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epilepticus (SE) induces severe vasogenic edema in the piriform cortex (PC) accompanied by neuronal and astroglial damages. To elucidate the mechanism of SE-induced vasogenic edema, we investigated the roles of tumor necrosis factor (TNF)-α in blood-brain barrier (BBB) disruption during vasogenic edema and its related events in rat epilepsy models provoked by pilocarpine-induced SE.\n\nMethods\nSE was induced by pilocarpine in rats that were intracerebroventricularly infused with saline-, and soluble TNF p55 receptor (sTNFp55R) prior to SE induction. Thereafter, we performed Fluoro-Jade B staining and immunohistochemical studies for TNF-α and NF-κB subunits.\n\nResults\nFollowing SE, most activated microglia showed strong TNF-α immunoreactivity. In addition, TNF p75 receptor expression was detected in endothelial cells as well as astrocytes. In addition, only p65-Thr435 phosphorylation was increased in endothelial cells accompanied by SMI-71 expression (an endothelial barrier antigen). Neutralization of TNF-α by soluble TNF p55 receptor (sTNFp55R) infusion attenuated SE-induced vasogenic edema and neuronal damages via inhibition of p65-Thr435 phosphorylation in endothelial cells. Furthermore, sTNFp55R infusion reduced SE-induced neutrophil infiltration in the PC.\n\nConclusion\nThese findings suggest that impairments of endothelial cell functions via TNF-α-mediated p65-Thr 485 NF-κB phosphorylation may be involved in SE-induced vasogenic edema. Subsequently, vasogenic edema results in extensive neutrophil infiltration and neuronal-astroglial loss."}

    bionlp-st-ge-2016-test-proteins

    {"project":"bionlp-st-ge-2016-test-proteins","denotations":[{"id":"T147","span":{"begin":229,"end":258},"obj":"Protein"},{"id":"T148","span":{"begin":521,"end":537},"obj":"Protein"},{"id":"T149","span":{"begin":540,"end":547},"obj":"Protein"},{"id":"T150","span":{"begin":656,"end":661},"obj":"Protein"},{"id":"T151","span":{"begin":744,"end":749},"obj":"Protein"},{"id":"T152","span":{"begin":781,"end":797},"obj":"Protein"},{"id":"T153","span":{"begin":884,"end":887},"obj":"Protein"},{"id":"T154","span":{"begin":1031,"end":1036},"obj":"Protein"},{"id":"T155","span":{"begin":1048,"end":1064},"obj":"Protein"},{"id":"T156","span":{"begin":1067,"end":1074},"obj":"Protein"},{"id":"T157","span":{"begin":1162,"end":1165},"obj":"Protein"},{"id":"T158","span":{"begin":1225,"end":1232},"obj":"Protein"},{"id":"T159","span":{"begin":1382,"end":1387},"obj":"Protein"},{"id":"T160","span":{"begin":1397,"end":1400},"obj":"Protein"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"Background\nStatus epilepticus (SE) induces severe vasogenic edema in the piriform cortex (PC) accompanied by neuronal and astroglial damages. To elucidate the mechanism of SE-induced vasogenic edema, we investigated the roles of tumor necrosis factor (TNF)-α in blood-brain barrier (BBB) disruption during vasogenic edema and its related events in rat epilepsy models provoked by pilocarpine-induced SE.\n\nMethods\nSE was induced by pilocarpine in rats that were intracerebroventricularly infused with saline-, and soluble TNF p55 receptor (sTNFp55R) prior to SE induction. Thereafter, we performed Fluoro-Jade B staining and immunohistochemical studies for TNF-α and NF-κB subunits.\n\nResults\nFollowing SE, most activated microglia showed strong TNF-α immunoreactivity. In addition, TNF p75 receptor expression was detected in endothelial cells as well as astrocytes. In addition, only p65-Thr435 phosphorylation was increased in endothelial cells accompanied by SMI-71 expression (an endothelial barrier antigen). Neutralization of TNF-α by soluble TNF p55 receptor (sTNFp55R) infusion attenuated SE-induced vasogenic edema and neuronal damages via inhibition of p65-Thr435 phosphorylation in endothelial cells. Furthermore, sTNFp55R infusion reduced SE-induced neutrophil infiltration in the PC.\n\nConclusion\nThese findings suggest that impairments of endothelial cell functions via TNF-α-mediated p65-Thr 485 NF-κB phosphorylation may be involved in SE-induced vasogenic edema. Subsequently, vasogenic edema results in extensive neutrophil infiltration and neuronal-astroglial loss."}

    bionlp-st-ge-2016-uniprot

    {"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T479","span":{"begin":1052,"end":1055},"obj":"http://www.uniprot.org/uniprot/P01589"},{"id":"T478","span":{"begin":525,"end":528},"obj":"http://www.uniprot.org/uniprot/P01589"},{"id":"T477","span":{"begin":1382,"end":1387},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T476","span":{"begin":1031,"end":1036},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T459","span":{"begin":884,"end":887},"obj":"http://www.uniprot.org/uniprot/Q04206"},{"id":"T460","span":{"begin":1162,"end":1165},"obj":"http://www.uniprot.org/uniprot/Q04206"},{"id":"T461","span":{"begin":1397,"end":1400},"obj":"http://www.uniprot.org/uniprot/Q04206"},{"id":"T463","span":{"begin":884,"end":887},"obj":"http://www.uniprot.org/uniprot/P21579"},{"id":"T464","span":{"begin":1162,"end":1165},"obj":"http://www.uniprot.org/uniprot/P21579"},{"id":"T465","span":{"begin":1397,"end":1400},"obj":"http://www.uniprot.org/uniprot/P21579"},{"id":"T466","span":{"begin":252,"end":255},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T467","span":{"begin":521,"end":524},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T468","span":{"begin":656,"end":659},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T469","span":{"begin":744,"end":747},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T470","span":{"begin":781,"end":784},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T471","span":{"begin":1031,"end":1034},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T472","span":{"begin":1048,"end":1051},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T473","span":{"begin":252,"end":258},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T474","span":{"begin":656,"end":661},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T475","span":{"begin":744,"end":749},"obj":"http://www.uniprot.org/uniprot/P01375"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"Background\nStatus epilepticus (SE) induces severe vasogenic edema in the piriform cortex (PC) accompanied by neuronal and astroglial damages. To elucidate the mechanism of SE-induced vasogenic edema, we investigated the roles of tumor necrosis factor (TNF)-α in blood-brain barrier (BBB) disruption during vasogenic edema and its related events in rat epilepsy models provoked by pilocarpine-induced SE.\n\nMethods\nSE was induced by pilocarpine in rats that were intracerebroventricularly infused with saline-, and soluble TNF p55 receptor (sTNFp55R) prior to SE induction. Thereafter, we performed Fluoro-Jade B staining and immunohistochemical studies for TNF-α and NF-κB subunits.\n\nResults\nFollowing SE, most activated microglia showed strong TNF-α immunoreactivity. In addition, TNF p75 receptor expression was detected in endothelial cells as well as astrocytes. In addition, only p65-Thr435 phosphorylation was increased in endothelial cells accompanied by SMI-71 expression (an endothelial barrier antigen). Neutralization of TNF-α by soluble TNF p55 receptor (sTNFp55R) infusion attenuated SE-induced vasogenic edema and neuronal damages via inhibition of p65-Thr435 phosphorylation in endothelial cells. Furthermore, sTNFp55R infusion reduced SE-induced neutrophil infiltration in the PC.\n\nConclusion\nThese findings suggest that impairments of endothelial cell functions via TNF-α-mediated p65-Thr 485 NF-κB phosphorylation may be involved in SE-induced vasogenic edema. Subsequently, vasogenic edema results in extensive neutrophil infiltration and neuronal-astroglial loss."}

    UBERON-AE

    {"project":"UBERON-AE","denotations":[{"id":"T95","span":{"begin":73,"end":88},"obj":"http://purl.obolibrary.org/obo/UBERON_0004725"},{"id":"T97","span":{"begin":82,"end":88},"obj":"http://purl.obolibrary.org/obo/UBERON_0001851"},{"id":"T98","span":{"begin":262,"end":267},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"T99","span":{"begin":262,"end":281},"obj":"http://purl.obolibrary.org/obo/UBERON_0000120"},{"id":"T100","span":{"begin":268,"end":273},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T101","span":{"begin":1519,"end":1528},"obj":"http://purl.obolibrary.org/obo/UBERON_2000106"}],"text":"Background\nStatus epilepticus (SE) induces severe vasogenic edema in the piriform cortex (PC) accompanied by neuronal and astroglial damages. To elucidate the mechanism of SE-induced vasogenic edema, we investigated the roles of tumor necrosis factor (TNF)-α in blood-brain barrier (BBB) disruption during vasogenic edema and its related events in rat epilepsy models provoked by pilocarpine-induced SE.\n\nMethods\nSE was induced by pilocarpine in rats that were intracerebroventricularly infused with saline-, and soluble TNF p55 receptor (sTNFp55R) prior to SE induction. Thereafter, we performed Fluoro-Jade B staining and immunohistochemical studies for TNF-α and NF-κB subunits.\n\nResults\nFollowing SE, most activated microglia showed strong TNF-α immunoreactivity. In addition, TNF p75 receptor expression was detected in endothelial cells as well as astrocytes. In addition, only p65-Thr435 phosphorylation was increased in endothelial cells accompanied by SMI-71 expression (an endothelial barrier antigen). Neutralization of TNF-α by soluble TNF p55 receptor (sTNFp55R) infusion attenuated SE-induced vasogenic edema and neuronal damages via inhibition of p65-Thr435 phosphorylation in endothelial cells. Furthermore, sTNFp55R infusion reduced SE-induced neutrophil infiltration in the PC.\n\nConclusion\nThese findings suggest that impairments of endothelial cell functions via TNF-α-mediated p65-Thr 485 NF-κB phosphorylation may be involved in SE-induced vasogenic edema. Subsequently, vasogenic edema results in extensive neutrophil infiltration and neuronal-astroglial loss."}

    GO-BP

    {"project":"GO-BP","denotations":[{"id":"T166","span":{"begin":235,"end":243},"obj":"http://purl.obolibrary.org/obo/GO_0019835"},{"id":"T173","span":{"begin":1409,"end":1430},"obj":"http://purl.obolibrary.org/obo/GO_0007252"},{"id":"T172","span":{"begin":1415,"end":1430},"obj":"http://purl.obolibrary.org/obo/GO_0016310"},{"id":"T171","span":{"begin":1173,"end":1188},"obj":"http://purl.obolibrary.org/obo/GO_0016310"},{"id":"T170","span":{"begin":895,"end":910},"obj":"http://purl.obolibrary.org/obo/GO_0016310"},{"id":"T168","span":{"begin":235,"end":243},"obj":"http://purl.obolibrary.org/obo/GO_0070265"},{"id":"T162","span":{"begin":235,"end":243},"obj":"http://purl.obolibrary.org/obo/GO_0001906"},{"id":"T164","span":{"begin":235,"end":243},"obj":"http://purl.obolibrary.org/obo/GO_0008219"}],"text":"Background\nStatus epilepticus (SE) induces severe vasogenic edema in the piriform cortex (PC) accompanied by neuronal and astroglial damages. To elucidate the mechanism of SE-induced vasogenic edema, we investigated the roles of tumor necrosis factor (TNF)-α in blood-brain barrier (BBB) disruption during vasogenic edema and its related events in rat epilepsy models provoked by pilocarpine-induced SE.\n\nMethods\nSE was induced by pilocarpine in rats that were intracerebroventricularly infused with saline-, and soluble TNF p55 receptor (sTNFp55R) prior to SE induction. Thereafter, we performed Fluoro-Jade B staining and immunohistochemical studies for TNF-α and NF-κB subunits.\n\nResults\nFollowing SE, most activated microglia showed strong TNF-α immunoreactivity. In addition, TNF p75 receptor expression was detected in endothelial cells as well as astrocytes. In addition, only p65-Thr435 phosphorylation was increased in endothelial cells accompanied by SMI-71 expression (an endothelial barrier antigen). Neutralization of TNF-α by soluble TNF p55 receptor (sTNFp55R) infusion attenuated SE-induced vasogenic edema and neuronal damages via inhibition of p65-Thr435 phosphorylation in endothelial cells. Furthermore, sTNFp55R infusion reduced SE-induced neutrophil infiltration in the PC.\n\nConclusion\nThese findings suggest that impairments of endothelial cell functions via TNF-α-mediated p65-Thr 485 NF-κB phosphorylation may be involved in SE-induced vasogenic edema. Subsequently, vasogenic edema results in extensive neutrophil infiltration and neuronal-astroglial loss."}

    GO-CC

    {"project":"GO-CC","denotations":[{"id":"T181","span":{"begin":837,"end":842},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T182","span":{"begin":940,"end":945},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T183","span":{"begin":1204,"end":1209},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T184","span":{"begin":1363,"end":1367},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":"Background\nStatus epilepticus (SE) induces severe vasogenic edema in the piriform cortex (PC) accompanied by neuronal and astroglial damages. To elucidate the mechanism of SE-induced vasogenic edema, we investigated the roles of tumor necrosis factor (TNF)-α in blood-brain barrier (BBB) disruption during vasogenic edema and its related events in rat epilepsy models provoked by pilocarpine-induced SE.\n\nMethods\nSE was induced by pilocarpine in rats that were intracerebroventricularly infused with saline-, and soluble TNF p55 receptor (sTNFp55R) prior to SE induction. Thereafter, we performed Fluoro-Jade B staining and immunohistochemical studies for TNF-α and NF-κB subunits.\n\nResults\nFollowing SE, most activated microglia showed strong TNF-α immunoreactivity. In addition, TNF p75 receptor expression was detected in endothelial cells as well as astrocytes. In addition, only p65-Thr435 phosphorylation was increased in endothelial cells accompanied by SMI-71 expression (an endothelial barrier antigen). Neutralization of TNF-α by soluble TNF p55 receptor (sTNFp55R) infusion attenuated SE-induced vasogenic edema and neuronal damages via inhibition of p65-Thr435 phosphorylation in endothelial cells. Furthermore, sTNFp55R infusion reduced SE-induced neutrophil infiltration in the PC.\n\nConclusion\nThese findings suggest that impairments of endothelial cell functions via TNF-α-mediated p65-Thr 485 NF-κB phosphorylation may be involved in SE-induced vasogenic edema. Subsequently, vasogenic edema results in extensive neutrophil infiltration and neuronal-astroglial loss."}

    sentences

    {"project":"sentences","denotations":[{"id":"T117","span":{"begin":1478,"end":1582},"obj":"Sentence"},{"id":"T116","span":{"begin":1308,"end":1477},"obj":"Sentence"},{"id":"T115","span":{"begin":1297,"end":1307},"obj":"Sentence"},{"id":"T114","span":{"begin":1211,"end":1295},"obj":"Sentence"},{"id":"T113","span":{"begin":1013,"end":1210},"obj":"Sentence"},{"id":"T112","span":{"begin":866,"end":1012},"obj":"Sentence"},{"id":"T111","span":{"begin":768,"end":865},"obj":"Sentence"},{"id":"T110","span":{"begin":691,"end":767},"obj":"Sentence"},{"id":"T109","span":{"begin":683,"end":690},"obj":"Sentence"},{"id":"T108","span":{"begin":572,"end":681},"obj":"Sentence"},{"id":"T107","span":{"begin":413,"end":571},"obj":"Sentence"},{"id":"T106","span":{"begin":405,"end":412},"obj":"Sentence"},{"id":"T105","span":{"begin":142,"end":403},"obj":"Sentence"},{"id":"T104","span":{"begin":11,"end":141},"obj":"Sentence"},{"id":"T103","span":{"begin":0,"end":10},"obj":"Sentence"},{"id":"T3","span":{"begin":0,"end":10},"obj":"Sentence"},{"id":"T4","span":{"begin":11,"end":141},"obj":"Sentence"},{"id":"T5","span":{"begin":142,"end":403},"obj":"Sentence"},{"id":"T6","span":{"begin":405,"end":412},"obj":"Sentence"},{"id":"T7","span":{"begin":413,"end":571},"obj":"Sentence"},{"id":"T8","span":{"begin":572,"end":681},"obj":"Sentence"},{"id":"T9","span":{"begin":683,"end":690},"obj":"Sentence"},{"id":"T10","span":{"begin":691,"end":767},"obj":"Sentence"},{"id":"T11","span":{"begin":768,"end":865},"obj":"Sentence"},{"id":"T12","span":{"begin":866,"end":1012},"obj":"Sentence"},{"id":"T13","span":{"begin":1013,"end":1210},"obj":"Sentence"},{"id":"T14","span":{"begin":1211,"end":1295},"obj":"Sentence"},{"id":"T15","span":{"begin":1297,"end":1307},"obj":"Sentence"},{"id":"T16","span":{"begin":1308,"end":1477},"obj":"Sentence"},{"id":"T17","span":{"begin":1478,"end":1582},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Background\nStatus epilepticus (SE) induces severe vasogenic edema in the piriform cortex (PC) accompanied by neuronal and astroglial damages. To elucidate the mechanism of SE-induced vasogenic edema, we investigated the roles of tumor necrosis factor (TNF)-α in blood-brain barrier (BBB) disruption during vasogenic edema and its related events in rat epilepsy models provoked by pilocarpine-induced SE.\n\nMethods\nSE was induced by pilocarpine in rats that were intracerebroventricularly infused with saline-, and soluble TNF p55 receptor (sTNFp55R) prior to SE induction. Thereafter, we performed Fluoro-Jade B staining and immunohistochemical studies for TNF-α and NF-κB subunits.\n\nResults\nFollowing SE, most activated microglia showed strong TNF-α immunoreactivity. In addition, TNF p75 receptor expression was detected in endothelial cells as well as astrocytes. In addition, only p65-Thr435 phosphorylation was increased in endothelial cells accompanied by SMI-71 expression (an endothelial barrier antigen). Neutralization of TNF-α by soluble TNF p55 receptor (sTNFp55R) infusion attenuated SE-induced vasogenic edema and neuronal damages via inhibition of p65-Thr435 phosphorylation in endothelial cells. Furthermore, sTNFp55R infusion reduced SE-induced neutrophil infiltration in the PC.\n\nConclusion\nThese findings suggest that impairments of endothelial cell functions via TNF-α-mediated p65-Thr 485 NF-κB phosphorylation may be involved in SE-induced vasogenic edema. Subsequently, vasogenic edema results in extensive neutrophil infiltration and neuronal-astroglial loss."}

    ICD10

    {"project":"ICD10","denotations":[{"id":"T175","span":{"begin":11,"end":29},"obj":"http://purl.bioontology.org/ontology/ICD10/G41.9"},{"id":"T177","span":{"begin":11,"end":29},"obj":"http://purl.bioontology.org/ontology/ICD10/G41"},{"id":"T178","span":{"begin":352,"end":360},"obj":"http://purl.bioontology.org/ontology/ICD10/G40.9"},{"id":"T179","span":{"begin":352,"end":360},"obj":"http://purl.bioontology.org/ontology/ICD10/G40"}],"text":"Background\nStatus epilepticus (SE) induces severe vasogenic edema in the piriform cortex (PC) accompanied by neuronal and astroglial damages. To elucidate the mechanism of SE-induced vasogenic edema, we investigated the roles of tumor necrosis factor (TNF)-α in blood-brain barrier (BBB) disruption during vasogenic edema and its related events in rat epilepsy models provoked by pilocarpine-induced SE.\n\nMethods\nSE was induced by pilocarpine in rats that were intracerebroventricularly infused with saline-, and soluble TNF p55 receptor (sTNFp55R) prior to SE induction. Thereafter, we performed Fluoro-Jade B staining and immunohistochemical studies for TNF-α and NF-κB subunits.\n\nResults\nFollowing SE, most activated microglia showed strong TNF-α immunoreactivity. In addition, TNF p75 receptor expression was detected in endothelial cells as well as astrocytes. In addition, only p65-Thr435 phosphorylation was increased in endothelial cells accompanied by SMI-71 expression (an endothelial barrier antigen). Neutralization of TNF-α by soluble TNF p55 receptor (sTNFp55R) infusion attenuated SE-induced vasogenic edema and neuronal damages via inhibition of p65-Thr435 phosphorylation in endothelial cells. Furthermore, sTNFp55R infusion reduced SE-induced neutrophil infiltration in the PC.\n\nConclusion\nThese findings suggest that impairments of endothelial cell functions via TNF-α-mediated p65-Thr 485 NF-κB phosphorylation may be involved in SE-induced vasogenic edema. Subsequently, vasogenic edema results in extensive neutrophil infiltration and neuronal-astroglial loss."}

    simple1

    {"project":"simple1","denotations":[{"id":"T200","span":{"begin":1397,"end":1400},"obj":"Protein"},{"id":"T199","span":{"begin":1382,"end":1387},"obj":"Protein"},{"id":"T198","span":{"begin":1225,"end":1232},"obj":"Protein"},{"id":"T197","span":{"begin":1162,"end":1165},"obj":"Protein"},{"id":"T196","span":{"begin":1067,"end":1074},"obj":"Protein"},{"id":"T195","span":{"begin":1048,"end":1064},"obj":"Protein"},{"id":"T194","span":{"begin":1031,"end":1036},"obj":"Protein"},{"id":"T193","span":{"begin":884,"end":887},"obj":"Protein"},{"id":"T192","span":{"begin":781,"end":797},"obj":"Protein"},{"id":"T191","span":{"begin":744,"end":749},"obj":"Protein"},{"id":"T190","span":{"begin":656,"end":661},"obj":"Protein"},{"id":"T189","span":{"begin":540,"end":547},"obj":"Protein"},{"id":"T188","span":{"begin":521,"end":537},"obj":"Protein"},{"id":"T187","span":{"begin":229,"end":258},"obj":"Protein"}],"text":"Background\nStatus epilepticus (SE) induces severe vasogenic edema in the piriform cortex (PC) accompanied by neuronal and astroglial damages. To elucidate the mechanism of SE-induced vasogenic edema, we investigated the roles of tumor necrosis factor (TNF)-α in blood-brain barrier (BBB) disruption during vasogenic edema and its related events in rat epilepsy models provoked by pilocarpine-induced SE.\n\nMethods\nSE was induced by pilocarpine in rats that were intracerebroventricularly infused with saline-, and soluble TNF p55 receptor (sTNFp55R) prior to SE induction. Thereafter, we performed Fluoro-Jade B staining and immunohistochemical studies for TNF-α and NF-κB subunits.\n\nResults\nFollowing SE, most activated microglia showed strong TNF-α immunoreactivity. In addition, TNF p75 receptor expression was detected in endothelial cells as well as astrocytes. In addition, only p65-Thr435 phosphorylation was increased in endothelial cells accompanied by SMI-71 expression (an endothelial barrier antigen). Neutralization of TNF-α by soluble TNF p55 receptor (sTNFp55R) infusion attenuated SE-induced vasogenic edema and neuronal damages via inhibition of p65-Thr435 phosphorylation in endothelial cells. Furthermore, sTNFp55R infusion reduced SE-induced neutrophil infiltration in the PC.\n\nConclusion\nThese findings suggest that impairments of endothelial cell functions via TNF-α-mediated p65-Thr 485 NF-κB phosphorylation may be involved in SE-induced vasogenic edema. Subsequently, vasogenic edema results in extensive neutrophil infiltration and neuronal-astroglial loss."}

    BioNLP16_DUT

    {"project":"BioNLP16_DUT","denotations":[{"id":"T911","span":{"begin":229,"end":258},"obj":"Protein"},{"id":"T912","span":{"begin":521,"end":537},"obj":"Protein"},{"id":"T913","span":{"begin":540,"end":547},"obj":"Protein"},{"id":"T914","span":{"begin":656,"end":661},"obj":"Protein"},{"id":"T915","span":{"begin":744,"end":749},"obj":"Protein"},{"id":"T916","span":{"begin":781,"end":797},"obj":"Protein"},{"id":"T917","span":{"begin":884,"end":887},"obj":"Protein"},{"id":"T918","span":{"begin":1031,"end":1036},"obj":"Protein"},{"id":"T919","span":{"begin":1048,"end":1064},"obj":"Protein"},{"id":"T920","span":{"begin":1067,"end":1074},"obj":"Protein"},{"id":"T921","span":{"begin":1162,"end":1165},"obj":"Protein"},{"id":"T922","span":{"begin":1225,"end":1232},"obj":"Protein"},{"id":"T923","span":{"begin":1382,"end":1387},"obj":"Protein"},{"id":"T924","span":{"begin":1397,"end":1400},"obj":"Protein"},{"id":"T926","span":{"begin":798,"end":808},"obj":"Gene_expression"},{"id":"T927","span":{"begin":915,"end":924},"obj":"Positive_regulation"},{"id":"T928","span":{"begin":895,"end":910},"obj":"Phosphorylation"},{"id":"T929","span":{"begin":1173,"end":1188},"obj":"Phosphorylation"},{"id":"T930","span":{"begin":1148,"end":1158},"obj":"Negative_regulation"},{"id":"T931","span":{"begin":1013,"end":1027},"obj":"Negative_regulation"}],"relations":[{"id":"R647","pred":"themeOf","subj":"T916","obj":"T926"},{"id":"R648","pred":"themeOf","subj":"T917","obj":"T928"},{"id":"R649","pred":"themeOf","subj":"T918","obj":"T931"},{"id":"R650","pred":"themeOf","subj":"T921","obj":"T929"},{"id":"R651","pred":"themeOf","subj":"T928","obj":"T927"},{"id":"R652","pred":"themeOf","subj":"T929","obj":"T930"}],"text":"Background\nStatus epilepticus (SE) induces severe vasogenic edema in the piriform cortex (PC) accompanied by neuronal and astroglial damages. To elucidate the mechanism of SE-induced vasogenic edema, we investigated the roles of tumor necrosis factor (TNF)-α in blood-brain barrier (BBB) disruption during vasogenic edema and its related events in rat epilepsy models provoked by pilocarpine-induced SE.\n\nMethods\nSE was induced by pilocarpine in rats that were intracerebroventricularly infused with saline-, and soluble TNF p55 receptor (sTNFp55R) prior to SE induction. Thereafter, we performed Fluoro-Jade B staining and immunohistochemical studies for TNF-α and NF-κB subunits.\n\nResults\nFollowing SE, most activated microglia showed strong TNF-α immunoreactivity. In addition, TNF p75 receptor expression was detected in endothelial cells as well as astrocytes. In addition, only p65-Thr435 phosphorylation was increased in endothelial cells accompanied by SMI-71 expression (an endothelial barrier antigen). Neutralization of TNF-α by soluble TNF p55 receptor (sTNFp55R) infusion attenuated SE-induced vasogenic edema and neuronal damages via inhibition of p65-Thr435 phosphorylation in endothelial cells. Furthermore, sTNFp55R infusion reduced SE-induced neutrophil infiltration in the PC.\n\nConclusion\nThese findings suggest that impairments of endothelial cell functions via TNF-α-mediated p65-Thr 485 NF-κB phosphorylation may be involved in SE-induced vasogenic edema. Subsequently, vasogenic edema results in extensive neutrophil infiltration and neuronal-astroglial loss."}

    BioNLP16_Messiy

    {"project":"BioNLP16_Messiy","denotations":[{"id":"T768","span":{"begin":798,"end":808},"obj":"Gene_expression"},{"id":"T765","span":{"begin":1397,"end":1400},"obj":"Protein"},{"id":"T764","span":{"begin":1382,"end":1387},"obj":"Protein"},{"id":"T763","span":{"begin":1225,"end":1232},"obj":"Protein"},{"id":"T762","span":{"begin":1162,"end":1165},"obj":"Protein"},{"id":"T761","span":{"begin":1067,"end":1074},"obj":"Protein"},{"id":"T760","span":{"begin":1048,"end":1064},"obj":"Protein"},{"id":"T759","span":{"begin":1031,"end":1036},"obj":"Protein"},{"id":"T758","span":{"begin":884,"end":887},"obj":"Protein"},{"id":"T757","span":{"begin":781,"end":797},"obj":"Protein"},{"id":"T756","span":{"begin":744,"end":749},"obj":"Protein"},{"id":"T755","span":{"begin":656,"end":661},"obj":"Protein"},{"id":"T754","span":{"begin":540,"end":547},"obj":"Protein"},{"id":"T753","span":{"begin":521,"end":537},"obj":"Protein"},{"id":"T775","span":{"begin":1415,"end":1430},"obj":"Phosphorylation"},{"id":"T774","span":{"begin":1388,"end":1396},"obj":"Positive_regulation"},{"id":"T773","span":{"begin":1148,"end":1158},"obj":"Negative_regulation"},{"id":"T772","span":{"begin":1173,"end":1188},"obj":"Phosphorylation"},{"id":"T771","span":{"begin":1013,"end":1027},"obj":"Negative_regulation"},{"id":"T770","span":{"begin":915,"end":924},"obj":"Positive_regulation"},{"id":"T769","span":{"begin":895,"end":910},"obj":"Phosphorylation"},{"id":"T752","span":{"begin":229,"end":258},"obj":"Protein"}],"relations":[{"id":"R556","pred":"themeOf","subj":"T757","obj":"T768"},{"id":"R557","pred":"themeOf","subj":"T758","obj":"T769"},{"id":"R558","pred":"themeOf","subj":"T759","obj":"T771"},{"id":"R559","pred":"themeOf","subj":"T762","obj":"T772"},{"id":"R560","pred":"causeOf","subj":"T764","obj":"T774"},{"id":"R561","pred":"themeOf","subj":"T765","obj":"T774"},{"id":"R562","pred":"themeOf","subj":"T765","obj":"T775"},{"id":"R564","pred":"themeOf","subj":"T769","obj":"T770"},{"id":"R565","pred":"themeOf","subj":"T772","obj":"T773"}],"text":"Background\nStatus epilepticus (SE) induces severe vasogenic edema in the piriform cortex (PC) accompanied by neuronal and astroglial damages. To elucidate the mechanism of SE-induced vasogenic edema, we investigated the roles of tumor necrosis factor (TNF)-α in blood-brain barrier (BBB) disruption during vasogenic edema and its related events in rat epilepsy models provoked by pilocarpine-induced SE.\n\nMethods\nSE was induced by pilocarpine in rats that were intracerebroventricularly infused with saline-, and soluble TNF p55 receptor (sTNFp55R) prior to SE induction. Thereafter, we performed Fluoro-Jade B staining and immunohistochemical studies for TNF-α and NF-κB subunits.\n\nResults\nFollowing SE, most activated microglia showed strong TNF-α immunoreactivity. In addition, TNF p75 receptor expression was detected in endothelial cells as well as astrocytes. In addition, only p65-Thr435 phosphorylation was increased in endothelial cells accompanied by SMI-71 expression (an endothelial barrier antigen). Neutralization of TNF-α by soluble TNF p55 receptor (sTNFp55R) infusion attenuated SE-induced vasogenic edema and neuronal damages via inhibition of p65-Thr435 phosphorylation in endothelial cells. Furthermore, sTNFp55R infusion reduced SE-induced neutrophil infiltration in the PC.\n\nConclusion\nThese findings suggest that impairments of endothelial cell functions via TNF-α-mediated p65-Thr 485 NF-κB phosphorylation may be involved in SE-induced vasogenic edema. Subsequently, vasogenic edema results in extensive neutrophil infiltration and neuronal-astroglial loss."}

    DLUT931

    {"project":"DLUT931","denotations":[{"id":"T819","span":{"begin":1388,"end":1396},"obj":"Positive_regulation"},{"id":"T818","span":{"begin":1415,"end":1430},"obj":"Phosphorylation"},{"id":"T817","span":{"begin":1148,"end":1158},"obj":"Negative_regulation"},{"id":"T816","span":{"begin":1173,"end":1188},"obj":"Phosphorylation"},{"id":"T794","span":{"begin":229,"end":258},"obj":"Protein"},{"id":"T795","span":{"begin":521,"end":537},"obj":"Protein"},{"id":"T796","span":{"begin":540,"end":547},"obj":"Protein"},{"id":"T797","span":{"begin":656,"end":661},"obj":"Protein"},{"id":"T798","span":{"begin":744,"end":749},"obj":"Protein"},{"id":"T799","span":{"begin":781,"end":797},"obj":"Protein"},{"id":"T800","span":{"begin":884,"end":887},"obj":"Protein"},{"id":"T801","span":{"begin":1031,"end":1036},"obj":"Protein"},{"id":"T802","span":{"begin":1048,"end":1064},"obj":"Protein"},{"id":"T803","span":{"begin":1067,"end":1074},"obj":"Protein"},{"id":"T804","span":{"begin":1162,"end":1165},"obj":"Protein"},{"id":"T805","span":{"begin":1225,"end":1232},"obj":"Protein"},{"id":"T806","span":{"begin":1382,"end":1387},"obj":"Protein"},{"id":"T807","span":{"begin":1397,"end":1400},"obj":"Protein"},{"id":"T811","span":{"begin":798,"end":808},"obj":"Gene_expression"},{"id":"T812","span":{"begin":895,"end":910},"obj":"Phosphorylation"},{"id":"T813","span":{"begin":915,"end":924},"obj":"Positive_regulation"},{"id":"T814","span":{"begin":1013,"end":1027},"obj":"Negative_regulation"},{"id":"T815","span":{"begin":1076,"end":1084},"obj":"Positive_regulation"}],"relations":[{"id":"R566","pred":"themeOf","subj":"T816","obj":"T817"},{"id":"R567","pred":"themeOf","subj":"T818","obj":"T819"},{"id":"R625","pred":"themeOf","subj":"T799","obj":"T811"},{"id":"R626","pred":"themeOf","subj":"T800","obj":"T812"},{"id":"R627","pred":"themeOf","subj":"T801","obj":"T814"},{"id":"R628","pred":"themeOf","subj":"T802","obj":"T815"},{"id":"R629","pred":"themeOf","subj":"T804","obj":"T816"},{"id":"R630","pred":"causeOf","subj":"T806","obj":"T819"},{"id":"R631","pred":"themeOf","subj":"T807","obj":"T818"},{"id":"R634","pred":"themeOf","subj":"T812","obj":"T813"}],"text":"Background\nStatus epilepticus (SE) induces severe vasogenic edema in the piriform cortex (PC) accompanied by neuronal and astroglial damages. To elucidate the mechanism of SE-induced vasogenic edema, we investigated the roles of tumor necrosis factor (TNF)-α in blood-brain barrier (BBB) disruption during vasogenic edema and its related events in rat epilepsy models provoked by pilocarpine-induced SE.\n\nMethods\nSE was induced by pilocarpine in rats that were intracerebroventricularly infused with saline-, and soluble TNF p55 receptor (sTNFp55R) prior to SE induction. Thereafter, we performed Fluoro-Jade B staining and immunohistochemical studies for TNF-α and NF-κB subunits.\n\nResults\nFollowing SE, most activated microglia showed strong TNF-α immunoreactivity. In addition, TNF p75 receptor expression was detected in endothelial cells as well as astrocytes. In addition, only p65-Thr435 phosphorylation was increased in endothelial cells accompanied by SMI-71 expression (an endothelial barrier antigen). Neutralization of TNF-α by soluble TNF p55 receptor (sTNFp55R) infusion attenuated SE-induced vasogenic edema and neuronal damages via inhibition of p65-Thr435 phosphorylation in endothelial cells. Furthermore, sTNFp55R infusion reduced SE-induced neutrophil infiltration in the PC.\n\nConclusion\nThese findings suggest that impairments of endothelial cell functions via TNF-α-mediated p65-Thr 485 NF-κB phosphorylation may be involved in SE-induced vasogenic edema. Subsequently, vasogenic edema results in extensive neutrophil infiltration and neuronal-astroglial loss."}

    bionlp-st-ge-2016-test-ihmc

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To elucidate the mechanism of SE-induced vasogenic edema, we investigated the roles of tumor necrosis factor (TNF)-α in blood-brain barrier (BBB) disruption during vasogenic edema and its related events in rat epilepsy models provoked by pilocarpine-induced SE.\n\nMethods\nSE was induced by pilocarpine in rats that were intracerebroventricularly infused with saline-, and soluble TNF p55 receptor (sTNFp55R) prior to SE induction. Thereafter, we performed Fluoro-Jade B staining and immunohistochemical studies for TNF-α and NF-κB subunits.\n\nResults\nFollowing SE, most activated microglia showed strong TNF-α immunoreactivity. In addition, TNF p75 receptor expression was detected in endothelial cells as well as astrocytes. In addition, only p65-Thr435 phosphorylation was increased in endothelial cells accompanied by SMI-71 expression (an endothelial barrier antigen). Neutralization of TNF-α by soluble TNF p55 receptor (sTNFp55R) infusion attenuated SE-induced vasogenic edema and neuronal damages via inhibition of p65-Thr435 phosphorylation in endothelial cells. Furthermore, sTNFp55R infusion reduced SE-induced neutrophil infiltration in the PC.\n\nConclusion\nThese findings suggest that impairments of endothelial cell functions via TNF-α-mediated p65-Thr 485 NF-κB phosphorylation may be involved in SE-induced vasogenic edema. Subsequently, vasogenic edema results in extensive neutrophil infiltration and neuronal-astroglial loss."}

    bionlp-st-ge-2016-spacy-parsed

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epilepticus (SE) induces severe vasogenic edema in the piriform cortex (PC) accompanied by neuronal and astroglial damages. To elucidate the mechanism of SE-induced vasogenic edema, we investigated the roles of tumor necrosis factor (TNF)-α in blood-brain barrier (BBB) disruption during vasogenic edema and its related events in rat epilepsy models provoked by pilocarpine-induced SE.\n\nMethods\nSE was induced by pilocarpine in rats that were intracerebroventricularly infused with saline-, and soluble TNF p55 receptor (sTNFp55R) prior to SE induction. Thereafter, we performed Fluoro-Jade B staining and immunohistochemical studies for TNF-α and NF-κB subunits.\n\nResults\nFollowing SE, most activated microglia showed strong TNF-α immunoreactivity. In addition, TNF p75 receptor expression was detected in endothelial cells as well as astrocytes. In addition, only p65-Thr435 phosphorylation was increased in endothelial cells accompanied by SMI-71 expression (an endothelial barrier antigen). Neutralization of TNF-α by soluble TNF p55 receptor (sTNFp55R) infusion attenuated SE-induced vasogenic edema and neuronal damages via inhibition of p65-Thr435 phosphorylation in endothelial cells. Furthermore, sTNFp55R infusion reduced SE-induced neutrophil infiltration in the PC.\n\nConclusion\nThese findings suggest that impairments of endothelial cell functions via TNF-α-mediated p65-Thr 485 NF-κB phosphorylation may be involved in SE-induced vasogenic edema. Subsequently, vasogenic edema results in extensive neutrophil infiltration and neuronal-astroglial loss."}

    bionlp-st-ge-2016-test-tees

    {"project":"bionlp-st-ge-2016-test-tees","denotations":[{"id":"T874","span":{"begin":1415,"end":1430},"obj":"Phosphorylation"},{"id":"T873","span":{"begin":1415,"end":1430},"obj":"Phosphorylation"},{"id":"T872","span":{"begin":1412,"end":1414},"obj":"Protein"},{"id":"T871","span":{"begin":1382,"end":1411},"obj":"Protein"},{"id":"T870","span":{"begin":1224,"end":1232},"obj":"Protein"},{"id":"T869","span":{"begin":1148,"end":1158},"obj":"Negative_regulation"},{"id":"T868","span":{"begin":1148,"end":1158},"obj":"Negative_regulation"},{"id":"T867","span":{"begin":1173,"end":1188},"obj":"Phosphorylation"},{"id":"T866","span":{"begin":1173,"end":1188},"obj":"Phosphorylation"},{"id":"T865","span":{"begin":1013,"end":1027},"obj":"Negative_regulation"},{"id":"T864","span":{"begin":1166,"end":1172},"obj":"Protein"},{"id":"T863","span":{"begin":1162,"end":1165},"obj":"Protein"},{"id":"T862","span":{"begin":1066,"end":1074},"obj":"Protein"},{"id":"T861","span":{"begin":1048,"end":1064},"obj":"Protein"},{"id":"T860","span":{"begin":1031,"end":1036},"obj":"Protein"},{"id":"T859","span":{"begin":915,"end":924},"obj":"Positive_regulation"},{"id":"T858","span":{"begin":915,"end":924},"obj":"Positive_regulation"},{"id":"T857","span":{"begin":895,"end":910},"obj":"Phosphorylation"},{"id":"T856","span":{"begin":895,"end":910},"obj":"Phosphorylation"},{"id":"T855","span":{"begin":888,"end":894},"obj":"Protein"},{"id":"T854","span":{"begin":884,"end":887},"obj":"Protein"},{"id":"T853","span":{"begin":798,"end":808},"obj":"Gene_expression"},{"id":"T852","span":{"begin":781,"end":797},"obj":"Protein"},{"id":"T851","span":{"begin":744,"end":749},"obj":"Protein"},{"id":"T850","span":{"begin":666,"end":680},"obj":"Protein"},{"id":"T849","span":{"begin":656,"end":661},"obj":"Protein"},{"id":"T846","span":{"begin":229,"end":258},"obj":"Protein"},{"id":"T847","span":{"begin":521,"end":537},"obj":"Protein"},{"id":"T848","span":{"begin":539,"end":547},"obj":"Protein"}],"relations":[{"id":"R576","pred":"themeOf","subj":"T866","obj":"T868"},{"id":"R577","pred":"themeOf","subj":"T867","obj":"T869"},{"id":"R578","pred":"Cause","subj":"T868","obj":"T865"},{"id":"R579","pred":"Cause","subj":"T869","obj":"T865"},{"id":"R580","pred":"themeOf","subj":"T871","obj":"T873"},{"id":"R581","pred":"themeOf","subj":"T872","obj":"T874"},{"id":"R568","pred":"themeOf","subj":"T852","obj":"T853"},{"id":"R569","pred":"themeOf","subj":"T854","obj":"T856"},{"id":"R570","pred":"themeOf","subj":"T855","obj":"T857"},{"id":"R571","pred":"themeOf","subj":"T856","obj":"T858"},{"id":"R572","pred":"themeOf","subj":"T857","obj":"T859"},{"id":"R573","pred":"themeOf","subj":"T860","obj":"T865"},{"id":"R574","pred":"themeOf","subj":"T863","obj":"T866"},{"id":"R575","pred":"themeOf","subj":"T864","obj":"T867"}],"text":"Background\nStatus epilepticus (SE) induces severe vasogenic edema in the piriform cortex (PC) accompanied by neuronal and astroglial damages. To elucidate the mechanism of SE-induced vasogenic edema, we investigated the roles of tumor necrosis factor (TNF)-α in blood-brain barrier (BBB) disruption during vasogenic edema and its related events in rat epilepsy models provoked by pilocarpine-induced SE.\n\nMethods\nSE was induced by pilocarpine in rats that were intracerebroventricularly infused with saline-, and soluble TNF p55 receptor (sTNFp55R) prior to SE induction. Thereafter, we performed Fluoro-Jade B staining and immunohistochemical studies for TNF-α and NF-κB subunits.\n\nResults\nFollowing SE, most activated microglia showed strong TNF-α immunoreactivity. In addition, TNF p75 receptor expression was detected in endothelial cells as well as astrocytes. In addition, only p65-Thr435 phosphorylation was increased in endothelial cells accompanied by SMI-71 expression (an endothelial barrier antigen). Neutralization of TNF-α by soluble TNF p55 receptor (sTNFp55R) infusion attenuated SE-induced vasogenic edema and neuronal damages via inhibition of p65-Thr435 phosphorylation in endothelial cells. Furthermore, sTNFp55R infusion reduced SE-induced neutrophil infiltration in the PC.\n\nConclusion\nThese findings suggest that impairments of endothelial cell functions via TNF-α-mediated p65-Thr 485 NF-κB phosphorylation may be involved in SE-induced vasogenic edema. Subsequently, vasogenic edema results in extensive neutrophil infiltration and neuronal-astroglial loss."}

    testone

    {"project":"testone","denotations":[{"id":"T19","span":{"begin":229,"end":258},"obj":"Protein"},{"id":"T20","span":{"begin":521,"end":537},"obj":"Protein"},{"id":"T21","span":{"begin":540,"end":547},"obj":"Protein"},{"id":"T22","span":{"begin":656,"end":661},"obj":"Protein"},{"id":"T23","span":{"begin":744,"end":749},"obj":"Protein"},{"id":"T24","span":{"begin":781,"end":797},"obj":"Protein"},{"id":"T25","span":{"begin":884,"end":887},"obj":"Protein"},{"id":"T26","span":{"begin":1031,"end":1036},"obj":"Protein"},{"id":"T27","span":{"begin":1048,"end":1064},"obj":"Protein"},{"id":"T28","span":{"begin":1067,"end":1074},"obj":"Protein"},{"id":"T29","span":{"begin":1162,"end":1165},"obj":"Protein"},{"id":"T30","span":{"begin":1225,"end":1232},"obj":"Protein"},{"id":"T31","span":{"begin":1382,"end":1387},"obj":"Protein"},{"id":"T32","span":{"begin":1397,"end":1400},"obj":"Protein"},{"id":"T35","span":{"begin":288,"end":298},"obj":"Negative_regulation"},{"id":"T36","span":{"begin":392,"end":399},"obj":"Positive_regulation"},{"id":"T37","span":{"begin":420,"end":427},"obj":"Positive_regulation"},{"id":"T38","span":{"begin":561,"end":570},"obj":"Positive_regulation"},{"id":"T39","span":{"begin":611,"end":619},"obj":"Gene_expression"},{"id":"T40","span":{"begin":798,"end":808},"obj":"Gene_expression"},{"id":"T41","span":{"begin":895,"end":910},"obj":"Phosphorylation"},{"id":"T42","span":{"begin":915,"end":924},"obj":"Positive_regulation"},{"id":"T43","span":{"begin":968,"end":978},"obj":"Gene_expression"},{"id":"T44","span":{"begin":1013,"end":1027},"obj":"Negative_regulation"},{"id":"T45","span":{"begin":1148,"end":1158},"obj":"Negative_regulation"},{"id":"T46","span":{"begin":1173,"end":1188},"obj":"Phosphorylation"},{"id":"T47","span":{"begin":1388,"end":1396},"obj":"Positive_regulation"},{"id":"T48","span":{"begin":1415,"end":1430},"obj":"Phosphorylation"}],"relations":[{"id":"R3","pred":"themeOf","subj":"T20","obj":"T38"},{"id":"R4","pred":"themeOf","subj":"T24","obj":"T40"},{"id":"R5","pred":"themeOf","subj":"T25","obj":"T41"},{"id":"R6","pred":"themeOf","subj":"T26","obj":"T44"},{"id":"R7","pred":"causeOf","subj":"T27","obj":"T44"},{"id":"R8","pred":"themeOf","subj":"T29","obj":"T46"},{"id":"R9","pred":"causeOf","subj":"T31","obj":"T47"},{"id":"R10","pred":"themeOf","subj":"T32","obj":"T48"},{"id":"R12","pred":"themeOf","subj":"T41","obj":"T42"},{"id":"R13","pred":"causeOf","subj":"T43","obj":"T42"},{"id":"R14","pred":"themeOf","subj":"T46","obj":"T45"},{"id":"R15","pred":"themeOf","subj":"T48","obj":"T47"}],"text":"Background\nStatus epilepticus (SE) induces severe vasogenic edema in the piriform cortex (PC) accompanied by neuronal and astroglial damages. To elucidate the mechanism of SE-induced vasogenic edema, we investigated the roles of tumor necrosis factor (TNF)-α in blood-brain barrier (BBB) disruption during vasogenic edema and its related events in rat epilepsy models provoked by pilocarpine-induced SE.\n\nMethods\nSE was induced by pilocarpine in rats that were intracerebroventricularly infused with saline-, and soluble TNF p55 receptor (sTNFp55R) prior to SE induction. Thereafter, we performed Fluoro-Jade B staining and immunohistochemical studies for TNF-α and NF-κB subunits.\n\nResults\nFollowing SE, most activated microglia showed strong TNF-α immunoreactivity. In addition, TNF p75 receptor expression was detected in endothelial cells as well as astrocytes. In addition, only p65-Thr435 phosphorylation was increased in endothelial cells accompanied by SMI-71 expression (an endothelial barrier antigen). Neutralization of TNF-α by soluble TNF p55 receptor (sTNFp55R) infusion attenuated SE-induced vasogenic edema and neuronal damages via inhibition of p65-Thr435 phosphorylation in endothelial cells. Furthermore, sTNFp55R infusion reduced SE-induced neutrophil infiltration in the PC.\n\nConclusion\nThese findings suggest that impairments of endothelial cell functions via TNF-α-mediated p65-Thr 485 NF-κB phosphorylation may be involved in SE-induced vasogenic edema. Subsequently, vasogenic edema results in extensive neutrophil infiltration and neuronal-astroglial loss."}

    test3

    {"project":"test3","denotations":[{"id":"T93","span":{"begin":1415,"end":1430},"obj":"Phosphorylation"},{"id":"T92","span":{"begin":1397,"end":1400},"obj":"Protein"},{"id":"T91","span":{"begin":1388,"end":1396},"obj":"Positive_regulation"},{"id":"T90","span":{"begin":1382,"end":1387},"obj":"Protein"},{"id":"T89","span":{"begin":1224,"end":1232},"obj":"Protein"},{"id":"T88","span":{"begin":1173,"end":1188},"obj":"Phosphorylation"},{"id":"T87","span":{"begin":1162,"end":1165},"obj":"Protein"},{"id":"T86","span":{"begin":1148,"end":1158},"obj":"Negative_regulation"},{"id":"T85","span":{"begin":1066,"end":1074},"obj":"Protein"},{"id":"T84","span":{"begin":1048,"end":1064},"obj":"Protein"},{"id":"T83","span":{"begin":1031,"end":1036},"obj":"Protein"},{"id":"T82","span":{"begin":1013,"end":1027},"obj":"Negative_regulation"},{"id":"T81","span":{"begin":968,"end":978},"obj":"Gene_expression"},{"id":"T80","span":{"begin":915,"end":924},"obj":"Positive_regulation"},{"id":"T79","span":{"begin":895,"end":910},"obj":"Phosphorylation"},{"id":"T78","span":{"begin":884,"end":887},"obj":"Protein"},{"id":"T77","span":{"begin":798,"end":808},"obj":"Gene_expression"},{"id":"T76","span":{"begin":781,"end":797},"obj":"Protein"},{"id":"T75","span":{"begin":744,"end":749},"obj":"Protein"},{"id":"T74","span":{"begin":656,"end":661},"obj":"Protein"},{"id":"T73","span":{"begin":561,"end":570},"obj":"Positive_regulation"},{"id":"T72","span":{"begin":539,"end":547},"obj":"Protein"},{"id":"T71","span":{"begin":521,"end":537},"obj":"Protein"},{"id":"T51","span":{"begin":229,"end":258},"obj":"Protein"},{"id":"T52","span":{"begin":521,"end":537},"obj":"Protein"},{"id":"T53","span":{"begin":540,"end":547},"obj":"Protein"},{"id":"T54","span":{"begin":656,"end":661},"obj":"Protein"},{"id":"T55","span":{"begin":744,"end":749},"obj":"Protein"},{"id":"T56","span":{"begin":781,"end":797},"obj":"Protein"},{"id":"T57","span":{"begin":884,"end":887},"obj":"Protein"},{"id":"T58","span":{"begin":1031,"end":1036},"obj":"Protein"},{"id":"T59","span":{"begin":1048,"end":1064},"obj":"Protein"},{"id":"T60","span":{"begin":1067,"end":1074},"obj":"Protein"},{"id":"T61","span":{"begin":1162,"end":1165},"obj":"Protein"},{"id":"T62","span":{"begin":1225,"end":1232},"obj":"Protein"},{"id":"T63","span":{"begin":1382,"end":1387},"obj":"Protein"},{"id":"T64","span":{"begin":1397,"end":1400},"obj":"Protein"},{"id":"T69","span":{"begin":229,"end":258},"obj":"Protein"},{"id":"T70","span":{"begin":420,"end":427},"obj":"Positive_regulation"}],"relations":[{"id":"R33","pred":"themeOf","subj":"T93","obj":"T91"},{"id":"R27","pred":"causeOf","subj":"T84","obj":"T82"},{"id":"R28","pred":"equivalentTo","subj":"T85","obj":"T84"},{"id":"R29","pred":"themeOf","subj":"T87","obj":"T88"},{"id":"R30","pred":"themeOf","subj":"T88","obj":"T86"},{"id":"R31","pred":"causeOf","subj":"T90","obj":"T91"},{"id":"R32","pred":"themeOf","subj":"T92","obj":"T93"},{"id":"R19","pred":"causeOf","subj":"T71","obj":"T70"},{"id":"R20","pred":"themeOf","subj":"T71","obj":"T73"},{"id":"R21","pred":"equivalentTo","subj":"T72","obj":"T71"},{"id":"R22","pred":"themeOf","subj":"T76","obj":"T77"},{"id":"R23","pred":"themeOf","subj":"T78","obj":"T79"},{"id":"R24","pred":"themeOf","subj":"T79","obj":"T80"},{"id":"R25","pred":"causeOf","subj":"T81","obj":"T80"},{"id":"R26","pred":"themeOf","subj":"T83","obj":"T82"}],"text":"Background\nStatus epilepticus (SE) induces severe vasogenic edema in the piriform cortex (PC) accompanied by neuronal and astroglial damages. To elucidate the mechanism of SE-induced vasogenic edema, we investigated the roles of tumor necrosis factor (TNF)-α in blood-brain barrier (BBB) disruption during vasogenic edema and its related events in rat epilepsy models provoked by pilocarpine-induced SE.\n\nMethods\nSE was induced by pilocarpine in rats that were intracerebroventricularly infused with saline-, and soluble TNF p55 receptor (sTNFp55R) prior to SE induction. Thereafter, we performed Fluoro-Jade B staining and immunohistochemical studies for TNF-α and NF-κB subunits.\n\nResults\nFollowing SE, most activated microglia showed strong TNF-α immunoreactivity. In addition, TNF p75 receptor expression was detected in endothelial cells as well as astrocytes. In addition, only p65-Thr435 phosphorylation was increased in endothelial cells accompanied by SMI-71 expression (an endothelial barrier antigen). Neutralization of TNF-α by soluble TNF p55 receptor (sTNFp55R) infusion attenuated SE-induced vasogenic edema and neuronal damages via inhibition of p65-Thr435 phosphorylation in endothelial cells. Furthermore, sTNFp55R infusion reduced SE-induced neutrophil infiltration in the PC.\n\nConclusion\nThese findings suggest that impairments of endothelial cell functions via TNF-α-mediated p65-Thr 485 NF-κB phosphorylation may be involved in SE-induced vasogenic edema. Subsequently, vasogenic edema results in extensive neutrophil infiltration and neuronal-astroglial loss."}