Hong Zhang

Beijing Medical University, Peping, Beijing, China

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Publications (114)390.12 Total impact

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    ABSTRACT: Complement activation is common in patients with IgA nephropathy (IgAN) and associated with disease severity. Our recent genome-wide association study of IgAN identified susceptibility loci on 1q23 containing the complement regulatory protein-encoding genes CFH and CFHR1-5, with rs6677604 in CFH as the top single-nucleotide polymorphism and CFHR3-1 deletion (CFHR3-1∆) as the top signal for copy number variation. In this study, to explore the clinical effects of variation in CFH, CFHR3, and CFHR1 on IgAN susceptibility and progression, we enrolled two populations. Group 1 included 1178 subjects with IgAN and available genome-wide association study data. Group 2 included 365 subjects with IgAN and available clinical follow-up data. In group 1, rs6677604 was associated with mesangial C3 deposition by genotype-phenotype correlation analysis. In group 2, we detected a linkage between the rs6677604-A allele and CFHR3-1∆ and found that the rs6677604-A allele was associated with higher serum levels of CFH and lower levels of the complement activation split product C3a. Furthermore, CFH levels were positively associated with circulating C3 levels and negatively associated with mesangial C3 deposition. Moreover, serum levels of the pathogenic galactose-deficient glycoform of IgA1 were also associated with the degree of mesangial C3 deposition in patients with IgAN. Our findings suggest that genetic variants in CFH, CFHR3, and CFHR1 affect complement activation and thereby, predispose patients to develop IgAN.
    Journal of the American Society of Nephrology : JASN. 09/2014;
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    ABSTRACT: Objectives: Recent genome-wide association studies have identified several novel susceptibility genes for systemic lupus erythematosus (SLE) and IgA nephropathy (IgAN). Since both lupus nephritis (LN) and IgAN are autoimmune kidney diseases, they may share common disease mechanisms that overlap with genetic susceptibility. To test this hypothesis, we sought to identify genetic variants associated with IgAN in LN. Methods: In the first stage, 500 LN patients, 240 SLE patients without LN, and 500 healthy controls were enrolled. Fifteen reported SNPs with top association signals with IgAN were selected for further testing in LN. Three independent cohorts from Beijing, Shanghai and Hong Kong were included as replicates. We also analyzed the functional significance of identified non-coding variants on regulatory motifs and gene expression. Results: Except for associations with HLA gene polymorphisms, genetic variants of MTMR3 in 22q12 showed associations with LN (rs9983A with P = 2.07×10(-3) ; OR 1.61; 95% CI 1.19-2.19) compared to healthy controls in the first stage. In replications, associations were replicated and reinforced with northern (LN vs. non-LN patients, P = 0.01) but not southern Han Chinese, although significant genetic heterogeneity was observed. In silico analyses predicted conservative and regulatory features of rs9983. In expression analysis, we observed lower MTMR3 transcription levels in blood samples with rs9983A and renal biopsies from LN and IgAN. Conclusions: Our results suggested that the MTMR3 gene was shared between IgAN and LN in the northern Chinese, further highlighting the role of autophagy in SLE. However, widespread replication of these experiments, fine mapping, and functional assays are required to establish this connection. © 2014 American College of Rheumatology.
    Arthritis & rheumatology (Hoboken, N.J.). 06/2014;
  • International Urology and Nephrology 06/2014; · 1.33 Impact Factor
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    ABSTRACT: To observe and compare the effects of grain-bean package, dietary fiber (DF) extracted from grain-bean package, and DF from grain corn on the blood lipids and fatty acid synthase (FAS) activity in high-fat, high-cholesterol feeding induced dyslipidemia rats, and observe its effects on regulation of sterol regulatory element protein-1c (SREBP-1c) mRNA expression in rat liver.
    05/2014; 43(3):372-7.
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    Xu-Jie Zhou, Ming-Hui Zhao, Hong Zhang
    Rheumatology (Oxford, England) 04/2014; · 4.24 Impact Factor
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    ABSTRACT: Abstract Objectives: Recent animal experiments showed that CCR5-deficient lupus mice (CCR5(-/-)) were closely associated with aggravated lupus nephritis. CCR5 Δ32 variation, a nonsynonymous mutation of CCR5, resulted in altered CCR5 function. However, the CCR5 Δ32 mutation in human lupus nephritis has been rarely reported in the literature. Methods: A large case-control study that included 2010 samples from a Chinese population was conducted, followed by a meta-analysis combining the current and previously published studies to explore the effect of CCR5 Δ32 on lupus nephritis susceptibility. Results: Four CCR5 Δ32 heterozygote carriers were detected in lupus nephritis patients only. We detected no CCR5 Δ32 homozygotes in our study population. In the meta-analysis, including 1,092 cases and 2,229 controls, we found great heterogeneity between studies (p < 0.001, I(2)( )= 89.6%). Furthermore, stratified and sensitivity analyses suggested that ethnicity and CCR5 Δ32 allele frequency were the main origin of heterogeneity. In the subgroups without obvious heterogeneity, we observed a positive correlation between CCR5 Δ32 and lupus nephritis risk (p < 0.05). Conclusions: Our study confirmed that the CCR5 Δ32 mutation is a very rare variation found in the Chinese population with Han ethnicity. However, CCR5 Δ32 might play a role in lupus nephritis susceptibility. Future replications and functional studies are needed.
    Autoimmunity 04/2014; · 2.77 Impact Factor
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    Xu-Jie Zhou, Fa-Juan Cheng, Hong Zhang
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    ABSTRACT: Aberrations of both innate immunity and adaptive immunity in genetically predisposed individuals evoked by environmental factors are suggested to be implicated in pathophysiological processes of systemic lupus erythematosus (SLE). Autophagy, a degradation pathway in which cytoplasmic content is engulfed and degraded by the lysosome, has been recently demonstrated to be involved in multiple cytoplasmic homeostatic progresses and interact with nearly all parts of the innate and adaptive immune system. More recently, some lines of evidence from genetic, cell biology and model animal studies also suggests a pivotal role of autophagy in mediating the occurrence and development of SLE. We discuss and synthesize studies that have begun to demonstrate how autophagy cause and/or promote autoimmunity in SLE.
    International Reviews Of Immunology 02/2014; · 5.73 Impact Factor
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    ABSTRACT: One hypothesis states that IgA nephropathy (IgAN) is a syndrome with an autoimmune component. Recent studies strongly support the notion of shared genetics between immune-related diseases. This study investigated single-nucleotide polymorphisms (SNPs) reported to be associated with systemic lupus erythematosus (SLE) in a Chinese cohort of patients with IgAN and in controls. This study investigated whether SNP markers that had been reported to be associated with SLE were also associated with IgAN in a Chinese population. The study cohort consisted of 1194 patients with IgAN and 902 controls enrolled in Peking University First Hospital from 1997 to 2008. Ninety-six SNPs mapping to 60 SLE loci with reported P values <1×10(-5) were investigated. CFH (P=8.41×10(-6)), HLA-DRA (P=4.91×10(-6)), HLA-DRB1 (P=9.46×10(-9)), PXK (P=3.62×10(-4)), BLK (P=9.32×10(-3)), and UBE2L3 (P=4.07×10(-3)) were identified as shared genes between IgAN and SLE. All associations reported herein were corroborated by associations at neighboring SNPs. Many of the alleles that are risk alleles for SLE are protective alleles for IgAN. By analyses of two open independent expression quantitative trait loci (eQTL) databases, correlations between genotypes and corresponding gene expression were observed (P<0.05 in multiple populations), suggesting a cis-eQTL effect. From gene-expression databases, differential expressions of these genes were observed in IgAN. Additive interactions between PXK rs6445961and HLA-DRA rs9501626 (P=1.51×10(-2)), as well as multiplicative interactions between CFH rs6677604 and HLA-DRB1 rs9271366 (P=1.77×10(-2)), and between HLA-DRA rs9501626 and HLA-DRB1 rs9271366 (P=3.23×10(-2)) were observed. Disease risk decreased with accumulation of protective alleles. Network analyses highlighted four pathways: MHC class II antigen presentation, complement regulation, signaling by the B-cell receptor, and ubiquitin/proteasome-dependent degradation. From this "systems genetics" perspective, these data provide important clues for future studies on pleiotropy in IgAN and lupus nephritis.
    Clinical Journal of the American Society of Nephrology 01/2014; · 5.07 Impact Factor
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    ABSTRACT: To evaluate the effects of compound whole grain-soybean on insulin resistance and serum adipocytokines levels in impared fasting glucose population. According to inclusion and exclusion criteria, 163 cases of impared fasting glucose (IFG) Chinese Han population from the age of 40 to 75 years old, were screened from 12 community health centers of three main districts of Nanjing city by the multi-stage cluster and simple randomization method from March to September, 2008. The IFG subjects were randomly divided into the intervention group (87 individuals) and control group (76 individuals) by quasi-experimental design. The intervention group was provided with compound whole grain-soybean and health education, while only health education was provided for the control group. Body mass index (BMI), waist-to-hip ratio (WHR), lipid profiles, fasting blood glucose (FBG), fasting insulin (FINS) and homeostasis model assessment of insulin resistance (HOMA-IR), adipocytokines including leptin, lipocalin 2 (LCN-2) and adiponectin (ADP) levels were measured before and after the half a year intervention period. Chi square test was used to analyze the distribution differences. Two-sample t-test was used to campare the differences of the two groups before and after the half a year intervention period, and paried t-test was used to campare the differences between before and after intervention in the intervention group or control group. Wilcoxon rank sum test was used to campare the differences of all indexes between after and before dietary intervention. After dietary interventin for half a year on the IFG population, BMI ((24.87 ± 3.69) kg/m(2)), FBG((6.27 ± 0.24) mmol/L), FINS((7.14 ± 1.05) mU/L) , HOMA-IR (1.99 ± 0.31), leptin ((13.07 ± 2.22) µg /L), LCN-2 ((67.42 ± 18.20) µg/L) of intervention group were decreased significantly compared to the levles of BMI ((25.16 ± 4.07) kg/m(2)), FBG((6.40 ± 0.28) mmol/L), FINS ((7.32 ± 1.54) mU/L), HOMA-IR (2.08 ± 0.45), leptin ((13.43 ± 2.52) µg/L), LCN-2((74.87 ± 17.81) µg/L) before dietary intervention, t values were 4.48, 7.08, 2.05, 3.39, 3.28 and 6.36, respectively, and all P values were < 0.05, while ADP ((5.07 ± 1.51) mg/L) of intervention group after dietary intervention was increased significantly compared to the level of ADP ((4.92 ± 1.53) mg/L) before dietary intervention, t = -2.47 and P < 0.05. The medians (P25, P 75) of differences after and before dietary intervention in the inervention group were BMI (-0.25(-0.68, 0.02) kg/m(2)), FBG (-0.08 (-0.20, 0.00) mmol/L), FINS (-0.15(-0.32, 0.00) mU/L), HOMA-IR (-0.07(-0.12, -0.03)), leptin (-0.36(-0.77, 0.12) µg/L), LCN-2 (-5.85(-14.29, -0.71) µg/L) and ADP (0.15(-0.13, 0.36) mg/L), and the medians of differences of after and before dietary intervention in the control group were BMI (0.00(-0.23, 0.29) kg/m(2)), FBG (0.00(-0.03, 0.04) mmol/L), FINS (-0.01(-0.13, 0.04) mU/L), HOMA-IR (-0.01(-0.05, 0.02)), leptin (-0.07 (-0.57, 0.46) µg/L), LCN-2 (-0.85(-5.39, 1.63) µg/L) and ADP (0.02(-0.19, 0.13) mg/L). There were significantly statistical differences between them (Z values were -3.65, -4.88, -3.08, -5.23, -2.16, -4.43 and 3.05, all P values were <0.05). Dietary intervention of compound whole grain-soybean can improves glucose level, increase insulin sensitivity and ameliorate insulin resistance state of IFG population.
    Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] 01/2014; 48(1):23-7.
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    ABSTRACT: The effect of genetic markers associated with IgA nephropathy on risk of disease in sub-phenotype and progression is uncertain. Data from 2096 Chinese patients were used to create both un-weighted (uw) and weighted (w) genetic risk score (GRS). The association between GRS with disease susceptibility and clinical parameters were assessed. All nine selected single nucleotide polymorphisms (SNPs) were associated with susceptibility to IgAN. uwGRS and wGRS showed a similar fit in disease associations. With every 1-unit increase in the uwGRS, the disease risk increased by approximately 20%; whereas every one standard deviation increase in the wGRS, disease risk increased by approximately 40% ~ 60%. Association between rs3803800 and serum IgA was replicated, and risk groups in GRSs were associated with increased IgA/IgA1 levels. uwGRS9 ≥ 16 was an independent predictor for end stage renal disease (ESRD) in IgAN, with a relative risk of 2.52 (p = 6.68 × 10(-3)). In conclusion, we observed that GRSs comprising nine SNPs identified in a GWAS of IgAN were strongly associated with susceptibility to IgAN. The high risk GRS9 group had a high risk of ESRD in follow-up.
    Scientific Reports 01/2014; 4:4904. · 5.08 Impact Factor
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    ABSTRACT: Endothelial injury, which may present clinically as hypertension, proteinuria and increased von Willebrand Factor (vWF) level, is a common manifestation in IgA nephropathy (IgAN). However, causal factors for endothelial injury in IgAN are not completely understood. An imbalance of vascular endothelial growth factor/Soluble fms-like tyrosine kinase-1 (VEGF/sFlt-1) has been observed in many diseases with endothelial dysfunction, including pre-eclampsia and diabetic retinopathy, but whether it contributes to endothelial injury in IgAN requires further exploration.
    PLoS ONE 01/2014; 9(7):e101779. · 3.53 Impact Factor
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    The Journal of Rheumatology 10/2013; 40(10):1772-1773. · 3.26 Impact Factor
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    ABSTRACT: Familial juvenile hyperuricemic nephropathy (FJHN) is an autosomal dominant disorder characterized by hyperuricemia and progressive chronic kidney disease. Uromodulin gene (UMOD) mutations, leading to abnormalities of uromodulin intracellular trafficking contribute to the progress of the disease. We did UMOD screening in three Chinese FJHN families. We thus constructed mutant uromodulin express plasmids by site-mutagenesis from wild type uromodulin vector and transfected them into HEK293 (human embryonic kidney) cells. And then we detected uromodulin expression by western blot and observed intracellular distribution by immunofluorescence. We found three heterozygous mutations. Mutation Val109Glu (c.326T/A; p.Val109Glu) and mutation Pro236Gln (c.707C/A; p.Pro236Gln) were newly indentified mutations in two distinct families (family F1 and family F3). Another previously reported UMOD mutation Cys248Trp (c.744C/G; p.Cys248Trp) was detected in family F2. Phenotypes varied both within the same family and between different families. Uromodulin expression is abnormal in the patient biopsy. Functional analysis of mutation showed that mutant types of uromodulin were secreted into the supernatant medium much less when compared with wild type. In mutant type uromoudlin transfected cells, intracellular uromodulin localized less in the Golgi apparatus and more in endoplasmic reticulum(ER). Our results suggested that the novel uromodulin mutations found in the Chinese families lead to misfolded protein, which was retained in the endoplasmic reticulum, finally contributed to the phenotype of FJHN.
    Gene 08/2013; · 2.20 Impact Factor
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    ABSTRACT: To explore the effects of transcription factor ETS-1 mRNA and B lymphocyte-associated cytokines on the differentiation of B cells in systemic lupus erythematosus (SLE) patients and explore its pathogenic and clinical significance. Thirty-one SLE patients (20 active and 11 inactive) and 15 healthy controls were enrolled. CD19+ B cells were isolated with magnetic beads. The levels of ETS-1 mRNA in B cells were determined by real-time polymerase chain reaction (PCR). Flow cytometry was used to detect the altered ratio of CD19-CD138 + plasma cells and CD19 + B cells. And enzyme-linked immunosorbent assay (ELISA) was performed to detect the serum levels of B cell differentiation-related cytokines interleukin-10 (IL-10) and APRIL. Compared to the healthy controls, SLE patients showed decreased mRNA expression level of ETS-1 in B cells (Z = -4.218, P < 0.01) . Moreover, the expression level of ETS-1 mRNA was significantly negatively correlated with the proportion of CD19-CD138+ plasma cells (r = -0.359, P < 0.05) and negatively correlated with the CD19-CD138 +B cells/CD19+ plasma cells ratio (r = -0.493, P < 0.01) . However, there was no correlation in normal controls. Significant negative correlation existed between the expression level of ETS-1 mRNA in B cells and the serum levels of IL-10 and APRIL in active SLE patients. But no correlation existed in inactive group. ETS-1 may participate in the pathogenesis of SLE through its effects on the differentiation of B cells and cooperation with IL-10 and APRIL.
    Zhonghua yi xue za zhi 08/2013; 93(31):2483-6.
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    ABSTRACT: The Oxford Classification of the pathology of immunoglobulin A (IgA) nephropathy, developed in 2009, is highly predictive of renal prognosis. It has been validated in different populations, but the results remain inconsistent. Systematic review and meta-analysis. Patients with biopsy-proven primary IgA nephropathy. Studies assessing the Oxford Classification of IgA nephropathy published between January 2009 and December 2012 were included following systematic searching of the MEDLINE and EMBASE databases. 4 pathologic lesions of the Oxford Classification: mesangial hypercellularity (M), endocapillary hypercellularity (E), segmental glomerulosclerosis (S), and tubular atrophy/interstitial fibrosis (T). Kidney failure defined as doubled serum creatinine level, 50% decline in estimated glomerular filtration rate, or end-stage kidney disease. 16 retrospective cohort studies with 3,893 patients and 570 kidney failure events were included. In a multivariate model, HRs for kidney failure were 0.6 (95% CI, 0.5-0.8; P < 0.001), 1.8 (95% CI, 1.4-2.4; P < 0.001), and 3.2 (95% CI, 1.8-5.6; P < 0.001) for scores of M0 (mesangial hypercellularity score ≤0.5), S1 (presence of segmental glomerulosclerosis), and T1/2 (>25% tubular atrophy/interstitial fibrosis), respectively, without evidence of heterogeneity. Pooled results showed that E lesions were not associated with kidney failure (HR, 1.4; 95% CI, 0.9-2.0; P = 0.1), with evidence of heterogeneity (I(2) = 54.1%; P = 0.01). Crescent (C) lesions were associated with kidney failure (HR, 2.3; 95% CI, 1.6-3.4; P < 0.001), with no evidence of heterogeneity (I(2) = 14.7%; P = 0.3). All studies were retrospective. This was not an individual-patient-data meta-analysis. This study suggests that M, S, T, and C lesions, but not E lesions, are associated strongly with progression to kidney failure and thus should be included in the Oxford Classification system.
    American Journal of Kidney Diseases 06/2013; · 5.29 Impact Factor
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    ABSTRACT: Risk alleles at genome loci containing phospholipase A2 receptor 1 (PLA2R1) and HLA-DQA1 closely associate with idiopathic membranous nephropathy (IMN) in the European population, but it is unknown whether a similar association exists in the Chinese population and whether high-risk alleles promote the development of anti-PLA2R antibodies. Here, we genotyped 2132 Chinese individuals, including 1112 patients with IMN and 1020 healthy controls, for three single nucleotide polymorphisms (SNPs) within PLA2R1 and three SNPs within HLA genes. We also selected 71 patients, with varying genotypes, to assess for circulating anti-PLA2R antibody and for PLA2R expression in glomeruli. Three SNPs within PLA2R1 and one SNP within HLA-DQA1 strongly associated with IMN, and we noted gene-gene interactions involving these SNPs. Furthermore, these risk alleles strongly associated with the presence of anti-PLA2R antibodies and glomerular PLA2R expression. Among individuals who carried risk alleles for both genes, 73% had anti-PLA2R antibodies and 75% expressed PLA2R in glomeruli. In contrast, among individuals who carried protective genotypes of both genes, none had anti-PLA2R antibodies and glomerular expression of PLA2R was weak or absent. In conclusion, the interaction between PLA2R1 and HLA-DQA1 risk alleles associates with the development of IMN in the Chinese population. Individuals carrying risk alleles are predisposed to the generation of circulating anti-PLA2R autoantibodies, which may contribute to the development of IMN.
    Journal of the American Society of Nephrology 06/2013; · 8.99 Impact Factor
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    ABSTRACT: AimsThe effects of statin therapy in patients with chronic kidney disease (CKD) remain uncertain. We undertook a systematic review and meta-analysis to investigate the effects of statin on major clinical outcomes.Methods and resultsWe systematically searched MEDLINE, Embase, and the Cochrane Library for trials published between 1970 and November 2011. We included prospective, randomized, controlled trials assessing the effects of statins on cardiovascular outcomes in people with kidney disease. Summary estimates of relative risk (RR) reductions were calculated with a random effects model. Thirty-one trials that include at least one event were identified, providing data for 48 429 patients with CKD, including 6690 major cardiovascular events and 6653 deaths. Statin therapy produced a 23% RR reduction (16-30) for major cardiovascular events (P<0.001), an 18% RR reduction (8-27) for coronary events, and 9% (1-16) reduction in cardiovascular or all-cause deaths, but had no significantly effect on stroke (21%, -12 to 44) or no clear effect on kidney failure events (5%, -1 to 10). Adverse events were not significantly increased by statins, including hepatic (RR 1.13, 95% CI 0.92-1.39) or muscular disorders (RR 1.02, 95% CI 0.95-1.09). Subgroup analysis demonstrated the relative effects of statin therapy in CKD were significantly reduced in people with advanced CKD (P < 0.001) but that the absolute risk reductions were comparable.Conclusion Statin therapy reduces the risk of major cardiovascular events in patients with chronic kidney disease including those receiving dialysis.
    European Heart Journal 03/2013; · 14.10 Impact Factor
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    ABSTRACT: To discuss the possible mechanism of the whole grain-soybean compound package on dyslipidaemia rats. 44 SD rats were randomly divided into four groups: the hyperlipidaemic group, the rice-flour group, the whole grain-soybean compound package group and the negative control group by lipid profiles, fed with corresponding feed for eight weeks. Serum total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C) and low density lipoprotein cholesterol (LDL-C) were measured before and after the test. At the end of the experiment, blood samples were taken from the femoral artery, the rat organs were collected and weighted. Serum Visfatin levels and SREBP-2 mRNA and LDLR mRNA in the liver were measured. Compared with the hyperlipidaemic group and rice-flour group, the body weight, serum TC, TG and LDL-C of whole grain-soybean compound package group were significantly decreased (P < 0.05), HDL-C was significantly increased (P < 0.05). Visfatin levels were significantly decreased (P < 0.05). Gene expressions of SREBP-2 and LDLR were significantly increased (P < 0.05). Gene expression of Visfatin in whole grain-soybean compound package group was significantly lower than that in hyperlipidaemia group and rice-flour group (P < 0.05). Whole grain-soybean compound package can improve the serum lipid profiles and Visfatin of rats fed with a high fat diet. The possible mechanism is that the whole grain-soybean compound package can activate the expression of SREBP-2, LDLR and Visfatin. And then enhance the expressing activity of regulate the cholesterol metabolism by SREBP-2, LDLR and Visfatin. Ultimately, to reduce the level of rats' cholesterol, and then ameliorate the dyslipidaemia of rats.
    Wei sheng yan jiu = Journal of hygiene research 03/2013; 42(2):196-202.
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    ABSTRACT: To study the effects of four kinds of experimental diet, including high fat/cholesterol diet, Chinese wild rice diet, white rice-flour diet and basal diet on the lipotoxicity and disordered lipid metabolism in rats. 44 male SD rats were divided into four groups, the basal group, high fat/cholesterol diet group, white rice-flour group and Chinese wild rice group. All rats of four groups were given different diets. Body weights were measured every week, serum total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), free fatty acids (FFA) and leptin concentrations were measured, and liver pathology were observed. When compared with the basal diet group, the hyperlipidemic rat model was successfully made in high fat/cholesterol diet group. When compared with the high fat/cholesterol diet group and white rice-flour diet group, the serum TG and TC contents were significantly decreased (P < 0.05), and HDL-C concentration significantly increased (P < 0.05) in Chinese wild rice group. Moreover, Chinese wild rice group had lower contents of serum and liver FFA than those of the high fat/cholesterol diet group and white rice-flour diet group (P < 0.05). Although Chinese wild rice group had a lower serum leptin level than the high fat/cholesterol diet group and white rice-flour diet group, there was no significant differences among the three groups (P > 0.05). The conditions of liver cell fatty degeneration in Chinese wild rice group were slight. Compared to the white rice-flour diet, Chinese wild rice could improve the lipid metabolism and liver lipotoxicity of hyperlipidemic rats induced by high fat/cholesterol diet.
    Wei sheng yan jiu = Journal of hygiene research 03/2013; 42(2):190-5.
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    ABSTRACT: Uromodulin (UMOD) genetic variants cause familial juvenile hyperuricemic nephropathy, characterized by hyperuricemia with decreased renal excretion of UMOD and uric acid, suggesting a role for UMOD in the regulation of plasma uric acid. To determine this, we screened common variants across the UMOD locus in one community-based Chinese population of 1000 individuals and the other population from 642 American twins and siblings of European and Hispanic ancestry. Transcriptional activity of promoter variants was estimated in luciferase reporter plasmids transfected into HEK-293 cells and mIMCD3 cells. In the primary Chinese population, we found that carriers of the GCC haplotype had higher plasma uric acid, and three promoter variants were associated with plasma uric acid. UMOD promoter variants displayed reciprocal effects on urine uric acid excretion and plasma uric acid concentration, suggesting a primary effect on renal tubular handling of urate. These UMOD genetic marker-on-trait associations for uric acid were replicated in the independent American cohort. Site-directed mutagenesis at trait-associated UMOD promoter variants altered promoter activity in transfected luciferase reporter plasmids. Thus, UMOD promoter variants seem to initiate a cascade of transcriptional and biochemical changes influencing UMOD secretion, leading to altered plasma uric acid levels.Kidney International advance online publication, 23 January 2013; doi:10.1038/ki.2012.449.
    Kidney International 01/2013; · 8.52 Impact Factor

Publication Stats

1k Citations
390.12 Total Impact Points


  • 2002–2014
    • Beijing Medical University
      • • Institute of Nephrology
      • • Department of Medicine
      • • Department of Internal Medicine
      Peping, Beijing, China
  • 2009–2013
    • Southeast University (China)
      Nan-ching-hsü, Jiangxi Sheng, China
    • University Health Network
      Toronto, Ontario, Canada
    • Oxford University Hospitals NHS Trust
      • Department of Cellular Pathology
      Oxford, ENG, United Kingdom
  • 2003–2013
    • Peking University
      • Institute of Urology
      Beijing, Beijing Shi, China
  • 2012
    • Anhui Medical University
      Luchow, Anhui Sheng, China
  • 2010
    • Università degli Studi di Torino
      Torino, Piedmont, Italy
  • 2001
    • Okayama University
      Okayama, Okayama, Japan