研究者詳細 - 堀口　崇

論文 - 堀口　崇

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Meningiomas of the ventral foramen magnum and lower clivus: factors influencing surgical morbidity, the extent of tumour resection, and tumour recurrence

堀口崇

ACTA NEUROCHIRURGICA 152 （ 1 ） 79 - 86 2010年01月

研究論文（学術雑誌）, ISSN 0001-6268

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Brain metastasis of a papillary renal cell carcinoma, identified as type 2

堀口崇

INTERNATIONAL JOURNAL OF CLINICAL ONCOLOGY 14 （ 3 ） 270 - 272 2009年06月

研究論文（学術雑誌）, ISSN 1341-9625

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連載脳神経外科疾患治療のスタンダード 6.無症候性脳腫瘍

堀口崇, 河瀬斌

Neurological Surgery 脳神経外科（株式会社医学書院） 37 （ 5 ） 503 - 510 2009年05月

ISSN 03012603

Asymptomatic Brain Tumor

堀口崇

NEUROLOGICAL SURGERY 37 （ 5 ） 503 - 510 2009年05月

研究論文（学術雑誌）, ISSN 0301-2603

[Clinical standard of neurosurgical disorder (6). Asymptomatic brain tumor].

Horiguchi T, Kawase T

No shinkei geka. Neurological surgery 37 （ 5 ） 503 - 10 2009年05月

ISSN 0301-2603

Subcortical Intracerebral Hemorrhage Caused by Mucormycosis in a Patient with a History of Bone-marrow Transplantation

堀口崇

JOURNAL OF STROKE & CEREBROVASCULAR DISEASES 18 （ 5 ） 405 - 406 2009年01月

研究論文（学術雑誌）, ISSN 1052-3057

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Mechanisms involved in the cerebrovascular dilator effects of cortical spreading depression

堀口崇

PROGRESS IN NEUROBIOLOGY 86 （ 4 ） 379 - 395 2008年12月

研究論文（学術雑誌）, ISSN 0301-0082

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Periventricular hyperintensity deteriorates word fluency in normal subjects

Fukunaga, A; Kato, M; Horiguchi, T; Sasaki, H; Toda, M; Yazaki, T; Asada, H; Inoue, H; Yoshida, K; Otani, M; Hattori, M; Kawase, T; Mizukami, M

EUROPEAN JOURNAL OF NEUROLOGY 15 290 - 290 2008年08月

ISSN 1351-5101

脳腫瘍手術の安全対策

堀口崇

厚生労働科学研究費補助金医療技術評価総合研究事業　脳神経外科手術におけるヒヤリ•ハット事例、事故事例、訴訟事例の分析による手術治療安全対策ガイドライン作成に関する研究 16 - 33 2007年

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Therapeutic hypothermia for severely head-injured patients with acute subdural haematoma

堀口崇

JOURNAL OF CLINICAL NEUROSCIENCE 13 （ 7 ） 733 - 737 2006年08月

研究論文（学術雑誌）, ISSN 0967-5868

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Cyclooxygenase-2 mediates the development of cortical spreading depression-induced tolerance to transient focal cerebral ischemia in rats

Horiguchi T., Snipes J. A., Kis B., Shimizu K., Busija D. W.

Neuroscience 140 （ 2 ） 723 - 730 2006年

ISSN 0306-4522

We examined the role of cyclooxygenase-2 in the development of ischemic tolerance induced by cortical spreading depression against transient, focal brain ischemia. Cortical spreading depression was continuously induced for 2 h with topical KCl (13±1 depolarizations/2 h) in male Wistar rats. At 1, 2, 3, 4, and 5 days following recovery, the middle cerebral artery was transiently occluded for 120 min. Four days later, the animals were killed and infarct volume was determined. Additionally, cyclooxygenase-2 levels in the cerebral cortex and 15 deoxy-Δ(12, 14) PGJ ₂ levels in cerebrospinal fluid were determined at these times with Western blotting and immunoassay, respectively. Infarct volume was reduced compared with non-cortical spreading depression control animals (274.3±15.3 mm ³) when cortical spreading depression was performed 3 and 4 days before middle cerebral artery occlusion (163.9±14.2 mm ³, 154.9±14.2 mm ³) but not at 1, 2 and 5 days (280.4±17.3 mm ³, 276.3±16.9 mm ³ and 268.5±17.3 mm ³). Cyclooxygenase-2 levels increased most dramatically starting at 2 days, peaked at 3 days, and started to return toward baseline at 4 days after cortical spreading depression. 15 Deoxy-Δ(12, 14) PGJ ₂ levels increased from 134.7±83 pg/ml at baseline to 718±98 pg/ml at 3 days. Administration of N-[2-cyclohexyloxy-4-nitrophenyl] methanesulphonamide (10 mg/kg, i.v.), a selective cyclooxygenase-2 inhibitor, at 1 h prior to middle cerebral artery occlusion in cortical spreading depression preconditioned animals did not affect infarct volume (162.6±62.1 mm ³). However, administration of N-[2-cyclohexyloxy-4-nitrophenyl] methanesulphonamide given three times prior to middle cerebral artery occlusion prevented the reduced infarct volume induced by cortical spreading depression preconditioning (272.9±63.2 mm ³). Administration of l-nitro-arginine methyl ester (4 mg/kg, i.v.) prior to cortical spreading depression blocked increases in cyclooxygenase-2 normally seen at 3 and 4 days. We conclude that NO-mediated cyclooxygenase-2 upregulation by cortical spreading depression protects the brain against ischemic damage. © 2006 IBRO.

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Cortical spreading depression (CSD)-induced tolerance to transient focal cerebral ischemia in halothane anesthetized rats is affected by anesthetic level but not ATP-sensitive potassium channels

Horiguchi Takashi, Kis Bela, Rajapakse Nishadi, Shimizu Katsuyoshi, Busija David W.

Brain Research 1062 （ 1-2 ） 127 - 133 2005年11月

ISSN 0006-8993

We investigated the participation of ATP-sensitive potassium (K _ATP) channels, adenosine A1 receptors, and the effects of different levels of halothane anesthesia in the development of CSD-induced ischemic tolerance. To elicit CSD, 0.5 M KCl was applied for 2 h to the right hemisphere of halothane anesthetized male Wistar rats. The inhalation concentration of halothane during CSD was maintained at 0.5% (n = 8), 1.0% (n = 8), or 2.0% (n = 8). For control animals, saline was applied instead of KCl (n = 8). To inhibit K_ATP channels or adenosine A1 receptors, glibenclamide (0.1 mg/kg icv; n = 8), 5-hydroxydeconaoate (5-HD; 100 mg/kg ip; n = 12), or 8-Cyclopentyl-1, 3-dipropylxanthine (DPCPX) (1.0 mg/kg ip; n = 8) was applied before preconditioning during 1.0% halothane anesthesia. Temporary occlusion (120 min) of the right middle cerebral artery was induced 4 days after preconditioning and the infarct volume was measured. Preconditioning elicited under 1.0% halothane reduced cortical infarct volume from 277 ± 15 mm³ in the control group to 159 ± 14 mm³ in the CSD group (mean ± SEM, P < 0.05). In contrast, CSD induced during inhalation of 0.5% or 2.0% halothane did not confer ischemic tolerance. The reduction in infarct area with CSD during inhalation of 1% halothane was not changed in animals treated with glibenclamide or 5-HD or DPCPX. These results uncover a crucial role of halothane level but not of K_ATP channels or adenosine A1 receptors in the preconditioning effects of CSD. © 2005 Elsevier B.V. All rights reserved.

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The role of nitric oxide in the development of cortical spreading depression-induced tolerance to transient focal cerebral ischemia in rats

Horiguchi Takashi, Snipes James A., Kis Bela, Shimizu Katsuyoshi, Busija David W.

Brain Research 1039 （ 1-2 ） 84 - 89 2005年03月

ISSN 0006-8993

Cortical spreading depression (CSD) has been documented to confer ischemic tolerance on brain. Although nitric oxide (NO) is a crucial mediator in preconditioning under certain circumstances, the role of NO in CSD-induced neuroprotection is unclear. We examined the effect of L-NAME, an inhibitor of NO synthase, on CSD-induced tolerance against transient focal cerebral ischemia. A solution of 0.5 M KCl was applied for 2 h on the right hemisphere to induce CSD. Animals received either vehicle or L-NAME (4 mg/kg, iv) 30 min before CSD. Temporary occlusion (120 min) of the right middle cerebral artery was induced 4 days after preconditioning and the infarct volume was measured. Additionally, ERK 1/2 activation and cyclooxygenase-2 (COX-2) expression in the cerebral cortex were examined by Western blotting analysis immediately after cessation of CSD, or at 1, 2, 4, 8, and 24 h after CSD. CSD reduced infarct volume from 275 ± 15 mm³ (mean ± SEM) in the non-CSD group to 155 ± 14 mm³ in the CSD group (P < 0.05). L-NAME abolished this protection (281 ± 14 mm³; P < 0.05 vs. CSD group). Elevated ERK activation and COX-2 expression were observed immediately after or 8 h after preconditioning, respectively. Those responses are significantly augmented by L-NAME (3-fold for ERK and 4-fold for COX-2). These results suggest a crucial role of NO in the establishment of preconditioning with CSD. © 2005 Elsevier B.V. All rights reserved.

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重症頭部外傷における脳圧亢進時の脳温と膀胱温の解離

斉藤良一、中村芳樹、三島　牧、黒島義明、堀口　崇、市来嵜　潔

脳死・脳蘇生 17 35 - 38 2005年

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くも膜下出血における脳低温療法

斉藤良一、中村芳樹、堀口　崇、三島　牧、黒島義明、市来嵜　潔

救急・集中治療 17 425 - 429 2005年

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脳圧制御困難な重症頭部外傷における低体温療法の適応　特に年齢と治療成績の観点から

斎藤良一, 堀口崇, 稲桝丈司, 三島牧, 真柳圭太, 黒島義明, 中村芳樹, 市来嵜潔

神経外傷（(一社)日本脳神経外傷学会） 27 （ 1 ） 90 - 94 2004年12月

ISSN 0389-5610

重症頭部外傷で循環動態が安定していて重篤な合併症のなかった36例(2〜75歳,平均41±19歳)に低体温療法を施行し,入院時Glasgowコーマスケール(GCS),年齢,脳圧値,治療成績を解析し,低体温療法の適応を検討した.導入時の脳圧と膀胱温の平均値は44±14mmHgと36.2±1.4℃で,導入後は35±18mmHgと33.5±0.9℃で,導入後いずれも有意に低下した.導入後12例は脳圧のコントロールが良好となったが,24例は不能であった.入院時GCS4,5点の23例の死亡率は83%と高かったが,良好な結果を得たのは2歳と15歳の2例であった.GCS6,7点は13例で死亡率は54%で,良好な結果となった6例中5例が21〜27歳であった.脳圧亢進に対する低体温療法の転帰には年齢が大きく影響し,脳圧のコントロールが困難な小児例,若年例(特に入院時GCS6,7点)は低体温療法の良い適応となり得ることが分かった

Targeting mitochondrial ATP-sensitive potassium channels - A novel approach to neuroprotection

Busija David W., Lacza Zsombor, Rajapakse Nishadi, Shimizu Katsuyoshi, Kis Béla, Bari Ferenc, Domoki Ferenc, Horiguchi Takashi

Brain Research Reviews 46 （ 3 ） 282 - 294 2004年11月

ISSN 0165-0173

Mitochondrial responses to ischemic stress play an important role in necrosis and apoptosis of brain cells. Recent studies using several different experimental preparations have shown that activation of ATP-sensitive potassium channels in mitochondria (mitoK _ATP channels) is able to protect neurons and astroglia against injury and death. Thus, targeting of mitoK _ATP channels appears to be a novel approach to neuroprotection. However, little is known about the mechanisms involved. The purpose of this review is to detail the current state of knowledge about this important, emerging area of investigation, and to provide suggestions for future studies. © 2004 Elsevier B.V. All rights reserved.

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The mitochondrial K_ATP channel opener BMS-191095 induces neuronal preconditioning

Kis Bela, Nagy Krisztina, Snipes James A., Rajapakse Nishadi C., Horiguchi Takashi, Grover Gary J., Busija David W.

NeuroReport 15 （ 2 ） 345 - 349 2004年02月

ISSN 0959-4965

BMS-191095, reportedly a selective mitoK_ATp channel opener which is free from the known side effects of the prototype mitoK_ATP channel opener diazoxide, induced acute and delayed preconditioning against glutamate excitotoxicity and delayed preconditioning against oxygen-glucose deprivation in primary cultures of rat cortical neurons. BMS-191095 dose dependency depolarized the mitochondria, increased the phosphorylation of PKC isoforms, but had no detectable effects on the activation of MAP kinases and did not influence the expressions of HSP70 and Mn-SOD. In BMS-191095- preconditioned neurons the glutamate-induced free-radical production was abolished. Our data give the first evidence that selective opening of mitoK _ATP channels with BMS-191095 leads to remarkable neuroprotection via mechanisms that involve mitochondrial depolarization, PKC activation and attenuated free radical production during neuronal stress. © 2004 Lippincott Williams & Wilkins.

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The mitochondrial K-ATP channel opener BMS-191095 induces neuronal preconditioning

B Kis, K Nagy, JA Snipes, NC Rajapakse, T Horiguchi, GJ Grover, DW Busija

NEUROREPORT （LIPPINCOTT WILLIAMS & WILKINS） 15 （ 2 ） 345 - 349 2004年02月

研究論文（学術雑誌）, 共著, ISSN 0959-4965

BMS-191095, reportedly a selective mitoK(ATP) channel opener which is free from the known side effects of the prototype mitoK(ATP) channel opener diazoxide, induced acute and delayed preconditioning against glutamate excitotoxicity and delayed preconditioning against oxygen-glucose deprivation in primary cultures of rat cortical neurons. BMS-191095 dose dependently depolarized the mitochondria, increased the phosphorylation of PKC isoforms, but had no detectable effects on the activation of MAP kinases and did not influence the expressions of HSP70 and Mn-SOD. In BMS-191095-preconditioned neurons the glutamate-induced free-radical production was abolished. Our data give the first evidence that selective opening of mitoK(ATP) channels with BMS-191095 leads to remarkable neuroprotection via mechanisms that involve mitochondrial depolarization, PKC activation and attenuated free radical production during neuronal stress.

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Malignant Peripheral Nerve Sheath Tumor in the Anterior Skull Base Associated with Neurofibromatosis Type 1

Ueda Ryo, Saito Ryoichi, Horiguchi Takashi, Nakamura Yoshiki, Ichikizaki Kiyoshi

Neurologia Medico-Chirurgica 44 （ 1 ） 38 - 42 2004年01月

ISSN 0470-8105

A 36-year-old man presented with a tumor in the anterior skull base manifesting as headache and visual disturbance. Neurofibromatosis type 1 (NF-1) was identified in early childhood in the patient, and also in his father. Subtotal excision of the tumor was performed, leaving the portion extending outside of the cranium. The histological diagnosis was malignant peripheral nerve sheath tumor. Local radiotherapy was instituted postoperatively. Facial paralysis and dysphagia appeared 7 months after the first operation. Magnetic resonance imaging revealed new lesions in the lateral ventricle and around the brainstem. These tumors were also subtotally excised, but the patient died 10 months after the first operation. The tumor very likely originated from the meningeal branch of the trigeminal nerve. Treatment of such tumors developing inside the cranium should include the widest resection possible, followed by irradiation of the entire neuraxis including the spinal cord to inhibit dissemination through the cerebrospinal fluid. Treatment should be started as quickly as possible if the tumor is associated with NF-1, because of the poor prognosis associated with this condition.

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