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PubmedHPO

Id Subject Object Predicate Lexical cue
T1 105-111 HP_0001297 denotes Stroke
T2 424-441 HP_0002637 denotes cerebral ischemia
T1 105-111 HP_0001297 denotes Stroke
T2 424-441 HP_0002637 denotes cerebral ischemia

PubMed_Structured_Abstracts

Id Subject Object Predicate Lexical cue
T1 105-582 BACKGROUND denotes Stroke is the second to third leading cause of death. Toll-like receptor 4 (TLR4) is a signaling receptor in innate immunity that is a specific immunologic response to systemic bacterial infection and cerebral injury. The role of TLR4 in brain ischemia has not been examined yet. We have therefore investigated whether cerebral ischemia and inflammation produced by permanent occlusion of the middle cerebral artery differ in mice that lack a functional TLR4 signaling pathway.
T2 604-1601 RESULTS denotes Permanent occlusion of the middle cerebral artery was performed on 2 strains of TLR4-deficient mice (C3H/HeJ and C57BL/10ScNJ) and respective controls (C3H/HeN and C57BL/10ScSn). Stroke outcome was evaluated by determination of infarct volume and assessment of neurological scores. Brains were collected 24 hours and 7 days after stroke. When compared with control mice, TLR4-deficient mice had lower infarct volumes and better outcomes in neurological and behavioral tests. Mice that lacked TLR4 had minor expression of stroke-induced interferon regulatory factor-1, inducible nitric oxide synthase, and cyclooxygenase-2, mediators implicated in brain damage. The levels of interferon-beta and of the lipid peroxidation marker malondialdehyde were also lower in brains from TLR4-deficient mice than in those from control mice. In addition, the expression of matrix metalloproteinase-9, which is induced and mediates brain damage, was also reduced in TLR4-deficient mice after experimental stroke.
T3 1615-1856 CONCLUSIONS denotes TLR4-deficient mice have minor infarctions and less inflammatory response after an ischemic insult. These data demonstrate that TLR4 signaling and innate immunity are involved in brain damage and in inflammation triggered by ischemic injury.

Inflammaging

Id Subject Object Predicate Lexical cue
T1 0-92 Sentence denotes Toll-like receptor 4 is involved in brain damage and inflammation after experimental stroke.
T2 93-104 Sentence denotes BACKGROUND:
T3 105-158 Sentence denotes Stroke is the second to third leading cause of death.
T4 159-322 Sentence denotes Toll-like receptor 4 (TLR4) is a signaling receptor in innate immunity that is a specific immunologic response to systemic bacterial infection and cerebral injury.
T5 323-384 Sentence denotes The role of TLR4 in brain ischemia has not been examined yet.
T6 385-582 Sentence denotes We have therefore investigated whether cerebral ischemia and inflammation produced by permanent occlusion of the middle cerebral artery differ in mice that lack a functional TLR4 signaling pathway.
T7 583-603 Sentence denotes METHODS AND RESULTS:
T8 604-782 Sentence denotes Permanent occlusion of the middle cerebral artery was performed on 2 strains of TLR4-deficient mice (C3H/HeJ and C57BL/10ScNJ) and respective controls (C3H/HeN and C57BL/10ScSn).
T9 783-885 Sentence denotes Stroke outcome was evaluated by determination of infarct volume and assessment of neurological scores.
T10 886-941 Sentence denotes Brains were collected 24 hours and 7 days after stroke.
T11 942-1078 Sentence denotes When compared with control mice, TLR4-deficient mice had lower infarct volumes and better outcomes in neurological and behavioral tests.
T12 1079-1264 Sentence denotes Mice that lacked TLR4 had minor expression of stroke-induced interferon regulatory factor-1, inducible nitric oxide synthase, and cyclooxygenase-2, mediators implicated in brain damage.
T13 1265-1431 Sentence denotes The levels of interferon-beta and of the lipid peroxidation marker malondialdehyde were also lower in brains from TLR4-deficient mice than in those from control mice.
T14 1432-1601 Sentence denotes In addition, the expression of matrix metalloproteinase-9, which is induced and mediates brain damage, was also reduced in TLR4-deficient mice after experimental stroke.
T15 1602-1714 Sentence denotes CONCLUSIONS: TLR4-deficient mice have minor infarctions and less inflammatory response after an ischemic insult.
T16 1715-1856 Sentence denotes These data demonstrate that TLR4 signaling and innate immunity are involved in brain damage and in inflammation triggered by ischemic injury.
T1 0-92 Sentence denotes Toll-like receptor 4 is involved in brain damage and inflammation after experimental stroke.
T2 93-104 Sentence denotes BACKGROUND:
T3 105-158 Sentence denotes Stroke is the second to third leading cause of death.
T4 159-322 Sentence denotes Toll-like receptor 4 (TLR4) is a signaling receptor in innate immunity that is a specific immunologic response to systemic bacterial infection and cerebral injury.
T5 323-384 Sentence denotes The role of TLR4 in brain ischemia has not been examined yet.
T6 385-582 Sentence denotes We have therefore investigated whether cerebral ischemia and inflammation produced by permanent occlusion of the middle cerebral artery differ in mice that lack a functional TLR4 signaling pathway.
T7 583-603 Sentence denotes METHODS AND RESULTS:
T8 604-782 Sentence denotes Permanent occlusion of the middle cerebral artery was performed on 2 strains of TLR4-deficient mice (C3H/HeJ and C57BL/10ScNJ) and respective controls (C3H/HeN and C57BL/10ScSn).
T9 783-885 Sentence denotes Stroke outcome was evaluated by determination of infarct volume and assessment of neurological scores.
T10 886-941 Sentence denotes Brains were collected 24 hours and 7 days after stroke.
T11 942-1078 Sentence denotes When compared with control mice, TLR4-deficient mice had lower infarct volumes and better outcomes in neurological and behavioral tests.
T12 1079-1264 Sentence denotes Mice that lacked TLR4 had minor expression of stroke-induced interferon regulatory factor-1, inducible nitric oxide synthase, and cyclooxygenase-2, mediators implicated in brain damage.
T13 1265-1431 Sentence denotes The levels of interferon-beta and of the lipid peroxidation marker malondialdehyde were also lower in brains from TLR4-deficient mice than in those from control mice.
T14 1432-1601 Sentence denotes In addition, the expression of matrix metalloproteinase-9, which is induced and mediates brain damage, was also reduced in TLR4-deficient mice after experimental stroke.
T15 1602-1714 Sentence denotes CONCLUSIONS: TLR4-deficient mice have minor infarctions and less inflammatory response after an ischemic insult.
T16 1715-1856 Sentence denotes These data demonstrate that TLR4 signaling and innate immunity are involved in brain damage and in inflammation triggered by ischemic injury.