Xinmei Zhao

Publications (3)9.62 Total impact

• Article: Anti-Saccharomyces cerevisiae Antibodies Associate with Phenotypes and Higher Risk for Surgery in Crohn's Disease: A Meta-Analysis.

  Zhaoxia Zhang, Chen Li, Xinmei Zhao, Chaolan Lv, Qiong He, Shan Lei, Yandong Guo, Fachao Zhi
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  ABSTRACT: Recent studies suggested that anti-Saccharomyces cerevisiae antibody (ASCA) status was associated with diagnostic findings, stratified classification phenotypes, disease activity and clinical course of Crohn's disease (CD). However, the relationship between ASCA status and phenotypes of CD remains controversial in these studies. The purpose of this study was to evaluate whether ASCA status is associated with the phenotypes and the risk of surgery in diverse populations in CD. We conducted a meta-analysis of studies assessing the association of ASCA status with phenotypes and risk of surgery in CD. Three independent reviewers undertook data extraction. We pooled odds ratios separately for the cohort and case-control studies. We identified ten cohort studies (n = 2,365) and 14 case-control studies (n = 1,887) that investigated the association of ASCA status with phenotypes and risk of surgery in CD. The meta-analysis of the cohort studies showed significant association between the ASCA-positive status and higher risk of early-onset age (OR 2.25, 95 % CI 1.41-3.57, P < 0.001), ileal involvement disease (1.70, 1.05-2.77, P = 0.03), complicated disease behavior (2.09, 1.71-2.57, P < 0.001), perianal disease (1.49, 1.14-1.94, P = 0.004), and risk for surgery (1.61, 1.29-2.01, P < 0.001). Meta-analysis of the case-control studies also showed a significantly higher risk in ileal involvement disease (1.77, 1.25-2.49, P = 0.001), complicated disease behavior (2.13, 1.70-2.68, P < 0.001), perianal disease (1.96, 1.38-2.78, P < 0.001), and risk for surgery (1.71, 1.17-2.49, P = 0.005), except for the early-onset age (1.16, 0.80-1.69, P = 0.44). This meta-analysis indicated that positive ASCA status is a risk factor for early-onset age, ileal involvement, complicated behavior, perianal disease and requirement for surgery in CD.
  Digestive Diseases and Sciences 06/2012; 57(11):2944-54. · 2.12 Impact Factor
• Article: Confirmation of three inflammatory bowel disease susceptibility loci in a Chinese cohort.

  Chaolan Lv, Xiaoming Yang, Yiyang Zhang, Xinmei Zhao, Zhengyan Chen, Jinghua Long, Yingchun Zhang, Changqing Zhong, Jia Zhi, Guopeng Yao, Bo Jiang, Fachao Zhi
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  ABSTRACT: Recent genome-wide association studies have identified a number of inflammatory bowel diseases (IBD) susceptibility loci in White populations. The aim of our study was to evaluate whether these susceptibility loci also existed in a Chinese Han IBD population. Peripheral blood DNA samples from groups of patients with Crohn's disease (CD) (n = 48), ulcerative colitis (UC) (n = 49), and healthy controls (n = 50) were genotyped for eight genes. Then, an extended analysis of the relationship between genotype and phenotype was performed. NOD2-P268S (P = 0.025) was found to contribute susceptibility to CD in the Chinese population. IL23R-rs11805303 was detected to confer a strong protective effect against UC (P = 0.010), whereas PTPN2-rs2542151 was significantly associated with an increased risk of UC (P = 0.001). Further phenotype-genotype analysis revealed that P268S was associated with early age of onset (P = 0.028), ileal disease (P = 0.003), and enteric cavity narrowing (P = 0.007). The study indicates that IL23R-rs11805303 and PTPN2-rs2542151 might contribute to the development of UC and NOD2-P268S might be involved in the etiology of CD in the Chinese Han population.
  International Journal of Colorectal Disease 03/2012; 27(11):1465-72. · 2.38 Impact Factor
• Article: Evaluation of p38 MAPK pathway as a molecular signature in ulcerative colitis.

  Xinmei Zhao, Bin Kang, Chaolan Lu, Siqi Liu, Huanjing Wang, Xiaoming Yang, Ye Chen, Bo Jiang, Jun Zhang, Youyong Lu, Fachao Zhi
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  ABSTRACT: Early diagnosis and treatment of ulcerative colitis (UC) is clinically challenging. To overcome this problem, we explored the interrelated multiplex signaling pathway to identify molecular signatures in UC by using integrated strategy in proteomics. Intestinal mucosa of 12 UC cases and 12 normal controls underwent comparative proteomic analysis. A total of 26 unique differential proteins were identified, including 12 up-regulated and 14 down-regulated in UC group. A differential protein cluster, consisting of 11 proteins involved in p38 mitogen-activated protein kinase (MAPK) pathway, was deduced and validated by Western blot. Furthermore, three proteins elicited from the protein cluster, phosphorylated p38, MAWBP and galectin-3, as a molecular signature, were analyzed by immunohistochemistry on 118 UC and normal samples. Increased expression of P-p38 and down-regulated MAWBP and/or galectin-3 were detected in UC compared to normal samples (p < 0.001). This signature correlated with disease progression of UC (p < 0.01), and classified UC risk with high sensitivity (94.83 ± 2.91%) and specificity (98.33 ± 1.65%). In addition, P38 MAPK pathway modulated the expression of the protein clusters in macrophage cell line as evidenced by the alteration with specific inhibitor SB203580. These results indicate that molecular signature of P38 MAPK pathway might be a potential biomarker for evaluating UC risk.
  Journal of Proteome Research 03/2011; 10(5):2216-25. · 5.11 Impact Factor