chinese liver transplant patients. What is new and conclusion A PPK model for TAC was established successfully in Chinese liver transplant patients. POD, CLcr and ABCB1 C3435T genotypes were shown to have significant effects on CL/F. The AUC of TAC in Chinese liver transplant patients could be estimated through Bayesian modelling, based on which individualized immunosuppressive regimens can be designed. [ABSTRACT FROM AUTHOR]

The relationship between murine double minute 2 ( MDM2) T309G polymorphism and esophageal cancer risk has been discussed with discrepant results. The aim of our study is to investigate the systematic association between the potentially functional MDM2 T309G polymorphism and esophageal cancer risk. Eligible studies were included through searching the databases of PubMed, EMBASE, and Chinese National Knowledge Infrastructure (up to April 2014). The crude odds ratio ( OR) and 95% confidence interval ( CI) were used to estimate the strength of the association. Six published case-control studies, including 1899 cases and 3016 controls, were identified. Overall, our study suggested that MDM2 T309G polymorphism was significantly associated with increased risk of esophageal cancer ( TT vs. GG: OR = 0.77, 95% CI = 0.65-0.90, P = 0.002; T vs. G: OR = 0.88, 95% CI = 0.81-0.96, P = 0.002). In subgroup analyses stratified by source of controls, ethnicity, and quality score assessment, respectively, similar results were obtained ( TT vs. GG: OR = 0.65, 95% CI = 0.48-0.89, P = 0.007 for hospital-based studies; T vs. G: OR = 0.90, 95% CI = 0.81-0.99, P = 0.04 for population-based studies; and T vs. G: OR = 0.85, 95% CI = 0.78-0.93, P = 0.004 for Asians). The results of Begg's test and Egger's test did not suggest publication bias in the studies. Therefore, the MDM2 T309G polymorphism may be significantly associated with increased esophageal cancer risk, especially among Asians. [ABSTRACT FROM AUTHOR]

1. The purpose of the study was to elucidate the influence of multidrug resistance gene (MDR1) haplotype and CYP3A5 genotype on cyclosporine (CsA) blood level in Chinese renal transplant recipients. 2. CsA trough level (C0) and peak level (C2) of 115 patients 1 week and 1 month after renal transplantation were determined. MDR1 C1236T, G2677T/A, C3435T and CYP3A5*3 genotypes were determined by polymerase chain reaction (PCR) assays based on amplification refractory mutation. 3. Dose-adjusted C0 (C0/D), C2 (C2/D) were 50.5 ± 22.5, 267.8 ± 110.1 ng·kg·(ml·mg)-1 after 1 week of therapy, and 79.3 ± 29.4, 406.0 ± 135.3 ng·kg· (ml·mg)-1 after 1 month of therapy. Frequencies of MDR1 haplotype TTT, CGC, and TGC were 27.0%, 25.2% and 20.0%, respectively. After 1 month of therapy, C2/D of TTT/TTT patients were 30% (p = 0.057) and 53% (p = 0.003) higher than CGC/TTT and CGC/ CGC patients. C0/D of CYP3A5 *1/*1, *1/*3 and *3/*3 patients after 1 month of therapy were 51.8 ± 25.0, 71.5 ± 27.6, and 86.7 ± 28.6 ng·kg·(ml·mg)-1 (p < 0.05). 4. MDR1 haplotypes and CYP3A5*3 genotypes can be related to C2 and C0 of CsA, respectively. [ABSTRACT FROM AUTHOR]

This study explores the impact of clopidogrel on the pharmacokinetics of omeprazole related to CYP2C19 genetic polymorphisms. Twelve healthy volunteers (6 CYP2C19*1/ *1, 5 CYP2C19*2/*2, and 1 CYP2C19*2/*3) are enrolled in a 2-phase randomized crossover trial. In each phase, the volunteers are administered a single oral dose of omeprazole 40 mg after pretreatment of either placebo or clopidogrel (300 mg on the first day and then 75 mg once daily for 3 consecutive days). Plasma concentrations of omeprazole and its metabolites are quantified by high-performance liquid chromatography with UV detection. After clopidogrel treatment, the AUC0-∞ of omeprazole increases by 30.02% ± 18.03% (P = .004) and that of 5-hydroxyomeprazole decreases by 24.30% ± 11.66% (P = .032) in CYP2C19*1/*1. The AUC0-∞ ratios of omeprazole to 5-hydroxyomeprazole increase by 74.98% ± 35.48% (P = .001) and those of omeprazole to omeprazole sulfone do not change significantly (P = .832) in CYP2C19*1/*1. No significant alteration is observed in CYP2C19*2/*2 or *3. Clopidogrel inhibits CYP2C19-dependent hydroxylation of omeprazole in CYP2C19*1/*1 and has no impact on CYP3A4-catalyzed sulfoxidation of omeprazole. [ABSTRACT FROM AUTHOR]

The aim was to investigate the effect of UGT1A9, UGT1A8, UGT2B7 and ABCC2 polymorphism on the pharmacokinetics of mycophenolic acid (MPA) and its metabolites phenolic glucuronide (MPAG) and acyl glucuronide (AcMPAG) in Chinese renal transplant recipients. Single nucleotide polymorphisms (SNP) in UGT1A9-118(dT)9/10, UGT1A9 T-440C/C-331T, UGT1A8*3, UGT2B7 G211T, UGT2B7 C802T, ABCC2 C-24T, and ABCC2 G1249A were detected. A total of 46 recipients were enrolled in the pharmacokinetics study at day 30 after kidney transplantation. Differences in the MPA pharmacokinetic profiles confirmed large inter-patient variation of MPA exposure. A statistical significant increase in the dose-adjusted AUC6-12 level of MPA was found in patients bearing the -118(dT)10 allele of the UGT1A9 gene (T9 = 7.34 ± 4.11 mg h ml-1 g-1; T9/T10 = 11.54 ± 7.62 mg h ml-1 g-1; and T10 = 11.89 ±8.76 mg h ml-1 g-1, p = 0.041). A similar trend was also observed for the dose-adjusted AUC0-12 and AUC6-12 of MPAG. Patients carrying the heterozygous mutant alleles of ABCC2 G1249A exhibited higher AUC6-12/D of AcMPAG than those with wild-type genotype (p = 0.016). The other SNPs that were genotyped did not cause any significant variation in MPA and MPAG pharmacokinetic parameters. In conclusion, the enterohepatic recirculation of MPA in the patients seems to be more extensive in UGT1A9-118(dT)10 allele carriers, and the exposure of AcMPAG is higher in patients carrying ABCC2 G1249A genotype than those with wild-type genotype. [ABSTRACT FROM AUTHOR]

Genetic differentiation among populations of Anopheles jeyporiensis was examined using 76 mtDNA COII sequences from 16 sites throughout southern China and northern Vietnam. The COII sequences are AT-rich (74.58%) and reveal high levels of diversity with 39 of 685 sites polymorphic and 50 different haplotypes present. Genetic variation is high within populations and significant geographical structure was detected at both population and regional levels. In the larger samples, the distributions of haplotypes suggest recent population expansion. [ABSTRACT FROM AUTHOR]

Determines whether terbinafine inhibits dextromethorphan metabolism in Chinese subjects. Comparison of genetic polymorphism of dextromethorphan in Chinese and in Caucasian; Use of dextromethorphan phenotyping method; Low prevalence of poor metabolizers in Chinese.

A higher prevalence of depression in systemic lupus erythematosus (SLE) patients has been reported, though the mechanism underlying this phenomenon remains unclear. The present study was conducted to explore whether the polymorphism and methylation status of the serotonin transporter gene (5HTT) promoter region (PR-5HTT) contribute to depression in SLE patients from both genetic and epigenetic perspectives. In this study, 96 SLE patients and 96 healthy controls (HCs) were recruited. Depression levels of all subjects were evaluated using the Hamilton Depression Rating Scale (HDRS). The serotonin transporter-linked polymorphism (5HTTLPR) and the DNA methylation status of PR-5HTT were detected in peripheral lymphocytes of SLE patients and HCs. The differences in 5HTTLPR and DNA methylation of PR-5HTT between SLEs and HCs were compared. In SLE patients, the frequencies of short allele (S) and SS genotype of 5HTTLPR were higher in depressive SLE (SLE-D) patients than in non-depressive SLE (SLE-ND) patients. The mean HDRS score of SS homozygote patients was higher than that of patients with SL/LL genotypes. Conversely, PR-5HTT was hypomethylated in HCs as well as SLE patients. There was no difference in the methylation status between HCs and SLEs. Thus, the functional expression of PR-5HTT may be primarily regulated by gene polymorphism and not by DNA methylation. The risk allele of 5HTTLPR appears to be a major contributor to depression in SLE patients. [ABSTRACT FROM AUTHOR]

Introduction: In the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway, STAT3 is one of the most prominent prognosis factors for cancer and leukemia. STAT3 activation might promote cellular transformation and therefore have an important role in human tumors. This study aimed to investigate the relationship between STAT3 polymorphisms and treatment response of acute myeloid leukemia (AML) in the Chinese population. Methods: Three single-nucleotide polymorphisms (SNPs) were tested in 130 patients with AML. Genomic DNA was isolated from peripheral blood and assayed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS). Results: The results of response to chemotherapy showed that there were strong relationships between unfavorable cytogenetics, partial remission (and even no remission), and GG genotype frequency in rs9909659 ( P = 0.01 and 0.03). Patients younger than 45 years were associated significantly with GA/AA genotype ( P = 0.01). Conclusions: The results of this study suggest that the GG genotype in rs9909659 might confer increased resistance to standard chemotherapy. [ABSTRACT FROM AUTHOR]

A yellow-seeded doubled haploid (DH) line no. 2127-17, derived from a resynthesizedBrassica napusL., was crossed with two black-seededBrassicacultivars‘Quantum’ and‘Sprint’ of spring type. The inheritance of seed colour was investigated in the F2, and BC1 populations of the two crosses and also in the DH population derived from the F1 of the cross‘Quantum’ × no. 2127-17. Seed colour analysis was performed with the colorimeter CR-300 (Minolta, Japan) together with a visual classification system. The immediate F1 seeds of the reciprocals in the two crosses had the same colour as the self-pollinated seeds of the respective black- and yellow-seeded female parents, indicating the maternal control of seed colour. The F1 plants produced yellow-brown seeds that were darker in colour than the seeds of no. 2127-17, indicating the partial dominance of yellow seed over black. In the segregating BC1 progenies of the two crosses, the frequencies of the black- and yellow-seeded plants fit well with a 1 : 1 ratio. In the cross with‘Quantum’, the frequencies of yellow-seeded and black-seeded plants fit with a 13 : 3 ratio in the F2 progeny, and with a 3 : 1 ratio in the DH progeny. However, a 49 : 15 segregation ratio was observed for the yellow-seeded and black-seeded plants in the F2 progeny of the cross with‘Sprint’. It was postulated from these results that seed colour was controlled by three pairs of genes. A dominant yellow-seeded gene (Y) was identified in no. 2127-17 that had epistatic effects on the two independent dominant black-seeded genes (B and C), thereby inhibiting the biosynthesis of seed coat pigments. [ABSTRACT FROM AUTHOR]

To assess the potential effects of Cytotoxic T-lymphocyte antigen 4 ( CTLA4) gene polymorphisms on susceptibility to gastric cardia adenocarcinoma ( GCA), we genotyped four polymorphisms (rs733618 A>G, rs16840252 C>T, rs231775 G>A and rs3087243 G>A) in CTLA4 and calculated odds ratios ( ORs) with the corresponding 95% confidence intervals (95% CIs) for the genotype and allele distributions between GCA cases and controls. The CTLA4 genotypes were determined by the polymerase chain reaction-ligase detection reaction ( PCR- LDR) analysis in 330 GCA patients and 608 unrelated cancer-free controls. In this case -control study, there was no significant difference in the genotype and allele distributions of four CTLA4 polymorphisms between GCA patients and controls. However, haplotype association analysis indicated that compared with CTLA4 Grs733618Crs16840252Grs231775Crs3087243, CTLA4 Grs733618Crs16840252Ars231775Grs3087243 and Ars733618Crs16840252Grs231775Ars3087243 haplotypes conferred increased risks of GCA ( OR = 6.46, 95% CI = 1.33-31.28; P = 0.012; both); however, CTLA4 Ars733618Crs16840252Ars231775Grs3087243 and Ars733618Trs16840252Grs231775Grs3087243 haplotypes conferred decreased risks of GCA ( P = 0.001 and P = 0.011, respectively). These results highlight that the rare CTLA4 haplotypes may affect the development of GCA in the Chinese population. [ABSTRACT FROM AUTHOR]

Serum amyloid A (SAA) protein is not only an inflammatory factor but also an apolipoprotein that can replace apolipoprotein A1 (apoA1) as the major apolipoprotein of high-density lipoprotein cholesterol (HDL-C). However, the relationship between genetic polymorphisms of SAA and coronary artery disease (CAD) remains unclear. A total of four single nucleotide polymorphisms (rs12218, rs4638289, rs7131332, and rs11603089) of the SAA gene were genotyped using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method in two independent case-control studies, one of the Han population (1416 CAD patients and 1373 control subjects) and the other of the Uygur population (588 CAD patients and 529 control subjects). We found that the rs12218 CC genotype was more frequent among the CAD patients than among the controls in both the Han (8.3% vs. 4.8%, P<0.001) and Uygur populations (15.5% vs. 11.3%, P<0.05). After adjustments for confounding factors, such as sex, age, smoking, drinking, hypertension, diabetes, and serum levels of triglycerides, total cholesterol, HDL, and plasma SAA, the differences remained significant in the Han (CC vs. CT+TT, P<0.001, OR=3.863, 95% CI: 1.755-12.477) and Uygur groups (CC vs. CT+TT, P=0.031, OR=3.022, 95% CI: 1.033-8.840). Genetic polymorphisms in SAA1 are associated with CAD in the Han and Uygur populations in western China. [ABSTRACT FROM AUTHOR]

Aim To test the hypothesis that there are single-nucleotide polymorphisms ( SNPs) in genes of the l-arginine/nitric oxide pathway associated with pulmonary hypertension ( PH) in neonates with bronchopulmonary dysplasia ( BPD). Methods Neonates with BPD were enrolled (n = 140) and clinical characteristics compared between case ( BPD + PH) and control ( BPD) groups. DNA was isolated from blood leucocytes and assayed for 17 SNPs in l-arginine/nitric oxide pathway genes by Sequenom massarray. Genes included carbamoyl-phosphate synthetase, ornithine transcarbamylase, argininosuccinate synthase, nitric oxide synthase and arginase. SNPs were selected from the National Center for Biotechnology Information database for their putative functionality. Calculated minor allele frequencies ( MAF) of cases and controls were compared using χ2 and logistic regression. Results Of the 140 patients with BPD, 26% had echocardiographic evidence of PH. Ventilation days were longer for cases than controls (mean 31 vs. 15 days, p < 0.05). Of the 17 SNPs, rs2781666 in arginase I gene was less common in cases ( MAF = 0.23) than controls ( MAF = 0.37, p = 0.04). The odds of PH decreased by 43% (p = 0.047) for each copy of the SNP minor allele in arginase I gene in patients with BPD. Conclusion Arginase I SNP (rs2781666) may be associated with protection against pulmonary hypertension in preterm neonates with BPD. [ABSTRACT FROM AUTHOR]

Introduction: Aberrant activation of Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway leads to deregulated proliferation, differentiation, or apoptosis of normal cells. One of the members of this family, JAK2, plays a very important role in metabolizing carcinogens and medications. This study aimed to detect whether any association exists between genetic polymorphisms in JAK2 gene and individual susceptibility to acute leukemia. Methods: A case-control study in a Chinese population with 260 acute leukemia cases and 280 healthy controls matched by age, gender, and ethnicity. Genomic DNA was assayed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF) with five genetic polymorphisms in JAK2 gene. Results: The distributions of rs56118985 GA genotype in the acute leukemia and acute myeloid leukemia (AML) groups were both slightly different when compared with the control group ( P = 0.049 and P = 0.045). The frequencies of rs2230724 AA and GA genotypes in the acute leukemia and its subtypes were all significantly higher than that in the control group ( P < 0.001). This suggested that subjects with A allele of rs2230724 were susceptible to acute leukemia and its subtypes. In addition, A allele of rs2230724 should be an important genetic determinant for acute leukemia and AML. Conclusion: The results indicate that the risk of acute leukemia might be associated with JAK2 polymorphisms. [ABSTRACT FROM AUTHOR]

ZHANG M., JIN M., YU Y., ZHANG S., WU Y., LIU H., LIU H., CHEN B., LI Q., MA X. & CHEN K. (2011) European Journal of Cancer Care 21, 274-280 Associations of miRNA polymorphisms and female physiological characteristics with breast cancer risk in Chinese population mircoRNAs (miRNAs) play important roles on regulation of gene expressions. Aberrant expression of miRNAs was involved in various biological and pathological processes, including tumorigenesis of breast cancer. Single-nucleotide polymorphisms (SNPs) were implicated in altered expression or biological functions of mature miRNAs. To explore the relevance of miRNA polymorphisms and female physiological characteristics to breast cancer risk, SNPs located within hsa-miR-605 (rs2043556), hsa-miR-149 (rs2292832), hsa-miR-27a (rs895819), hsa-miR-196a-2 (rs11614913) and hsa-miR-618 (rs2682818) were selected, and their associations with breast cancer risk were analysed. In addition, associations between physiological characteristics-related factors and breast cancer risk were estimated too. We found that the ones with menarche age less than 16 years had increased breast cancer risk (OR = 2.10, 95% CI: 1.23-3.60). Marginally significant association between rs11614913 CT/CC genotypes and reduced breast cancer risk was observed (OR = 0.65, 95% CI: 0.40-1.06), while no significance was detected about the other miRNA polymorphisms. We concluded that menarche at less than 16 years old increased breast cancer risk, while the genetic variants in miR-196-a-2 might decreased the risk. [ABSTRACT FROM AUTHOR]

Systemic lupus erythematosus (SLE) is a complex immune disease. The genetic variation in the PXK gene was found to associate with SLE in Caucasian populations. However, the association of rs6445975 with SLE has not been extensively studied in a Chinese mainland population. A total of 288 SLE patients and 357 controls were recruited. Unlabeled probe-based high-resolution melting analysis (HRMA) was used in genotyping. HRMA with unlabeled probe successfully distinguished all genotypes. Neither genotype nor allele frequencies of SNP rs6445975 showed statistically significant differences between SLE patients and controls. The association of SNP rs6445975 with the diagnostic criteria of SLE was also examined. No obvious association was observed between rs6445975 and the incidence of clinical symptoms. However, the minor allele (G) of rs6445975 was found to significantly associate with increased abnormalities of anti-Smith (p = 0.004, odds ratio (OR) = 1.95, 95% confidence interval (CI) = 1.22—3.09), anti-Ro (p = 0.015, OR = 1.69, 95% CI = 1.10—2.58), anti-La (p = 0.008, OR = 1.86, 95% CI = 1.17—2.93) and C3C4 (p = 0.007, OR = 1.79, 95% CI = 1.17—2.74). Polymorphisms of rs6445975 in the PXK gene were associated with autoantibody production, but not disease risk, of systemic lupus erythematosus in a Chinese population. Lupus (2011) 20, 23—27. [ABSTRACT FROM AUTHOR]

Background Atopic dermatitis (AD) is a chronic skin disease affecting more than 15% of children and 2% of adults. A strong connection between genetic factors and AD has been described for a long time. Histamine receptor H4 ( HRH4) has been shown to be related to different kinds of allergic and autoimmune disorders. However, an association between HRH4 and AD has not yet been reported. Objectives To examine a possible association between HRH4 and AD. Methods Genomic DNA from 301 patients with AD and 313 healthy controls was extracted and three exons of HRH4 were sequenced. Results We found three new single nucleotide polymorphisms (SNPs) in HRH4 which were significantly associated with AD: ss142022671 [odds ratio (OR) 1·87, 95% confidence interval (CI) 1·24–2·81; P = 0·002], ss142022677 (OR 4·40, 95% CI 2·42–8·00; P = 1·5 × 10−7) and ss142022679 (OR 4·26, 95% CI 2·38–7·61; P = 1·3 × 10−7). The SNPs ss142022677 and ss142022679 were found to be in strong linkage disequilibrium ( D’ = 0·98; r2 = 0·92). Two-SNP haplotype analysis (ss142022677 and ss142022679) showed that the major AA haplotype was protective against AD (OR 0·22, 95% CI 0·12–0·40; P = 3·1 × 10−8) and the minor TT haplotype was significantly associated with AD (OR 4·13, 95% CI 2·27–7·54; P = 6·6 × 10−7). In addition, in a three-SNP haplotype analysis (ss142022671, ss142022677 and ss142022679), the major TAA haplotype was protective against AD (OR 0·46, 95% CI 0·31–0·69; P = 0·0001), while the complementary ATT haplotype was found to be significantly associated with AD (OR 3·81, 95% CI 2·03–7·14; P = 8·3 × 10−6). Conclusions Polymorphisms of ss142022671, ss142022677 and ss142022679 in HRH4 are associated with AD. [ABSTRACT FROM AUTHOR]

The objective of this study was to dissect the genetic control of days to flowering (DTF) and photoperiod sensitivity (PS) into the various components including the main-effect quantitative trait loci (QTLs), epistatic QTLs and QTL-by-environment interactions (QEs). Doubled haploid (DH) lines were produced from an F1 between two spring Brassica napus cultivars Hyola 401 and Q2. DTF of the DH lines and parents were investigated in two locations, one location with a short and the other with a long photoperiod regime over two years. PS was calculated by the delay in DTF under long day as compared to that under short day. A genetic linkage map was constructed that comprised 248 marker loci including SSR, SRAP, and AFLP markers. Further QTL analysis resolved the genetic components of flowering time and PS into the main-effect QTLs, epistatic QTLs, and QEs. A total of 7 main-effect QTLs and 11 digenic interactions involving 21 loci located on 13 out of the 19 linkage groups were detected for the two traits. Three main-effect QTLs and four pairs of epistatic QTLs were involved in QEs conferring DTF. One QTL on linkage group (LG) 18 was revealed to simultaneously affect DTF and PS and explain for the highest percentage of the phenotypic variation. The implications of the results for B. napus breeding have been discussed. [ABSTRACT FROM AUTHOR]

Pre-eclampsia is a multisystem disorder of pregnancy and remains the leading cause of both maternal and fetal morbidity and mortality in many countries. Despite extensive studies, the underlying mechanisms still remain unknown. Besides its restricted expression in the tissues of placenta and its function in regulating immune suppression and in ensuring successful invasion of placental tissues into maternal deciduas, it has been postulated that HLA-G may play a role in modulation of immune tolerance at the fetal–maternal interface. Aberrant HLA-G expression may result in pregnancy disorders that are associated with poor invasion of extravillous cytotrophoblast into maternal spiral arteries, such as pre-eclampsia. Studies have shown that pre-eclampsia is largely under genetic control, but genetic mechanisms underlying the disorder have yet to be determined. In the current study, we focus on the potential role of HLA-G polymorphism in the pathogenesis of pre-eclampsia. Samples were obtained from Chinese Han primiparous women with pre-eclampsia and irrelative normal women, and case-matched placentas were genotyped for the HLA-G polymorphism in the exons 2, 3, and 4, and the 14-base-pair (bp) insertion/deletion polymorphism in the 3′-untranslated region of exon 8 was analyzed separately. The frequency of HLA-G polymorphism in these samples was not significantly different from those of normal controls, indicating that maternal HLA-G polymorphism is not associated with the risk for pre-eclampsia in this Chinese Han population. However, the maternal 14-bp insertion/deletion polymorphism is ethnically different. [ABSTRACT FROM AUTHOR]

Background Peroxisome proliferator-activated receptor γ inhibits the growth and induces apoptosis of gastric cancer cells. A common polymorphism at codon 12 of this gene (Pro12Ala) has been shown to confer protection against diabetes and colorectal cancer. Aim To study the association between peroxisome proliferator-activated receptor γ gene polymorphism, Helicobacter pylori infection and gastric cancer in Chinese. Methods One hundred and four consecutive patients with non-cardia gastric adenocarcinoma and 104 matched controls were examined. Peroxisome proliferator-activated receptor γ Pro12Ala polymorphism was analysed by polymerase chain reaction-restriction fragment length polymorphism. Results The frequency of peroxisome proliferator-activated receptor γ G (Ala12) allele was significantly higher among cancer patients (19.2%) than in control (8.7%; OR 2.5, 95% CI 1.1–5.8). While H. pylori infection was more prevalent in gastric cancer patients (OR 3.0; 95% CI 1.6–5.7), the combination of peroxisome proliferator-activated receptor γ G allele and H. pylori infection further increased the risk of gastric cancer (OR 12.8, 95% CI 3.2–50.5). The presence of the Ala12 did not increase the risk of gastric cancer in H. pylori-negative subjects. Conclusion Our study suggests the potential association between peroxisome proliferator-activated receptor γ polymorphism and H. pylori infection in the development of non-cardia gastric cancer. [ABSTRACT FROM AUTHOR]

Li G-P, Wang J-Y, Yan S-K, Chen B-S, Xue H, Wu G. Genetic effect of two polymorphisms in the apolipoprotein A5 gene and apolipoprotein C3 gene on serum lipids and lipoproteins levels in a Chinese population. Two polymorphisms, apolipoprotein A5 (APOA5) −1131T>C and apolipoprotein C3 (APOC3) −482C>T, were examined in a healthy Chinese group. Analysis of covariance ( ancova) showed that both −1131T>C and −482C>T minor alleles were associated with triglyceride (TG)-raising effects (p < 0.001 and p = 0.012, respectively) after adjustment of sex, age, and body mass index (BMI). Moreover, −1131T>C minor alleles were also found to be associated with total cholesterol (TC)-raising effects (p = 0.045). However, the relationship between −482C>T minor alleles and TC-raising effects was not observed after adjustment of sex, age, and BMI. By contrast, significant inverse associations were noted between minor alleles (−1131T>C and −482C>T) and high-density lipoprotein cholesterol (HDL-C) concentrations (p = 0.021 and p = 0.021, respectively). Linear regression analysis showed that the effects of −1131T>C and −482C>T polymorphisms on TG and HDL-C (0.001 and 0.008; 0.041 and 0.005, respectively) are independent and additive and that −1131T>C can seriously affect the levels of TG (0.001 vs 0.008). The additive effect of the two polymorphisms was confirmed further by haplotype analysis. Our results strongly support that the two single nucleotide polymorphisms, −1131T>C in APOA5 and −482C>T in APOC3, are related to the levels of serum TG and HDL-C and those of other several lipids and lipoproteins in the Chinese population. [ABSTRACT FROM AUTHOR]