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Outstanding Scientists In The World Of Organ Dysfunction

机译:器官功能障碍领域的杰出科学家

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In the etiology of multiple organ dysfunction syndrome (MODS), sepsis has been considered to be representative of bacteria- and bacterial toxin-associated organ inflammation and dysfunction, while acute pancreatitis (AP) is a non-septic representative of diseases leading to the development of MODS. Dr Roland Andersson is one of a few leading scientists exploring the mechanisms of both septic and non-septic MODS, investigating the similarities between and variation in MODS induced by abdominal sepsis and AP and identifying potential inter-organ signaling mechanisms. His scientific focus has changed from single-organ damage (gut ischemia) to multiple organ dysfunction (hepato-pancreato-biliary diseases, abdominal sepsis and various inflammatory conditions), and from a single system (reticuloendothelial function) to multiple systems (leukocyte system activation, endothelial barrier dysfunction and epithelial system compromise). One of his early contributions was to understand alterations in reticuloendothelial function in multiple diseases and organs. Dr Andersson was one of the very first to provide both clinical and experimental evidence to show the migration of bacteria from the intestinal lumen to the systemic circulation and other organs in liver injury induced by major liver resection or chemicals. In addition, he was one of the first and one of the most active scientists to suggest that bacterial translocation occurs in sple-nectomy, intraperitoneal implantation, obstructive jaundice, gut ischemia and reperfusion, and AP. Dr Andersson should be greatly appreciated for his efforts to understand cellular and molecular mechanisms of AP-associated MODS, comparison of the differentiation of MODS induced by sepsis and pancreatitis, mechanisms underpinning the development of MODS and potential therapies for its prevention and treatment.
机译:在多器官功能障碍综合征(MODS)的病因学中,败血症被认为是细菌和细菌毒素相关器官炎症和功能障碍的代表,而急性胰腺炎(AP)是导致发展的疾病的非败血症性代表MODS。 Roland Andersson博士是探索败血症和非败血症MODS机理的少数领先科学家之一,研究了由腹部脓毒症和AP引起的MODS之间的相似性和变异性,并确定了潜在的器官间信号传导机制。他的科学重点已从单器官损伤(肠缺血)变为多器官功能障碍(肝胰胆管疾病,腹部脓毒症和各种炎症),从单一系统(网状内皮功能)改变为多个系统(白细胞系统激活) ,内皮屏障功能障碍和上皮系统受损)。他的早期贡献之一是了解多种疾病和器官中网状内皮功能的改变。 Andersson博士是最早提供临床和实验证据的人之一,以显示细菌在主要肝脏切除术或化学药物引起的肝损伤中从肠腔向全身循环及其他器官的迁移。此外,他是最早发现细菌移位发生在脾切除术,腹膜内植入,阻塞性黄疸,肠缺血和再灌注以及AP中的科学家之一,也是最活跃的科学家之一。应该对Andersson博士所做的努力进行了解,包括了解与AP相关的MODS的细胞和分子机制,比较脓毒症和胰腺炎引起的MODS分化,支持MODS发展的机制以及预防和治疗的潜在疗法,这一点应受到高度赞赏。

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