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Cold Storage Exacerbates Renal and Mitochondrial Dysfunction Following Transplantation. 冷藏加重移植后肾脏和线粒体功能障碍。
Pub Date : 2016-02-01 Epub Date: 2016-02-27
S Shrum, L A MacMillan-Crow, N Parajuli

Long-term renal function is compromised in patients receiving deceased donor kidneys which require cold storage exposure prior to transplantation. It is well established that extended cold storage induces renal damage and several labs, including our own, have demonstrated renal mitochondrial damage after cold storage alone. However, to our knowledge, few studies have assessed renal and mitochondrial function after transplantation of rat kidneys exposed to short-term (4 hr) cold storage compared to transplant without cold storage (autotransplantation). Our data reveal that cold storage plus transplantation exacerbated renal and mitochondrial dysfunction when compared to autotransplantation alone.

接受已故供体肾脏的患者在移植前需要冷藏,长期肾功能受损。众所周知,长期冷藏会导致肾脏损伤,包括我们自己的实验室在内的几个实验室已经证明了单独冷藏后肾脏线粒体损伤。然而,据我们所知,很少有研究评估短期(4小时)冷藏大鼠肾脏移植后与不冷藏移植(自体移植)相比的肾脏和线粒体功能。我们的数据显示,与单独的自体移植相比,冷藏加移植加重了肾脏和线粒体功能障碍。
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引用次数: 0
Discovering Biomarkers within the Genomic Landscape of Renal Cell Carcinoma. 发现肾细胞癌基因组景观中的生物标志物。
Pub Date : 2016-02-01 Epub Date: 2016-02-25 DOI: 10.4172/jok.1000115
Sankin A

Recent advances in molecular sequencing technology have led to the discovery of numerous biomarkers in renal cell carcinoma (RCC). These biomarkers have the potential to predict clinical outcomes and aid in clinical management decisions. The following commentary is a review of the preliminary data on some of the most promising genetic biomarker candidates.

近年来,分子测序技术的进步导致了肾细胞癌(RCC)中许多生物标志物的发现。这些生物标志物具有预测临床结果和帮助临床管理决策的潜力。下面的评论是对一些最有希望的遗传生物标记候选物的初步数据的回顾。
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引用次数: 0
Renal Mitochondrial Lipid Peroxidation during Sepsis. 脓毒症期间肾脏线粒体脂质过氧化。
Pub Date : 2016-02-01 Epub Date: 2016-02-29 DOI: 10.4172/jok.1000116
P Singh, N Parajuli, P R Mayeux, L A MacMillan-Crow

Sepsis can provoke kidney injury, which increases mortality. Human and animal studies have documented increased renal oxidative injury and mitochondrial damage during sepsis. However, few studies have attempted to dissect specific renal targets and/or types of oxidative injury using the cecal ligation and puncture (CLP) murine model of sepsis. The purpose of this short communication is to examine the extent of lipid peroxidation within renal mitochondria using CLP and blue native gel electrophoresis which separates intact mitochondrial respiratory complexes. Our results show that CLP induced increased 4-hydroxy-nonenal protein adduction (marker of lipid peroxidation) in renal homogenates and mitochondrial fractions. Blue native gel electrophoresis revealed that respiratory complex III was selectively targeted within mitochondrial fractions. This supports our prior report showing renal complex III inactivation following CLP. Future studies will identify specific renal proteins within complex III that are modified during sepsis to provide mechanistic insight on how mitochondrial respiration is inhibited during sepsis.

败血症可引起肾损伤,从而增加死亡率。人类和动物研究表明,败血症期间肾脏氧化损伤和线粒体损伤增加。然而,很少有研究试图使用盲肠结扎和穿刺(CLP)小鼠脓毒症模型解剖特定的肾脏靶点和/或氧化损伤类型。本简短通讯的目的是使用CLP和分离完整线粒体呼吸复合物的蓝色天然凝胶电泳来检查肾线粒体内脂质过氧化的程度。我们的研究结果表明,CLP诱导肾匀浆和线粒体组分中4-羟基壬烯醛蛋白内聚(脂质过氧化的标志)增加。蓝色天然凝胶电泳显示呼吸复合物III在线粒体组分中有选择性靶向。这支持了我们先前关于CLP后肾复合体III失活的报道。未来的研究将确定在脓毒症期间被修饰的复合物III中的特定肾脏蛋白,以提供脓毒症期间线粒体呼吸如何被抑制的机制见解。
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引用次数: 3
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Journal of kidney
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