1999
The contribution of various NOS gene products to HIV-1 coat protein (gp120)-mediated retinal ganglion cell injury.
Dreyer E, Zurakowski D, Gorla M, Vorwerk C, Lipton S. The contribution of various NOS gene products to HIV-1 coat protein (gp120)-mediated retinal ganglion cell injury. Investigative Ophthalmology & Visual Science 1999, 40: 983-9. PMID: 10102296.Peer-Reviewed Original ResearchConceptsNitric oxide synthaseHIV-1 coat proteinRetinal ganglion cell injuryIsoforms of NOSNitric oxideNeuronal nitric oxide synthaseGanglion cell injuryRetinal ganglion cellsPresence of nNOSNOS-deficient miceWild-type miceNeuronal lossExcitotoxic pathwayIntravitreal injectionGanglion cellsGp120 toxicityNeuronal pathologyNOS inhibitorOxide synthaseHIV-1Cell injuryControl animalsNervous systemGp120Pathologic statesMice Deficient in Mac-1 (CD11b/CD18) Are Less Susceptible to Cerebral Ischemia/Reperfusion Injury
Soriano S, Coxon A, Wang Y, Frosch M, Lipton S, Hickey P, Mayadas T. Mice Deficient in Mac-1 (CD11b/CD18) Are Less Susceptible to Cerebral Ischemia/Reperfusion Injury. Stroke 1999, 30: 134-139. PMID: 9880401, DOI: 10.1161/01.str.30.1.134.Peer-Reviewed Original ResearchConceptsTransient focal cerebral ischemiaRegional cerebral blood flowMac-1-deficient miceFocal cerebral ischemiaCerebral blood flowMac-1Cerebral ischemiaBrain sectionsBlood flowCerebral ischemia/reperfusion injuryFocal ischemia/reperfusionIschemia/reperfusion injuryLeft middle cerebral arteryCerebral cell deathLeukocyte beta2 integrinsIschemic brain tissueReperfusion-induced injuryMiddle cerebral arteryIschemia/reperfusionWild-type miceLaser Doppler flowmeterWild-type cohortsMac-1 deficiencyMacrophage-1 antigenInfarct volume
1998
ICAM-1 dependent pathway is not involved in the development of neuronal apoptosis after transient focal cerebral ischemia
Soriano S, Wang Y, Lipton S, Dikkes P, Gutierrez-Ramos J, Hickey P. ICAM-1 dependent pathway is not involved in the development of neuronal apoptosis after transient focal cerebral ischemia. Brain Research 1998, 780: 337-341. PMID: 9507184, DOI: 10.1016/s0006-8993(97)01298-5.Peer-Reviewed Original ResearchConceptsFocal cerebral ischemiaCerebral ischemiaTerminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) stainingICAM-1-dependent pathwayTransient focal cerebral ischemiaICAM-1-deficient miceDUTP-biotin nick end labeling stainingNick end labeling stainingICAM-1 deficiencyNeuronal cell deathEnd labeling stainingPresence of apoptosisIschemic hemisphereNontransgenic littermatesDeficient miceTemporary MCAONeuronal apoptosisBrain sectionsDependent pathwayApoptotic cellsIschemiaNecrosisCell deathMiceApoptosis
1996
Intercellular adhesion molecule‐1‐deficient mice are less susceptible to cerebral ischemia‐reperfusion lnjury
Soriano S, Lipton S, Wang Y, Xaio M, Springer T, Gutierrez‐Ramos J, Hickey P. Intercellular adhesion molecule‐1‐deficient mice are less susceptible to cerebral ischemia‐reperfusion lnjury. Annals Of Neurology 1996, 39: 618-624. PMID: 8619547, DOI: 10.1002/ana.410390511.Peer-Reviewed Original ResearchConceptsIntercellular adhesion molecule-1Transient focal cerebral ischemiaICAM-1-deficient miceFocal cerebral ischemiaCerebral ischemiaIntercellular adhesion molecule-1-deficient miceNeutrophil adhesionLeft middle cerebral arteryICAM-1 deficiencyMiddle cerebral arteryTransient focal ischemiaAdhesion molecule-1Wild-type littermatesInducible adhesion moleculesInfarction volumeCerebral injuryReperfusion periodCerebral arteryFocal ischemiaNeutrophil emigrationIschemic areaInflammatory processNeurological damageMolecule-1Ischemia