On ischemic brain injury in genetically altered mice.
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[1] P. Carmeliet,et al. Tissue plasminogen activator (tPA) deficiency exacerbates cerebrovascular fibrin deposition and brain injury in a murine stroke model: studies in tPA-deficient mice and wild-type mice on a matched genetic background. , 1999, Arteriosclerosis, thrombosis, and vascular biology.
[2] R. Busto,et al. Middle cerebral artery occlusion in the mouse by intraluminal suture coated with poly-l-lysine: neurological and histological validation , 1999, Brain Research.
[3] M. Ross,et al. Age-Dependent Increase in Ischemic Brain Injury in Wild-Type Mice and in Mice Lacking the Inducible Nitric Oxide Synthase Gene , 1999, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[4] C J Epstein,et al. Manganese Superoxide Dismutase Mediates the Early Release of Mitochondrial Cytochrome C and Subsequent DNA Fragmentation after Permanent Focal Cerebral Ischemia in Mice , 1999, The Journal of Neuroscience.
[5] E. Connolly,et al. CD18-mediated neutrophil recruitment contributes to the pathogenesis of reperfused but not nonreperfused stroke. , 1999, Stroke.
[6] Markus Schwaninger,et al. NF-κB is activated and promotes cell death in focal cerebral ischemia , 1999, Nature Medicine.
[7] A. Buchan,et al. Tissue plasminogen activator does not increase neuronal damage in rat models of global and focal ischemia , 1999, Neurology.
[8] H. Bolay,et al. Occlusion of the MCA by an intraluminal filament may cause disturbances in the hippocampal blood flow due to anomalies of circle of Willis and filament thickness , 1999, Brain Research.
[9] M. Maines,et al. Overexpression of Heme Oxygenase‐1 Is Neuroprotective in a Model of Permanent Middle Cerebral Artery Occlusion in Transgenic Mice , 1999, Journal of neurochemistry.
[10] C. Iadecola,et al. The Transcription Factor Interferon Regulatory Factor 1 Is Expressed after Cerebral Ischemia and Contributes to Ischemic Brain Injury , 1999, The Journal of experimental medicine.
[11] KazuoKitagawa,et al. Amelioration of Hippocampal Neuronal Damage After Global Ischemia by Neuronal Overexpression of BCL-2 in Transgenic Mice , 1998 .
[12] M. Hori,et al. Deficiency of Intercellular Adhesion Molecule 1 Attenuates Microcirculatory Disturbance and Infarction Size in Focal Cerebral Ischemia , 1998, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[13] G. Mies,et al. Attenuated c-fos mRNA Induction after Middle Cerebral Artery Occlusion in CREB Knockout Mice Does Not Modulate Focal Ischemic Injury , 1998, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[14] M. Mishina,et al. Attenuation of Focal Ischemic Brain Injury in Mice Deficient in the ε1 (NR2A) Subunit of NMDA Receptor , 1998, The Journal of Neuroscience.
[15] J. Dichgans,et al. Extended therapeutic window for caspase inhibition and synergy with MK-801 in the treatment of cerebral histotoxic hypoxia , 1998, Cell Death and Differentiation.
[16] R. Pearlstein,et al. Regional CBF in apolipoprotein E‐deficient and wild type mice during focal cerebral ischemia , 1998, Neuroreport.
[17] M. Hori,et al. Cerebral Ischemia after Bilateral Carotid Artery Occlusion and Intraluminal Suture Occlusion in Mice: Evaluation of the Patency of the Posterior Communicating Artery , 1998, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[18] A. Roses,et al. Apolipoprotein E Isoform-Specific Differences in Outcome from Focal Ischemia in Transgenic Mice , 1998, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[19] Guo-Yuan Yang,et al. Reduced Ischemic Brain Injury in Interleukin-1β Converting Enzyme—Deficient Mice , 1998, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[20] S. Lipton,et al. Tissue plasminogen activator (tPA) increase neuronal damage after focal cerebral ischemia in wild-type and tPA-deficient mice , 1998, Nature Medicine.
[21] J. B. Hutchins,et al. Mitochondrial Manganese Superoxide Dismutase Prevents Neural Apoptosis and Reduces Ischemic Brain Injury: Suppression of Peroxynitrite Production, Lipid Peroxidation, and Mitochondrial Dysfunction , 1998, The Journal of Neuroscience.
[22] S. Lipton,et al. ICAM-1 dependent pathway is not involved in the development of neuronal apoptosis after transient focal cerebral ischemia , 1998, Brain Research.
[23] Makoto Kawase,et al. Mitochondrial Susceptibility to Oxidative Stress Exacerbates Cerebral Infarction That Follows Permanent Focal Cerebral Ischemia in Mutant Mice with Manganese Superoxide Dismutase Deficiency , 1998, The Journal of Neuroscience.
[24] S. Lipton,et al. Enhanced neuronal death from focal ischemia in AMPA-receptor transgenic mice. , 1997, Brain research. Molecular brain research.
[25] R. Busto,et al. Transient Middle Cerebral Artery Occlusion by Intraluminal Suture: I. Three-Dimensional Autoradiographic Image-Analysis of Local Cerebral Glucose Metabolism—Blood Flow Interrelationships during Ischemia and Early Recirculation , 1997, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[26] Fangyi Zhang,et al. Delayed Reduction of Ischemic Brain Injury and Neurological Deficits in Mice Lacking the Inducible Nitric Oxide Synthase Gene , 1997, The Journal of Neuroscience.
[27] M D Ginsberg,et al. Transient Middle Cerebral Artery Occlusion by Intraluminal Suture: II. Neurological Deficits, and Pixel-Based Correlation of Histopathology with Local Blood Flow and Glucose Utilization , 1997, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[28] D. Choi. Background genes: out of sight, but not out of brain.... , 1997, Trends in Neurosciences.
[29] Hee-Sup Shin,et al. Mutant Mice and Neuroscience: Recommendations Concerning Genetic Background , 1997, Neuron.
[30] S. Snyder,et al. Poly(ADP-ribose) polymerase gene disruption renders mice resistant to cerebral ischemia , 1997, Nature Medicine.
[31] M. Moskowitz,et al. Strain-related differences in susceptibility to transient forebrain ischemia in SV-129 and C57black/6 mice. , 1997, Stroke.
[32] C. Epstein,et al. Overexpression of CuZn-superoxide dismutase reduces hippocampal injury after global ischemia in transgenic mice. , 1997, Stroke.
[33] E. Connolly,et al. Exacerbation of cerebral injury in mice that express the P-selectin gene: identification of P-selectin blockade as a new target for the treatment of stroke. , 1997, Circulation research.
[34] M. Moskowitz,et al. Attenuation of Transient Focal Cerebral Ischemic Injury in Transgenic Mice Expressing a Mutant ICE Inhibitory Protein , 1997, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[35] T. Yanagihara,et al. C57BL/6 strain is most susceptible to cerebral ischemia following bilateral common carotid occlusion among seven mouse strains: selective neuronal death in the murine transient forebrain ischemia , 1997, Brain Research.
[36] M. Moskowitz,et al. Enlarged Infarcts in Endothelial Nitric Oxide Synthase Knockout Mice are Attenuated by Nitro-L-Arginine , 1996, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[37] M D Ginsberg,et al. Middle cerebral artery occlusion in the rat by intraluminal suture. Neurological and pathological evaluation of an improved model. , 1996, Stroke.
[38] M. Mattson,et al. Altered neuronal and microglial responses to excitotoxic and ischemic brain injury in mice lacking TNF receptors , 1996, Nature Medicine.
[39] Koroshetz Wj,et al. Tissue plasminogen activator for acute ischemic stroke. , 1996, The New England journal of medicine.
[40] Joseph P. Broderick,et al. Tissue plasminogen activator for acute ischemic stroke. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. , 1995 .
[41] M. Moskowitz,et al. Effects of cerebral ischemia in mice deficient in neuronal nitric oxide synthase. , 1994, Science.
[42] C. Epstein,et al. Brain infarction is not reduced in SOD-1 transgenic mice after a permanent focal cerebral ischemia. , 1993, Neuroreport.
[43] C. Epstein,et al. Attenuation of focal cerebral ischemic injury in transgenic mice overexpressing CuZn superoxide dismutase. , 1991, Proceedings of the National Academy of Sciences of the United States of America.
[44] W. Pulsinelli,et al. Hypothermia but not the N-methyl-D-aspartate antagonist, MK-801, attenuates neuronal damage in gerbils subjected to transient global ischemia , 1990, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[45] S. Lipton,et al. Mice deficient in Mac-1 (CD11b/CD18) are less susceptible to cerebral ischemia/reperfusion injury. , 1999, Stroke.
[46] A. Martin-Villalba,et al. NF-kappaB is activated and promotes cell death in focal cerebral ischemia. , 1999, Nature medicine.
[47] P. Carmeliet,et al. Role of plasminogen system components in focal cerebral ischemia , 1999 .
[48] M. Mishina,et al. Attenuation of focal ischemic brain injury in mice deficient in the epsilon1 (NR2A) subunit of NMDA receptor. , 1998, Journal of Neuroscience.
[49] E. Connolly,et al. Cerebral protection in homozygous null ICAM-1 mice after middle cerebral artery occlusion. Role of neutrophil adhesion in the pathogenesis of stroke. , 1996, The Journal of clinical investigation.
[50] Joakim Bjorkdahl. Reduced brain edema and infarction volume in mice lacking the neuronal isoform of nitric oxide synthase after transient MCA occlusion , 1996 .