Fumihiro Kawakita

ORCID: 0000-0001-8757-6245
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About
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Research Areas
  • Intracranial Aneurysms: Treatment and Complications
  • Traumatic Brain Injury and Neurovascular Disturbances
  • Intracerebral and Subarachnoid Hemorrhage Research
  • S100 Proteins and Annexins
  • Neurosurgical Procedures and Complications
  • Cerebrovascular and Carotid Artery Diseases
  • Connective tissue disorders research
  • Vascular Malformations Diagnosis and Treatment
  • Bone and Dental Protein Studies
  • Angiogenesis and VEGF in Cancer
  • Aortic Disease and Treatment Approaches
  • Cell Adhesion Molecules Research
  • Neuroscience and Neuropharmacology Research
  • Signaling Pathways in Disease
  • Cardiac Fibrosis and Remodeling
  • Acute Ischemic Stroke Management
  • Dermatology and Skin Diseases
  • Cerebrovascular and genetic disorders
  • Galectins and Cancer Biology
  • Atherosclerosis and Cardiovascular Diseases
  • Psoriasis: Treatment and Pathogenesis
  • Neurological Disease Mechanisms and Treatments
  • Barrier Structure and Function Studies
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Spinal Fractures and Fixation Techniques

Mie University
2016-2025

Mie University Hospital
2022

Matsunami General Hospital
2017

OBJECT Tenascin-C (TNC), a matricellular protein, is induced in the brain following subarachnoid hemorrhage (SAH). The authors investigated if TNC causes edema and blood-brain barrier (BBB) disruption experimental SAH. METHODS C57BL/6 wild-type (WT) or knockout (TNKO) mice were subjected to SAH by endovascular puncture. Ninety-seven randomly allocated WT sham-operated (n = 16), TNKO 34), 31) groups. Mice examined means of neuroscore water content 24-48 hours post-SAH; Evans blue dye...

10.3171/2015.4.jns15484 article EN Journal of neurosurgery 2015-10-16

Background and Purpose— Plasma levels of galectin-3—a matricellular protein—are increased after aneurysmal subarachnoid hemorrhage (SAH), but the functional significance remains undetermined. This study was conducted to evaluate whether modified citrus pectin (MCP; galectin-3 inhibitor) prevents post-SAH early brain injury, focusing on blood-brain barrier disruption. Methods— C57BL/6 male adult mice (n=251) underwent sham or filament perforation SAH modeling, followed by a random...

10.1161/strokeaha.118.021757 article EN Stroke 2018-10-15

Background and Purpose— A matricellular protein tenascin-C is implicated in early brain injury after experimental subarachnoid hemorrhage (SAH). This study first evaluated the role of another periostin relationships with post-SAH injury. Methods— Wild-type (n=226) knockout (n=9) C57BL/6 male adult mice underwent sham or filament perforation SAH modeling. Vehicle, anti-periostin antibody, recombinant was randomly administrated by an intracerebroventricular injection at 30 minutes...

10.1161/strokeaha.117.016629 article EN Stroke 2017-02-28

Osteopontin (OPN), a matricellular protein, is produced as full-length OPN (FL-OPN) and cleaved by thrombin, thus generating the N-terminal half of (OPN N-half) with new functions. Although plasma FL-OPN levels have been associated neurovascular events after aneurysmal subarachnoid hemorrhage (SAH), N-half never investigated. In this study, prospective clinical data samples were collected from 108 consecutive SAH patients ruptured aneurysms undergoing acute treatment via surgery, measured in...

10.3390/ijms26062781 article EN International Journal of Molecular Sciences 2025-03-19

Early brain injury including neuronal apoptosis is a main contributor to neurological deterioration after subarachnoid hemorrhage (SAH). This study was aimed investigate whether EGFR (epidermal growth factor receptor)/NFκB (nuclear factor-kappa B) inducing kinase (NIK)/NFκB (p65 and p50) pathway involved in the SAH mice.C57BL/6 adult male mice underwent endovascular perforation modeling or sham-operation (n=286), 86 mild were excluded. In experiment 1, vehicle an inhibitor (632.0 ng AG1478)...

10.1161/strokeaha.122.041977 article EN Stroke 2023-05-08

OBJECTIVE Chronic hydrocephalus develops in association with the induction of tenascin-C (TNC), a matricellular protein, after aneurysmal subarachnoid hemorrhage (SAH). The aim this study was to examine if cilostazol, selective inhibitor phosphodiesterase Type III, suppresses development chronic by inhibiting TNC SAH patients. METHODS authors retrospectively reviewed factors influencing shunt-dependent 87 patients Fisher Grade 3 using multivariate logistic regression analyses. Cilostazol (50...

10.3171/2016.5.jns152907 article EN Journal of neurosurgery 2016-08-05

Aneurysmal subarachnoid hemorrhage (SAH) has increased with the aging of population, but outcome for elderly SAH patients is very poor. Therefore, predicting important determining whether to pursue aggressive treatment. Pigment epithelium-derived factor (PEDF) a matricellular protein that induced in brain, and plasma levels could be used as biomarker severity metabolic diseases. This study investigated acute-phase PEDF predict outcomes after aneurysmal elderly. Plasma samples clinical...

10.3390/ijms25031701 article EN International Journal of Molecular Sciences 2024-01-30
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