PMC:2817507 / 15746-17947 JSONTXT

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studies demonstrated that ICH initiates inflammatory responses, which are associated with secondary growth of hemorrhage and cell death [18]. It is now believed that TLR4-mediated-NFκB pathway activates and regulates immunological and inflammatory responses. To investigate the mechanisms underlying the increased inflammatory responses in the brain after ICH, in the present study, we evaluated the activation of TLR4-mediated NFκB signaling by detecting the p-IκB and the activity of NFκB in hemorrhagic brains. NFκB is an important transcription factor downstream in the TLR4-mediated signaling pathway. Activation of TLR4 stimulates IκBα phosphorylation and degradation, resulting in nuclear translocation of NFκB, which initiates transcription of genes associated with innate immune responses and inflammation [5, 6]. We observed that the levels of phosphorylation of IκB and the activity of NFκB were significantly increased in brain tissue after ICH. The temporal profile of the expression of p-IκB and the activation of NFκB was similar to that of the expression of TLR4. Our data suggest that ICH stimulates activation of the TLR4/NFκB signaling pathway, which is consistent with previous reports that activation of NFκB is regulated through the TLR4-mediated signaling pathway. TLR4 plays an important role in the recognition of microbial components [19, 20] and can also recognize endogenous molecules such as the degradation products of macromolecules, products of proteolytic cascades, intracellular components of ruptured cells, and products of genes that are activated by inflammation. For instance, HSP70, HSP32, HSP27, and enzymes involved in oxidative stress are found to be upregulated in the brain after ICH, which may be produced by injured neuronal cells or blood cells [21]. It may be speculated that these molecules produced in damaged brain or came from blood cells and constituents of plasma server as endogenous TLR4 ligands, activate TLR4-mediated NFκB signaling, and initiate the inflammatory responses in IHC brain. However, the specific endogenous ligands for TLR4 in hemorrhagic brain have not been determined and need to be identified through further research.\n"}

{"project":"bionlp-st-ge-2016-coref","denotations":[{"id":"T6288","span":{"begin":1831,"end":1846},"obj":"Anaphor"},{"id":"T6287","span":{"begin":1636,"end":1641},"obj":"Antecedent"},{"id":"T6286","span":{"begin":1629,"end":1634},"obj":"Antecedent"},{"id":"T6285","span":{"begin":1622,"end":1627},"obj":"Antecedent"},{"id":"T6284","span":{"begin":1736,"end":1741},"obj":"Anaphor"}],"relations":[{"id":"R4669","pred":"boundBy","subj":"T6284","obj":"T6285"},{"id":"R4670","pred":"boundBy","subj":"T6284","obj":"T6286"},{"id":"R4671","pred":"boundBy","subj":"T6284","obj":"T6287"},{"id":"R4672","pred":"boundBy","subj":"T6288","obj":"T6285"},{"id":"R4673","pred":"boundBy","subj":"T6288","obj":"T6286"},{"id":"R4674","pred":"boundBy","subj":"T6288","obj":"T6287"}],"namespaces":[{"prefix":"_base","uri":"https://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"Recent studies demonstrated that ICH initiates inflammatory responses, which are associated with secondary growth of hemorrhage and cell death [18]. It is now believed that TLR4-mediated-NFκB pathway activates and regulates immunological and inflammatory responses. To investigate the mechanisms underlying the increased inflammatory responses in the brain after ICH, in the present study, we evaluated the activation of TLR4-mediated NFκB signaling by detecting the p-IκB and the activity of NFκB in hemorrhagic brains. NFκB is an important transcription factor downstream in the TLR4-mediated signaling pathway. Activation of TLR4 stimulates IκBα phosphorylation and degradation, resulting in nuclear translocation of NFκB, which initiates transcription of genes associated with innate immune responses and inflammation [5, 6]. We observed that the levels of phosphorylation of IκB and the activity of NFκB were significantly increased in brain tissue after ICH. The temporal profile of the expression of p-IκB and the activation of NFκB was similar to that of the expression of TLR4. Our data suggest that ICH stimulates activation of the TLR4/NFκB signaling pathway, which is consistent with previous reports that activation of NFκB is regulated through the TLR4-mediated signaling pathway. TLR4 plays an important role in the recognition of microbial components [19, 20] and can also recognize endogenous molecules such as the degradation products of macromolecules, products of proteolytic cascades, intracellular components of ruptured cells, and products of genes that are activated by inflammation. For instance, HSP70, HSP32, HSP27, and enzymes involved in oxidative stress are found to be upregulated in the brain after ICH, which may be produced by injured neuronal cells or blood cells [21]. It may be speculated that these molecules produced in damaged brain or came from blood cells and constituents of plasma server as endogenous TLR4 ligands, activate TLR4-mediated NFκB signaling, and initiate the inflammatory responses in IHC brain. However, the specific endogenous ligands for TLR4 in hemorrhagic brain have not been determined and need to be identified through further research.\n"}

{"project":"bionlp-st-ge-2016-test-proteins","denotations":[{"id":"T6310","span":{"begin":2098,"end":2102},"obj":"Protein"},{"id":"T6309","span":{"begin":1969,"end":1973},"obj":"Protein"},{"id":"T6308","span":{"begin":1946,"end":1950},"obj":"Protein"},{"id":"T6307","span":{"begin":1636,"end":1641},"obj":"Protein"},{"id":"T6306","span":{"begin":1629,"end":1634},"obj":"Protein"},{"id":"T6305","span":{"begin":1622,"end":1627},"obj":"Protein"},{"id":"T6304","span":{"begin":1295,"end":1299},"obj":"Protein"},{"id":"T6303","span":{"begin":1262,"end":1266},"obj":"Protein"},{"id":"T6302","span":{"begin":1142,"end":1146},"obj":"Protein"},{"id":"T6301","span":{"begin":1081,"end":1085},"obj":"Protein"},{"id":"T6300","span":{"begin":644,"end":648},"obj":"Protein"},{"id":"T6299","span":{"begin":628,"end":632},"obj":"Protein"},{"id":"T6298","span":{"begin":581,"end":585},"obj":"Protein"},{"id":"T6297","span":{"begin":421,"end":425},"obj":"Protein"},{"id":"T6296","span":{"begin":173,"end":177},"obj":"Protein"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"Recent studies demonstrated that ICH initiates inflammatory responses, which are associated with secondary growth of hemorrhage and cell death [18]. It is now believed that TLR4-mediated-NFκB pathway activates and regulates immunological and inflammatory responses. To investigate the mechanisms underlying the increased inflammatory responses in the brain after ICH, in the present study, we evaluated the activation of TLR4-mediated NFκB signaling by detecting the p-IκB and the activity of NFκB in hemorrhagic brains. NFκB is an important transcription factor downstream in the TLR4-mediated signaling pathway. Activation of TLR4 stimulates IκBα phosphorylation and degradation, resulting in nuclear translocation of NFκB, which initiates transcription of genes associated with innate immune responses and inflammation [5, 6]. We observed that the levels of phosphorylation of IκB and the activity of NFκB were significantly increased in brain tissue after ICH. The temporal profile of the expression of p-IκB and the activation of NFκB was similar to that of the expression of TLR4. Our data suggest that ICH stimulates activation of the TLR4/NFκB signaling pathway, which is consistent with previous reports that activation of NFκB is regulated through the TLR4-mediated signaling pathway. TLR4 plays an important role in the recognition of microbial components [19, 20] and can also recognize endogenous molecules such as the degradation products of macromolecules, products of proteolytic cascades, intracellular components of ruptured cells, and products of genes that are activated by inflammation. For instance, HSP70, HSP32, HSP27, and enzymes involved in oxidative stress are found to be upregulated in the brain after ICH, which may be produced by injured neuronal cells or blood cells [21]. It may be speculated that these molecules produced in damaged brain or came from blood cells and constituents of plasma server as endogenous TLR4 ligands, activate TLR4-mediated NFκB signaling, and initiate the inflammatory responses in IHC brain. However, the specific endogenous ligands for TLR4 in hemorrhagic brain have not been determined and need to be identified through further research.\n"}

{"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T8669","span":{"begin":1636,"end":1641},"obj":"http://www.uniprot.org/uniprot/P04792"},{"id":"T8668","span":{"begin":644,"end":648},"obj":"http://www.uniprot.org/uniprot/P25963"},{"id":"T8665","span":{"begin":2098,"end":2102},"obj":"http://www.uniprot.org/uniprot/O00206"},{"id":"T8664","span":{"begin":1969,"end":1973},"obj":"http://www.uniprot.org/uniprot/O00206"},{"id":"T8663","span":{"begin":1946,"end":1950},"obj":"http://www.uniprot.org/uniprot/O00206"},{"id":"T8662","span":{"begin":1295,"end":1299},"obj":"http://www.uniprot.org/uniprot/O00206"},{"id":"T8661","span":{"begin":1262,"end":1266},"obj":"http://www.uniprot.org/uniprot/O00206"},{"id":"T8660","span":{"begin":1142,"end":1146},"obj":"http://www.uniprot.org/uniprot/O00206"},{"id":"T8659","span":{"begin":1081,"end":1085},"obj":"http://www.uniprot.org/uniprot/O00206"},{"id":"T8658","span":{"begin":628,"end":632},"obj":"http://www.uniprot.org/uniprot/O00206"},{"id":"T8657","span":{"begin":581,"end":585},"obj":"http://www.uniprot.org/uniprot/O00206"},{"id":"T8656","span":{"begin":421,"end":425},"obj":"http://www.uniprot.org/uniprot/O00206"},{"id":"T8655","span":{"begin":173,"end":177},"obj":"http://www.uniprot.org/uniprot/O00206"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"Recent studies demonstrated that ICH initiates inflammatory responses, which are associated with secondary growth of hemorrhage and cell death [18]. It is now believed that TLR4-mediated-NFκB pathway activates and regulates immunological and inflammatory responses. To investigate the mechanisms underlying the increased inflammatory responses in the brain after ICH, in the present study, we evaluated the activation of TLR4-mediated NFκB signaling by detecting the p-IκB and the activity of NFκB in hemorrhagic brains. NFκB is an important transcription factor downstream in the TLR4-mediated signaling pathway. Activation of TLR4 stimulates IκBα phosphorylation and degradation, resulting in nuclear translocation of NFκB, which initiates transcription of genes associated with innate immune responses and inflammation [5, 6]. We observed that the levels of phosphorylation of IκB and the activity of NFκB were significantly increased in brain tissue after ICH. The temporal profile of the expression of p-IκB and the activation of NFκB was similar to that of the expression of TLR4. Our data suggest that ICH stimulates activation of the TLR4/NFκB signaling pathway, which is consistent with previous reports that activation of NFκB is regulated through the TLR4-mediated signaling pathway. TLR4 plays an important role in the recognition of microbial components [19, 20] and can also recognize endogenous molecules such as the degradation products of macromolecules, products of proteolytic cascades, intracellular components of ruptured cells, and products of genes that are activated by inflammation. For instance, HSP70, HSP32, HSP27, and enzymes involved in oxidative stress are found to be upregulated in the brain after ICH, which may be produced by injured neuronal cells or blood cells [21]. It may be speculated that these molecules produced in damaged brain or came from blood cells and constituents of plasma server as endogenous TLR4 ligands, activate TLR4-mediated NFκB signaling, and initiate the inflammatory responses in IHC brain. However, the specific endogenous ligands for TLR4 in hemorrhagic brain have not been determined and need to be identified through further research.\n"}

{"project":"UBERON-AE","denotations":[{"id":"T6189","span":{"begin":1886,"end":1891},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"T6188","span":{"begin":1787,"end":1792},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"T6183","span":{"begin":947,"end":953},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"T6175","span":{"begin":2118,"end":2123},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T6174","span":{"begin":2046,"end":2051},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T6173","span":{"begin":1867,"end":1872},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T6172","span":{"begin":1719,"end":1724},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T6171","span":{"begin":941,"end":946},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T6170","span":{"begin":351,"end":356},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"}],"text":"Recent studies demonstrated that ICH initiates inflammatory responses, which are associated with secondary growth of hemorrhage and cell death [18]. It is now believed that TLR4-mediated-NFκB pathway activates and regulates immunological and inflammatory responses. To investigate the mechanisms underlying the increased inflammatory responses in the brain after ICH, in the present study, we evaluated the activation of TLR4-mediated NFκB signaling by detecting the p-IκB and the activity of NFκB in hemorrhagic brains. NFκB is an important transcription factor downstream in the TLR4-mediated signaling pathway. Activation of TLR4 stimulates IκBα phosphorylation and degradation, resulting in nuclear translocation of NFκB, which initiates transcription of genes associated with innate immune responses and inflammation [5, 6]. We observed that the levels of phosphorylation of IκB and the activity of NFκB were significantly increased in brain tissue after ICH. The temporal profile of the expression of p-IκB and the activation of NFκB was similar to that of the expression of TLR4. Our data suggest that ICH stimulates activation of the TLR4/NFκB signaling pathway, which is consistent with previous reports that activation of NFκB is regulated through the TLR4-mediated signaling pathway. TLR4 plays an important role in the recognition of microbial components [19, 20] and can also recognize endogenous molecules such as the degradation products of macromolecules, products of proteolytic cascades, intracellular components of ruptured cells, and products of genes that are activated by inflammation. For instance, HSP70, HSP32, HSP27, and enzymes involved in oxidative stress are found to be upregulated in the brain after ICH, which may be produced by injured neuronal cells or blood cells [21]. It may be speculated that these molecules produced in damaged brain or came from blood cells and constituents of plasma server as endogenous TLR4 ligands, activate TLR4-mediated NFκB signaling, and initiate the inflammatory responses in IHC brain. However, the specific endogenous ligands for TLR4 in hemorrhagic brain have not been determined and need to be identified through further research.\n"}

{"project":"GO-BP","denotations":[{"id":"T6392","span":{"begin":1276,"end":1299},"obj":"http://purl.obolibrary.org/obo/GO_0034143"},{"id":"T6391","span":{"begin":1276,"end":1299},"obj":"http://purl.obolibrary.org/obo/GO_0034142"},{"id":"T6390","span":{"begin":861,"end":883},"obj":"http://purl.obolibrary.org/obo/GO_0007252"},{"id":"T6389","span":{"begin":781,"end":804},"obj":"http://purl.obolibrary.org/obo/GO_0045824"},{"id":"T6388","span":{"begin":781,"end":804},"obj":"http://purl.obolibrary.org/obo/GO_0045089"},{"id":"T6387","span":{"begin":781,"end":804},"obj":"http://purl.obolibrary.org/obo/GO_0002218"},{"id":"T6386","span":{"begin":781,"end":804},"obj":"http://purl.obolibrary.org/obo/GO_0045088"},{"id":"T6385","span":{"begin":781,"end":804},"obj":"http://purl.obolibrary.org/obo/GO_0002227"},{"id":"T6384","span":{"begin":781,"end":804},"obj":"http://purl.obolibrary.org/obo/GO_0045087"},{"id":"T6383","span":{"begin":1432,"end":1443},"obj":"http://purl.obolibrary.org/obo/GO_0009056"},{"id":"T6382","span":{"begin":669,"end":680},"obj":"http://purl.obolibrary.org/obo/GO_0009056"},{"id":"T6381","span":{"begin":861,"end":876},"obj":"http://purl.obolibrary.org/obo/GO_0016310"},{"id":"T6380","span":{"begin":649,"end":664},"obj":"http://purl.obolibrary.org/obo/GO_0016310"},{"id":"T6379","span":{"begin":1267,"end":1293},"obj":"http://purl.obolibrary.org/obo/GO_0071847"},{"id":"T6378","span":{"begin":586,"end":612},"obj":"http://purl.obolibrary.org/obo/GO_0071847"},{"id":"T6377","span":{"begin":1267,"end":1293},"obj":"http://purl.obolibrary.org/obo/GO_0070098"},{"id":"T6376","span":{"begin":586,"end":612},"obj":"http://purl.obolibrary.org/obo/GO_0070098"},{"id":"T6375","span":{"begin":1267,"end":1293},"obj":"http://purl.obolibrary.org/obo/GO_0035689"},{"id":"T6374","span":{"begin":586,"end":612},"obj":"http://purl.obolibrary.org/obo/GO_0035689"},{"id":"T6373","span":{"begin":1267,"end":1293},"obj":"http://purl.obolibrary.org/obo/GO_0038166"},{"id":"T6372","span":{"begin":586,"end":612},"obj":"http://purl.obolibrary.org/obo/GO_0038166"},{"id":"T6371","span":{"begin":1267,"end":1293},"obj":"http://purl.obolibrary.org/obo/GO_0038161"},{"id":"T6370","span":{"begin":586,"end":612},"obj":"http://purl.obolibrary.org/obo/GO_0038161"},{"id":"T6369","span":{"begin":1267,"end":1293},"obj":"http://purl.obolibrary.org/obo/GO_0038007"},{"id":"T6368","span":{"begin":586,"end":612},"obj":"http://purl.obolibrary.org/obo/GO_0038007"},{"id":"T6367","span":{"begin":1267,"end":1293},"obj":"http://purl.obolibrary.org/obo/GO_0009755"},{"id":"T6366","span":{"begin":586,"end":612},"obj":"http://purl.obolibrary.org/obo/GO_0009755"},{"id":"T6365","span":{"begin":1267,"end":1293},"obj":"http://purl.obolibrary.org/obo/GO_0019221"},{"id":"T6364","span":{"begin":586,"end":612},"obj":"http://purl.obolibrary.org/obo/GO_0019221"},{"id":"T6363","span":{"begin":1267,"end":1293},"obj":"http://purl.obolibrary.org/obo/GO_0007229"},{"id":"T6362","span":{"begin":586,"end":612},"obj":"http://purl.obolibrary.org/obo/GO_0007229"},{"id":"T6361","span":{"begin":192,"end":223},"obj":"http://purl.obolibrary.org/obo/GO_1903307"},{"id":"T6360","span":{"begin":107,"end":113},"obj":"http://purl.obolibrary.org/obo/GO_0040007"},{"id":"T6359","span":{"begin":97,"end":113},"obj":"http://purl.obolibrary.org/obo/GO_0080117"},{"id":"T6357","span":{"begin":1276,"end":1293},"obj":"http://purl.obolibrary.org/obo/GO_0007165"},{"id":"T6356","span":{"begin":1152,"end":1169},"obj":"http://purl.obolibrary.org/obo/GO_0007165"},{"id":"T6355","span":{"begin":595,"end":612},"obj":"http://purl.obolibrary.org/obo/GO_0007165"},{"id":"T6350","span":{"begin":1988,"end":1997},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T6349","span":{"begin":1276,"end":1285},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T6348","span":{"begin":1152,"end":1161},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T6347","span":{"begin":595,"end":604},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T6346","span":{"begin":440,"end":449},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T6341","span":{"begin":137,"end":142},"obj":"http://purl.obolibrary.org/obo/GO_0016265"},{"id":"T6339","span":{"begin":132,"end":142},"obj":"http://purl.obolibrary.org/obo/GO_0008219"},{"id":"T6337","span":{"begin":788,"end":804},"obj":"http://purl.obolibrary.org/obo/GO_0006955"},{"id":"T6335","span":{"begin":742,"end":755},"obj":"http://purl.obolibrary.org/obo/GO_0006351"},{"id":"T6334","span":{"begin":542,"end":555},"obj":"http://purl.obolibrary.org/obo/GO_0006351"},{"id":"T6324","span":{"begin":1594,"end":1606},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T6323","span":{"begin":809,"end":821},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T6319","span":{"begin":321,"end":343},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T6318","span":{"begin":242,"end":264},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T6317","span":{"begin":47,"end":69},"obj":"http://purl.obolibrary.org/obo/GO_0006954"}],"text":"Recent studies demonstrated that ICH initiates inflammatory responses, which are associated with secondary growth of hemorrhage and cell death [18]. It is now believed that TLR4-mediated-NFκB pathway activates and regulates immunological and inflammatory responses. To investigate the mechanisms underlying the increased inflammatory responses in the brain after ICH, in the present study, we evaluated the activation of TLR4-mediated NFκB signaling by detecting the p-IκB and the activity of NFκB in hemorrhagic brains. NFκB is an important transcription factor downstream in the TLR4-mediated signaling pathway. Activation of TLR4 stimulates IκBα phosphorylation and degradation, resulting in nuclear translocation of NFκB, which initiates transcription of genes associated with innate immune responses and inflammation [5, 6]. We observed that the levels of phosphorylation of IκB and the activity of NFκB were significantly increased in brain tissue after ICH. The temporal profile of the expression of p-IκB and the activation of NFκB was similar to that of the expression of TLR4. Our data suggest that ICH stimulates activation of the TLR4/NFκB signaling pathway, which is consistent with previous reports that activation of NFκB is regulated through the TLR4-mediated signaling pathway. TLR4 plays an important role in the recognition of microbial components [19, 20] and can also recognize endogenous molecules such as the degradation products of macromolecules, products of proteolytic cascades, intracellular components of ruptured cells, and products of genes that are activated by inflammation. For instance, HSP70, HSP32, HSP27, and enzymes involved in oxidative stress are found to be upregulated in the brain after ICH, which may be produced by injured neuronal cells or blood cells [21]. It may be speculated that these molecules produced in damaged brain or came from blood cells and constituents of plasma server as endogenous TLR4 ligands, activate TLR4-mediated NFκB signaling, and initiate the inflammatory responses in IHC brain. However, the specific endogenous ligands for TLR4 in hemorrhagic brain have not been determined and need to be identified through further research.\n"}

{"project":"GO-MF","denotations":[{"id":"T6398","span":{"begin":2086,"end":2093},"obj":"http://purl.obolibrary.org/obo/GO_0005488"},{"id":"T6397","span":{"begin":1951,"end":1958},"obj":"http://purl.obolibrary.org/obo/GO_0005488"}],"text":"Recent studies demonstrated that ICH initiates inflammatory responses, which are associated with secondary growth of hemorrhage and cell death [18]. It is now believed that TLR4-mediated-NFκB pathway activates and regulates immunological and inflammatory responses. To investigate the mechanisms underlying the increased inflammatory responses in the brain after ICH, in the present study, we evaluated the activation of TLR4-mediated NFκB signaling by detecting the p-IκB and the activity of NFκB in hemorrhagic brains. NFκB is an important transcription factor downstream in the TLR4-mediated signaling pathway. Activation of TLR4 stimulates IκBα phosphorylation and degradation, resulting in nuclear translocation of NFκB, which initiates transcription of genes associated with innate immune responses and inflammation [5, 6]. We observed that the levels of phosphorylation of IκB and the activity of NFκB were significantly increased in brain tissue after ICH. The temporal profile of the expression of p-IκB and the activation of NFκB was similar to that of the expression of TLR4. Our data suggest that ICH stimulates activation of the TLR4/NFκB signaling pathway, which is consistent with previous reports that activation of NFκB is regulated through the TLR4-mediated signaling pathway. TLR4 plays an important role in the recognition of microbial components [19, 20] and can also recognize endogenous molecules such as the degradation products of macromolecules, products of proteolytic cascades, intracellular components of ruptured cells, and products of genes that are activated by inflammation. For instance, HSP70, HSP32, HSP27, and enzymes involved in oxidative stress are found to be upregulated in the brain after ICH, which may be produced by injured neuronal cells or blood cells [21]. It may be speculated that these molecules produced in damaged brain or came from blood cells and constituents of plasma server as endogenous TLR4 ligands, activate TLR4-mediated NFκB signaling, and initiate the inflammatory responses in IHC brain. However, the specific endogenous ligands for TLR4 in hemorrhagic brain have not been determined and need to be identified through further research.\n"}

{"project":"GO-CC","denotations":[{"id":"T6405","span":{"begin":1506,"end":1519},"obj":"http://purl.obolibrary.org/obo/GO_0005622"},{"id":"T6404","span":{"begin":1892,"end":1897},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T6403","span":{"begin":1793,"end":1798},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T6402","span":{"begin":1778,"end":1783},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T6401","span":{"begin":1543,"end":1548},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":"Recent studies demonstrated that ICH initiates inflammatory responses, which are associated with secondary growth of hemorrhage and cell death [18]. It is now believed that TLR4-mediated-NFκB pathway activates and regulates immunological and inflammatory responses. To investigate the mechanisms underlying the increased inflammatory responses in the brain after ICH, in the present study, we evaluated the activation of TLR4-mediated NFκB signaling by detecting the p-IκB and the activity of NFκB in hemorrhagic brains. NFκB is an important transcription factor downstream in the TLR4-mediated signaling pathway. Activation of TLR4 stimulates IκBα phosphorylation and degradation, resulting in nuclear translocation of NFκB, which initiates transcription of genes associated with innate immune responses and inflammation [5, 6]. We observed that the levels of phosphorylation of IκB and the activity of NFκB were significantly increased in brain tissue after ICH. The temporal profile of the expression of p-IκB and the activation of NFκB was similar to that of the expression of TLR4. Our data suggest that ICH stimulates activation of the TLR4/NFκB signaling pathway, which is consistent with previous reports that activation of NFκB is regulated through the TLR4-mediated signaling pathway. TLR4 plays an important role in the recognition of microbial components [19, 20] and can also recognize endogenous molecules such as the degradation products of macromolecules, products of proteolytic cascades, intracellular components of ruptured cells, and products of genes that are activated by inflammation. For instance, HSP70, HSP32, HSP27, and enzymes involved in oxidative stress are found to be upregulated in the brain after ICH, which may be produced by injured neuronal cells or blood cells [21]. It may be speculated that these molecules produced in damaged brain or came from blood cells and constituents of plasma server as endogenous TLR4 ligands, activate TLR4-mediated NFκB signaling, and initiate the inflammatory responses in IHC brain. However, the specific endogenous ligands for TLR4 in hemorrhagic brain have not been determined and need to be identified through further research.\n"}

{"project":"sentences","denotations":[{"id":"T6230","span":{"begin":2053,"end":2200},"obj":"Sentence"},{"id":"T6229","span":{"begin":1805,"end":2052},"obj":"Sentence"},{"id":"T6228","span":{"begin":1608,"end":1804},"obj":"Sentence"},{"id":"T6227","span":{"begin":1295,"end":1607},"obj":"Sentence"},{"id":"T6226","span":{"begin":1087,"end":1294},"obj":"Sentence"},{"id":"T6225","span":{"begin":965,"end":1086},"obj":"Sentence"},{"id":"T6224","span":{"begin":830,"end":964},"obj":"Sentence"},{"id":"T6223","span":{"begin":614,"end":829},"obj":"Sentence"},{"id":"T6222","span":{"begin":521,"end":613},"obj":"Sentence"},{"id":"T6221","span":{"begin":266,"end":520},"obj":"Sentence"},{"id":"T6220","span":{"begin":149,"end":265},"obj":"Sentence"},{"id":"T6219","span":{"begin":0,"end":148},"obj":"Sentence"},{"id":"T153","span":{"begin":0,"end":148},"obj":"Sentence"},{"id":"T154","span":{"begin":149,"end":265},"obj":"Sentence"},{"id":"T155","span":{"begin":266,"end":520},"obj":"Sentence"},{"id":"T156","span":{"begin":521,"end":613},"obj":"Sentence"},{"id":"T157","span":{"begin":614,"end":829},"obj":"Sentence"},{"id":"T158","span":{"begin":830,"end":964},"obj":"Sentence"},{"id":"T159","span":{"begin":965,"end":1086},"obj":"Sentence"},{"id":"T160","span":{"begin":1087,"end":1294},"obj":"Sentence"},{"id":"T161","span":{"begin":1295,"end":1607},"obj":"Sentence"},{"id":"T162","span":{"begin":1608,"end":1804},"obj":"Sentence"},{"id":"T163","span":{"begin":1805,"end":2052},"obj":"Sentence"},{"id":"T164","span":{"begin":2053,"end":2200},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Recent studies demonstrated that ICH initiates inflammatory responses, which are associated with secondary growth of hemorrhage and cell death [18]. It is now believed that TLR4-mediated-NFκB pathway activates and regulates immunological and inflammatory responses. To investigate the mechanisms underlying the increased inflammatory responses in the brain after ICH, in the present study, we evaluated the activation of TLR4-mediated NFκB signaling by detecting the p-IκB and the activity of NFκB in hemorrhagic brains. NFκB is an important transcription factor downstream in the TLR4-mediated signaling pathway. Activation of TLR4 stimulates IκBα phosphorylation and degradation, resulting in nuclear translocation of NFκB, which initiates transcription of genes associated with innate immune responses and inflammation [5, 6]. We observed that the levels of phosphorylation of IκB and the activity of NFκB were significantly increased in brain tissue after ICH. The temporal profile of the expression of p-IκB and the activation of NFκB was similar to that of the expression of TLR4. Our data suggest that ICH stimulates activation of the TLR4/NFκB signaling pathway, which is consistent with previous reports that activation of NFκB is regulated through the TLR4-mediated signaling pathway. TLR4 plays an important role in the recognition of microbial components [19, 20] and can also recognize endogenous molecules such as the degradation products of macromolecules, products of proteolytic cascades, intracellular components of ruptured cells, and products of genes that are activated by inflammation. For instance, HSP70, HSP32, HSP27, and enzymes involved in oxidative stress are found to be upregulated in the brain after ICH, which may be produced by injured neuronal cells or blood cells [21]. It may be speculated that these molecules produced in damaged brain or came from blood cells and constituents of plasma server as endogenous TLR4 ligands, activate TLR4-mediated NFκB signaling, and initiate the inflammatory responses in IHC brain. However, the specific endogenous ligands for TLR4 in hemorrhagic brain have not been determined and need to be identified through further research.\n"}

{"project":"simple1","denotations":[{"id":"T6544","span":{"begin":2098,"end":2102},"obj":"Protein"},{"id":"T6543","span":{"begin":1969,"end":1973},"obj":"Protein"},{"id":"T6542","span":{"begin":1946,"end":1950},"obj":"Protein"},{"id":"T6541","span":{"begin":1636,"end":1641},"obj":"Protein"},{"id":"T6540","span":{"begin":1629,"end":1634},"obj":"Protein"},{"id":"T6539","span":{"begin":1622,"end":1627},"obj":"Protein"},{"id":"T6538","span":{"begin":1295,"end":1299},"obj":"Protein"},{"id":"T6537","span":{"begin":1262,"end":1266},"obj":"Protein"},{"id":"T6536","span":{"begin":1142,"end":1146},"obj":"Protein"},{"id":"T6535","span":{"begin":1081,"end":1085},"obj":"Protein"},{"id":"T6534","span":{"begin":644,"end":648},"obj":"Protein"},{"id":"T6533","span":{"begin":628,"end":632},"obj":"Protein"},{"id":"T6532","span":{"begin":581,"end":585},"obj":"Protein"},{"id":"T6531","span":{"begin":421,"end":425},"obj":"Protein"},{"id":"T6530","span":{"begin":173,"end":177},"obj":"Protein"}],"text":"Recent studies demonstrated that ICH initiates inflammatory responses, which are associated with secondary growth of hemorrhage and cell death [18]. It is now believed that TLR4-mediated-NFκB pathway activates and regulates immunological and inflammatory responses. To investigate the mechanisms underlying the increased inflammatory responses in the brain after ICH, in the present study, we evaluated the activation of TLR4-mediated NFκB signaling by detecting the p-IκB and the activity of NFκB in hemorrhagic brains. NFκB is an important transcription factor downstream in the TLR4-mediated signaling pathway. Activation of TLR4 stimulates IκBα phosphorylation and degradation, resulting in nuclear translocation of NFκB, which initiates transcription of genes associated with innate immune responses and inflammation [5, 6]. We observed that the levels of phosphorylation of IκB and the activity of NFκB were significantly increased in brain tissue after ICH. The temporal profile of the expression of p-IκB and the activation of NFκB was similar to that of the expression of TLR4. Our data suggest that ICH stimulates activation of the TLR4/NFκB signaling pathway, which is consistent with previous reports that activation of NFκB is regulated through the TLR4-mediated signaling pathway. TLR4 plays an important role in the recognition of microbial components [19, 20] and can also recognize endogenous molecules such as the degradation products of macromolecules, products of proteolytic cascades, intracellular components of ruptured cells, and products of genes that are activated by inflammation. For instance, HSP70, HSP32, HSP27, and enzymes involved in oxidative stress are found to be upregulated in the brain after ICH, which may be produced by injured neuronal cells or blood cells [21]. It may be speculated that these molecules produced in damaged brain or came from blood cells and constituents of plasma server as endogenous TLR4 ligands, activate TLR4-mediated NFκB signaling, and initiate the inflammatory responses in IHC brain. However, the specific endogenous ligands for TLR4 in hemorrhagic brain have not been determined and need to be identified through further research.\n"}

{"project":"BioNLP16_DUT","denotations":[{"id":"T8921","span":{"begin":2098,"end":2102},"obj":"Protein"},{"id":"T8920","span":{"begin":1969,"end":1973},"obj":"Protein"},{"id":"T8919","span":{"begin":1946,"end":1950},"obj":"Protein"},{"id":"T8918","span":{"begin":1636,"end":1641},"obj":"Protein"},{"id":"T8917","span":{"begin":1629,"end":1634},"obj":"Protein"},{"id":"T8916","span":{"begin":1622,"end":1627},"obj":"Protein"},{"id":"T8915","span":{"begin":1295,"end":1299},"obj":"Protein"},{"id":"T8914","span":{"begin":1262,"end":1266},"obj":"Protein"},{"id":"T8913","span":{"begin":1142,"end":1146},"obj":"Protein"},{"id":"T8912","span":{"begin":1081,"end":1085},"obj":"Protein"},{"id":"T8911","span":{"begin":644,"end":648},"obj":"Protein"},{"id":"T8910","span":{"begin":628,"end":632},"obj":"Protein"},{"id":"T8909","span":{"begin":581,"end":585},"obj":"Protein"},{"id":"T8908","span":{"begin":421,"end":425},"obj":"Protein"},{"id":"T8907","span":{"begin":173,"end":177},"obj":"Protein"},{"id":"T8939","span":{"begin":1700,"end":1711},"obj":"Positive_regulation"},{"id":"T8938","span":{"begin":1389,"end":1398},"obj":"Binding"},{"id":"T8937","span":{"begin":1067,"end":1077},"obj":"Gene_expression"},{"id":"T8936","span":{"begin":669,"end":680},"obj":"Protein_catabolism"},{"id":"T8935","span":{"begin":649,"end":664},"obj":"Phosphorylation"},{"id":"T8934","span":{"begin":633,"end":643},"obj":"Positive_regulation"},{"id":"T8933","span":{"begin":614,"end":624},"obj":"Positive_regulation"}],"relations":[{"id":"R6953","pred":"themeOf","subj":"T8935","obj":"T8934"},{"id":"R6954","pred":"themeOf","subj":"T8910","obj":"T8933"},{"id":"R6955","pred":"themeOf","subj":"T8936","obj":"T8934"},{"id":"R6956","pred":"themeOf","subj":"T8911","obj":"T8935"},{"id":"R6957","pred":"themeOf","subj":"T8911","obj":"T8936"},{"id":"R6958","pred":"themeOf","subj":"T8912","obj":"T8937"},{"id":"R6959","pred":"themeOf","subj":"T8915","obj":"T8938"},{"id":"R6960","pred":"themeOf","subj":"T8916","obj":"T8939"},{"id":"R6962","pred":"themeOf","subj":"T8917","obj":"T8939"},{"id":"R6964","pred":"themeOf","subj":"T8918","obj":"T8939"}],"text":"Recent studies demonstrated that ICH initiates inflammatory responses, which are associated with secondary growth of hemorrhage and cell death [18]. It is now believed that TLR4-mediated-NFκB pathway activates and regulates immunological and inflammatory responses. To investigate the mechanisms underlying the increased inflammatory responses in the brain after ICH, in the present study, we evaluated the activation of TLR4-mediated NFκB signaling by detecting the p-IκB and the activity of NFκB in hemorrhagic brains. NFκB is an important transcription factor downstream in the TLR4-mediated signaling pathway. Activation of TLR4 stimulates IκBα phosphorylation and degradation, resulting in nuclear translocation of NFκB, which initiates transcription of genes associated with innate immune responses and inflammation [5, 6]. We observed that the levels of phosphorylation of IκB and the activity of NFκB were significantly increased in brain tissue after ICH. The temporal profile of the expression of p-IκB and the activation of NFκB was similar to that of the expression of TLR4. Our data suggest that ICH stimulates activation of the TLR4/NFκB signaling pathway, which is consistent with previous reports that activation of NFκB is regulated through the TLR4-mediated signaling pathway. TLR4 plays an important role in the recognition of microbial components [19, 20] and can also recognize endogenous molecules such as the degradation products of macromolecules, products of proteolytic cascades, intracellular components of ruptured cells, and products of genes that are activated by inflammation. For instance, HSP70, HSP32, HSP27, and enzymes involved in oxidative stress are found to be upregulated in the brain after ICH, which may be produced by injured neuronal cells or blood cells [21]. It may be speculated that these molecules produced in damaged brain or came from blood cells and constituents of plasma server as endogenous TLR4 ligands, activate TLR4-mediated NFκB signaling, and initiate the inflammatory responses in IHC brain. However, the specific endogenous ligands for TLR4 in hemorrhagic brain have not been determined and need to be identified through further research.\n"}

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studies demonstrated that ICH initiates inflammatory responses, which are associated with secondary growth of hemorrhage and cell death [18]. It is now believed that TLR4-mediated-NFκB pathway activates and regulates immunological and inflammatory responses. To investigate the mechanisms underlying the increased inflammatory responses in the brain after ICH, in the present study, we evaluated the activation of TLR4-mediated NFκB signaling by detecting the p-IκB and the activity of NFκB in hemorrhagic brains. NFκB is an important transcription factor downstream in the TLR4-mediated signaling pathway. Activation of TLR4 stimulates IκBα phosphorylation and degradation, resulting in nuclear translocation of NFκB, which initiates transcription of genes associated with innate immune responses and inflammation [5, 6]. We observed that the levels of phosphorylation of IκB and the activity of NFκB were significantly increased in brain tissue after ICH. The temporal profile of the expression of p-IκB and the activation of NFκB was similar to that of the expression of TLR4. Our data suggest that ICH stimulates activation of the TLR4/NFκB signaling pathway, which is consistent with previous reports that activation of NFκB is regulated through the TLR4-mediated signaling pathway. TLR4 plays an important role in the recognition of microbial components [19, 20] and can also recognize endogenous molecules such as the degradation products of macromolecules, products of proteolytic cascades, intracellular components of ruptured cells, and products of genes that are activated by inflammation. For instance, HSP70, HSP32, HSP27, and enzymes involved in oxidative stress are found to be upregulated in the brain after ICH, which may be produced by injured neuronal cells or blood cells [21]. It may be speculated that these molecules produced in damaged brain or came from blood cells and constituents of plasma server as endogenous TLR4 ligands, activate TLR4-mediated NFκB signaling, and initiate the inflammatory responses in IHC brain. However, the specific endogenous ligands for TLR4 in hemorrhagic brain have not been determined and need to be identified through further research.\n"}

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studies demonstrated that ICH initiates inflammatory responses, which are associated with secondary growth of hemorrhage and cell death [18]. It is now believed that TLR4-mediated-NFκB pathway activates and regulates immunological and inflammatory responses. To investigate the mechanisms underlying the increased inflammatory responses in the brain after ICH, in the present study, we evaluated the activation of TLR4-mediated NFκB signaling by detecting the p-IκB and the activity of NFκB in hemorrhagic brains. NFκB is an important transcription factor downstream in the TLR4-mediated signaling pathway. Activation of TLR4 stimulates IκBα phosphorylation and degradation, resulting in nuclear translocation of NFκB, which initiates transcription of genes associated with innate immune responses and inflammation [5, 6]. We observed that the levels of phosphorylation of IκB and the activity of NFκB were significantly increased in brain tissue after ICH. The temporal profile of the expression of p-IκB and the activation of NFκB was similar to that of the expression of TLR4. Our data suggest that ICH stimulates activation of the TLR4/NFκB signaling pathway, which is consistent with previous reports that activation of NFκB is regulated through the TLR4-mediated signaling pathway. TLR4 plays an important role in the recognition of microbial components [19, 20] and can also recognize endogenous molecules such as the degradation products of macromolecules, products of proteolytic cascades, intracellular components of ruptured cells, and products of genes that are activated by inflammation. For instance, HSP70, HSP32, HSP27, and enzymes involved in oxidative stress are found to be upregulated in the brain after ICH, which may be produced by injured neuronal cells or blood cells [21]. It may be speculated that these molecules produced in damaged brain or came from blood cells and constituents of plasma server as endogenous TLR4 ligands, activate TLR4-mediated NFκB signaling, and initiate the inflammatory responses in IHC brain. However, the specific endogenous ligands for TLR4 in hemorrhagic brain have not been determined and need to be identified through further research.\n"}

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It is now believed that TLR4-mediated-NFκB pathway activates and regulates immunological and inflammatory responses. To investigate the mechanisms underlying the increased inflammatory responses in the brain after ICH, in the present study, we evaluated the activation of TLR4-mediated NFκB signaling by detecting the p-IκB and the activity of NFκB in hemorrhagic brains. NFκB is an important transcription factor downstream in the TLR4-mediated signaling pathway. Activation of TLR4 stimulates IκBα phosphorylation and degradation, resulting in nuclear translocation of NFκB, which initiates transcription of genes associated with innate immune responses and inflammation [5, 6]. We observed that the levels of phosphorylation of IκB and the activity of NFκB were significantly increased in brain tissue after ICH. The temporal profile of the expression of p-IκB and the activation of NFκB was similar to that of the expression of TLR4. Our data suggest that ICH stimulates activation of the TLR4/NFκB signaling pathway, which is consistent with previous reports that activation of NFκB is regulated through the TLR4-mediated signaling pathway. TLR4 plays an important role in the recognition of microbial components [19, 20] and can also recognize endogenous molecules such as the degradation products of macromolecules, products of proteolytic cascades, intracellular components of ruptured cells, and products of genes that are activated by inflammation. For instance, HSP70, HSP32, HSP27, and enzymes involved in oxidative stress are found to be upregulated in the brain after ICH, which may be produced by injured neuronal cells or blood cells [21]. It may be speculated that these molecules produced in damaged brain or came from blood cells and constituents of plasma server as endogenous TLR4 ligands, activate TLR4-mediated NFκB signaling, and initiate the inflammatory responses in IHC brain. However, the specific endogenous ligands for TLR4 in hemorrhagic brain have not been determined and need to be identified through further research.\n"}