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本文引用的文献

1
Radiation-Induced Lung Injury: Assessment and Management.放射性肺损伤:评估与管理。
Chest. 2019 Jul;156(1):150-162. doi: 10.1016/j.chest.2019.03.033. Epub 2019 Apr 15.
2
Radiation Nephropathy in a Nonhuman Primate Model of Partial-Body Irradiation With Minimal Bone Marrow Sparing-Part 2: Histopathology, Mediators, and Mechanisms.部分躯体全身照射非人类灵长类动物模型中的放射性肾病-第 2 部分:组织病理学、介质和机制。
Health Phys. 2019 Mar;116(3):409-425. doi: 10.1097/HP.0000000000000935.
3
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Health Phys. 2019 Mar;116(3):401-408. doi: 10.1097/HP.0000000000000960.
4
Efficacy of Neulasta or Neupogen on H-ARS and GI-ARS Mortality and Hematopoietic Recovery in Nonhuman Primates After 10-Gy Irradiation With 2.5% Bone Marrow Sparing.在 2.5%骨髓保护下接受 10Gy 照射后,非人类灵长类动物的 Neulasta 或 Neupogen 对 H-ARS 和 GI-ARS 死亡率和造血恢复的疗效。
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5
Acute and Chronic Kidney Injury in a Non-Human Primate Model of Partial-Body Irradiation with Bone Marrow Sparing.骨髓保护的局部身体照射非人灵长类动物模型中的急性和慢性肾损伤
Radiat Res. 2017 Dec;188(6):661-671. doi: 10.1667/RR24857.1. Epub 2017 Oct 16.
6
The Banff 2015 Kidney Meeting Report: Current Challenges in Rejection Classification and Prospects for Adopting Molecular Pathology.《2015年班夫肾脏会议报告:排斥反应分类的当前挑战及采用分子病理学的前景》
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Intra-renal arterial injection of autologous bone marrow mesenchymal stromal cells ameliorates cisplatin-induced acute kidney injury in a rhesus Macaque mulatta monkey model.自体骨髓间充质干细胞经肾内动脉注射可改善食蟹猴恒河猴模型顺铂诱导的急性肾损伤。
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The prolonged gastrointestinal syndrome in rhesus macaques: the relationship between gastrointestinal, hematopoietic, and delayed multi-organ sequelae following acute, potentially lethal, partial-body irradiation.食蟹猴的迁延性胃肠道综合征:急性、潜在致死性全身部分照射后胃肠道、造血和迟发性多器官后遗症之间的关系。
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辐射性肾病非人灵长类动物模型中细胞炎症的缺乏。

Lack of Cellular Inflammation in a Non-human Primate Model of Radiation Nephropathy.

机构信息

Departments of Medicine, University of Maryland, School of Medicine, Baltimore, MD.

Radiation Oncology, University of Maryland, School of Medicine, Baltimore, MD.

出版信息

Health Phys. 2020 Nov;119(5):588-593. doi: 10.1097/HP.0000000000001329.

DOI:10.1097/HP.0000000000001329
PMID:32941291
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8932376/
Abstract

Inflammation is commonly cited as a mechanism of delayed effects of acute radiation exposure (DEARE). Confirmation of its presence could provide significant insight to targeted use of treatments or mitigators of DEARE. We sought to quantify the presence of cellular inflammation in kidneys of non-human primates that developed acute and chronic kidney injury after a partial body irradiation exposure. We show herein that cellular inflammation is not found as a component of either acute or chronic kidney injury. Other mechanistic pathways of injury must be sought.

摘要

炎症通常被认为是急性辐射暴露延迟效应(DEARE)的机制之一。确认其存在可以为靶向治疗或减轻 DEARE 提供重要的见解。我们试图定量分析部分身体辐射暴露后发生急性和慢性肾损伤的非人灵长类动物肾脏中细胞炎症的存在。本文表明,细胞炎症不是急性或慢性肾损伤的组成部分。必须寻找其他损伤的机制途径。