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在法医案件的神经病理学检查中,Bystin(BYSL)作为严重缺氧缺血性改变的一种可能标志物。

Bystin (BYSL) as a possible marker of severe hypoxic-ischemic changes in neuropathological examination of forensic cases.

作者信息

Olczak Mieszko, Chutorański Dominik, Kwiatkowska Magdalena, Samojłowicz Dorota, Tarka Sylwia, Wierzba-Bobrowicz Teresa

机构信息

Department of Forensic Medicine, Medical University of Warsaw, 1 Oczki St., 02-007, Warsaw, Poland.

Departament of Neuropathology, Institute of Psychiatry and Neurology, 9 Sobieskiego St., 02-957, Warsaw, Poland.

出版信息

Forensic Sci Med Pathol. 2018 Mar;14(1):26-30. doi: 10.1007/s12024-017-9942-x. Epub 2018 Jan 18.

Abstract

Bystin (BYSL) is a 306-amino acid protein encoded in humans by the BYSL gene located on the 6p21.1 chromosome. It is conserved across a wide range of eukaryotes. BYSL was reported to be a sensitive marker for the reactive astrocytes induced by ischemia/reperfusion and chemical hypoxia in vitro and is considered to be one of the common characteristics of astrogliosis. In our study we examined whether BYSL could be used as a marker for hypoxic-ischemic changes in forensic cases. Groups suspected of acute hypoxic-ischemic changes presented strong BYSL expression in the cytoplasm of neocortical neurons especially in layers 3-5, that seemed to be short-lasting. In the hypoxic-ischemic-reperfusion group we did not find BYSL expression. BYSL expression in the cytoplasm of cortical neurons was minimal in the control group (cardiac arrest). BYSL seems to be a promising early marker of severe hypoxic-ischemic changes in neuropathological examination of forensic cases and certainly requires further studies.

摘要

Bystin(BYSL)是一种由位于6号染色体p21.1区域的BYSL基因编码的306个氨基酸的蛋白质。它在广泛的真核生物中保守。据报道,BYSL是体外缺血/再灌注和化学性缺氧诱导的反应性星形胶质细胞的敏感标志物,被认为是星形胶质细胞增生的共同特征之一。在我们的研究中,我们检测了BYSL是否可作为法医案件中缺氧缺血性变化的标志物。疑似急性缺氧缺血性变化的组在新皮质神经元的细胞质中呈现强烈的BYSL表达,尤其是在3-5层,这种表达似乎是短暂的。在缺氧缺血再灌注组中,我们未发现BYSL表达。在对照组(心脏骤停)中,皮质神经元细胞质中的BYSL表达最低。在法医案件的神经病理学检查中,BYSL似乎是严重缺氧缺血性变化的一个有前景的早期标志物,当然还需要进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbc1/5830468/c683b0d0494b/12024_2017_9942_Fig1_HTML.jpg

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