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20篇 您的检索式:作者名="Suofu"
    题名 作者 年代 出处 被引量
1Matrix metalloproteinase-2 or-9 deletions protect against hemorrhagic transformation during early stage of cerebral ischemia and reperfusion显示文摘Suofu Y Clark JF Broderick JP 2012Neuroscience2012,212,:1
2Matrix metalloproteinase- 2 or -9 deletions protect against hemorrhagic transformation during early stage of cerebral ischemia and reperfusion 显示文摘Suofu Y Clark JF Broderick JP 2012Neuroscience2012,212,:1
3Prevention of Oxidative Stress-Induced Retinal Pigment Epithelial Cell Death by the PPAR γ Agonist, 15-Deoxy-Delta 12, 14-Prostaglandin J 2显示文摘Jason Y. Chang Puran S. Bora Nalini S. Bora Suofu Qin 2008PPAR Research2008,,:1
4Peroxynitrite decomposition catalyst prevents matrixmetalloproteinase activation and neurovascular injury afterprolonged cerebral ischemia in rats 显示文摘Yalikun Suofu Joseph Clark Joseph Broderick 2010J Neurochem2010,115,5:1
5Proteomic identification of an upregulated isoform of annexin A3 in the rat brain following reversible cerebral ischemia 显示文摘Junker H Suofu Y Venz S 2007Olia2007,55,16:1
6Matrix metalloproteinase- 2 or - 9 deletions protect against hemorrhagic transfor-mation during early stage of cerebral ischemia and reperfusion显示文摘Suofu Y Clark JF Broderick JP 2012Neuroscience2012,212,:1
7Proteomics identification of the involvement of the mitochondrial rieske protein in epilepsy显示文摘Junker H Spote K Suofu Y 2005Epilepsia2005,46,:1
8Matrix met-alloproteinase-2 or -9 deletions protect against hemorrhagictransformation during early stage of cerebral ischemia andreperfusion 显示文摘SUOFU Y CLARK JF BRODERICK JP 2012Neuroscience2012,212,:1
9Matrix metalloprotei- nase-2 or -9 deletions protect against hemorrhagic transforma- tion during early stage of cerebral ischemia and reperfusion 显示文摘Suofu Y Clark JF Broderick JP 2012Neuroseience2012,212,:1
10Suofu Qin’s work on studies of cell survival signaling in cancer and epithelial cells显示文摘Reactive oxygen species (ROS) encompass a variety of diverse chemical species including superoxide anions, hydrogen peroxide, hydroxyl radicals and peroxynitrite, which are mainly produced via mitochondrial oxidative metabolism, enzymatic reactions, and light-initiated lipid peroxidation. Over-production of ROS and/or decrease in the antioxidant capacity cause cells to undergo oxi- dative stress that damages cellular macromolecules such as proteins, lipids, and DNA. Oxidative stress is associated with ageing and the development of agerelated diseases such as cancer and age-related macular degeneration. ROS activate signaling pathways that promote cell survival or lead to cell death, depending on the source and site of ROS production, the specific ROS generated, the concentration and kinetics of ROS generation, and the cell types being challenged. However, how the nature and compartmentalization of ROS contribute to the pathogenesis of individual diseases is poorly understood. Consequently, it is crucial to gain a comprehensive understanding of the molecular bases of cell oxidative stress signaling, which will then provide novel therapeutic opportunities to interfere with disease progression via targeting specific signaling pathways.Currently, Dr. Qin's work is focused on inflammatory and oxidative stress responses using the retinal pigment epithelial (RPE) cells as a model. The study of RPE cell inflammatory and oxidative stress responses has successfully led to a better understanding of RPE cell biology and identification of potential therapeutic targets.Suofu Qin, Retinal Disease Research, Department of Biological Sciences, Allergan, Inc., 2525 Dupont Drive, Irvine, CA 92612-1599, United States 2010World Journal of Biological Chemistry2010,1,12:1
11Proteomic identification of the involvement of the mitochondrial rieske protein in epilepsy显示文摘Junker H Spate K Suofu Y 2005Epilepsia2005,46,:1
12Matrix metalloproteinase-2 Deletions protect against hemorrhagic transformation after 1 h of cerebral ischemia and 23h of reperfusion显示文摘Lu A Suofu Y Guan F 2013Neuroscience2013,253,:1
13Matrix metalloproteinase-2 deletions protect against hemorrhagic transformation after 1 hour of cere- bral ischemia and 23 hours of reperfusion显示文摘Lu A Suofu Y Guan F 2013Neuroscienee2013,253,3:1
14Proteomic identification of the involvement of the mitochondrial rieske protein in epilepsy显示文摘Junker H Spate K Suofu Y 2005Epilepsia2005,46,3:1
15Matrix metalloproteinase-2 or-9 deletions protect against hemorrhagic transformation during early stage of cerebral ischemia and reperfusion显示文摘Suofu Y Clark JF Broderick JP 2012Neuroscience2012,212,:1
16Matrix metalloprotein- ase-2 or-9 deletions protect against hemorrhagic transforma- tion during early stage of cerebral ischemia and reperfusion 显示文摘Suofu Y Clark JF Broderick JP 2012Neuroscience2012,212,:1
17Proteomic identification of the involvement of the mitochondriai rieske protein in epilepsy 显示文摘Junker H Spate K Suofu Y 2005Epilepsia2005,46,3:1
18Proteomic identification of the involvement of the mitochondrial rieske protein in epilepsy 显示文摘Junker H Spate K Suofu Y 2005Epilepsia2005,46,3:1
19Peroxynitrite decomposition catalyst prevents matrix metalloproteinase activation and neurovascular injury after prolonged cerebral ischemia in rats显示文摘Suofu Y Clark J Broderick J 0,,:1
20Matrix metalloproteinase- 2 or -9 deletions protect against hemorrhagic transformation during early stage of cerebral ischemia and reperfusion显示文摘Suofu Y Clark JF Broderick JP etal 2012Neuroseience2012,212,:1
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