PMC:3312845 / 26894-28469 JSONTXT

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expression\nMIP-2 is a powerful chemokine that contributes to recruitment of neutrophils [27]. MIP-2 is undetectable or present at low levels under physiological conditions, and shows transient increases under pathological conditions via TNF-α and/or interleukin-1β (IL-1β)-dependent mechanisms [14]. Thus, it would be plausible that TNF-α-mediated MIP-2 expression may provoke SE-induced neutrophil infiltrations. To confirm this hypothesis, we investigated MIP-2 expression in the PC. Consistent with our previous study [20], some MIP-2-positive astrocytes were observed in the core and periphery of the vasogenic edema lesions, but not in the non-vasogenic edema region (Figure 6B and 6C). Although the number of MIP-2 positive cells per unit area in the PC region of sTNFp55R-infused animals was significantly lower than that of the saline-infused group due to reduction of the area of vasogenic edema, there was no difference in the number of MIP-2 positive cells per unit area of vasogenic edema between sTNFp55R-infused animals and saline-infused animals (Figure 6F). Furthermore, the number of MIP-2-positive cells showed a direct proportion to the unit area of vasogenic edema with a linear coefficient of correlation of 0.682 (p \u003c 0.05, Figure 6G). Therefore, together with reduction in neutrophil infiltration in the PC region of sTNFp55R-infused animals, our findings provide evidence that TNF-α may regulate SE-induced neutrophil infiltration at least in the PC via vasogenic edema formation and not via direct TNF-α-mediated MIP-2 expression in astrocytes."}

{"project":"bionlp-st-ge-2016-test-proteins","denotations":[{"id":"T10535","span":{"begin":1544,"end":1549},"obj":"Protein"},{"id":"T10523","span":{"begin":339,"end":344},"obj":"Protein"},{"id":"T10522","span":{"begin":272,"end":277},"obj":"Protein"},{"id":"T10521","span":{"begin":256,"end":270},"obj":"Protein"},{"id":"T10520","span":{"begin":243,"end":248},"obj":"Protein"},{"id":"T10519","span":{"begin":100,"end":105},"obj":"Protein"},{"id":"T10518","span":{"begin":37,"end":46},"obj":"Protein"},{"id":"T10517","span":{"begin":17,"end":22},"obj":"Protein"},{"id":"T10516","span":{"begin":0,"end":5},"obj":"Protein"},{"id":"T10534","span":{"begin":1529,"end":1534},"obj":"Protein"},{"id":"T10533","span":{"begin":1407,"end":1412},"obj":"Protein"},{"id":"T10532","span":{"begin":1347,"end":1354},"obj":"Protein"},{"id":"T10531","span":{"begin":1107,"end":1112},"obj":"Protein"},{"id":"T10530","span":{"begin":1016,"end":1023},"obj":"Protein"},{"id":"T10529","span":{"begin":953,"end":958},"obj":"Protein"},{"id":"T10528","span":{"begin":777,"end":784},"obj":"Protein"},{"id":"T10527","span":{"begin":721,"end":726},"obj":"Protein"},{"id":"T10526","span":{"begin":538,"end":543},"obj":"Protein"},{"id":"T10525","span":{"begin":464,"end":469},"obj":"Protein"},{"id":"T10524","span":{"begin":354,"end":359},"obj":"Protein"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"MIP-2 expression\nMIP-2 is a powerful chemokine that contributes to recruitment of neutrophils [27]. MIP-2 is undetectable or present at low levels under physiological conditions, and shows transient increases under pathological conditions via TNF-α and/or interleukin-1β (IL-1β)-dependent mechanisms [14]. Thus, it would be plausible that TNF-α-mediated MIP-2 expression may provoke SE-induced neutrophil infiltrations. To confirm this hypothesis, we investigated MIP-2 expression in the PC. Consistent with our previous study [20], some MIP-2-positive astrocytes were observed in the core and periphery of the vasogenic edema lesions, but not in the non-vasogenic edema region (Figure 6B and 6C). Although the number of MIP-2 positive cells per unit area in the PC region of sTNFp55R-infused animals was significantly lower than that of the saline-infused group due to reduction of the area of vasogenic edema, there was no difference in the number of MIP-2 positive cells per unit area of vasogenic edema between sTNFp55R-infused animals and saline-infused animals (Figure 6F). Furthermore, the number of MIP-2-positive cells showed a direct proportion to the unit area of vasogenic edema with a linear coefficient of correlation of 0.682 (p \u003c 0.05, Figure 6G). Therefore, together with reduction in neutrophil infiltration in the PC region of sTNFp55R-infused animals, our findings provide evidence that TNF-α may regulate SE-induced neutrophil infiltration at least in the PC via vasogenic edema formation and not via direct TNF-α-mediated MIP-2 expression in astrocytes."}

{"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T10832","span":{"begin":268,"end":274},"obj":"http://www.uniprot.org/uniprot/P01584"},{"id":"T10831","span":{"begin":1529,"end":1534},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T10830","span":{"begin":1407,"end":1412},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T10829","span":{"begin":339,"end":344},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T10828","span":{"begin":243,"end":248},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T10827","span":{"begin":1407,"end":1410},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T10826","span":{"begin":339,"end":342},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T10825","span":{"begin":243,"end":246},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T10824","span":{"begin":1544,"end":1549},"obj":"http://www.uniprot.org/uniprot/P10889"},{"id":"T10823","span":{"begin":1107,"end":1112},"obj":"http://www.uniprot.org/uniprot/P10889"},{"id":"T10822","span":{"begin":953,"end":958},"obj":"http://www.uniprot.org/uniprot/P10889"},{"id":"T10821","span":{"begin":721,"end":726},"obj":"http://www.uniprot.org/uniprot/P10889"},{"id":"T10820","span":{"begin":538,"end":543},"obj":"http://www.uniprot.org/uniprot/P10889"},{"id":"T10819","span":{"begin":464,"end":469},"obj":"http://www.uniprot.org/uniprot/P10889"},{"id":"T10818","span":{"begin":354,"end":359},"obj":"http://www.uniprot.org/uniprot/P10889"},{"id":"T10817","span":{"begin":100,"end":105},"obj":"http://www.uniprot.org/uniprot/P10889"},{"id":"T10816","span":{"begin":17,"end":22},"obj":"http://www.uniprot.org/uniprot/P10889"},{"id":"T10815","span":{"begin":0,"end":5},"obj":"http://www.uniprot.org/uniprot/P10889"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"MIP-2 expression\nMIP-2 is a powerful chemokine that contributes to recruitment of neutrophils [27]. MIP-2 is undetectable or present at low levels under physiological conditions, and shows transient increases under pathological conditions via TNF-α and/or interleukin-1β (IL-1β)-dependent mechanisms [14]. Thus, it would be plausible that TNF-α-mediated MIP-2 expression may provoke SE-induced neutrophil infiltrations. To confirm this hypothesis, we investigated MIP-2 expression in the PC. Consistent with our previous study [20], some MIP-2-positive astrocytes were observed in the core and periphery of the vasogenic edema lesions, but not in the non-vasogenic edema region (Figure 6B and 6C). Although the number of MIP-2 positive cells per unit area in the PC region of sTNFp55R-infused animals was significantly lower than that of the saline-infused group due to reduction of the area of vasogenic edema, there was no difference in the number of MIP-2 positive cells per unit area of vasogenic edema between sTNFp55R-infused animals and saline-infused animals (Figure 6F). Furthermore, the number of MIP-2-positive cells showed a direct proportion to the unit area of vasogenic edema with a linear coefficient of correlation of 0.682 (p \u003c 0.05, Figure 6G). Therefore, together with reduction in neutrophil infiltration in the PC region of sTNFp55R-infused animals, our findings provide evidence that TNF-α may regulate SE-induced neutrophil infiltration at least in the PC via vasogenic edema formation and not via direct TNF-α-mediated MIP-2 expression in astrocytes."}

{"project":"GO-BP","denotations":[{"id":"T10536","span":{"begin":1500,"end":1509},"obj":"http://purl.obolibrary.org/obo/GO_0009058"}],"text":"MIP-2 expression\nMIP-2 is a powerful chemokine that contributes to recruitment of neutrophils [27]. MIP-2 is undetectable or present at low levels under physiological conditions, and shows transient increases under pathological conditions via TNF-α and/or interleukin-1β (IL-1β)-dependent mechanisms [14]. Thus, it would be plausible that TNF-α-mediated MIP-2 expression may provoke SE-induced neutrophil infiltrations. To confirm this hypothesis, we investigated MIP-2 expression in the PC. Consistent with our previous study [20], some MIP-2-positive astrocytes were observed in the core and periphery of the vasogenic edema lesions, but not in the non-vasogenic edema region (Figure 6B and 6C). Although the number of MIP-2 positive cells per unit area in the PC region of sTNFp55R-infused animals was significantly lower than that of the saline-infused group due to reduction of the area of vasogenic edema, there was no difference in the number of MIP-2 positive cells per unit area of vasogenic edema between sTNFp55R-infused animals and saline-infused animals (Figure 6F). Furthermore, the number of MIP-2-positive cells showed a direct proportion to the unit area of vasogenic edema with a linear coefficient of correlation of 0.682 (p \u003c 0.05, Figure 6G). Therefore, together with reduction in neutrophil infiltration in the PC region of sTNFp55R-infused animals, our findings provide evidence that TNF-α may regulate SE-induced neutrophil infiltration at least in the PC via vasogenic edema formation and not via direct TNF-α-mediated MIP-2 expression in astrocytes."}

{"project":"GO-CC","denotations":[{"id":"T10540","span":{"begin":1122,"end":1127},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T10539","span":{"begin":968,"end":973},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T10538","span":{"begin":736,"end":741},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T10537","span":{"begin":585,"end":589},"obj":"http://purl.obolibrary.org/obo/GO_0019013"}],"text":"MIP-2 expression\nMIP-2 is a powerful chemokine that contributes to recruitment of neutrophils [27]. MIP-2 is undetectable or present at low levels under physiological conditions, and shows transient increases under pathological conditions via TNF-α and/or interleukin-1β (IL-1β)-dependent mechanisms [14]. Thus, it would be plausible that TNF-α-mediated MIP-2 expression may provoke SE-induced neutrophil infiltrations. To confirm this hypothesis, we investigated MIP-2 expression in the PC. Consistent with our previous study [20], some MIP-2-positive astrocytes were observed in the core and periphery of the vasogenic edema lesions, but not in the non-vasogenic edema region (Figure 6B and 6C). Although the number of MIP-2 positive cells per unit area in the PC region of sTNFp55R-infused animals was significantly lower than that of the saline-infused group due to reduction of the area of vasogenic edema, there was no difference in the number of MIP-2 positive cells per unit area of vasogenic edema between sTNFp55R-infused animals and saline-infused animals (Figure 6F). Furthermore, the number of MIP-2-positive cells showed a direct proportion to the unit area of vasogenic edema with a linear coefficient of correlation of 0.682 (p \u003c 0.05, Figure 6G). Therefore, together with reduction in neutrophil infiltration in the PC region of sTNFp55R-infused animals, our findings provide evidence that TNF-α may regulate SE-induced neutrophil infiltration at least in the PC via vasogenic edema formation and not via direct TNF-α-mediated MIP-2 expression in astrocytes."}

{"project":"sentences","denotations":[{"id":"T10483","span":{"begin":1264,"end":1575},"obj":"Sentence"},{"id":"T10482","span":{"begin":1080,"end":1263},"obj":"Sentence"},{"id":"T10481","span":{"begin":698,"end":1079},"obj":"Sentence"},{"id":"T10480","span":{"begin":492,"end":697},"obj":"Sentence"},{"id":"T10479","span":{"begin":420,"end":491},"obj":"Sentence"},{"id":"T10478","span":{"begin":306,"end":419},"obj":"Sentence"},{"id":"T10477","span":{"begin":100,"end":305},"obj":"Sentence"},{"id":"T10476","span":{"begin":17,"end":99},"obj":"Sentence"},{"id":"T10475","span":{"begin":0,"end":16},"obj":"Sentence"},{"id":"T200","span":{"begin":0,"end":16},"obj":"Sentence"},{"id":"T201","span":{"begin":17,"end":99},"obj":"Sentence"},{"id":"T202","span":{"begin":100,"end":305},"obj":"Sentence"},{"id":"T203","span":{"begin":306,"end":419},"obj":"Sentence"},{"id":"T204","span":{"begin":420,"end":491},"obj":"Sentence"},{"id":"T205","span":{"begin":492,"end":697},"obj":"Sentence"},{"id":"T206","span":{"begin":698,"end":1079},"obj":"Sentence"},{"id":"T207","span":{"begin":1080,"end":1263},"obj":"Sentence"},{"id":"T208","span":{"begin":1264,"end":1575},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"MIP-2 expression\nMIP-2 is a powerful chemokine that contributes to recruitment of neutrophils [27]. MIP-2 is undetectable or present at low levels under physiological conditions, and shows transient increases under pathological conditions via TNF-α and/or interleukin-1β (IL-1β)-dependent mechanisms [14]. Thus, it would be plausible that TNF-α-mediated MIP-2 expression may provoke SE-induced neutrophil infiltrations. To confirm this hypothesis, we investigated MIP-2 expression in the PC. Consistent with our previous study [20], some MIP-2-positive astrocytes were observed in the core and periphery of the vasogenic edema lesions, but not in the non-vasogenic edema region (Figure 6B and 6C). Although the number of MIP-2 positive cells per unit area in the PC region of sTNFp55R-infused animals was significantly lower than that of the saline-infused group due to reduction of the area of vasogenic edema, there was no difference in the number of MIP-2 positive cells per unit area of vasogenic edema between sTNFp55R-infused animals and saline-infused animals (Figure 6F). Furthermore, the number of MIP-2-positive cells showed a direct proportion to the unit area of vasogenic edema with a linear coefficient of correlation of 0.682 (p \u003c 0.05, Figure 6G). Therefore, together with reduction in neutrophil infiltration in the PC region of sTNFp55R-infused animals, our findings provide evidence that TNF-α may regulate SE-induced neutrophil infiltration at least in the PC via vasogenic edema formation and not via direct TNF-α-mediated MIP-2 expression in astrocytes."}

{"project":"simple1","denotations":[{"id":"T10560","span":{"begin":1544,"end":1549},"obj":"Protein"},{"id":"T10559","span":{"begin":1529,"end":1534},"obj":"Protein"},{"id":"T10558","span":{"begin":1407,"end":1412},"obj":"Protein"},{"id":"T10557","span":{"begin":1347,"end":1354},"obj":"Protein"},{"id":"T10556","span":{"begin":1107,"end":1112},"obj":"Protein"},{"id":"T10555","span":{"begin":1016,"end":1023},"obj":"Protein"},{"id":"T10554","span":{"begin":953,"end":958},"obj":"Protein"},{"id":"T10553","span":{"begin":777,"end":784},"obj":"Protein"},{"id":"T10552","span":{"begin":721,"end":726},"obj":"Protein"},{"id":"T10551","span":{"begin":538,"end":543},"obj":"Protein"},{"id":"T10550","span":{"begin":464,"end":469},"obj":"Protein"},{"id":"T10549","span":{"begin":354,"end":359},"obj":"Protein"},{"id":"T10548","span":{"begin":339,"end":344},"obj":"Protein"},{"id":"T10547","span":{"begin":272,"end":277},"obj":"Protein"},{"id":"T10546","span":{"begin":256,"end":270},"obj":"Protein"},{"id":"T10545","span":{"begin":243,"end":248},"obj":"Protein"},{"id":"T10544","span":{"begin":100,"end":105},"obj":"Protein"},{"id":"T10543","span":{"begin":37,"end":46},"obj":"Protein"},{"id":"T10542","span":{"begin":17,"end":22},"obj":"Protein"},{"id":"T10541","span":{"begin":0,"end":5},"obj":"Protein"}],"text":"MIP-2 expression\nMIP-2 is a powerful chemokine that contributes to recruitment of neutrophils [27]. MIP-2 is undetectable or present at low levels under physiological conditions, and shows transient increases under pathological conditions via TNF-α and/or interleukin-1β (IL-1β)-dependent mechanisms [14]. Thus, it would be plausible that TNF-α-mediated MIP-2 expression may provoke SE-induced neutrophil infiltrations. To confirm this hypothesis, we investigated MIP-2 expression in the PC. Consistent with our previous study [20], some MIP-2-positive astrocytes were observed in the core and periphery of the vasogenic edema lesions, but not in the non-vasogenic edema region (Figure 6B and 6C). Although the number of MIP-2 positive cells per unit area in the PC region of sTNFp55R-infused animals was significantly lower than that of the saline-infused group due to reduction of the area of vasogenic edema, there was no difference in the number of MIP-2 positive cells per unit area of vasogenic edema between sTNFp55R-infused animals and saline-infused animals (Figure 6F). Furthermore, the number of MIP-2-positive cells showed a direct proportion to the unit area of vasogenic edema with a linear coefficient of correlation of 0.682 (p \u003c 0.05, Figure 6G). Therefore, together with reduction in neutrophil infiltration in the PC region of sTNFp55R-infused animals, our findings provide evidence that TNF-α may regulate SE-induced neutrophil infiltration at least in the PC via vasogenic edema formation and not via direct TNF-α-mediated MIP-2 expression in astrocytes."}

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expression\nMIP-2 is a powerful chemokine that contributes to recruitment of neutrophils [27]. MIP-2 is undetectable or present at low levels under physiological conditions, and shows transient increases under pathological conditions via TNF-α and/or interleukin-1β (IL-1β)-dependent mechanisms [14]. Thus, it would be plausible that TNF-α-mediated MIP-2 expression may provoke SE-induced neutrophil infiltrations. To confirm this hypothesis, we investigated MIP-2 expression in the PC. Consistent with our previous study [20], some MIP-2-positive astrocytes were observed in the core and periphery of the vasogenic edema lesions, but not in the non-vasogenic edema region (Figure 6B and 6C). Although the number of MIP-2 positive cells per unit area in the PC region of sTNFp55R-infused animals was significantly lower than that of the saline-infused group due to reduction of the area of vasogenic edema, there was no difference in the number of MIP-2 positive cells per unit area of vasogenic edema between sTNFp55R-infused animals and saline-infused animals (Figure 6F). Furthermore, the number of MIP-2-positive cells showed a direct proportion to the unit area of vasogenic edema with a linear coefficient of correlation of 0.682 (p \u003c 0.05, Figure 6G). Therefore, together with reduction in neutrophil infiltration in the PC region of sTNFp55R-infused animals, our findings provide evidence that TNF-α may regulate SE-induced neutrophil infiltration at least in the PC via vasogenic edema formation and not via direct TNF-α-mediated MIP-2 expression in astrocytes."}

{"project":"bionlp-st-ge-2016-test-tees","denotations":[{"id":"T11198","span":{"begin":1417,"end":1425},"obj":"Regulation"},{"id":"T11197","span":{"begin":1550,"end":1560},"obj":"Gene_expression"},{"id":"T11196","span":{"begin":1529,"end":1534},"obj":"Protein"},{"id":"T11195","span":{"begin":1407,"end":1412},"obj":"Protein"},{"id":"T11194","span":{"begin":1346,"end":1354},"obj":"Protein"},{"id":"T11193","span":{"begin":1015,"end":1023},"obj":"Protein"},{"id":"T11192","span":{"begin":776,"end":784},"obj":"Protein"},{"id":"T11191","span":{"begin":470,"end":480},"obj":"Gene_expression"},{"id":"T11190","span":{"begin":464,"end":469},"obj":"Protein"},{"id":"T11189","span":{"begin":339,"end":344},"obj":"Protein"},{"id":"T11187","span":{"begin":256,"end":270},"obj":"Protein"},{"id":"T11186","span":{"begin":243,"end":248},"obj":"Protein"},{"id":"T11188","span":{"begin":272,"end":277},"obj":"Protein"}],"relations":[{"id":"R9012","pred":"themeOf","subj":"T11190","obj":"T11191"},{"id":"R9013","pred":"themeOf","subj":"T11196","obj":"T11197"},{"id":"R9014","pred":"themeOf","subj":"T11197","obj":"T11198"},{"id":"R9015","pred":"Cause","subj":"T11198","obj":"T11195"}],"text":"MIP-2 expression\nMIP-2 is a powerful chemokine that contributes to recruitment of neutrophils [27]. MIP-2 is undetectable or present at low levels under physiological conditions, and shows transient increases under pathological conditions via TNF-α and/or interleukin-1β (IL-1β)-dependent mechanisms [14]. Thus, it would be plausible that TNF-α-mediated MIP-2 expression may provoke SE-induced neutrophil infiltrations. To confirm this hypothesis, we investigated MIP-2 expression in the PC. Consistent with our previous study [20], some MIP-2-positive astrocytes were observed in the core and periphery of the vasogenic edema lesions, but not in the non-vasogenic edema region (Figure 6B and 6C). Although the number of MIP-2 positive cells per unit area in the PC region of sTNFp55R-infused animals was significantly lower than that of the saline-infused group due to reduction of the area of vasogenic edema, there was no difference in the number of MIP-2 positive cells per unit area of vasogenic edema between sTNFp55R-infused animals and saline-infused animals (Figure 6F). Furthermore, the number of MIP-2-positive cells showed a direct proportion to the unit area of vasogenic edema with a linear coefficient of correlation of 0.682 (p \u003c 0.05, Figure 6G). Therefore, together with reduction in neutrophil infiltration in the PC region of sTNFp55R-infused animals, our findings provide evidence that TNF-α may regulate SE-induced neutrophil infiltration at least in the PC via vasogenic edema formation and not via direct TNF-α-mediated MIP-2 expression in astrocytes."}

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MIP-2 is undetectable or present at low levels under physiological conditions, and shows transient increases under pathological conditions via TNF-α and/or interleukin-1β (IL-1β)-dependent mechanisms [14]. Thus, it would be plausible that TNF-α-mediated MIP-2 expression may provoke SE-induced neutrophil infiltrations. To confirm this hypothesis, we investigated MIP-2 expression in the PC. Consistent with our previous study [20], some MIP-2-positive astrocytes were observed in the core and periphery of the vasogenic edema lesions, but not in the non-vasogenic edema region (Figure 6B and 6C). Although the number of MIP-2 positive cells per unit area in the PC region of sTNFp55R-infused animals was significantly lower than that of the saline-infused group due to reduction of the area of vasogenic edema, there was no difference in the number of MIP-2 positive cells per unit area of vasogenic edema between sTNFp55R-infused animals and saline-infused animals (Figure 6F). Furthermore, the number of MIP-2-positive cells showed a direct proportion to the unit area of vasogenic edema with a linear coefficient of correlation of 0.682 (p \u003c 0.05, Figure 6G). Therefore, together with reduction in neutrophil infiltration in the PC region of sTNFp55R-infused animals, our findings provide evidence that TNF-α may regulate SE-induced neutrophil infiltration at least in the PC via vasogenic edema formation and not via direct TNF-α-mediated MIP-2 expression in astrocytes."}