PMC:3317373 / 1307-1893 JSONTXT

{"project":"2_test","denotations":[{"id":"22529521-10698075-67992081","span":{"begin":475,"end":476},"obj":"10698075"},{"id":"22529521-16230799-67992082","span":{"begin":581,"end":582},"obj":"16230799"},{"id":"22529521-15680377-67992082","span":{"begin":581,"end":582},"obj":"15680377"},{"id":"22529521-18715849-67992082","span":{"begin":581,"end":582},"obj":"18715849"}],"text":"Brain 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]."}

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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]."}

{"project":"UBERON-AE","denotations":[{"id":"T619","span":{"begin":573,"end":579},"obj":"http://purl.obolibrary.org/obo/UBERON_0000062"},{"id":"T618","span":{"begin":247,"end":266},"obj":"http://purl.obolibrary.org/obo/UBERON_0000120"},{"id":"T617","span":{"begin":314,"end":319},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"T616","span":{"begin":247,"end":252},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"T612","span":{"begin":549,"end":554},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T611","span":{"begin":274,"end":279},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T610","span":{"begin":253,"end":258},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T609","span":{"begin":0,"end":5},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"}],"text":"Brain 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]."}

{"project":"GO-BP","denotations":[{"id":"T638","span":{"begin":320,"end":341},"obj":"http://purl.obolibrary.org/obo/GO_0001775"},{"id":"T637","span":{"begin":314,"end":341},"obj":"http://purl.obolibrary.org/obo/GO_1903708"},{"id":"T636","span":{"begin":234,"end":243},"obj":"http://purl.obolibrary.org/obo/GO_0009056"},{"id":"T632","span":{"begin":498,"end":510},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T631","span":{"begin":201,"end":222},"obj":"http://purl.obolibrary.org/obo/GO_0006954"}],"text":"Brain 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]."}

{"project":"GO-CC","denotations":[{"id":"T906","span":{"begin":370,"end":375},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T905","span":{"begin":320,"end":325},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":"Brain 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]."}

{"project":"sentences","denotations":[{"id":"T622","span":{"begin":479,"end":586},"obj":"Sentence"},{"id":"T621","span":{"begin":134,"end":478},"obj":"Sentence"},{"id":"T620","span":{"begin":0,"end":133},"obj":"Sentence"},{"id":"T15","span":{"begin":0,"end":133},"obj":"Sentence"},{"id":"T16","span":{"begin":134,"end":478},"obj":"Sentence"},{"id":"T17","span":{"begin":479,"end":586},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Brain 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]."}

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