Sodium Carbonate-Promoted Formation of 5-Amino-1,2,4-thiadiazoles and 5-Amino-1,2,4-selenadiazoles with Elemental Sulfur and Selenium.

Sodium carbonate-promoted facile synthesis of 5-amino-1,2,4-thiadiazoles and 5-amino-1,2,4-selenadiazoles with elemental sulfur and selenium, respectively, was developed. This method was carried out with O2 in the air as the green oxidant, and it has several advantages, including low cost, low toxicity, and stable sulfur and selenium sources, good to excellent yields with water as the sole byproduct, simple operation, and a broad substrate scope. Preliminary mechanistic studies indicate that the formation of the 1,2,4-thiadiazole ring and the 1,2,4-selenadiazole ring undergoes different processes.

Three-Component Domino Reaction of Thioamide, Isonitriles, and Water: Selective Synthesis of 1,2,4-Thiadiazolidin-3-ones and (E)-N-(1,2-Diamino-2-thioxoethylidene)benzamides.

The three-component domino reaction of thioamides, benzyl isocyanide, and water in the presence of a catalytic amount of both Pd(dppf)Cl2 and Cu(OAc)2 afforded novel 1,2,4-thiadiazolidin-3-one cyclic compounds, whereas the same reaction with tertiary alkylisonitriles in the presence of rare earth metal salt [La(OTf)3] resulted in (E)-N-(1,2-diamino-2-thioxoethylidene)benzamide open-chain products. This divergent reaction enabled the one-pot construction of five (N-S, C-S, C-O, and two C-N) or four (C-S, C-N, C-O, and C-C) new chemical bonds. Mechanism studies indicate that the oxygen atom of the product was derived from H2O.

A comprehensive overview of oncogenic pathways in human cancer.

Alterations of biological pathways can lead to oncogenesis. An overview of these oncogenic pathways would be highly valuable for researchers to reveal the pathogenic mechanism and develop novel therapeutic approaches for cancers. Here, we reviewed approximately 8500 literatures and documented experimentally validated cancer-pathway associations as benchmarking data set. This data resource includes 4709 manually curated relationships between 1557 paths and 49 cancers with 2427 upstream regulators in 7 species. Based on this resource, we first summarized the cancer-pathway associations and revealed some commonly deregulated pathways across tumor types. Then, we systematically analyzed these oncogenic pathways by integrating TCGA pan-cancer data sets. Multi-omics analysis showed oncogenic pathways may play different roles across tumor types under different omics contexts. We also charted the survival relevance landscape of oncogenic pathways in 26 tumor types, identified dominant omics features and found survival relevance for oncogenic pathways varied in tumor types and omics levels. Moreover, we predicted upstream regulators and constructed a hierarchical network model to understand the pathogenic mechanism of human cancers underlying oncogenic pathway context. Finally, we developed `CPAD' (freely available at http://bio-bigdata.hrbmu.edu.cn/CPAD/), an online resource for exploring oncogenic pathways in human cancers, that integrated manually curated cancer-pathway associations, TCGA pan-cancer multi-omics data sets, drug-target data, drug sensitivity and multi-omics data for cancer cell lines. In summary, our study provides a comprehensive characterization of oncogenic pathways and also presents a valuable resource for investigating the pathogenesis of human cancer.

Aerobic Copper-Catalyzed Four-Component Reaction of O-Phenylenediamines, Isocyanides, and Selenium Powder for the Assembly of Benzo[4,5]imidazo[2,1-c][1,2,4]selenadiazol-3-imine Derivatives.

A convenient, four-component reaction of o-phenylenediamines, isocyanides, and selenium powder catalyzed by a natural abundant copper/air (O2) catalyst system has been developed, providing a highly step and atom economical protocol for the synthesis of benzo[4,5]imidazo[2,1-c][1,2,4]selenadiazol-3-imine derivatives with excellent yields and good functional group tolerance. This method enables the construction of an imidazo[2,1-c][1,2,4]selenadiazol ring, one N-Se bond, one C-Se bond, and three C-N bonds in a single step with only water as the byproduct. Preliminary mechanistic studies imply that the copper/air (O2)-catalyzed cyclization proceeds via a selenium-centered radical intermediate.

Palladium-catalyzed double coupling reaction of terminal alkynes with isocyanides: a direct approach to symmetrical N-aryl dialkynylimines.

A novel and efficient one-pot synthesis of symmetrical N-aryl dialkynylimines via palladium-catalyzed and copper-promoted isocyanide insertion, cross-coupling and elimination has been developed. This method features readily available starting materials, mild reaction conditions and high atom efficiency as well as simple one-pot operation, which make this strategy highly attractive. Moreover, 2-iodobenzo[f]quinoline derivatives can be obtained via electrophilic cyclization of N-aryl dialkynylimines.

Facile synthesis of 2-alkynyl oxazoles via a Ce(OTf)3-catalyzed cascade reaction of alkynyl carboxylic acids with tert-butyl isocyanide.

We developed an efficient and novel protocol to synthesize 2-alkynyl oxazoles from tert-butyl isocyanide and alkynyl carboxylic acids. This method allowed the synthesis of diversely functionalized oxazoles under mild reaction conditions, coupled with operational simplicity and these functionalized oxazoles showed a certain degree of biological activity. Moreover, compounds 2b, 2h, 2k, 2n, 2p and 2t exhibited good anticancer activities in human gastric cancer cells (MGC803) and human bladder tumor cells (T24), with IC50 below 20.0 µM.

Downregulation of long non-coding RNA MEG3 promotes proliferation, migration, and invasion of human hepatocellular carcinoma cells by upregulating TGF-ß1.

Hepatocellular carcinoma is a common malignant cancer with high incidence. And long non-coding RNAs (lncRNAs) play pivotal roles in the development of different types of cancers. In this study, we aimed to investigate the role of lncRNA maternally expressed gene 3 (MEG3) in the development and progression of hepatocellular carcinoma. Expression of MEG3 in tumor tissues and adjacent healthy tissues of hepatocellular carcinoma patients, as well as the serum of both hepatocellular carcinoma patients and healthy controls, was detected by quantitative reverse transcriptase-polymerase chain reaction. The results showed that expression level of MEG3 was significantly lower in tumor tissues than in adjacent healthy tissues. Serum level of MEG3 was also significantly lower in hepatocellular carcinoma patients than in normal controls. The receiver operating characteristic curve analysis was used to evaluate the diagnostic value of MEG3 for hepatocellular carcinoma, and the prognostic value of MEG3 for this disease was analyzed using Kaplan-Meier method. The results indicated that serum level of MEG3 was a diagnostic and prognostic marker for hepatocellular carcinoma. We also found that MEG3 small interfering Ribonucleic Acid (siRNA) silencing promoted the proliferation, migration, and invasion of hepatocellular carcinoma cells by CCK-8 assay, transwell migration, and invasion assay, respectively, while TGF-ß inhibitor treatment reduced those enhancing effects. MEG3 siRNA silencing also increased the expression level of TGF-ß1. These results indicated that downregulation of MEG3 can promote proliferation, migration, and invasion of human hepatocellular carcinoma cells by upregulating TGF-ß1 expression.

Effects of uric acid-lowering therapy on the progression of chronic kidney disease: a systematic review and meta-analysis.

OBJECTIVES: Whether uric acid levels were associated with the progression of chronic kidney disease (CKD) remained controversial. This meta-analysis was aimed to assess the effect of lowering serum uric acid therapy on the progression of CKD to clarify the role of uric acid in the progression of CKD indirectly. METHODS: Pubmed, Embase, the Cochrane library, CBM were searched for randomized controlled trials (RCTs) that assessed the efficiency of lowering serum uric acid therapy on the progression of CKD without language restriction. Summary estimates of weighted mean differences (WMDs) and relative risk (RR) were obtained by using random-effect or fixed-effect models. Sensitivity analyses were performed to identify the source of heterogeneity. RESULTS: A total of 12 randomized controlled trials with 832 CKD participants were included in the analysis. Pooled estimate for eGFR was in favor of lowering serum uric acid therapy with a mean difference (MD) of 3.88 ml/min/1.73 m2, 95% CI 1.26-6.49 ml/min/1.73 m2, p = .004 and this was consistent with results for serum creatinine. The risk of worsening of kidney function or ESRD or death was significantly decreased in the treatment group compared to the control group (RR 0.39, 95% CI 0.28-0.52, p< .01). CONCLUSIONS: Uric acid-lowering therapy may be effective in retarding the progression of CKD. Further randomized controlled trials should be performed to confirm the effect of lowering serum uric acid therapy on the progression of CKD.

Effect of BMP7 on podocyte transdifferentiation and Smad7 expression induced by hyperglycemia.

OBJECTIVE: To investigate the effect of BMP7 on the transdifferentiation and Smad7 expression of podocytes induced by high glucose in vitro and to explore its possible protective mechanisms. METHODS: Mouse podocytes were cultured and divided into normal glucose group (NG), high glucose group (HG), mannitol group, NG+BMP7 group, and HG+BMP7 group. Real-time PCR and Western blot were applied respectively to detect the mRNA and protein expression levels of synaptopodin, desmin, and Smad7. RESULTS: The cells significantly up-regulated the mRNA and protein expression of desmin and reduced the expression of both synaptopodin and Smad7 after 48 hours (vs. NG, p < 0.01). BMP7 dramatically suppressed the mRNA and protein expression of desmin and protected the expression of synaptopodin and Smad7 after incubation with high glucose for 48 hours (vs. HG, p < 0.01). CONCLUSIONS: BMP7 can inhibit the epithelial-to-mesenchymal cell transformation (EMT) of podocytes induced by high glucose; Smad7 may mediate the blunting effects of BMP7 on high glucose in podocytes.

Efficacy and initial dose determination of paricalcitol for treatment of secondary hyperparathyroidism in Chinese subjects.

AIM: Prevalence of secondary hyperparathyroidism (SHPT), a renal disease complication, is increasing in China. Available therapies may not optimally control SHPT, particularly in patients with hypercalcemia, hyperphosphatemia, and parathyroid hyperplasia. This study examined efficacy and safety of two dosing regimens of selective vitamin D receptor activator paricalcitol. MATERIALS AND METHODS: Subjects with SHPT (n = 216) undergoing hemodialysis were treated with paricalcitol i.v. for 12 weeks. One group was treated according to the EU paricalcitol package insert (PI) (initial µg dose based on iPTH/80), and the other was treated according to the US PI (initial dose of 0.04 µg/kg). Dose titration was based on iPTH and serum calcium (Ca) and phosphorus (P) levels. RESULTS: The primary endpoint of two consecutive ≥ 30% iPTH decreases was achieved by 88.6% and 55.9% of subjects in the EU and US PI groups, respectively. Noninferiority of the EU PI group vs. the US PI group was demonstrated (lower bound of the 1-sided 97.5% CI = 21.3%). Superiority of the EU PI group was shown (lower limit > 0%) and confirmed by Fisher's exact test (p < 0.001); both groups showed similar achievement of recommended KDIGO iPTH levels. Ca and P levels were relatively constant. CONCLUSION: Both EU and US PI paricalcitol dosing strategies effectively reduced iPTH levels in Chinese subjects with SHPT, with minimal impact on Ca and P levels.

Shared and divergent contribution of vitamin A and oxytocin to the aetiology of autism spectrum disorder.

Rare genetic variations contribute to the heterogeneity of autism spectrum disorder (ASD) and the responses to various interventions for ASD probands. However, the associated molecular underpinnings remain unclear. Herein, we estimated the association between rare genetic variations in 410 vitamin A (VA)-related genes (VARGs) and ASD aetiology using publicly available de novo mutations (DNMs), rare inherited variants, and copy number variations (CNVs) from about 50,000 ASD probands and 20,000 normal controls (discovery and validation cohorts). Additionally, given the functional relevance of VA and oxytocin, we systematically compared the similarities and differences between VA and oxytocin with respect to ASD aetiology and evaluated their potential for clinical applications. Functional DNMs and pathogenic CNVs in VARGs contributed to ASD pathogenesis in the discovery and validation cohorts. Additionally, 324 potential VA-related biomarkers were identified, 243 of which were shared with previously identified oxytocin-related biomarkers, while 81 were unique VA biomarkers. Moreover, multivariable logistic regression analysis revealed that both VA- and oxytocin-related biomarkers were able to predict ASD aetiology for individuals carrying functional DNM in corresponding biomarkers with an average precision of 0.94. As well as, convergent and divergent functions were also identified between VA- and oxytocin-related biomarkers. The findings of this study provide a basis for future studies aimed at understanding the pathophysiological mechanisms underlying ASD while also defining a set of potential molecular biomarkers for adjuvant diagnosis and intervention in ASD.

[Triptolide combined with irbesartan synergistically blocks podocyte injury in a type 2 diabetes rat model].

OBJECTIVE: To investigate the protective effect of combination of triptolide and irbesartan on the podocytes in a type 2 diabetic(T2DM) rat model, and evaluate its mechanism. METHODS: T2DM rats were induced by fed with high-sucrose-high-fat diet combined with a low dose of streptozocin. The rats were randomly divided into 5 groups: normal control group (NC, n = 10), diabetes group (DM, n = 11), triptolide treatment group (DT, n = 12), irbesartan treatment group (DI, n = 12) and triptolide combined with irbesartan treatment group (DTI, n = 13). Ultrastructure of podocytes was observed by electronic microscopy and urinary albumin (UAL) excretion by ELISA was determined after 8 weeks. The expression of nephrin and bone morphogenetic protein-7 (BMP-7), connective tissue growth factor (CTGF), transforming growth factor (TGF)ß(1) mRNA and proteins were detected by immunohistochemistry, real-time PCR and Western blot. RESULTS: Increased UAL was significantly attenuated in all treatment groups. Compared to NC group, UAL in DM group was increased significantly (0.45 ± 0.09 vs 6.36 ± 0.87, P < 0.01), while decreased in triptolide or irbesartan alone treatment group (2.48 ± 0.37 and 2.68 ± 0.42, both P < 0.01). Compared with those in control groups, kidney expression of nephrin, BMP-7 mRNA and proteins were downregulated while CTGF, TGFß(1) mRNA and proteins were significantly upregulated in T2DM rats. Triptolide or irbesartan each alone moderately ameliorated albuminuria and podocyte damage. However, their combined usage showed a dramatic therapeutic synergism, manifested by prevention of progressive albuminuria, restoration of the glomerular filtration barrier, reversal of the decline in slit diaphragm proteins, reduction expression of CTGF, TGFß(1), and upregulation of BMP-7. CONCLUSION: Our findings show that triptolide can increase the efficacy of irbesartan, leading to a more effective prevention of kidney disease in T2DM rat model, which may through upregulation of BMP-7 and inhibition the over-expression of CTGF and TGFß(1).

Hierarchal Porous Graphene-Structured Electrocatalysts with Fe-N5 Active Sites Modified with Fe Clusters for Enhanced Performance Toward Oxygen Reduction Reaction.

The local coordination environment around the active centers has a major impact on tuning the intrinsic activity of M-N-C catalysts. Herein, a porous graphene with Fe-N5 active sites modified with Fe clusters is successfully fabricated by using Fe3+-SCN- and NaHCO3 as the metal precursor and pore-forming agent, respectively. The unique Fe-N5 configuration accompanying Fe clusters and the improved ORR activity are confirmed by various characterization techniques and theoretical calculations. Benefiting from the pores, mass and electron transfer channels are successfully constructed, making more active sites accessible and facilitating the ORR process. As a consequence, the as-prepared catalyst has an excellent ORR activity with a half-wave potential of 0.89 V, comparable selectivity, and superior stability. In addition, a homemade primary zinc-air battery using this material as the cathode catalyst has a maximum power density of 0.205 W/cm2, revealing the potential of the as-constructed CSA-Fe-N-C catalyst to replace precious Pt catalysts.

Integrative analysis prioritised oxytocin-related biomarkers associated with the aetiology of autism spectrum disorder.

BACKGROUND: Autism spectrum disorder (ASD) is a neurodevelopmental disorder with high phenotypic and genetic heterogeneity. The common variants of specific oxytocin-related genes (OTRGs), particularly OXTR, are associated with the aetiology of ASD. The contribution of rare genetic variations in OTRGs to ASD aetiology remains unclear. METHODS: We catalogued publicly available de novo mutations (DNMs) [from 6,511 patients with ASD and 3,391 controls], rare inherited variants (RIVs) [from 1,786 patients with ASD and 1,786 controls], and both de novo copy number variations (dnCNVs) and inherited CNVs (ihCNVs) [from 15,581 patients with ASD and 6,017 controls] in 963 curated OTRGs to explore their contribution to ASD pathology, respectively. Finally, a combined model was designed to prioritise the contribution of each gene to ASD aetiology by integrating DNMs and CNVs. FINDINGS: The rare genetic variations of OTRGs were significantly associated with ASD aetiology, in the order of dnCNVs > ihCNVs > DNMs. Furthermore, 172 OTRGs and their connected 286 ASD core genes were prioritised to positively contribute to ASD aetiology, including top-ranked MAPK3. Probands carrying rare disruptive variations in these genes were estimated to account for 10∼11% of all ASD probands. INTERPRETATION: Our findings suggest that rare disruptive variations in 172 OTRGs and their connected 286 ASD core genes are associated with ASD aetiology and may be potential biomarkers predicting the effects of oxytocin treatment. FUNDING: Guangdong Key Project, National Natural Science Foundation of China, Key Laboratory of Clinical Laboratory Diagnosis and Translational Research of Zhejiang Province.

Npas3 deficiency impairs cortical astrogenesis and induces autistic-like behaviors.

Transcription factors with basic-helix-loop-helix (bHLH) motifs can control neural progenitor fate determination to neurons and oligodendrocytes. How bHLH transcription factors regulate astrogenesis remains largely unknown. Here, we report that NPAS3, a bHLH transcription factor, is a critical regulator of astrogenesis. Npas3 deficiency impairs cortical astrogenesis, correlating with abnormal brain development and autistic-like behaviors. Single-cell transcriptomes reveal that Npas3 knockout induces abnormal transition states in the differentiation trajectories from radial glia to astrocytes. Analysis of chromatin immunoprecipitation sequencing data in primary cortical astrocytes shows that NPAS3 binding targets are involved in functions of brain development and synapse organization. Co-culture assay further indicates that NPAS3-impaired astrogenesis induces synaptic deficits in wild-type neurons. Astrocyte-specific knockdown of NPAS3 in wild-type cortex causes synaptic and behavioral abnormalities associated with the core symptoms in autism. Together, our findings suggest that transcription factor NPAS3 regulates astrogenesis and its subsequent consequences for brain development and behavior.

[Diagnosis and treatment of eye diseases associated with HIV infection and AIDS].

OBJECTIVE: To investigate the manifestations and treatment principles of ocular diseases associated with human immunodeficiency virus infection (HIV) and acquired immunodeficiency syndrome (AIDS). METHODS: It was a retrospective case series. One hundred and ten patients were recruited. Two hundred and twenty eyes underwent ophthalmologic examination that included vision acuity, anterior segment and fundus examinations with papillary dilation and fundus fluorescein angiography. CD(4)(+)T-lymphocyte was counted in peripheral blood of 110 patients. Intravitreal injection of ganciclovir 400 microg was performed in 4 eyes (2 patients) with cytomegalovirus (CMV) retinitis associated with AIDS. All statistical analyses were performed using SPSS 13.0 software. The association between the age, duration of HIV infection and HIV/AIDS related ocular manifestations was analyzed by Pearson Correlation Analysis. The association between the gender and HIV/AIDS related ocular manifestations was analyzed by Pearson Chi-Square test. For comparison of the CD(4)(+)T cells counts of the patients with normal fundus, HIV retinopathy, CMV retinitis, Kruskal-Wallis Test for Several Independent Samples was used. RESULTS: Baseline visual acuity: no light perception (NLP) 5 eyes; light perception (LP) to 0.04, 10 eyes; 0.05 to 0.2, 14 eyes; 0.3 to 0.7, 62 eyes and >/= 0.8, 129 eyes. Small grayish keratin precipitates or pigment keratin precipitates were present in 25 eyes, 22 eyes had positive aqueous flare, 4 eyes had posterior synechia of the iris, 28 eyes had cataract. HIV retinopathy was present in 34 eyes. Cotton-wool spots, retinal hemorrhages, and retinal microaneurysms were found in eyes with HIV retinopathy. CMV retinitis was present in 32 eyes. The fundus manifestations of CMV retinitis included retinal vasculitis; dense, full-thickness, yellow-white lesions along vascular distribution with irregular granules at the border, and hemorrhage on the retinal surface in 26 eyes. Late stage retinopathy was demonstrated in 3 eyes characterized as atrophic retina, sclerotic and attenuated vessels, and optic nerve atrophy. Retinal detachment was found in 3 eyes. The median of CD(4)(+)T-lymphocyte counts of the patients with normal fundus was 100.0/mm(3). The median of CD(4)(+)T-lymphocyte counts of the patients with HIV retinopathy was 41.0/mm(3). The median of CD(4)(+)T-lymphocyte counts of the patients with CMV retinitis was 18.0/mm(3). The difference of CD(4)(+)T-lymphocyte counts between patients with normal fundus and HIV retinopathy was statistically significant (chi(2) = 4.848, P = 0.028). The difference of CD(4)(+)T-lymphocyte counts between patients with normal fundus and CMV retinitis was statistically significant (chi(2) = 15.696, P = 0.000). The difference of CD(4)(+)T-lymphocyte counts between patients with CMV retinitis and HIV retinopathy was statistically significant (chi(2) = 4.860, P = 0.027). Four eyes (2 patients) with CMV retinitis underwent intravitreal injection of ganciclovir 400 microg. After intravitreal injection of ganciclovir, visual acuity was improved and fundus lesions disappeared in 4 eyes. CONCLUSIONS: HIV retinopathy is a common intraocular complication in HIV-infected patients. CMV retinitis is the severest intraocular complication in patients with AIDS. Highly active anti-retroviral therapy allows immune reconstitution. Intravitreal injection of ganciclovir can effectively control CMV retinitis and save the vision.

A novel SLC12A3 splicing mutation skipping of two exons and preliminary screening for alternative splice variants in human kidney.

BACKGROUND: Gitelman's syndrome is a mild autosomal recessive disorder caused by inactivating mutations of SLC12A3. However, severe phenotype may be associated with compound heterozygous nonfunctional variants such as frameshift and splicing mutations. Because most multi-exon genes are alternatively spliced as shown by recent studies, SLC12A3, with 26 exons, is likely to be alternatively spliced as well. METHODS: A case of Gitelman's syndrome with both physical and mental retardation was investigated by genetic analysis. In addition, the alternative splice variants of SLC12A3 were screened by RT-PCR. RESULTS: A novel intron 7 and exon 8 boundary mutation (a successive 13-nucleotide transition: intron 7 as -1 G>A plus exon 8 +1 to +12 delCGGACATTTTTGinsCCGAAAATTTT) was identified in this patient besides a missense mutation Thr60Met. Further cDNA analysis revealed the novel mutation led to skipping of exons 7 and 8. Furthermore, we found an aberrant splice product skipping of exon 7 and identified two high-abundance alternative splice transcripts. CONCLUSION: This is the first report of a splice mutation of SLC12A3 with multiple-exon skipping in Gitelman's syndrome. This study provides further evidence for the severe phenotype of Gitelman's syndrome and its association with underlying mutations. Additionally, we demonstrated that the pre-mRNA of SLC12A3 was complex spliced.

(Z)-1-(3-Nitro-phen-yl)-2-(4-nitro-phen-yl)ethene.

In the mol-ecule of the title compound, C(14)H(10)N(2)O(4), the dihedral angle formed by the benzene rings is 53.66 (5)°. In the crystal structure, mol-ecules are linked into chains parallel to the [01] direction by inter-molecular C-H⋯O hydrogen-bonding inter-actions.

[Effect of content of hepatitis B virus DNA in the serum on the pathologic change in hepatitis B virus associated-glomerulonephritis].

OBJECTIVE: To investigate the correlation between the content of hepatitis B virus DNA(HBV-DNA) in the serum and the pathologic change in hepatitis B virus associated-glomerulonephritis (HBV-GN). METHODS: Forty one HBV-GN patients were divided into 3 groups by the content of HBV-DNA in the serum:low replicate group,midrange replicate group, and high replicate group. The relationship with the content of HBV-DNA in the serum and pathologic stage or change was analyzed in 35 membranous glomerulopathy patients; Effect of the content of hepatitis B virus DNA in the serum on HBVAg deposition in glomeruli of kidney was examined by immunohistochemistry; Effect of HBVAg deposition on pathologic change was observed in membranous glomerulopathy patients. RESULTS: With the multiplication of HBV-DNA in the serum, the pathologic lesion was aggravating from Stage I to Stage III in membranous glomerulopathy patients; the deposition of HBVAg in glomeruli of kidney was increasing; with the increasing of deposition of HBVAg in glomeruli of kidney, the pathologic lesion was aggravating in membranous glomerulopathy patients. CONCLUSION: With the multiplication of HBV-DNA in the serum, the deposition of HBVAg in glomeruli of kidney increases, and the pathologic lesion aggravates, which have significant correlation.