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供体特异性抗体阳性且活检正常的肾移植患者中基于发病机制的转录特征。

A pathogenesis-based transcript signature in donor-specific antibody-positive kidney transplant patients with normal biopsies.

作者信息

Ó Broin P, Hayde N, Bao Y, Ye B, Calder R B, de Boccardo G, Lubetzky M, Ajaimy M, Pullman J, Colovai A, Akalin E, Golden A

机构信息

Department of Genetics, Albert Einstein College of Medicine, Bronx, NY, USA.

Division of Pediatric Nephrology, University of Texas Health Science Center, Houston, TX, USA.

出版信息

Genom Data. 2014 Oct 12;2:357-60. doi: 10.1016/j.gdata.2014.10.005. eCollection 2014 Dec.

Abstract

Affymetrix Human Gene 1.0-ST arrays were used to assess the gene expression profiles of kidney transplant patients who presented with donor-specific antibodies (DSAs) but showed normal biopsy histopathology and did not develop antibody-mediated rejection (AMR). Biopsy and whole-blood profiles for these DSA-positive, AMR-negative (DSA +/AMR-) patients were compared to both DSA-positive, AMR-positive (DSA +/AMR +) patients as well as DSA-negative (DSA -) controls. While individual gene expression changes across sample groups were relatively subtle, gene-set enrichment analysis using previously identified pathogenesis-based transcripts (PBTs) identified a clear molecular signature involving increased rejection-associated transcripts in AMR - patients. Results from this study have been published in Kidney International (Hayde et al., 2014 [1]) and the associated data have been deposited in the GEO archive and are accessible via the following link: http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE50084.

摘要

采用Affymetrix人类基因1.0-ST芯片评估肾移植患者的基因表达谱,这些患者存在供者特异性抗体(DSA),但活检组织病理学正常且未发生抗体介导的排斥反应(AMR)。将这些DSA阳性、AMR阴性(DSA +/AMR -)患者的活检和全血谱与DSA阳性、AMR阳性(DSA +/AMR +)患者以及DSA阴性(DSA -)对照进行比较。虽然各样本组间的个体基因表达变化相对细微,但使用先前鉴定的基于发病机制的转录本(PBT)进行的基因集富集分析确定了一个明确的分子特征,即AMR -患者中与排斥相关的转录本增加。本研究结果已发表于《国际肾脏杂志》(Hayde等人,2014 [1]),相关数据已存入GEO数据库,可通过以下链接获取:http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE50084

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a8d/4536051/465a47155ad6/gr1.jpg

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