Fas System Activation in Perihematomal Areas After Spontaneous Intracerebral Hemorrhage
Apoptosis has been implicated as the prominent form of cell death in the brain perihematomal region in animal models and in autopsy or postsurgical human studies. Both the Fas system and caspase activation play a central role in apoptotic pathways. The aims of this study were to investigate soluble...
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| Veröffentlicht in: | Stroke (1970) 2008-06, Vol.39 (6), p.1730-1734 |
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| creator | DELGADO, Pilar CUADRADO, Eloy ROSELL, Anna ALVAREZ-SABIN, José ORTEGA-AZNAR, Arantxa HERNANDEZ-GUILLAMON, Mar PENALBA, Anna MOLINA, Carlos A MONTANER, Joan |
| description | Apoptosis has been implicated as the prominent form of cell death in the brain perihematomal region in animal models and in autopsy or postsurgical human studies. Both the Fas system and caspase activation play a central role in apoptotic pathways. The aims of this study were to investigate soluble Fas (s-Fas) plasma levels after acute intracerebral hemorrhage (ICH), to determine its influence on clinical and radiologic features, and to assess Fas receptor and Fas ligand (Fas-L) protein expression in human ICH brain tissue.
s-Fas plasma levels were determined on admission in 78 consecutive ICH patients and serially in a subgroup of 21 of them, at the time of neurologic assessment, by means of ELISA. ICH and perihematomal edema volumes were determined at baseline and on follow-up computed tomography scans, and ICH and perihematomal edema growth was calculated. The presence of Fas receptor and Fas-L was assessed in different brain tissue samples by immunoblotting from 6 deceased ICH patients and from 2 control subjects.
Mortality reached 20.5% of patients at the third month, and 48% of survivors had an unfavorable outcome (modified Rankin Scale score >/=3). The baseline s-Fas level in ICH patients was significantly lower than in healthy controls [160 (160-245) vs 269 (230-332) pg/mL, P |
| doi_str_mv | 10.1161/STROKEAHA.107.500876 |
| format | Article |
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s-Fas plasma levels were determined on admission in 78 consecutive ICH patients and serially in a subgroup of 21 of them, at the time of neurologic assessment, by means of ELISA. ICH and perihematomal edema volumes were determined at baseline and on follow-up computed tomography scans, and ICH and perihematomal edema growth was calculated. The presence of Fas receptor and Fas-L was assessed in different brain tissue samples by immunoblotting from 6 deceased ICH patients and from 2 control subjects.
Mortality reached 20.5% of patients at the third month, and 48% of survivors had an unfavorable outcome (modified Rankin Scale score >/=3). The baseline s-Fas level in ICH patients was significantly lower than in healthy controls [160 (160-245) vs 269 (230-332) pg/mL, P<0.001], returning to normal values by 24 hours (P<0.05 for all determinations). Regarding radiologic features, the baseline s-Fas value was found to be inversely correlated to perihematomal edema growth at follow-up (r=-0.33, P=0.041). Finally, Fas-L content was highest in the perihematomal area compared with contralateral and remote ipsilateral areas in ICH patient and control samples.
A decreased plasma s-Fas level together with an increased Fas-L amount in perihematomal brain tissue suggest Fas-mediated apoptosis involvement in this disease.</description><identifier>ISSN: 0039-2499</identifier><identifier>EISSN: 1524-4628</identifier><identifier>DOI: 10.1161/STROKEAHA.107.500876</identifier><identifier>PMID: 18403741</identifier><identifier>CODEN: SJCCA7</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Aged ; Aged, 80 and over ; Apoptosis ; Biological and medical sciences ; Biomarkers - analysis ; Biomarkers - blood ; Brain - blood supply ; Brain - diagnostic imaging ; Brain - pathology ; Brain Edema - blood ; Brain Edema - complications ; Brain Edema - physiopathology ; Brain Infarction - blood ; Brain Infarction - etiology ; Brain Infarction - physiopathology ; Cerebral Hemorrhage - blood ; Cerebral Hemorrhage - complications ; Cerebral Hemorrhage - physiopathology ; Death Domain Receptor Signaling Adaptor Proteins - metabolism ; Disease Progression ; Down-Regulation - physiology ; Fas Ligand Protein - analysis ; Fas Ligand Protein - blood ; fas Receptor - analysis ; fas Receptor - blood ; Female ; Hematologic and hematopoietic diseases ; Humans ; Male ; Medical sciences ; Middle Aged ; Nerve Degeneration - blood ; Nerve Degeneration - etiology ; Nerve Degeneration - physiopathology ; Neurology ; Platelet diseases and coagulopathies ; Predictive Value of Tests ; Reference Values ; Tomography, X-Ray Computed ; Up-Regulation - physiology ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Stroke (1970), 2008-06, Vol.39 (6), p.1730-1734</ispartof><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c448t-14b85c6569f197d0f317cf1b300ca88966fff6140cb5ec504b5752fff1e84b2d3</citedby><cites>FETCH-LOGICAL-c448t-14b85c6569f197d0f317cf1b300ca88966fff6140cb5ec504b5752fff1e84b2d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3673,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20390857$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18403741$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>DELGADO, Pilar</creatorcontrib><creatorcontrib>CUADRADO, Eloy</creatorcontrib><creatorcontrib>ROSELL, Anna</creatorcontrib><creatorcontrib>ALVAREZ-SABIN, José</creatorcontrib><creatorcontrib>ORTEGA-AZNAR, Arantxa</creatorcontrib><creatorcontrib>HERNANDEZ-GUILLAMON, Mar</creatorcontrib><creatorcontrib>PENALBA, Anna</creatorcontrib><creatorcontrib>MOLINA, Carlos A</creatorcontrib><creatorcontrib>MONTANER, Joan</creatorcontrib><title>Fas System Activation in Perihematomal Areas After Spontaneous Intracerebral Hemorrhage</title><title>Stroke (1970)</title><addtitle>Stroke</addtitle><description>Apoptosis has been implicated as the prominent form of cell death in the brain perihematomal region in animal models and in autopsy or postsurgical human studies. Both the Fas system and caspase activation play a central role in apoptotic pathways. The aims of this study were to investigate soluble Fas (s-Fas) plasma levels after acute intracerebral hemorrhage (ICH), to determine its influence on clinical and radiologic features, and to assess Fas receptor and Fas ligand (Fas-L) protein expression in human ICH brain tissue.
s-Fas plasma levels were determined on admission in 78 consecutive ICH patients and serially in a subgroup of 21 of them, at the time of neurologic assessment, by means of ELISA. ICH and perihematomal edema volumes were determined at baseline and on follow-up computed tomography scans, and ICH and perihematomal edema growth was calculated. The presence of Fas receptor and Fas-L was assessed in different brain tissue samples by immunoblotting from 6 deceased ICH patients and from 2 control subjects.
Mortality reached 20.5% of patients at the third month, and 48% of survivors had an unfavorable outcome (modified Rankin Scale score >/=3). The baseline s-Fas level in ICH patients was significantly lower than in healthy controls [160 (160-245) vs 269 (230-332) pg/mL, P<0.001], returning to normal values by 24 hours (P<0.05 for all determinations). Regarding radiologic features, the baseline s-Fas value was found to be inversely correlated to perihematomal edema growth at follow-up (r=-0.33, P=0.041). Finally, Fas-L content was highest in the perihematomal area compared with contralateral and remote ipsilateral areas in ICH patient and control samples.
A decreased plasma s-Fas level together with an increased Fas-L amount in perihematomal brain tissue suggest Fas-mediated apoptosis involvement in this disease.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Biomarkers - analysis</subject><subject>Biomarkers - blood</subject><subject>Brain - blood supply</subject><subject>Brain - diagnostic imaging</subject><subject>Brain - pathology</subject><subject>Brain Edema - blood</subject><subject>Brain Edema - complications</subject><subject>Brain Edema - physiopathology</subject><subject>Brain Infarction - blood</subject><subject>Brain Infarction - etiology</subject><subject>Brain Infarction - physiopathology</subject><subject>Cerebral Hemorrhage - blood</subject><subject>Cerebral Hemorrhage - complications</subject><subject>Cerebral Hemorrhage - physiopathology</subject><subject>Death Domain Receptor Signaling Adaptor Proteins - metabolism</subject><subject>Disease Progression</subject><subject>Down-Regulation - physiology</subject><subject>Fas Ligand Protein - analysis</subject><subject>Fas Ligand Protein - blood</subject><subject>fas Receptor - analysis</subject><subject>fas Receptor - blood</subject><subject>Female</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Nerve Degeneration - blood</subject><subject>Nerve Degeneration - etiology</subject><subject>Nerve Degeneration - physiopathology</subject><subject>Neurology</subject><subject>Platelet diseases and coagulopathies</subject><subject>Predictive Value of Tests</subject><subject>Reference Values</subject><subject>Tomography, X-Ray Computed</subject><subject>Up-Regulation - physiology</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0039-2499</issn><issn>1524-4628</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1L5EAQhpvFRUfXf7BILnrLbFWnv3IMoo4oKDsuewydnmqN5GPs7hH890Zm0KOngpenXoqnGPuNMEdU-Gf58Pfu5qJaVHMEPZcARqsfbIaSi1wobvbYDKAocy7K8oAdxvgMALwwcp8doBFQaIEz9v_Sxmz5FhP1WeVS-2pTOw5ZO2T3FNon6m0ae9tlVaAJrHyikC3X45DsQOMmZtdDCtZRoCZM1IL6MYQn-0i_2E9vu0jHu3nE_l1ePJwv8tu7q-vz6jZ3QpiUo2iMdEqq0mOpV-AL1M5jUwA4a0yplPdeoQDXSHISRCO15FOGZETDV8URO9v2rsP4sqGY6r6Njrpue1-tQatSovkW5KC5QI4TKLagC2OMgXy9Dm1vw1uNUH-Yrz_NT4mut-antZNd_6bpafW1tFM9Aac7wEZnOx_s4Nr4yfHpV2CkLt4BLSWM0w</recordid><startdate>20080601</startdate><enddate>20080601</enddate><creator>DELGADO, Pilar</creator><creator>CUADRADO, Eloy</creator><creator>ROSELL, Anna</creator><creator>ALVAREZ-SABIN, José</creator><creator>ORTEGA-AZNAR, Arantxa</creator><creator>HERNANDEZ-GUILLAMON, Mar</creator><creator>PENALBA, Anna</creator><creator>MOLINA, Carlos A</creator><creator>MONTANER, Joan</creator><general>Lippincott Williams & Wilkins</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>20080601</creationdate><title>Fas System Activation in Perihematomal Areas After Spontaneous Intracerebral Hemorrhage</title><author>DELGADO, Pilar ; CUADRADO, Eloy ; ROSELL, Anna ; ALVAREZ-SABIN, José ; ORTEGA-AZNAR, Arantxa ; HERNANDEZ-GUILLAMON, Mar ; PENALBA, Anna ; MOLINA, Carlos A ; MONTANER, Joan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c448t-14b85c6569f197d0f317cf1b300ca88966fff6140cb5ec504b5752fff1e84b2d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Biomarkers - analysis</topic><topic>Biomarkers - blood</topic><topic>Brain - blood supply</topic><topic>Brain - diagnostic imaging</topic><topic>Brain - pathology</topic><topic>Brain Edema - blood</topic><topic>Brain Edema - complications</topic><topic>Brain Edema - physiopathology</topic><topic>Brain Infarction - blood</topic><topic>Brain Infarction - etiology</topic><topic>Brain Infarction - physiopathology</topic><topic>Cerebral Hemorrhage - blood</topic><topic>Cerebral Hemorrhage - complications</topic><topic>Cerebral Hemorrhage - physiopathology</topic><topic>Death Domain Receptor Signaling Adaptor Proteins - metabolism</topic><topic>Disease Progression</topic><topic>Down-Regulation - physiology</topic><topic>Fas Ligand Protein - analysis</topic><topic>Fas Ligand Protein - blood</topic><topic>fas Receptor - analysis</topic><topic>fas Receptor - blood</topic><topic>Female</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Nerve Degeneration - blood</topic><topic>Nerve Degeneration - etiology</topic><topic>Nerve Degeneration - physiopathology</topic><topic>Neurology</topic><topic>Platelet diseases and coagulopathies</topic><topic>Predictive Value of Tests</topic><topic>Reference Values</topic><topic>Tomography, X-Ray Computed</topic><topic>Up-Regulation - physiology</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>DELGADO, Pilar</creatorcontrib><creatorcontrib>CUADRADO, Eloy</creatorcontrib><creatorcontrib>ROSELL, Anna</creatorcontrib><creatorcontrib>ALVAREZ-SABIN, José</creatorcontrib><creatorcontrib>ORTEGA-AZNAR, Arantxa</creatorcontrib><creatorcontrib>HERNANDEZ-GUILLAMON, Mar</creatorcontrib><creatorcontrib>PENALBA, Anna</creatorcontrib><creatorcontrib>MOLINA, Carlos A</creatorcontrib><creatorcontrib>MONTANER, Joan</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Stroke (1970)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>DELGADO, Pilar</au><au>CUADRADO, Eloy</au><au>ROSELL, Anna</au><au>ALVAREZ-SABIN, José</au><au>ORTEGA-AZNAR, Arantxa</au><au>HERNANDEZ-GUILLAMON, Mar</au><au>PENALBA, Anna</au><au>MOLINA, Carlos A</au><au>MONTANER, Joan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fas System Activation in Perihematomal Areas After Spontaneous Intracerebral Hemorrhage</atitle><jtitle>Stroke (1970)</jtitle><addtitle>Stroke</addtitle><date>2008-06-01</date><risdate>2008</risdate><volume>39</volume><issue>6</issue><spage>1730</spage><epage>1734</epage><pages>1730-1734</pages><issn>0039-2499</issn><eissn>1524-4628</eissn><coden>SJCCA7</coden><abstract>Apoptosis has been implicated as the prominent form of cell death in the brain perihematomal region in animal models and in autopsy or postsurgical human studies. Both the Fas system and caspase activation play a central role in apoptotic pathways. The aims of this study were to investigate soluble Fas (s-Fas) plasma levels after acute intracerebral hemorrhage (ICH), to determine its influence on clinical and radiologic features, and to assess Fas receptor and Fas ligand (Fas-L) protein expression in human ICH brain tissue.
s-Fas plasma levels were determined on admission in 78 consecutive ICH patients and serially in a subgroup of 21 of them, at the time of neurologic assessment, by means of ELISA. ICH and perihematomal edema volumes were determined at baseline and on follow-up computed tomography scans, and ICH and perihematomal edema growth was calculated. The presence of Fas receptor and Fas-L was assessed in different brain tissue samples by immunoblotting from 6 deceased ICH patients and from 2 control subjects.
Mortality reached 20.5% of patients at the third month, and 48% of survivors had an unfavorable outcome (modified Rankin Scale score >/=3). The baseline s-Fas level in ICH patients was significantly lower than in healthy controls [160 (160-245) vs 269 (230-332) pg/mL, P<0.001], returning to normal values by 24 hours (P<0.05 for all determinations). Regarding radiologic features, the baseline s-Fas value was found to be inversely correlated to perihematomal edema growth at follow-up (r=-0.33, P=0.041). Finally, Fas-L content was highest in the perihematomal area compared with contralateral and remote ipsilateral areas in ICH patient and control samples.
A decreased plasma s-Fas level together with an increased Fas-L amount in perihematomal brain tissue suggest Fas-mediated apoptosis involvement in this disease.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>18403741</pmid><doi>10.1161/STROKEAHA.107.500876</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; American Heart Association; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Aged Aged, 80 and over Apoptosis Biological and medical sciences Biomarkers - analysis Biomarkers - blood Brain - blood supply Brain - diagnostic imaging Brain - pathology Brain Edema - blood Brain Edema - complications Brain Edema - physiopathology Brain Infarction - blood Brain Infarction - etiology Brain Infarction - physiopathology Cerebral Hemorrhage - blood Cerebral Hemorrhage - complications Cerebral Hemorrhage - physiopathology Death Domain Receptor Signaling Adaptor Proteins - metabolism Disease Progression Down-Regulation - physiology Fas Ligand Protein - analysis Fas Ligand Protein - blood fas Receptor - analysis fas Receptor - blood Female Hematologic and hematopoietic diseases Humans Male Medical sciences Middle Aged Nerve Degeneration - blood Nerve Degeneration - etiology Nerve Degeneration - physiopathology Neurology Platelet diseases and coagulopathies Predictive Value of Tests Reference Values Tomography, X-Ray Computed Up-Regulation - physiology Vascular diseases and vascular malformations of the nervous system |
| title | Fas System Activation in Perihematomal Areas After Spontaneous Intracerebral Hemorrhage |
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