可能因为您的浏览器不支持样式,您可以更新您的浏览器到最新版本,以获取对此功能的支持,访问下面的网站,获取关于浏览器的信息:
[1]臧益民,樊荣. 加强多学科协作,争取心血管病研究取得新进展[J]. 心脏杂志, 2006, 18(5):483-488.
[2]王焕亮,周长青,王春玲,等. HMGB1细胞因子作用研究进展[J]. 医学综述, 2009, 15(7):963-966.
[3]卢淑云,张胜兰. 高迁移率族蛋白B1及其与炎症反应相关性的研究进展[J]. 实用医药杂志, 2008, 25(1):103-105.
[4]Herold K, Moser B, Chen Y, et al. Receptor for advanced glycation end products (RAGE) in a dash to the rescue: inflammatory signals gone awry in the primal response to stress[J]. J Ieukoc Biol, 2007, 82(2):204-201.
[5]宫玉玲,邢启崇. 高迁移率族蛋白B1与动脉粥样硬化[J]. 中国动脉硬化杂志, 2008, 16(09):747-749.
[6] 李法权,廖伟,王梦洪. 脂多糖诱导人脐静脉内皮细胞分泌高迁移族蛋白B1及NF-κB调控的实验研究[J]. 江西医药, 2009, 44(05):428-429.
[7]Inoue K, Kawahara K, Biswas KK, et al. HMGB1 expression by activated vascular smooth muscle ceHs in advanced human atherosclerosis plaques[J]. Cardiovasc Pathol, 2007, 16(3):136-143.
[8] Porto A, Palumbo R, Pieroni M, et al. Smooth muscle cells in human atherosclerotic plaques secrete an d proliferate in response to high mobility group box 1 protein[J]. FASEB J,2006, 20(14):2565-2566.
[9]Yamada S, Yakabe K, Ishii J , et al. New high mobility group box 1assay system[J]. Clin Chim Acta, 2006, 372(1-2):173-178.
[10]王焕亮,周长青,李东亮,等. 高迁移率族蛋白B1及其生物学效应研究进展[J]. 中华现代外科学杂志, 2006, 3(22):1806-1809.
[11]周宁,费丽萍. 血清高迁移率族蛋白B1与冠状动脉病变程度相关性的探讨[J]. 疑难病杂志, 2008, 7(4):222-223.
[12]Takeno M, Yasuda S, Oisuka Y, et al. Impact of metabolic syndrome on the long-term survival of patients with acute myocardial infarction[J]. Circ J, 2008, 72(3):415-419.
[13]潘喜峰. 细胞因子对急性心肌梗死的影响及其相关作用机制的研究进展[J]. 中国医药导报, 2006, 6(24):6-8.
[14]王晓武,张卫达,罗林,等. 大鼠心肌梗死后心肌高迁移率族蛋白HMGB1的时程变化[J]. 南方医科大学学报, 2008, 28(9):1688-1690.
[15]Giallauria F, Cirillo P, Lucci R, et al. Autonomic dysfunction is associated with high mobility group box-1 levels in patients after acute myocardial infarction[J]. Atherosclerosis, 2010, 208(1):280-284.
[16]Yamada S, Maruyama I. HMGB l, a novel inflammatory cytokine[J]. Clin Chim Acta, 2007, 375(1-2 ):36-42.
[17]Germani A, Limana F, Capogrossi MC. Pivotal advances: high-mobility group box 1 protein--a cytokine with a role in cardiac repair[J]. J Leukoc Biol, 2007, 81(1):41-45.
[18]陈雪峰,何桂珍,董良广,等. TLR4及内源性配体对缺血-再灌注损伤的作用[J]. 基础医学与临床, 2008, 28(12):1334-1335.
[19]Kohno T, Anzai T, Naito K, et al. Role of high-mobility group box 1 protein in post-infarction healing process and left ventricular remodeling[J]. Cardiovasc Res, 2009, 81(3):565-573.
[20]Hu X, Jiang H, Bai Q, et al. Increased serum HMGB1 is related to the severity of coronary artery stenosis[J]. Clin Chim Acta, 2009, 406(1-2):139-142.
[21]刘秋影,陈国千. 胞外高迁移率族蛋白B1与缺血/再灌注损伤的关系[J]. 医学综述, 2009, 15(15):2259-2261.
[22]Andrassy M,Volz HC, Igwe JC, et al. High mobility group box 1 inischemia reperfusion injury ofthe heart[J]. Circulation, 2008, 117(25):3216-3226.
[23]Oozawa S, Mori S, Kanke T, et al. Effects of HMGB1 on ischemia reperfusion injury in the rat heart[J]. Circ J, 2008, 2(7): 1178-1184.
[24]Tsuchihashi S, Zhai Y, Bo Q, et al. Heme oxygenase-1 mediated cytoprotection against liver ischemia and reperfusion injury: inhibition of type-1 interferon signaling[J]. Transplantation, 2007, 83(12):1628-1634.
[25]Kaczorowski DJ, Nakao A, Vallabhaneni R, et al. Mechanisms of Toll-like receptor 4(TLR4)-mediated inflammation after cold ischemia/reperfusion in the heart[J]. Transplantation, 2009, 87(10):1455-1463.
[26]Chavakis E, Hain A, Vinci M, et al. High mobility group box activaties integrin dependent homing of endothelial progenitor cells[J]. Circ Res, 2007, 100 (2):204-212.
[27]Li W, Sama AE, Wang H. Role of HMGB1 in cardiovascular diseases[J]. Curr Opin Pharmacol, 2006, 6(2):130-135.
[28]姚咏明,徐珊,盛志勇,等. 高迁移率族蛋白B1的组织损伤效应及其干预途径[J]. 中国医学科学院学报, 2007, 29(4):493-495.
29]Das UN. Is pyruvate an endogenous anti-inflammatory molecule?[J]. Nutrition, 2006, 22(9):965-972.
[30]李冬玲,臧伟进,刘兵行. 迷走神经和乙酰胆碱对缺血性心脏病的可能抗炎保护作用[J]. 心脏杂志, 2008, 20(2):219-222.
[31]Wang H,Li W,Li J, et al. The aqueous extract of a popular herbal nutrient supplement, Angelica sinensis, protects mice against lethal endotoxemia and sepsis[J]. J Nutr, 2006, 136(2):360-365.
[32]Chen X, Li W, Wang H. More tea for septic patients? -Green tea may reduce endotoxin-induced release of high mobility group box 1 (HMGB1) and other pro-inflammatory cytokines[J]. Med Hypotheses, 2006, 66(3):660-663.
[33] Li W, Li J, Ashok M,et al. A cardiovascular drug rescues mice from lethal sepsis by selectively attenuating a late-acting proinflammatory mediator, high mobility group box 1[J]. J Immunol, 2007, 178(6):3856-3864.