Background The proteomic landscape offers insights into potential therapeutic targets for benign prostatic hyperplasia (BPH). We used a Mendelian randomization (MR) approach and colocalization analysis to identify proteins and druggable targets associated with BPH risk.Methods Data from 4,907 circulating proteins in 35,559 individuals were analyzed. Single nucleotide polymorphisms associated with protein levels served as instrumental variables in a summary data-based MR analysis. Colocalization analysis was performed to identify overlapping genetic loci, and the DGIdb database was explored for therapeutic targets.Results MR analysis identified four proteins significantly associated with BPH. Specifically, BTN3A3, BTN3A1, and ASIP were found to be positively correlated with BPH, while RTP4 demonstrated a negative correlation. Colocalization analysis revealed strong support for BTN3A1 and RTP4 with BPH risk loci. The DGIdb database highlighted BTN3A3, BTN3A1, and RTP4 as potential therapeutic targets.Conclusion This study confirms the causal relationship between circulating proteins and BPH, with BTN3A1 as a promising therapeutic target.

Background Maribavir and valganciclovir are pharmacotherapeutic options utilized in the management of cytomegalovirus (CMV) infection post-transplantation. Despite their established utility, a comprehensive assessment of their safety profiles in real-world settings remains lacking, particularly with regards to long-term safety outcomes within a sizable cohort.Objective The study aims to analyze the adverse event (AE) profiles of maribavir and valganciclovir using data from the U.S. Food and Drug Administration Adverse Event Reporting System (FAERS). This endeavor seeks to juxtapose their respective association strengths and furnish clinicians with pertinent clinical reference points.Methods Employing a methodological framework involving the filtration of the FAERS database by specific drugs (maribavir and valganciclovir), AEs attributed to each agent were meticulously cataloged. We applied various disproportionation analysis techniques, including the reporting odds ratio (ROR), proportional reporting ratio (PRR), Bayesian confidence propagation neural network (BCPNN) and multi-item gamma Poisson shrinker (MGPS) algorithms, to identify and quantify potential signals of AEs associated with maribavir and valganciclovir.Results There were 999 and 3,454 reports for maribavir and valganciclovir, respectively. Maribavir was primarily associated with the following AEs: dysgeusia (133, 4.07%), taste disorder (127, 3.89%), death (120, 3.67%), fatigue (105, 3.21%), and diarrhea (69, 2.11%). In contrast, the most notable AEs linked to valganciclovir included death (260, 2.59%) and neutropenia (246, 2.59%), leukopenia (175, 1.74%), diarrhea (117, 1.17%), and thrombocytopenia (113, 1.13%). Remarkably, death emerged as an unexpected AE signature for both agents. Key associations were elucidated, notably taste disorder (ROR: 65.23) for maribavir and CMV colitis (ROR: 152.26) for valganciclovir, accentuating distinct AE propensities. Additionally, median onset times for AE manifestation were delineated, with maribavir exhibiting a median onset time of 40 days, compared to 28 days for valganciclovir-associated AEs.Conclusion This comprehensive analysis of FAERS data enhances our understanding of the safety. These findings hold implications for ongoing clinical surveillance efforts and provide a foundational basis for subsequent investigations into the safety profiles of these agents.

This study reports trends in acute glomerulonephritis (AGN) mortality in older adults (aged 65-94 years) and its association with age, period, and birth cohort across 204 countries and territories over the past 30 years, using data from the Global Burden of Disease (GBD) 2021 Study. An age-period-cohort model was used to estimate the overall annual percentage change in AGN mortality (net drift), annual percentage change for individuals aged 65-94 years (local drift), and longitudinal age-specific rates adjusted for period bias and period/cohort relative risks from 1992 to 2021. In 2021, there were 6213 AGN-related deaths globally (95% UI: 4460-7961). Between 1992 and 2021, the net drift for AGN mortality in high socio-demographic index (SDI) countries was 3.15% per year (95% CI 2.62-3.69), compared to - 1.18% per year in low SDI countries (95% CI - 2.01 to - 0.33). High-middle SDI countries had a decline of - 1.49% per year (95% CI - 1.80 to - 1.18), middle SDI countries - 1.52% per year (95% CI - 1.75 to - 1.28), and low-middle SDI countries - 1.78% per year (95% CI - 2.37 to - 1.20). Globally, high SDI countries showed an upward trend in AGN mortality, while others showed a downward trend. Despite the declining mortality in many regions, 15 high SDI countries, 5 high-middle SDI countries, 4 middle SDI countries, 5 low-middle SDI countries, and 3 low SDI countries showed poor or worsening outcomes in the most recent period and birth cohort. These findings suggest that AGN mortality trends are not related to a country's economic development, highlighting the need for high SDI countries to invest more in AGN-related healthcare.

Renal fibrosis, specifically tubulointerstitial fibrosis, represents the predominant pathological consequence observed in the context of progressive chronic kidney conditions. The pathogenesis of renal fibrosis encompasses a multifaceted interplay of mechanisms, including but not limited to interstitial fibroblast proliferation, activation, augmented production of extracellular matrix (ECM) components, and impaired ECM degradation. Notably, mitochondria, the intracellular organelles responsible for orchestrating biological oxidation processes in mammalian cells, assume a pivotal role within this intricate milieu. Mitochondrial dysfunction, when manifest, can incite a cascade of events, including inflammatory responses, perturbed mitochondrial autophagy, and associated processes, ultimately culminating in the genesis of renal fibrosis. This comprehensive review endeavors to furnish an exegesis of mitochondrial pathophysiology and biogenesis, elucidating the precise mechanisms through which mitochondrial aberrations contribute to the onset and progression of renal fibrosis. We explored how mitochondrial dysfunction, mitochondrial cytopathy and mitochondrial autophagy mediate ECM deposition and renal fibrosis from a multicellular perspective of mesangial cells, endothelial cells, podocytes, macrophages and fibroblasts. Furthermore, it succinctly encapsulates the most recent advancements in the realm of mitochondrial-targeted therapeutic strategies aimed at mitigating renal fibrosis.

Chronic Kidney Disease (CKD) stands as a substantial challenge within the global health landscape. The elevated metabolic demands essential for sustaining normal kidney function have propelled an increasing interest in unraveling the intricate relationship between mitochondrial dysfunction and CKD. However, the authentic causal relationship between these two factors remains to be conclusively elucidated. This study endeavors to address this knowledge gap through the Mendelian Randomization (MR) method. We utilized large-scale QTL datasets (including 31,684 eQTLs samples, 1980 mQTLs samples, and 35,559 pQTLs samples) to precisely identify key genes related to mitochondrial function as exposure factors. Subsequently, we employed GWAS datasets (comprising 480,698 CKD samples and 1,004,040 eGFRcrea samples) as outcome factors. Through a comprehensive multi-level analysis (encompassing expression, methylation, and protein quantification loci), we evaluated the causal impact of these genes on CKD and estimated glomerular filtration rate (eGFR). The integration and validation of diverse genetic data, complemented by the application of co-localization analysis, bi-directional MR analysis, and various MR methods, notably including inverse variance weighted, have collectively strengthened our confidence in the robustness of these findings. Lastly, we validate the outcomes through examination in human RNA sequencing datasets encompassing various subtypes of CKD. This study unveils significant associations between the glycine amidinotransferase (GATM) and CKD, as well as eGFR. Notably, an augmentation in GATM gene and protein expression corresponds to a diminished risk of CKD, whereas distinct methylation patterns imply an increased risk. Furthermore, a discernible reduction in GATM expression is observed across diverse pathological subtypes of CKD, exhibiting a noteworthy positive correlation with GFR. These findings establish a causal relationship between GATM and CKD, thereby highlighting its potential as a therapeutic target. This insight lays the foundation for the development of potential therapeutic interventions for CKD, presenting substantial clinical promise.

BackgroundTacrolimus is a potent macrolide immunosuppressant frequently used to prevent graft rejection in organ transplantation. Despite the known side effect of hemorrhage, there are no extensive descriptive series of patients who experience hemorrhage events associated with tacrolimus. We sought to review and describe tacrolimus-related hemorrhage events reported by healthcare professionals to the United States Food and Drug Association Adverse Event Reporting System (FAERS) database.MethodsThe FAERS database (2004q1-2022q4) was retrospectively analyzed to characterize reporting of hemorrhage adverse events (AEs) with tacrolimus. Subgroup analysis was completed on the hemorrhage.ResultsA total of 75,310 tacrolimus-associated AEs were identified, of which 1,511 cases met specific inclusion/exclusion criteria with most occurring in the gastrointestinal tract (422 cases, 27.93% of all included cases). Death was reported in 558 patients (36.93% of hemorrhage cases), the most of which occurred in cases of brain hemorrhage (219 cases, 39.25% of death cases). Among definitive organ transplants, renal transplant was the most common indication for tacrolimus (62 cases, 4.10%) followed by bone marrow transplant (44 cases, 2.91%) and liver transplant (30 cases, 1.99%).ConclusionsThis study presents the largest collective description of tacrolimus-related hemorrhage events. We additionally described a number of previously unreported tacrolimus-related hemorrhage events.

Background Many factors affect the survival rate after kidney transplantation, including laboratory tests, medicine therapy and pharmacogenomics. Tacrolimus, mycophenolate mofetil and methylprednisolone were used as an immunosuppressive regimen after kidney transplantation. The primary goal of this study was to investigate the factors affecting the tacrolimus concentrations and mycophenolate mofetil area under the curve of mycophenolic acid AUC-MPA. Secondary goals were to study the association between perioperative period laboratory tests, medicine therapy, CYP3A5 genetic polymorphisms, and survival rate in kidney renal transplant patients. Methods A total of 303 patients aged above 18 years were enrolled in this study. Their clinical characteristics, laboratory tests, and medicine therapy regimens were collected. We followed the patients for survival for 1 year after kidney transplantation. Results Multivariable logistic analyses reveal that age greater than 50 years, and the CY3A5 *3*3 genotype were independently, positively, and significantly related to tacrolimus C/D ratio at 7 days. At 1 month of follow-up, only CYP3A5 *3*3 was associated with tacrolimus C/D ratio. Basiliximab, Imipenem and cilastatin sodium, sex were associated with mycophenolate mofetil AUC-MPA at 7 days. In the COX regression analysis, a high-density lipoprotein cholesterol level≥1 mmol/L was identified as a positive independent risk factors for the survival rate, while a creatinine level ≥200 μmol/L was a negatively independent risk factors for survival rate. Conclusion These results suggest that age, genes, and drug-drug interaction can affect the concentration of tacrolimus.

人白细胞抗原G （HLA-G）是一种非经典的人主要组织相容性复合体（MHC）Ib分子，早期针对HLA-G的研究主要集中在妊娠期的免疫发育，其对母体和胎儿异种抗原的耐受性具有重要意义。近年来，越来越多的研究揭示了HLA-G在不同疾病中的作用和机制。HLA-G作为一种重要的免疫调节分子，在器官移植中的作用也有陆续报道。肾移植是终末期肾衰竭最有效的治疗选择，然而排斥反应是移植后主要的并发症，早期诊断急性、

目的 探讨不同免疫抑制剂方案对长期存活的肾移植患者肝肾功能及血糖、血脂代谢的影响.方法 收集2020年7月1日至2021年4月1日期间来吉林大学第一医院随访且存活10年以上功能稳定的肾移植患者临床血液标本,共计291例,根据不同免疫抑制方案对其进行分组,他克莫司(tacrolimus,FK)组、环孢素A(cyclosporin A,CSA)组、西罗莫司(sirolimus,SRL)组,分别进行肝肾功能、血糖血脂检测并登记各指标.结果 FK组、CSA组、SRL组中ALT、TP、UA、TC、TG、LDL-C差异有统计学意义(P<0.05).结论 不同的免疫抑制方案对长期生存肾移植术后患者肝肾功能、血糖影响不大,主要影响其脂类代谢.

BACKGROUND Diabetic nephropathy (DN) is the principal cause of end-stage renal disease. Previous studies have shown that clopidogrel can prevent the early progression of renal injury. AIM To elucidate whether clopidogrel is beneficial against DN by using a db/db mouse model. METHODS db/db mice with a higher urinary albumin/creatinine ratio (ACR) relative to age- and sex-matched wild-type control mice were randomly allocated to clopidogrel and vehicle treatment groups. Clopidogrel was administered at doses of 5, 10, and 20 mg/kg by gavage for 12 wk. Body mass, blood glucose level, and urinary creatinine and albumin concentrations in each group were measured before and after the intervention. Renal fibrosis was evaluated using periodic acid-Schiff and Masson’s trichrome staining. The renal protein expression of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and F4/80 was assessed using immunohistochemistry. Urinary TNF-α, monocyte chemoattractant protein-1 (MCP-1), and IL-6 levels were analyzed using enzyme-linked immunosorbent assay; TNF-α and IL-1β mRNA expression was measured using real-time quantitative polymerase chain reaction. The protein expression of fibronectin (FN) and collagen I was assessed using immunohistochemistry. RESULTS Clopidogrel treatment did not affect the body mass or blood glucose level of the db/db mice; however, it increased bleeding time and reduced urinary ACR in a dose-dependent manner. Immunohistochemical staining revealed an amelioration of renal fibrosis, significantly lower deposition of FN and collagen I, and significantly lower expression of the proinflammatory cytokines TNF-α and IL-1β and lower levels of urinary TNF-α and MCP-1 in the clopidogrel-treated db/db mice (P < 0.05). Furthermore, clopidogrel significantly reduced macrophage infiltration into the glomeruli of the db/db mice. CONCLUSION Clopidogrel significantly reduced renal collagen deposition and fibrosis and prevented renal dysfunction in db/db mice, most likely through inhibition of renal macrophage infiltration and the associated inflammation.

Objective:To explore the influencing factors of chronic renal allograft dysfunction (CRAD) after renal transplantation.Methods:The clinical data of 1 457 renal transplant recipients who underwent renal transplantation between January 2008 and December 2018 in the First Hospital of Jilin University were retrospective analyzed. The recipients were divided into CRAD group and control group according to whether or not the recipient with CRAD after renal transplantation. The clinical data including sex, age, body mass index (BMI) before transplantation, protopathy, dialysis before transplantation, type of kidney donor, immunity induction and immunosuppressant regiments. Group t test was used to compare the age and BMI of recipients before transplantation between CRAD group and control group. Chi-square test or Fisher exact probability method were used to compare the sex, protopathy, preoperative dialysis form, type of kidney donor, immunity induction and immunosuppressant protocols between the two groups. The variables with statistical difference in univariate analysis were included in Logistic regression for multivariate analysis. A P<0.05 was considered statistically significant.Results:The occurrence rate of CRAD was 4.19%(61/1 457). Among 61 recipients with CRAD 59 recipients received dialysis again after transplantation, and 2 recipients died of interstitial lung disease at 8 and 10 months postoperatively, respectively. The rest recipients (n=1396) were all survived with transplant kidneys. The age, preoperative BMI, preoperative dialysis form, immune induction protocol between of recipients between the two groups had significant difference (t=-2.835 and -2.722, χ2=29.400, 18.310 and 27.250, all P<0.05). Logistic regression multivariate analysis showed that age, BMI, preoperative dialysis form and immune induction protocol of recipients were independent risk factors for CRAD (all P<0.05).Conclusions:Stricter control of age and BMI of renal transplant recipients, early renal transplantation and immunity induction are beneficial to reduce the occurrence of CRAD and prolong the survival time of transplant kidnay.

目的 探讨鹅去氧胆酸(CDCA)对雄激素非依赖性前列腺癌细胞生物学特性的影响及可能机制.方法 CDCA作用于雄激素非依赖前列腺癌细胞DU145后,通过油红染色检测细胞内脂肪含量变化,观察CDCA对前列腺癌细胞内脂类的影响;采用CCK8方法测定细胞增殖,采用Real-time PCR及Western blot检测细胞脂类代谢关键因子FASN及ACC的表达.结果 CDCA能够降低DU145细胞内脂质水平,对正常前列腺细胞RWPE-1无明显作用.CDCA作用后,DU145增殖水平明显下降,且随着作用时间延长,抑制作用更显著.Real-time PCR结果显示CD-CA能够抑制FASN及ACC基因的表达水平,同时FASN的蛋白表达水平及ACC磷酸化水平在CDCA作用后均有不同程度的降低.结论 CDCA能够影响DU145细胞增殖,同时对细胞内脂类的合成有明显的抑制作用,其效应机制可能与调节脂类合成酶的表达有关.

移植肾输尿管梗阻是肾移植术后常见的泌尿系统并发症,可发生于术后任何时间,其发病率随肾移植术后时间的增加而增加[1],若不能早期诊断及治疗,易导致移植肾丧失功能。现将吉林大学第一医院2010年1月至2020年1月收治的23例移植肾输尿管梗阻患者的诊治情况报道如下。1资料与方法1.1临床资料23例移植肾输尿管梗阻患者,其中男性15例,女性8例,年龄22-70岁。

The tumor microenvironment (TME) is a complex system that plays an important role in tumor development and progression, but the current knowledge about its effect on bladder cancer (BC) is scarce. In this study, we performed a comprehensive analysis of the relationship between the TME and gene expression profiles to identify prognostic biomarkers for BC. The ESTIMATE algorithm was used to calculate immune and stromal scores of BC patients who were obtained from the Gene Expression Omnibus database. We found that the immune and stromal scores were associated with clinical characteristics and the prognosis of BC patients. Based on these scores, 104 immune-related differentially expressed genes were identified. Further, functional enrichment analysis revealed that these genes were mainly involved in the immune-related biological processes and signaling pathways. Three prognostic genes were then identified and used to establish a risk prediction model using Cox regression analyses. Kaplan-Meier survival analysis showed that the expression levels of COL1A1, COMP, and SERPINE2 significantly correlated with cancer-specific survival and overall survival of BC patients. Additionally, we validated the prognostic values of these genes using two independent cohorts from The Cancer Genome Atlas and Gene Expression Omnibus databases. Finally, the relationships between the three prognostic genes and several immune cells were evaluated using Tumor Immune Estimation Resource, indicating that the expression levels of COL1A1, COMP, and SERPINE2 correlated positively with the tumor infiltration levels of CD4(+)T cells and macrophages. In conclusion, the current study comprehensively analyzed the TME and presented immune-related prognostic genes for BC, providing new insights into immunotherapeutic strategies for BC patients.

目的:探讨沉默调节蛋白1(SIRT1)在膀胱癌组织中的表达情况及在肿瘤进展、侵袭、转移中的作用.方法:选取82例不同病理分期的膀胱尿路上皮癌患者术后石蜡标本,采用免疫组织化学技术检测癌组织及癌旁正常组织中SIRT1的表达,分析其与临床病理特征的关系.另选取15例膀胱尿路上皮癌行膀胱根治术患者的癌组织和癌旁组织,应用Real-Time PCR技术检测SIRT1 mRNA表达水平.结果:SIRT1的表达水平与临床分期、病理分级及是否转移呈相关性(P＜0.05),与性别、年龄、是否复发无相关性(P＞0.05).癌组织中SIRT1 mRNA的表达明显高于癌旁组织的表达,差异有统计学意义(P＜0.05).结论:SIRT1在膀胱癌组织呈高表达,与临床分期及转移相关,有可能作为肿瘤进展的潜在标志物及治疗靶点.

目的:探讨肾移植患者在发生不同排斥反应过程时,IL-17在血液中的表达情况及其在移植肾组织不同位置的表达特征及意义.方法:收集在我院定期随诊经病理证实的不同类型排斥反应患者的外周血液及组织病理标本,检测其IL-17基因和蛋白的表达情况,免疫组化染色观察移植肾组织中IL-17的表达位置.结果:肾移植患者在发生急性排斥反应时,IL-17在基因表达水平和血液中蛋白质含量显著升高(P<0.05).免疫组织化学染色结果显示,IL-17在急性T细胞排斥反应组肾小管和肾间质中的表达与未见异常组比较有差异(P=0.02,P=0.004),并且在小管中主要高表达于急性T细胞排斥反应,IL-17在肾小管上皮高表达与小管炎存在呈正相关(r=0.455,P=0.034).急性抗体介导排斥反应中IL-17表达与C4d沉积呈正相关(r=0.71,P=0.001).浸润于肾小球的炎细胞偶见IL-17表达,而血管上皮细胞未见IL-17表达.结论:移植肾急性排斥反应时IL-17表达升高,在各组移植肾穿刺活检组织中亦有不同程度表达,主要定位于肾小管上皮细胞及间质中浸润的炎细胞,并与小管炎严重程度及C4 d沉积呈正相关,其表达水平可作为早期监测移植肾功能状态、组织损伤以及预后判断的重要指标.

Photodynamic therapy (PDT) is one of the non-invasive and selective treatment methodologies for cancer. However, many highly efficient photosensitizers (PSs) are usually low physiological solubility, limited bioavailability and tending aggregation, impeding the effectiveness of PDT, as well as cancer resistance of PDT further reduce its therapeutic effect. Though some smart delivery systems have been developed, the problem of photosensitizer leakage/release has not been completely solved. Herein, we developed a smart therapeutic nanoplatform based on polyphotosensitizer nanogel as novel nanophotosensitizers and drug carriers. Moreover, by loading of histone deacetylase inhibitors (SAHA), it allows for enhanced synergistic therapy strategy of prostate cancer via inhibiting HIF-1α and VEGF pathways of cancer cells involved in PDT resistance. Our study presents the well-designed nanoplatform of nanogel-Ce6, which could serve as a photodynamic agent without Ce6 molecules release in the responsive environment, offering the potential to encapsulate diverse functional components for smart drug release and imaging-guided combination therapy in vitro and in vivo.

目的:探讨IL-17在大鼠肾移植急性排斥反应过程中的表达特点及其意义.方法:将大鼠随机分为正常对照组、同系基因对照组、同种异体移植组、免疫抑制剂干预组,并建立肾移植急性排斥反应模型,用RT-PCR及免疫组织化学方法检测急性排斥时IL-17在肾组织中的表达.结果:同种异体移植组在移植后第3天、5天和7天,移植肾IL-17均明显升高,与其他组相比,均有统计学意义(P＜0.05),其中以第5天为最高,差异具有统计学有意义(P＜0.05).结论:IL-17参与了大鼠肾移植急性排斥反应的发生,并为早期事件,IL-17检测可能为人类肾移植早期急性排斥反应的诊断和治疗提供理论依据.

AIM:A wealth of studies have demonstrated that abnormal cellular lipid metabolism plays an important role in prostate cancer (PCa) development. Therefore, manipulating lipid metabolism is a potential PCa therapy strategy. In this study, our goal is to investigate the role of farnesoid X receptor (FXR) in regulating the proliferation and lipid metabolism of human PCa cells following its ligand chenodexycholic acid (CDCA) treatment.METHODS:Oil Red O was used to stain lipid contents in PCa cells, and siRNA knockdown was performed to deplete FXR expression. To study the cell proliferation when treated by CDCA or FXR knockdown, cell counting kit 8 (CCK8) was adopted to evaluate tumor cell growth. Western blot was used for protein analysis.RESULTS:Our data suggest that activation of FXR by CDCA reduces lipid accumulation and significantly inhibits cells proliferation in prostate tumor cells. Instead, CDCA treatment doesn't affect normal prostate epithelial RWPE-1 cells growth in vitro. FXR activation decreases mRNA and protein levels of sterol regulatory element binding protein 1 (SREBP1) and some other key regulators involved in lipid metabolism. Depletion of FXR by siRNA attenuates the inhibitory effects.CONCLUSION:Our study indicates that activation of FXR inhibits lipid metabolism via SREBP1 pathway and further suppresses prostate tumor growth in vitro.

Objective To establish an accurate testing method for detection of Brucella and Brucella Abortus,Brucella Melitensis,Brucella suis.Methods The strains include the standard Brucella melitensis 16M,Brucella abortus 544A,the standard Brucella suis 1330s,and the clinical specimens Brucella melitensis 81190,Brucella abortus 80176,104M,Brucella suis 80177,19971,19972.All 9 strains were saved at the Base for Prevention and Control of Plague and Brucellosis,the Chinese Center for Disease Prevention and Control.DNA was extracted and used to amplify by PCR,Yersinia pestis O ∶ 9 served as control.The single nucleotide polymorphisms probes were designed on the basis of twosites (379,576) in conservative segment from Blucella flhA,and made into gene chip.According to part sequence of flhA,primers were labeled by biotin,target gene was amplified by PCR,and hybridized with the designed gene chip,and finally,biotin was used for identification.Results The length of all 9 strains were all 357 bp,consistent with expected results.The Yersinia pestis O ∶ 9 that had the same antigens with the Brucella showed no specific PCR products.At the 379 and 576 points of gene,the Brucella suis was 379G,576C,the Brucella Abortus was 379T,576T,the Brucella Melitensis was 379T,576C,all these results were identical to the designed probe sequence.Experimental verification of membrane gene chip,the Brucella suis showed color at the points of 379G,576C and F,the Brucella Abortus showed color at the points of 379T,576T and F,the Brucella Melitensis showed color at the points of 379T,576C and F.Conclusion Brucella gene chip can be used to identify Brucella rapidly.