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Andras Perl于匈牙利布达佩斯的Semmelweis大学获得了他的MD和博士学位。他被培训为Semmelweis的内科居民,是罗切斯特大学的风湿病学/免疫学。他在罗切斯特大学罗切斯特大学塞梅利斯举办了教师职位,罗斯威尔公园纪念研究所和纽约州立大学(南阳)。自1997年以来,他一直是医药,微生物学和免疫学教授,自2001年以来,自2001年以来,自2003年纽约纽约州立大学,纽约州立大学,纽约州立大学,纽约,纽约州纽约大学。他的研究专注于病毒的相互作用和宿主基因组和信号通路,其在狼疮中介导异常的T细胞活化。他的实验室确定了HRES-1内源性逆转录病毒,将其映射到染色体1Q42,并将Rab4a鉴定为其基因产物通过增加的受体回收赋予狼疮的易感性。他的实验室发现了狼疮T细胞中的线粒体功能障碍,其特征在于线粒体超极化(MHP)和ATP耗尽,使坏死易患死亡。来自T细胞的坏死材料的增加的增加是B细胞和树突细胞的重要激活剂,SLE中的炎症。雷帕霉素(MTOR)的哺乳动物靶标的激活,其用作MHP和受体再循环调节剂的传感器,是生物标志物和狼疮治疗的靶标。T细胞功能障碍的另一个生物标志物,细胞内谷胱甘肽的耗竭通过用N-乙酰半胱氨酸处理来靶向。 Both of these clinical studies have been approved by the FDA. The human transaldolase gene was originally identified and its role in cell type-specific regulation of the pentose phosphate pathway, MHP, and apoptosis has been characterized in this laboratory. The deficiency of transaldolase was recently revealed a genetic cause of male infertility, chronic progressive diseases of the liver, leading to steatosis, steatohepatitis, cirrhosis, cancer, as well as systemic autoimmunity, which may be preventable by treatment with N-acetylcysteine. His laboratory has published over 150 original peer-reviewed papers, authored chapters in rheumatology and immunology textbooks, trained over 30 PhD students and postdoctoral fellows, received funding from the National Institutes of Health, the National Multiple Sclerosis Society, the Arthritis Foundation, the American Lupus Society and the Alliance for Lupus Research. He authors and edited textbooks, such Autoimmunity Methods and Protocols, 1st edition in 2004 and 2nd edition in 2012. He has been listed among the Best Doctors in Central New York and in America since 2007.