Delayed Treatment of Ischemia/Reperfusion Brain Injury: Extended Therapeutic Window with the Proteosome Inhibitor MLN519
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[1] M. Fisher. Recommendations for Advancing Development of Acute Stroke Therapies: Stroke Therapy Academic Industry Roundtable 3 , 2003, Stroke.
[2] P. Elliott,et al. Proteasome inhibition ablates activation of NF-kappa B in myocardial reperfusion and reduces reperfusion injury. , 2003, American journal of physiology. Heart and circulatory physiology.
[3] F. Tortella,et al. Delayed Treatment with MLN519 Reduces Infarction and Associated Neurologic Deficit Caused by Focal Ischemic Brain Injury in Rats via Antiinflammatory Mechanisms Involving Nuclear Factor-κB Activation, Gliosis, and Leukocyte Infiltration , 2003, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[4] P. Elliott,et al. Early clinical experience with the novel proteasome inhibitor PS-519. , 2002, British journal of clinical pharmacology.
[5] F. Tortella,et al. Quantitative Real-Time RT—PCR Analysis of Inflammatory Gene Expression Associated with Ischemia—Reperfusion Brain Injury , 2002, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[6] M. Chopp,et al. Postischemic (6-Hour) Treatment With Recombinant Human Tissue Plasminogen Activator and Proteasome Inhibitor PS-519 Reduces Infarction in a Rat Model of Embolic Focal Cerebral Ischemia , 2001, Stroke.
[7] P. Elliott,et al. The proteasome: a new target for novel drug therapies. , 2001, American journal of clinical pathology.
[8] F. Tortella,et al. Neuroprotective efficacy and therapeutic window of the high-affinity N-methyl-D-aspartate antagonist conantokin-G: in vitro (primary cerebellar neurons) and in vivo (rat model of transient focal brain ischemia) studies. , 2000, The Journal of pharmacology and experimental therapeutics.
[9] F. Tortella,et al. Proteasome inhibitor PS519 reduces infarction and attenuates leukocyte infiltration in a rat model of focal cerebral ischemia. , 2000, Stroke.
[10] K. Satoh,et al. Inflammatory Mediators of Cerebral Endothelium: A Role in Ischemic Brain Inflammation , 2000, Brain pathology.
[11] X. C. Lu,et al. Neuroprotection (focal ischemia) and neurotoxicity (electroencephalographic) studies in rats with AHN649, a 3-amino analog of dextromethorphan and low-affinity N-methyl-D-aspartate antagonist. , 1999, The Journal of pharmacology and experimental therapeutics.
[12] M. Barinaga. Stroke-Damaged Neurons May Commit Cellular Suicide , 1998, Science.
[13] D. Stephenson,et al. Drug-induced neuroprotection from global ischemia is associated with prevention of persistent but not transient activation of nuclear factor-kappaB in rats. , 1998, Stroke.
[14] X. C. Lu,et al. Dextromethorphan protects against cerebral injury following transient, but not permanent, focal ischemia in rats. , 1997, Life sciences.
[15] William Slikker,et al. Fluoro-Jade: a novel fluorochrome for the sensitive and reliable histochemical localization of neuronal degeneration , 1997, Brain Research.
[16] F. Barone,et al. Reperfusion following focal stroke hastens inflammation and resolution of ischemic injured tissue , 1994, Brain Research Bulletin.
[17] F. Barone,et al. Development of tissue damage, inflammation and resolution following stroke: An immunohistochemical and quantitative planimetric study , 1993, Brain Research Bulletin.
[18] L. Pitts,et al. Rat middle cerebral artery occlusion: evaluation of the model and development of a neurologic examination. , 1986, Stroke.