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您的检索式：作者名="Maria Rohde"
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| 1 | NOD2-and disease-specific gene expression profiles of peripheral blood mononuclear cells from Crohn's disease patients显示文摘AIM To investigate disease-specific gene expression profiles of peripheral blood mononuclear cells(PBMCs) from Crohn's disease(CD) patients in clinical remission.METHODS Patients with CD in clinical remission or with very low disease activity according to the Crohn's disease activity index were genotyped regarding nucleotidebinding oligomerization domain 2(NOD2),and PBMCs from wild-type(WT)-NOD2 patients,patients with homozygous or heterozygous NOD2 mutations and healthy donors were isolated for further analysis.The cells were cultured with vitamin D,peptidoglycan(PGN) and lipopolysaccharide(LPS) for defined periods of time before RNA was isolated and subjected to microarray analysis using Clariom S assays and quantitative realtime PCR.NOD2-and disease-specific gene expression profiles were evaluated with repeated measure ANOVA by a general linear model.RESULTS Employing microarray assays,a total of 267 genes were identified that were significantly up-or downregulated in PBMCs of WT-NOD2 patients,compared to healthy donors after challenge with vitamin D and/or a combination of LPS and PGN(P < 0.05;threshold:≥ 2-fold change).For further analysis by real-time PCR,genes with known impact on inflammation and immunity were selected that fulfilled predefined expression criteria.In a larger cohort of patients and controls,a disease-associated expression pattern,with higher transcript levels in vitamin D-treated PBMCs from patients,was observed for three of these genes,CLEC5 A(P < 0.030),lysozyme(LYZ;P < 0.047) and TREM1(P < 0.023).Six genes were found to be expressed in a NOD2-dependent manner(CD101,P < 0.002;CLEC5 A,P < 0.020;CXCL5,P < 0.009;IL-24,P < 0.044;ITGB2,P < 0.041;LYZ,P < 0.042).Interestingly,the highest transcript levels were observed in patients with heterozygous NOD2 mutations.CONCLUSION Our data identify CLEC5 A and LYZ as CD-and NOD2-associated genes of PBMCs and encourage further studies on their pathomechanistic roles. | Holger Schufler Maria Rohde Sarah Rohde Astrid Huth Nicole Gittel Hannes Hollborn Dirk Koczan Ane Glass Georg Lamprecht Robert Jaster | 2018 | World Journal of Gastroenterology2018，24，11： | 1 |
| 2 | Absent MicroRNAs in Different Tissues of Patients with Acquired Cardiomyopathy显示文摘Micro RNAs(mi RNAs) can be found in a wide range of tissues and body ?uids, and their speci?c signatures can be used to determine diseases or predict clinical courses. The mi RNA pro?les in biological samples(tissue, serum, peripheral blood mononuclear cells or other body ?uids) differ signi?cantly even in the same patient and therefore have their own speci?city for the presented condition. Complex pro?les of deregulated mi RNAs are of high interest, whereas the importance of non-expressed mi RNAs was ignored. Since mi RNAs regulate gene expression rather negatively,absent mi RNAs could indicate genes with unaltered expression that therefore are normally expressed in speci?c compartments or under speci?c disease situations. For the ?rst time,non-detectable mi RNAs in different tissues and body ?uids from patients with different diseases(cardiomyopathies, Alzheimer's disease, bladder cancer, and ocular cancer) were analyzed and compared in this study. mi RNA expression data were generated by microarray or Taq Man PCR-based platforms. Lists of absent mi RNAs of primarily cardiac patients(myocardium, blood cells, and serum) were clustered and analyzed for potentially involved pathways using two prediction platforms, i.e., mi RNA enrichment analysis and annotation tool(mi EAA) and DIANA mi RPath.Extensive search in biomedical publication databases for the relevance of non-expressed mi RNAs in predicted pathways revealed no evidence for their involvement in heart-related pathways as indicated by software tools, con?rming proposed approach. | Christine S. Siegismund Maria Rohde Uwe Kiihl Felicitas Escher Heinz Peter Schultheiss Dirk Lassner | 2016 | Genomics, Proteomics & Bioinformatics2016，14，4： | 0 |
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