2020
Mural Cell-Specific Deletion of Cerebral Cavernous Malformation 3 in the Brain Induces Cerebral Cavernous Malformations
Wang K, Zhang H, He Y, Jiang Q, Tanaka Y, Park IH, Pober JS, Min W, Zhou HJ. Mural Cell-Specific Deletion of Cerebral Cavernous Malformation 3 in the Brain Induces Cerebral Cavernous Malformations. Arteriosclerosis Thrombosis And Vascular Biology 2020, 40: 2171-2186. PMID: 32640906, DOI: 10.1161/atvbaha.120.314586.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosis Regulatory ProteinsBrainCell CommunicationCell MovementCells, CulturedCoculture TechniquesEndothelial CellsFemaleFocal AdhesionsGene DeletionGenetic Predisposition to DiseaseHemangioma, Cavernous, Central Nervous SystemHumansMaleMembrane ProteinsMice, KnockoutMicrovesselsMyocytes, Smooth MusclePaxillinPericytesPhenotypeProtein StabilityProto-Oncogene ProteinsSignal TransductionConceptsCerebral cavernous malformationsBrain mural cellsCCM lesionsMural cellsCavernous malformationsSevere brain hemorrhageCCM pathogenesisSmooth muscle cellsWeeks of ageCell-specific deletionMural cell coverageBrain pericytesBrain hemorrhageNeonatal stageBrain vasculatureLesionsEntire brainMuscle cellsCerebral cavernous malformation 3Endothelial cellsMicePericytesSpecific deletionAdhesion formationPathogenesisTissue plasminogen activator mobilizes neutrophils and T cells that exacerbate hemorrhagic transformation in stroke
Shi K, Liu Q, Jia D, Yang X, Zou M, Shi S, Dong J, Sheth K, Wang X, Shi F. Tissue plasminogen activator mobilizes neutrophils and T cells that exacerbate hemorrhagic transformation in stroke. The Journal Of Immunology 2020, 204: 64.21-64.21. DOI: 10.4049/jimmunol.204.supp.64.21.Peer-Reviewed Original ResearchTissue plasminogen activatorT cellsEmbolic strokeHemorrhagic transformationNeurovascular unitThrombolytic therapyBrain hemorrhageEffects of tPAPlasminogen activatorFocal embolic strokeIschemic stroke patientsMyeloid cell recruitmentMigration of neutrophilsTPA thrombolysisHemorrhagic complicationsIschemic strokeLymphocyte egressEndothelial injuryNeurological functionStroke patientsImmune modulationRat modelCell recruitmentImmune invasionNeutrophils
2008
New Definition and Natural History of Patients With Diffuse Pulmonary Arteriovenous Malformations Twenty-Seven–Year Experience
Pierucci P, Murphy J, Henderson KJ, Chyun DA, White RI. New Definition and Natural History of Patients With Diffuse Pulmonary Arteriovenous Malformations Twenty-Seven–Year Experience. CHEST Journal 2008, 133: 653-661. PMID: 18198252, DOI: 10.1378/chest.07-1949.Peer-Reviewed Original ResearchConceptsDiffuse pulmonary arteriovenous malformationsPulmonary arteriovenous malformationsBilateral involvementArteriovenous malformationsOxygen saturationInitial oxygen saturationSegmental pulmonary arteriesHigh-risk groupOperative deathsLung transplantConsecutive patientsDuodenal ulcerPulmonary arterySignificant morbidityArtery originLiver necrosisFemale genderBrain hemorrhagePatientsMortality rateNatural historyYears' experienceHemoptysisHemorrhageDeath
2005
The Evolving Role of Acute Stroke Imaging in Intravenous Thrombolytic Therapy: Patient Selection and Outcomes Assessment
Sims J, Schwamm L. The Evolving Role of Acute Stroke Imaging in Intravenous Thrombolytic Therapy: Patient Selection and Outcomes Assessment. Neuroimaging Clinics Of North America 2005, 15: 421-440. PMID: 16198950, DOI: 10.1016/j.nic.2005.06.001.Peer-Reviewed Original ResearchConceptsPatient selectionIntravenous thrombolytic therapyStroke pathophysiologyThrombolytic trialsPenumbral tissueAcute strokeLarge infarctionCerebral ischemiaRisk stratificationThrombolytic therapyCT perfusionStroke mechanismBrain hemorrhageTherapeutic successCT angiographyUnenhanced CTOutcome assessmentPotential future roleEarly signsEarly trialsMR imagingThrombolysisInfarctionTrialsEvolving role
2001
Risk Factors for Misdiagnosis of Subarachnoid and Intracerebral Hemorrhage
Oen-Hsiao J, Kernan W, Viscoli C, Brass L, Morgenstern L, Awad I, Wilterdink J, Feldmann E, Brott T, Horwitz R. Risk Factors for Misdiagnosis of Subarachnoid and Intracerebral Hemorrhage. Stroke 2001, 32: 322-322. DOI: 10.1161/str.32.suppl_1.322-b.Peer-Reviewed Original ResearchRisk factorsAlarm symptomsIntracerebral hemorrhageOdds ratioBrain hemorrhageInitial evaluationHistory of hypertensionLower stroke riskLow-risk patientsAppropriate diagnostic evaluationBrain CT scanPresence of headachePrimary care physiciansAdditional risk factorsCase-control studyLogistic regression analysisHospital emergency roomNeck painStroke riskYounger patientsHSP patientsCare physiciansStroke ProjectControl subjectsEmergency room
1992
Cerebral Hemorrhage With Biopsy-Proved Amyloid Angiopathy
Yong W, Robert M, Secor D, Kleikamp T, Vinters H. Cerebral Hemorrhage With Biopsy-Proved Amyloid Angiopathy. JAMA Neurology 1992, 49: 51-58. PMID: 1728264, DOI: 10.1001/archneur.1992.00530250055016.Peer-Reviewed Original ResearchConceptsBiopsy specimensAcute clinical presentationComputed tomographic scanFocal neurological deficitsBrain biopsy specimensTransient ischemic attackBiopsy-provedClinical presentationRing enhancementLoss of consciousnessRadiological featuresImpending hemorrhageTomographic scanIntracerebral hemorrhageLobar hemorrhageNeurological deficitsBiopsy materialImmunohistochemical findingsImmunohistochemical studiesIntraparenchymal bleedingHemorrhageCerebral hemorrhageIschemic attackBrain hemorrhagePatients
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