To Improve Translational Research in Subarachnoid Hemorrhage

Suzuki, Hiroyoshi; Nakano, Fumi

doi:10.1007/s12975-017-0546-2

Cited by 39 publications

(31 citation statements)

References 32 publications

(44 reference statements)

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“…Our models do not account for mechanisms of early brain injury (EBI) caused by aneurysm rupture in aSAH patients (41,76). Interspecies differences and mode of bleeding induction are known to limit translation of animal model data in SAH research to clinical practice (77). We have tried to compensate for this limitation by the use of different species and the use of CSF samples of aSAH patients in ex vivo vascular function experiments.…”

Section: Discussionmentioning

confidence: 99%

Haptoglobin administration into the subarachnoid space prevents hemoglobin-induced cerebral vasospasm

Hugelshofer

Buzzi

Schaer

et al. 2019

Journal of Clinical Investigation

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Statistics. We used JMP software from SAS (versions 13 or 14) for all analyses. Data are presented with all data points plotted. Overlayed diamonds represent mean, 95% CI, and overlap marks (horizontal lines above and below the mean line), which define statistical significant difference between groups if not overlapping (P < 0.05). Groups were compared with 1-way ANOVA, applying a Tukey-Kramer posttest correcting for multiple comparisons. A P value of less than 0.05 was considered statistically significant.Study approval. All animal studies were approved by the cantonal veterinary authorities "Kantonale Tierversuchskommission Zürich." The clinical study (CSF sampling) was approved by the local ethical review board of the Kanton of Zurich, and written consent was obtained from all patients or their legal representatives.

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Section: Discussionmentioning

confidence: 99%

Haptoglobin administration into the subarachnoid space prevents hemoglobin-induced cerebral vasospasm

Hugelshofer

Buzzi

Schaer

et al. 2019

Journal of Clinical Investigation

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“…At 24 h after experimental SAH by endovascular perforation in rats, magnetic resonance imaging studies showed that more severe SAH caused a more frequent and larger cerebral infarction, where fibrinogen/fibrin-stained microthromboses were histologically found [22]. Thus, although several challenges exist to translate findings from animal research to clinical settings [23], the endovascular perforation model associated with arterial bleeding may be the most suitable to study severe EBI, and in fact it has the highest mortality among SAH models in mice [24]. As to target pathologies, inflammation may be a good candidate [21]: to put it more concretely, damageassociated molecular patterns (DAMPs) and pattern recognition receptors may be important initiators as well as enhancers of post-SAH neuroinflammation leading to severe EBI [1].…”

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confidence: 99%

Inflammation: a Good Research Target to Improve Outcomes of Poor-Grade Subarachnoid Hemorrhage

Suzuki

2019

Transl. Stroke Res.

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“…The already-known pathogeneses of DCI include cerebral vasospasm, inflammation, microthrombosis , and cortical spreading ischemia [11], and a measure of intracranial hematoma is one of the strong predictors of DCI [12]. Cerebral vasospasm has been considered as the main player in DCI for a long time, although the drugs targeting cerebral vasospasm have failed to cause any improvement in the neurological outcomes [13]. Therefore, nowadays, cerebral vasospasm is believed to be only a part of DCI, and EBI and the non-vasospastic causes of DCI are recognized as the more important determinants of neurological outcomes [5,14].…”

Section: Early Brain Injury (Ebi) and Delayed Cerebral Ischemia (Dci)mentioning

confidence: 99%

The Role of Periostin in Brain Injury Caused by Subarachnoid Hemorrhage

Kanamaru¹,

Kawakita²,

Asada³

et al. 2019

obm neurobiol

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Aneurysmal subarachnoid hemorrhage (aSAH) causes serious brain injury, and its mechanisms have not been completely unraveled so far. The causative factors for the brain injury initiated by an aneurysm rupture, which is referred to as the early brain injury (EBI), include elevated intracranial pressure, cerebral hypoperfusion, and blood contents that are directly exposed to the brain surface. At Day 4-14 post aSAH, delayed cerebral ischemia (DCI) often develops, which may worsen the neurological outcomes critically. DCI may be a consequence of EBI. Understanding the complex mechanisms underlying the post-aSAH brain injury (EBI and DCI) is, therefore, important in order to improve the neurological outcomes. In addition, several biomarkers possibly associated with EBI, DCI, and neurological outcome have been investigated, although none of these has been conclusive. A matricellular protein periostin has emerged as an important potential contributor to EBI and DCI, and may serve as the biomarker and a therapeutic molecular target for EBI and DCI. In the present report, the possible role of periostin in aSAH has been reviewed.

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To Improve Translational Research in Subarachnoid Hemorrhage

Cited by 39 publications

References 32 publications

Haptoglobin administration into the subarachnoid space prevents hemoglobin-induced cerebral vasospasm

Haptoglobin administration into the subarachnoid space prevents hemoglobin-induced cerebral vasospasm

Inflammation: a Good Research Target to Improve Outcomes of Poor-Grade Subarachnoid Hemorrhage

The Role of Periostin in Brain Injury Caused by Subarachnoid Hemorrhage

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