PMC:3317373 / 1291-2851 JSON TXT

Annnotations TAB JSON ListView MergeView

2_test

{"project":"2_test","denotations":[{"id":"22529521-10698075-67992081","span":{"begin":491,"end":492},"obj":"10698075"},{"id":"22529521-16230799-67992082","span":{"begin":597,"end":598},"obj":"16230799"},{"id":"22529521-15680377-67992082","span":{"begin":597,"end":598},"obj":"15680377"},{"id":"22529521-18715849-67992082","span":{"begin":597,"end":598},"obj":"18715849"},{"id":"22529521-19125683-67992083","span":{"begin":956,"end":957},"obj":"19125683"},{"id":"22529521-20953205-67992084","span":{"begin":1094,"end":1095},"obj":"20953205"}],"text":"1. Introduction\nBrain damage following traumatic injury is a result of direct (primary injury) and indirect (secondary or delayed injury) mechanisms. The secondary injury mechanism involves the initiation of an acute inflammatory response, including breakdown of blood-brain barrier (BBB), brain edema, infiltration of peripheral blood cells, and activation of resident immunocompetent cells, as well as the release of numerous immune mediators such as interleukins and chemotactic factors [1]. And the subsequent inflammation leads to secondary damage not only in brain but also in other organs [2–4].\nNuclear factor erythroid 2-related factor2 (Nrf2) is a transcription factor that regulates many kinds of antioxidant genes. Several studies have demonstrated that Nrf2 regulates the inflammation in the brain after traumatic brain injury (TBI). It was also showed that TBI could induce more aggravated damage in Nrf2 knockout mice than in wildtype mice [5]. On the contrary, such inflammation can be extenuated through elevating the level of Nrf2 by its inducers, such as sulforaphane (SFN) [6]. It is well documented that astrocytes play a critical role in maintaining normal brain physiology and responding to injury or disease. In fact, all the aforementioned studies are performed in vivo. Little is known about the relationship between Nrf2 and inflammation in astrocytes after TBI. Therefore, here we analysed the influence of Nrf2 on the expression of proinflammatory cytokines in primary cultured astrocytes from transgenic mice after scratch injury."}

pmc-enju-pas

UBERON-AE

{"project":"UBERON-AE","denotations":[{"id":"T619","span":{"begin":589,"end":595},"obj":"http://purl.obolibrary.org/obo/UBERON_0000062"},{"id":"T618","span":{"begin":263,"end":282},"obj":"http://purl.obolibrary.org/obo/UBERON_0000120"},{"id":"T617","span":{"begin":330,"end":335},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"T616","span":{"begin":263,"end":268},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"T615","span":{"begin":1179,"end":1184},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T614","span":{"begin":827,"end":832},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T613","span":{"begin":805,"end":810},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T612","span":{"begin":565,"end":570},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T611","span":{"begin":290,"end":295},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T610","span":{"begin":269,"end":274},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T609","span":{"begin":16,"end":21},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"}],"text":"1. Introduction\nBrain damage following traumatic injury is a result of direct (primary injury) and indirect (secondary or delayed injury) mechanisms. The secondary injury mechanism involves the initiation of an acute inflammatory response, including breakdown of blood-brain barrier (BBB), brain edema, infiltration of peripheral blood cells, and activation of resident immunocompetent cells, as well as the release of numerous immune mediators such as interleukins and chemotactic factors [1]. And the subsequent inflammation leads to secondary damage not only in brain but also in other organs [2–4].\nNuclear factor erythroid 2-related factor2 (Nrf2) is a transcription factor that regulates many kinds of antioxidant genes. Several studies have demonstrated that Nrf2 regulates the inflammation in the brain after traumatic brain injury (TBI). It was also showed that TBI could induce more aggravated damage in Nrf2 knockout mice than in wildtype mice [5]. On the contrary, such inflammation can be extenuated through elevating the level of Nrf2 by its inducers, such as sulforaphane (SFN) [6]. It is well documented that astrocytes play a critical role in maintaining normal brain physiology and responding to injury or disease. In fact, all the aforementioned studies are performed in vivo. Little is known about the relationship between Nrf2 and inflammation in astrocytes after TBI. Therefore, here we analysed the influence of Nrf2 on the expression of proinflammatory cytokines in primary cultured astrocytes from transgenic mice after scratch injury."}

GO-BP

{"project":"GO-BP","denotations":[{"id":"T639","span":{"begin":658,"end":671},"obj":"http://purl.obolibrary.org/obo/GO_0006351"},{"id":"T638","span":{"begin":336,"end":357},"obj":"http://purl.obolibrary.org/obo/GO_0001775"},{"id":"T637","span":{"begin":330,"end":357},"obj":"http://purl.obolibrary.org/obo/GO_1903708"},{"id":"T636","span":{"begin":250,"end":259},"obj":"http://purl.obolibrary.org/obo/GO_0009056"},{"id":"T635","span":{"begin":1352,"end":1364},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T634","span":{"begin":982,"end":994},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T633","span":{"begin":785,"end":797},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T632","span":{"begin":514,"end":526},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T631","span":{"begin":217,"end":238},"obj":"http://purl.obolibrary.org/obo/GO_0006954"}],"text":"1. Introduction\nBrain damage following traumatic injury is a result of direct (primary injury) and indirect (secondary or delayed injury) mechanisms. The secondary injury mechanism involves the initiation of an acute inflammatory response, including breakdown of blood-brain barrier (BBB), brain edema, infiltration of peripheral blood cells, and activation of resident immunocompetent cells, as well as the release of numerous immune mediators such as interleukins and chemotactic factors [1]. And the subsequent inflammation leads to secondary damage not only in brain but also in other organs [2–4].\nNuclear factor erythroid 2-related factor2 (Nrf2) is a transcription factor that regulates many kinds of antioxidant genes. Several studies have demonstrated that Nrf2 regulates the inflammation in the brain after traumatic brain injury (TBI). It was also showed that TBI could induce more aggravated damage in Nrf2 knockout mice than in wildtype mice [5]. On the contrary, such inflammation can be extenuated through elevating the level of Nrf2 by its inducers, such as sulforaphane (SFN) [6]. It is well documented that astrocytes play a critical role in maintaining normal brain physiology and responding to injury or disease. In fact, all the aforementioned studies are performed in vivo. Little is known about the relationship between Nrf2 and inflammation in astrocytes after TBI. Therefore, here we analysed the influence of Nrf2 on the expression of proinflammatory cytokines in primary cultured astrocytes from transgenic mice after scratch injury."}

GO-CC

{"project":"GO-CC","denotations":[{"id":"T906","span":{"begin":386,"end":391},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T905","span":{"begin":336,"end":341},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":"1. Introduction\nBrain damage following traumatic injury is a result of direct (primary injury) and indirect (secondary or delayed injury) mechanisms. The secondary injury mechanism involves the initiation of an acute inflammatory response, including breakdown of blood-brain barrier (BBB), brain edema, infiltration of peripheral blood cells, and activation of resident immunocompetent cells, as well as the release of numerous immune mediators such as interleukins and chemotactic factors [1]. And the subsequent inflammation leads to secondary damage not only in brain but also in other organs [2–4].\nNuclear factor erythroid 2-related factor2 (Nrf2) is a transcription factor that regulates many kinds of antioxidant genes. Several studies have demonstrated that Nrf2 regulates the inflammation in the brain after traumatic brain injury (TBI). It was also showed that TBI could induce more aggravated damage in Nrf2 knockout mice than in wildtype mice [5]. On the contrary, such inflammation can be extenuated through elevating the level of Nrf2 by its inducers, such as sulforaphane (SFN) [6]. It is well documented that astrocytes play a critical role in maintaining normal brain physiology and responding to injury or disease. In fact, all the aforementioned studies are performed in vivo. Little is known about the relationship between Nrf2 and inflammation in astrocytes after TBI. Therefore, here we analysed the influence of Nrf2 on the expression of proinflammatory cytokines in primary cultured astrocytes from transgenic mice after scratch injury."}

sentences

{"project":"sentences","denotations":[{"id":"T630","span":{"begin":1390,"end":1560},"obj":"Sentence"},{"id":"T629","span":{"begin":1296,"end":1389},"obj":"Sentence"},{"id":"T628","span":{"begin":1233,"end":1295},"obj":"Sentence"},{"id":"T627","span":{"begin":1098,"end":1232},"obj":"Sentence"},{"id":"T626","span":{"begin":960,"end":1097},"obj":"Sentence"},{"id":"T625","span":{"begin":847,"end":959},"obj":"Sentence"},{"id":"T624","span":{"begin":727,"end":846},"obj":"Sentence"},{"id":"T623","span":{"begin":603,"end":726},"obj":"Sentence"},{"id":"T622","span":{"begin":495,"end":602},"obj":"Sentence"},{"id":"T621","span":{"begin":150,"end":494},"obj":"Sentence"},{"id":"T620","span":{"begin":16,"end":149},"obj":"Sentence"},{"id":"T13","span":{"begin":0,"end":2},"obj":"Sentence"},{"id":"T14","span":{"begin":3,"end":15},"obj":"Sentence"},{"id":"T15","span":{"begin":16,"end":149},"obj":"Sentence"},{"id":"T16","span":{"begin":150,"end":494},"obj":"Sentence"},{"id":"T17","span":{"begin":495,"end":602},"obj":"Sentence"},{"id":"T18","span":{"begin":603,"end":726},"obj":"Sentence"},{"id":"T19","span":{"begin":727,"end":846},"obj":"Sentence"},{"id":"T20","span":{"begin":847,"end":959},"obj":"Sentence"},{"id":"T21","span":{"begin":960,"end":1097},"obj":"Sentence"},{"id":"T22","span":{"begin":1098,"end":1232},"obj":"Sentence"},{"id":"T23","span":{"begin":1233,"end":1295},"obj":"Sentence"},{"id":"T24","span":{"begin":1296,"end":1389},"obj":"Sentence"},{"id":"T25","span":{"begin":1390,"end":1560},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"1. Introduction\nBrain damage following traumatic injury is a result of direct (primary injury) and indirect (secondary or delayed injury) mechanisms. The secondary injury mechanism involves the initiation of an acute inflammatory response, including breakdown of blood-brain barrier (BBB), brain edema, infiltration of peripheral blood cells, and activation of resident immunocompetent cells, as well as the release of numerous immune mediators such as interleukins and chemotactic factors [1]. And the subsequent inflammation leads to secondary damage not only in brain but also in other organs [2–4].\nNuclear factor erythroid 2-related factor2 (Nrf2) is a transcription factor that regulates many kinds of antioxidant genes. Several studies have demonstrated that Nrf2 regulates the inflammation in the brain after traumatic brain injury (TBI). It was also showed that TBI could induce more aggravated damage in Nrf2 knockout mice than in wildtype mice [5]. On the contrary, such inflammation can be extenuated through elevating the level of Nrf2 by its inducers, such as sulforaphane (SFN) [6]. It is well documented that astrocytes play a critical role in maintaining normal brain physiology and responding to injury or disease. In fact, all the aforementioned studies are performed in vivo. Little is known about the relationship between Nrf2 and inflammation in astrocytes after TBI. Therefore, here we analysed the influence of Nrf2 on the expression of proinflammatory cytokines in primary cultured astrocytes from transgenic mice after scratch injury."}

ICD10

{"project":"ICD10","denotations":[{"id":"T904","span":{"begin":1553,"end":1559},"obj":"http://purl.bioontology.org/ontology/ICD10/T14.9"},{"id":"T903","span":{"begin":1214,"end":1220},"obj":"http://purl.bioontology.org/ontology/ICD10/T14.9"},{"id":"T902","span":{"begin":833,"end":839},"obj":"http://purl.bioontology.org/ontology/ICD10/T14.9"},{"id":"T901","span":{"begin":164,"end":170},"obj":"http://purl.bioontology.org/ontology/ICD10/T14.9"},{"id":"T900","span":{"begin":130,"end":136},"obj":"http://purl.bioontology.org/ontology/ICD10/T14.9"},{"id":"T899","span":{"begin":87,"end":93},"obj":"http://purl.bioontology.org/ontology/ICD10/T14.9"},{"id":"T898","span":{"begin":49,"end":55},"obj":"http://purl.bioontology.org/ontology/ICD10/T14.9"}],"text":"1. Introduction\nBrain damage following traumatic injury is a result of direct (primary injury) and indirect (secondary or delayed injury) mechanisms. The secondary injury mechanism involves the initiation of an acute inflammatory response, including breakdown of blood-brain barrier (BBB), brain edema, infiltration of peripheral blood cells, and activation of resident immunocompetent cells, as well as the release of numerous immune mediators such as interleukins and chemotactic factors [1]. And the subsequent inflammation leads to secondary damage not only in brain but also in other organs [2–4].\nNuclear factor erythroid 2-related factor2 (Nrf2) is a transcription factor that regulates many kinds of antioxidant genes. Several studies have demonstrated that Nrf2 regulates the inflammation in the brain after traumatic brain injury (TBI). It was also showed that TBI could induce more aggravated damage in Nrf2 knockout mice than in wildtype mice [5]. On the contrary, such inflammation can be extenuated through elevating the level of Nrf2 by its inducers, such as sulforaphane (SFN) [6]. It is well documented that astrocytes play a critical role in maintaining normal brain physiology and responding to injury or disease. In fact, all the aforementioned studies are performed in vivo. Little is known about the relationship between Nrf2 and inflammation in astrocytes after TBI. Therefore, here we analysed the influence of Nrf2 on the expression of proinflammatory cytokines in primary cultured astrocytes from transgenic mice after scratch injury."}

bionlp-st-ge-2016-test-ihmc

{"project":"bionlp-st-ge-2016-test-ihmc","denotations":[{"id":"T1218","span":{"begin":1406,"end":1559},"obj":"Regulation"},{"id":"T1217","span":{"begin":1440,"end":1559},"obj":"Gene_expression"},{"id":"T1216","span":{"begin":941,"end":958},"obj":"Protein"},{"id":"T1215","span":{"begin":705,"end":725},"obj":"Protein"},{"id":"T1214","span":{"begin":1368,"end":1378},"obj":"Entity"},{"id":"T1213","span":{"begin":914,"end":918},"obj":"Protein"},{"id":"T1212","span":{"begin":1458,"end":1486},"obj":"Protein"},{"id":"T1211","span":{"begin":1044,"end":1048},"obj":"Protein"},{"id":"T1210","span":{"begin":647,"end":651},"obj":"Protein"},{"id":"T1209","span":{"begin":1052,"end":1092},"obj":"Entity"},{"id":"T1208","span":{"begin":766,"end":770},"obj":"Protein"},{"id":"T1207","span":{"begin":316,"end":341},"obj":"Entity"},{"id":"T1206","span":{"begin":708,"end":719},"obj":"Entity"},{"id":"T1205","span":{"begin":914,"end":932},"obj":"Protein"},{"id":"T1204","span":{"begin":1088,"end":1091},"obj":"Protein"},{"id":"T1203","span":{"begin":1523,"end":1559},"obj":"Protein"},{"id":"T1202","span":{"begin":1343,"end":1347},"obj":"Protein"},{"id":"T1201","span":{"begin":1490,"end":1559},"obj":"Entity"},{"id":"T1200","span":{"begin":1125,"end":1135},"obj":"Entity"},{"id":"T1199","span":{"begin":453,"end":465},"obj":"Protein"},{"id":"T1198","span":{"begin":1432,"end":1439},"obj":"Protein"},{"id":"T1197","span":{"begin":370,"end":391},"obj":"Entity"}],"relations":[{"id":"R982","pred":"causeOf","subj":"T1198","obj":"T1218"},{"id":"R983","pred":"themeOf","subj":"T1212","obj":"T1217"},{"id":"R984","pred":"themeOf","subj":"T1217","obj":"T1218"}],"text":"1. Introduction\nBrain damage following traumatic injury is a result of direct (primary injury) and indirect (secondary or delayed injury) mechanisms. The secondary injury mechanism involves the initiation of an acute inflammatory response, including breakdown of blood-brain barrier (BBB), brain edema, infiltration of peripheral blood cells, and activation of resident immunocompetent cells, as well as the release of numerous immune mediators such as interleukins and chemotactic factors [1]. And the subsequent inflammation leads to secondary damage not only in brain but also in other organs [2–4].\nNuclear factor erythroid 2-related factor2 (Nrf2) is a transcription factor that regulates many kinds of antioxidant genes. Several studies have demonstrated that Nrf2 regulates the inflammation in the brain after traumatic brain injury (TBI). It was also showed that TBI could induce more aggravated damage in Nrf2 knockout mice than in wildtype mice [5]. On the contrary, such inflammation can be extenuated through elevating the level of Nrf2 by its inducers, such as sulforaphane (SFN) [6]. It is well documented that astrocytes play a critical role in maintaining normal brain physiology and responding to injury or disease. In fact, all the aforementioned studies are performed in vivo. Little is known about the relationship between Nrf2 and inflammation in astrocytes after TBI. Therefore, here we analysed the influence of Nrf2 on the expression of proinflammatory cytokines in primary cultured astrocytes from transgenic mice after scratch injury."}

bionlp-st-ge-2016-spacy-parsed

bionlp-st-ge-2016-test-tees

{"project":"bionlp-st-ge-2016-test-tees","denotations":[{"id":"T916","span":{"begin":1435,"end":1439},"obj":"Protein"},{"id":"T915","span":{"begin":1343,"end":1347},"obj":"Protein"},{"id":"T914","span":{"begin":1021,"end":1030},"obj":"Positive_regulation"},{"id":"T913","span":{"begin":1044,"end":1048},"obj":"Protein"},{"id":"T912","span":{"begin":914,"end":918},"obj":"Protein"},{"id":"T911","span":{"begin":766,"end":770},"obj":"Protein"},{"id":"T910","span":{"begin":684,"end":693},"obj":"Regulation"},{"id":"T909","span":{"begin":684,"end":693},"obj":"Regulation"},{"id":"T908","span":{"begin":603,"end":645},"obj":"Protein"},{"id":"T907","span":{"begin":647,"end":651},"obj":"Protein"}],"relations":[{"id":"R706","pred":"themeOf","subj":"T907","obj":"T909"},{"id":"R707","pred":"themeOf","subj":"T908","obj":"T910"},{"id":"R708","pred":"themeOf","subj":"T913","obj":"T914"}],"text":"1. Introduction\nBrain damage following traumatic injury is a result of direct (primary injury) and indirect (secondary or delayed injury) mechanisms. The secondary injury mechanism involves the initiation of an acute inflammatory response, including breakdown of blood-brain barrier (BBB), brain edema, infiltration of peripheral blood cells, and activation of resident immunocompetent cells, as well as the release of numerous immune mediators such as interleukins and chemotactic factors [1]. And the subsequent inflammation leads to secondary damage not only in brain but also in other organs [2–4].\nNuclear factor erythroid 2-related factor2 (Nrf2) is a transcription factor that regulates many kinds of antioxidant genes. Several studies have demonstrated that Nrf2 regulates the inflammation in the brain after traumatic brain injury (TBI). It was also showed that TBI could induce more aggravated damage in Nrf2 knockout mice than in wildtype mice [5]. On the contrary, such inflammation can be extenuated through elevating the level of Nrf2 by its inducers, such as sulforaphane (SFN) [6]. It is well documented that astrocytes play a critical role in maintaining normal brain physiology and responding to injury or disease. In fact, all the aforementioned studies are performed in vivo. Little is known about the relationship between Nrf2 and inflammation in astrocytes after TBI. Therefore, here we analysed the influence of Nrf2 on the expression of proinflammatory cytokines in primary cultured astrocytes from transgenic mice after scratch injury."}

testone

{"project":"testone","denotations":[{"id":"T606","span":{"begin":919,"end":927},"obj":"Negative_regulation"}],"text":"1. Introduction\nBrain damage following traumatic injury is a result of direct (primary injury) and indirect (secondary or delayed injury) mechanisms. The secondary injury mechanism involves the initiation of an acute inflammatory response, including breakdown of blood-brain barrier (BBB), brain edema, infiltration of peripheral blood cells, and activation of resident immunocompetent cells, as well as the release of numerous immune mediators such as interleukins and chemotactic factors [1]. And the subsequent inflammation leads to secondary damage not only in brain but also in other organs [2–4].\nNuclear factor erythroid 2-related factor2 (Nrf2) is a transcription factor that regulates many kinds of antioxidant genes. Several studies have demonstrated that Nrf2 regulates the inflammation in the brain after traumatic brain injury (TBI). It was also showed that TBI could induce more aggravated damage in Nrf2 knockout mice than in wildtype mice [5]. On the contrary, such inflammation can be extenuated through elevating the level of Nrf2 by its inducers, such as sulforaphane (SFN) [6]. It is well documented that astrocytes play a critical role in maintaining normal brain physiology and responding to injury or disease. In fact, all the aforementioned studies are performed in vivo. Little is known about the relationship between Nrf2 and inflammation in astrocytes after TBI. Therefore, here we analysed the influence of Nrf2 on the expression of proinflammatory cytokines in primary cultured astrocytes from transgenic mice after scratch injury."}

test3

{"project":"test3","denotations":[{"id":"T608","span":{"begin":1021,"end":1030},"obj":"Positive_regulation"},{"id":"T607","span":{"begin":919,"end":927},"obj":"Negative_regulation"}],"text":"1. Introduction\nBrain damage following traumatic injury is a result of direct (primary injury) and indirect (secondary or delayed injury) mechanisms. The secondary injury mechanism involves the initiation of an acute inflammatory response, including breakdown of blood-brain barrier (BBB), brain edema, infiltration of peripheral blood cells, and activation of resident immunocompetent cells, as well as the release of numerous immune mediators such as interleukins and chemotactic factors [1]. And the subsequent inflammation leads to secondary damage not only in brain but also in other organs [2–4].\nNuclear factor erythroid 2-related factor2 (Nrf2) is a transcription factor that regulates many kinds of antioxidant genes. Several studies have demonstrated that Nrf2 regulates the inflammation in the brain after traumatic brain injury (TBI). It was also showed that TBI could induce more aggravated damage in Nrf2 knockout mice than in wildtype mice [5]. On the contrary, such inflammation can be extenuated through elevating the level of Nrf2 by its inducers, such as sulforaphane (SFN) [6]. It is well documented that astrocytes play a critical role in maintaining normal brain physiology and responding to injury or disease. In fact, all the aforementioned studies are performed in vivo. Little is known about the relationship between Nrf2 and inflammation in astrocytes after TBI. Therefore, here we analysed the influence of Nrf2 on the expression of proinflammatory cytokines in primary cultured astrocytes from transgenic mice after scratch injury."}

PMC:3317373 / 1291-2851 JSONTXT

Annnotations TAB JSON ListView MergeView

PMC:3317373 / 1291-2851 JSON TXT