Kyushu University Academic Staff Educational and Research Activities Database
List of Papers
Satoshi O Suzuki Last modified date:2019.12.31

Associate Professor / Pathobiology / Department of Basic Medicine / Faculty of Medical Sciences

1. Takato Morioka, Nobuya Murakami, Haruhisa Yanagida, Toru Yamaguchi, Yushi Noguchi, Yasushi Takahata, Ayumi Tsukamoto, Satoshi Suzuki, Terminal syringomyelia associated with lumbar limited dorsal myeloschisis, Child's Nervous System, 10.1007/s00381-019-04297-8, 2019.01, Purpose: Limited dorsal myeloschisis (LDM) is characterized by a fibroneural tethering stalk linking the skin lesion to the underlying spinal cord. Terminal syringomyelia, which is located at the lower third of the cord, is often associated with a tethered cord caused by various spinal dysraphisms; however, terminal syringomyelia has not been documented in LDM. The purpose of this study was to clarify the pathophysiological mechanisms of syringomyelia in LDM. Methods: In our 16 patients with lumbar LDM, three patients had terminal syringomyelia. We retrospectively analyzed the clinical, neuroradiological, intraoperative, and histopathological findings for these patients, with particular attention to the clinical course of the syrinx. Results: Patient 1 had a saccular skin lesion and patients 2 and 3 had flat lesions. In all patients, the syringomyelic cavity was located in the lower thoracolumbar cord, immediately rostral to the stalk–cord attachment at the lumbar level. The caudal pole of the syrinx extended to the thickened stalk at the attachment instead of at the caudal cord. Patient 3 had another syrinx in the stalk itself. The longitudinal axis of the syrinx and central canal coincided with the traveling angle of the LDM stalk at the stalk–cord attachment. In patient 1, histology revealed an ependyma-lined central canal in both the LDM stalk and meningocele sac. Patients 1 and 2 underwent syringostomy, but long-term effects were not obtained. Preoperative spontaneous resolution occurred in patient 3. Conclusions: The histological findings in patient 1 supported the idea that segmental myelocystocele is involved in the development of saccular LDM. The hydromyelic central canal herniates and distends the stalk, resulting in the formation of the myelocystocele. It is possible that the hydromyelic central canal also distends the stalk of flat LDM lesions. The syrinx in patient 3 differed from that in patients 1 and 2, in that the syrinx resolved spontaneously. Further studies are needed to clarify the outcomes of syrinxes associated with LDM stalks..
2. Ai Kurogi, Takato Morioka, Nobuya Murakami, Naoyuki Nakanami, Satoshi O. Suzuki, Ruptured dermoid cyst of the conus medullaris in the myelomeningocele sac revealed at the initial repair surgery, Child's Nervous System, 10.1007/s00381-019-04428-1, 2019.01, Background: Dermoid cysts in the myelomeningocele (MMC) site are thought to arise in a delayed fashion because of iatrogenic implantation of dermoid elements at the time of the initial repair surgery. However, there have been few reports on dermoid elements already present at birth. Clinical presentation: We report a patient, in whom dermoid cyst was located at dorsal aspect of the conus medullaris in the MMC sac. Between 23+3 and 24+4 weeks of gestation, rupture of the MMC sac occurred. At this time of gestation, we speculate that rupture of the dermoid cyst also occurred and dissemination of the cyst contents caused chemical arachnoiditis in the MMC sac. At the age of 1 day, surgery to repair MMC and postoperative histological findings revealed these rare pathologies. Conclusion: Physicians should be aware of the possibility of rupture of a dermoid cyst in the MMC sac during fetal period..
3. Nobuya Murakami, Takato Morioka, Satoshi O. Suzuki, Yasushi Takahata, Masahiro Mizoguchi, Congenital interdural arachnoid cyst of the tentorium cerebelli, Child's Nervous System, 10.1007/s00381-019-04404-9, 2019.01, Background: Intracranial interdural cyst is a rare lesion. The exact pathophysiology of these cysts remains unknown. Clinical presentation: We report an infant with interdural cyst of the tentorium cerebelli. Although the cyst mimicked an arachnoid cyst on pre- and postnatal magnetic resonance images, lateral suboccipital craniotomy revealed the cyst within the tentorium. Fenestration on the infratentorial side was performed with successful results. Histologically, the inner surface of the cyst was lined with arachnoid cells. Conclusion: We report detailed neuroradiological, intraoperative, and histological findings, and discuss the pathophysiology of the cyst in this case..
4. Yutaka Fujioka, Nobuhiro Hata, Ryusuke Hatae, Satoshi O. Suzuki, Yuhei Sangatsuda, Yukiko Nakahara, Masahiro Mizoguchi, Koji Iihara, A case of diffuse midline glioma, H3 K27M mutant mimicking a hemispheric malignant glioma in an elderly patient, Neuropathology, 10.1111/neup.12609, 2019.01, Diffuse midline glioma, H3 K27M mutant arises from midline structures of the central nervous system and predominately affects pediatric patients. However, this disease entity was only recently established, and the clinical phenotypic spectrum remains largely unclear. We herein report a rare case of diffuse midline glioma, H3 K27M mutant with an unusual distribution in an elderly woman who presented with a diffuse glioma that invaded both sides of the thalami, and left hippocampus and frontoparietal lobes, thus mimicking a hemispheric malignant glioma. A biopsy of the lobular lesion led to a molecular diagnostic confirmation of diffuse midline glioma, H3 K27M mutant. The patient received concurrent bevacizumab and temozolomide therapy with radiation therapy and survived for 30 months. This case highlights the possibility that a glioma with cerebral hemispheric spread in an elderly patient may harbor the H3 K27M mutation..
5. Yuhei Michiwaki, Nobuhiro Hata, Toshiyuki Amano, Satoshi O. Suzuki, Yojiro Akagi, Daisuke Kuga, Daisuke Onozuka, Seiya Momosaki, Akira Nakamizo, Koji Yoshimoto, Toru Iwaki, Koji Iihara, Predictors of recurrence and postoperative outcomes in patients with non-skull base meningiomas based on modern neurosurgical standards, Interdisciplinary Neurosurgery: Advanced Techniques and Case Management, 10.1016/j.inat.2018.10.007, 15, 30-37, 2019.03, Background: Advances in neurosurgical techniques and neuroimaging resolution questions the modern-day reliability of the Simpson grade for predicting meningioma recurrence. Therefore, we evaluated the reliability of predictors for recurrence and outcomes in detail in patients with non-skull base meningiomas (NSBMs). Methods: We retrospectively analyzed data from consecutive 175 NSBMs underwent surgical resection. We performed Kaplan–Meier analyses of recurrence-free survival (RFS) according to Simpson and World Health Organization (WHO) grades. Predictors of RFS and clinical deterioration were estimated by univariate and multivariate analyses. Correlation between the Simpson grade and change in Karnofsky Performance Scale scores was assessed by Fisher's exact test. Results: Log-rank tests revealed significant correlations of both the Simpson and WHO grades with RFS for the overall cohort, convexity, and falx/tentorium meningioma. Unlike patients undergoing Simpson grade I and II resections, RFS in patients with WHO grade I and II/III tumors differed significantly from the early postoperative stage. Multivariate analysis identified tumor size, Simpson grade, and MIB-1 labeling index as significant predictors of RFS. Clinical deterioration was more frequent among patients undergoing less aggressive resection. Tumor location was the only significant predictor of clinical deterioration. Conclusions: Our findings indicate that tumor size, Simpson and WHO grades, and MIB-1 labeling index are significant predictors of NSBM recurrence. Moreover, the risk of recurrence markedly decreases within the follow-up duration of 80 months. Aggressive resection appears to minimize the risk of recurrence without evidence of clinical deterioration. Follow-up schedules should be based on the WHO grade and extent of resection..
6. Mio Sarukawa, Takato Morioka, Nobuya Murakami, Takafumi Shimogawa, Nobutaka Mukae, Noriko Kuga, Satoshi O. Suzuki, Koji Iihara, Correction to
Human tail-like cutaneous appendage with a contiguous stalk of limited dorsal myeloschisis (Child's Nervous System, (2019), 35, 6, (973-978), 10.1007/s00381-019-04071-w), Child's Nervous System, 10.1007/s00381-019-04111-5, 35, 6, 2019.06, The article was recently published, contained error. Author name “Nobutaka Mukai” should be “Nobutaka Mukae”. Given in this article is the correct name. The original article has been corrected..
7. Masahiro Shijo, Hideomi Hamasaki, Hiroyuki Honda, Satoshi O. Suzuki, Masaki Tachibana, Tetsuro Ago, Takanari Kitazono, Koji Iihara, Toru Iwaki, Upregulation of Annexin A1 in Reactive Astrocytes and Its Subtle Induction in Microglia at the Boundaries of Human Brain Infarcts, Journal of neuropathology and experimental neurology, 10.1093/jnen/nlz079, 78, 10, 961-970, 2019.10, Annexin A1 (ANXA1) has multiple functions, including anti-inflammatory effects, and is thought to be neuroprotective in various pathophysiologies of the central nervous system. The importance of ANXA1 in microglia and endothelial cells in ischemic environments in the brain has been recognized, but its detailed behavior in astrocytes in the ischemic brain remains unknown. Using immunohistochemistry, we therefore assessed the altered distribution of ANXA1 in human brain infarcts using 14 autopsied samples and 18 surgical samples. Elevated expression of ANXA1 was observed in reactive astrocytes in peri-infarct regions. ANXA1 accumulated at the cell periphery and in swollen cytoplasmic processes of reactive astrocytes, as well as at the rim of vacuoles at the boundary of necrosis, and colocalized with aberrantly distributed aquaporin 4 and excitatory amino acid transporter 1. Foamy macrophages in the necrotic core also expressed abundant ANXA1, whereas resident microglia at the boundary of necrosis rarely showed intrinsic expression of ANXA1. This characteristic distribution of ANXA1 in human brain infarcts may represent the good adaptability of reactive astrocytes to ischemic damage..
8. Hiroyuki Honda, Masaki Matsumoto, Masahiro Shijo, Hideomi Hamasaki, Shoko Sadashima, Satoshi O. Suzuki, Shinichi Aishima, Keita Kai, Keiichi I. Nakayama, Naokazu Sasagasako, Toru Iwaki, Frequent Detection of Pituitary-Derived PrPres in Human Prion Diseases, Journal of neuropathology and experimental neurology, 10.1093/jnen/nlz075, 78, 10, 922-929, 2019.10, Human prion diseases including sporadic Creutzfeldt-Jakob disease (sCJD), inherited prion diseases, and acquired human prion diseases are lethal neurodegenerative diseases. One of the major sources of iatrogenic Creutzfeldt-Jakob disease was human growth hormone (hGH-iCJD) derived from contaminated cadaveric pituitaries. The incidence of hGH-iCJD has decreased since changing from growth hormone extracted from human cadaveric pituitaries to recombinant pituitary hormones. However, extensive analysis on the localization and detecting of abnormal prion protein in the pituitary gland are limited. In this study, we examined 9 autopsied brains and pituitary glands from 6 patients with prion disease (3 Gerstmann-Sträussler-Scheinker disease, 2 sCJD, and 1 dura mater graft-associated CJD) and 3 individuals with nonprion diseases. Western blot analysis of pituitary samples demonstrated unique glycoforms of normal cellular prion protein with molecular weights of 30-40 kDa, which was higher than the typical 25-35 kDa prion protein in brains. Proteomic analysis also revealed prion protein approximately the molecular weight of 40 kDa in pituitary samples. Moreover, proteinase K-resistant Prion protein was frequently detected in pituitary samples of the prion diseases. Immunohistochemistry for Prion protein revealed mosaic cellular distribution preferentially in growth hormone- or prolactin-producing cells..
9. Shinichiro Mori, Hiroyuki Honda, Takashi Ishii, Motoi Yoshimura, Naokazu Sasagasako, Satoshi O. Suzuki, Takayuki Taniwaki, Toru Iwaki, Expanded polyglutamine impairs normal nuclear distribution of fused in sarcoma and poly (rC)-binding protein 1 in Huntington's disease, Neuropathology, 10.1111/neup.12600, 39, 5, 358-367, 2019.10, Huntington's disease (HD) is an inherited neurodegenerative disease caused by a polyglutamine repeat expansion in the huntingtin protein. Immunohistochemical studies using the 1C2 antibody for polyglutamine expansion have detected characteristic intranuclear inclusions (INIs) in affected neurons in HD. Further, in vitro and mouse models of HD have shown that the INIs recruit several proteins relating to RNA splicing and translation. In the present study, we immunohistochemically investigated the association of INIs with various heterogeneous nuclear ribonucleoproteins in the cerebral cortex of four autopsy cases of HD. Fused in sarcoma (FUS) was colocalized with 1C2-positive nuclear inclusions in all examined cases. Localization of poly (rC)-binding protein 1 (PCBP1) in 1C2-positive nuclear inclusions was also observed. Double immunofluorescence revealed complete or partial loss of the normal, diffuse nuclear distribution of FUS or PCBP1 in neurons with 1C2-positive nuclear inclusions. This maldistribution of FUS in cortical neurons suggests a severe disturbance of messenger RNA processing, which may be a common pathogenetic mechanism of FUS-related familial amyotrophic lateral sclerosis..
10. Keitaro Yamagami, Nobutaka Mukae, Kimiaki Hashiguchi, Tadahisa Shono, Satoshi O. Suzuki, Koji Iihara, Spinal intramedullary dermoid cyst associated with filar lipoma
A case report and literature review, Interdisciplinary Neurosurgery: Advanced Techniques and Case Management, 10.1016/j.inat.2019.100546, 18, 2019.12, Background: Several authors have reported the various patterns of coexistence of spinal dermoid cysts and lipoma; however, the association of intramedullary dermoid cysts with lipoma is extremely rare. In addition to the embryological and pathological aspects of this rare condition, we discuss the feasibility of combined microscopic and endoscopic procedures for the management of intramedullary dermoid cysts. Case description: An 18-year-old woman presented with right buttock pain. Magnetic resonance (MR) imaging revealed a large, well-defined mass extending from L2 to L4. The conus medullaris terminated in the mass and was tethered by a fatty filum. According to the signal intensities on MR images, the mass could be divided into two components. The upper component existed intramedullary and was iso- to hypo-intense relative to the spinal cord on T1-weighted images. The lower component exhibited homogeneous hyper-intensity signals on both T1- and T2-weighted images. Partial removal of the cyst wall and evacuation of the cyst contents followed by untethering of the spinal cord were performed by the combined microscopic and endoscopic procedures. The patient's symptoms were relieved postoperatively and pathological studies confirmed the diagnosis of dermoid cysts associated with lipoma. Conclusions: We present a rare case of an embryological “collision” of an intramedullary dermoid cyst associated with filar lipoma underlining the spectrum of intradural pathologies in spinal dysraphism. Surgical management is creative in these circumstances and multimodal. Our surgical management shows that the use of endoscopes can be effective in the surgical removal of long sectional spinal dermoid cysts..
11. Yuhei Michiwaki, Nobuhiro Hata, Masahiro Mizoguchi, Akio Hiwatashi, Daisuke Kuga, Ryusuke Hatae, Yojiro Akagi, Takeo Amemiya, Yutaka Fujioka, Osamu Togao, Satoshi O. Suzuki, Koji Yoshimoto, Toru Iwaki, Koji Iihara, Relevance of calcification and contrast enhancement pattern for molecular diagnosis and survival prediction of gliomas based on the 2016 World Health Organization Classification, Clinical Neurology and Neurosurgery, 10.1016/j.clineuro.2019.105556, 187, 2019.12, Objectives: The significance of conventional neuroimaging features for predicting molecular diagnosis and patient survival based on the updated World Health Organization (WHO) classification remains uncertain. We assessed the relevance of neuroimaging features (ring enhancement [RE], non-ring enhancement [non-RE], overall gadolinium enhancement [GdE], and intratumoral calcification [IC]) for molecular diagnosis and survival in glioma patients. Patients and methods: We evaluated 234 glioma patients according to the updated WHO classification. Isocitrate dehydrogenase (IDH), H3F3A, BRAF hotspot mutations, TERT promotor mutation, and chromosome 1p/19q co-deletion were examined. RE, non-RE, GdE, and IC were evaluated as significant neuroimaging findings. Kaplan-Meier analyses were performed to evaluate overall survival (OS) and the correlations of prognostic factors were evaluated by log-rank tests. Univariate and multivariate analyses were performed to detect prognostic factors for OS. Results: A total of 207 patients were eligible. In 110 patients presenting RE, 102 (93%) were glioblastoma (GBM), IDH-wild type. In 97 patients without RE, presence of GdE or IC were not significantly different between IDH-mutant and -wild type tumors, whereas presence of GdE was a significant indicator of higher WHO grades. IC was the only significant finding for 1p/19q co-deleted tumors. TERT promoter mutation was observed in 7/17 patients with diffuse astrocytic glioma, IDH-wild type; recently-defined as “molecular GBM.” IC, RE, and GdE were observed with lower prevalence in molecular GBMs. While presence of RE, GdE, and absence of IC were significant factors of OS in overall cohort, presence of GdE was not significant in OS in cases without RE, and IDH-mutant tumors. IC was a significant predictor of favorable OS in cases without RE and IDH-wild type tumors. Multivariate analysis also validated these findings. Conclusion: GdE alone is not a significant predictor of IDH mutation status, but the pattern of enhancement is a significant predictor with RE demonstrating high sensitivity and specificity for GBM, IDH-wild type. Predicting “molecular GBM” by conventional neuroimaging is difficult. Moreover, GdE is not a significant factor of survival analyzed with pattern of enhancement or molecular stratifications. IC is an important radiographic finding for predicting molecular diagnosis and survival in glioma patients..
12. Takato Morioka, Nobuya Murakami, Akiko Kanata, Haruhisa Tsukamoto, Satoshi Suzuki, Retained medullary cord with sacral subcutaneous meningocele and congenital dermal sinus, Child's Nervous System, 10.1007/s00381-019-04301-1, 2019.01, Background: A retained medullary cord (RMC) is a rare closed spinal dysraphism with a robust elongated cord-like structure extending continuously from the conus medullaris to the dural cul-de-sac that is caused by late arrest of secondary neurulation. Five patients with RMC extending to an associated sacral subcutaneous meningocele have been reported. Case presentation: We report an additional patient with RMC, in whom a congenital dermal sinus (CDS) was found in the caudal portion of the RMC. At the age of 3 days, the patient underwent surgery consisting of meningocele excision and cord untethering, and CDS was noted histologically in the proximal cut end of the RMC. During a second surgery at the age of 5 months, after determining the exact border of the nonfunctional RMC and the true conus by neurophysiological mapping, we removed the entire length of the remnant RMC, including newly developed epidermoid cysts in the CDS. Conclusion: Although the exact pathoembryogenesis of concurrent RMC and CDS is unknown, an associated subcutaneous meningocele, caused by failure of primary neurulation, could be involved. Surgeons should be aware of the possibility of the coexistence of CDS when dealing with RMCs that extend out to the extradural space..
13. Kikuchi K, Hiwatashi A, Togao O, Yamashita K, Kamei R, Momosaka D, Hata N, Iihara K, Suzuki SO, Iwaki T, Honda H., Intravoxel Incoherent Motion MR Imaging of Pediatric Intracranial Tumors: Correlation with Histology and Diagnostic Utility., AJNR Am J Neuroradiol., 10.3174/ajnr.A6052, 40, 5, 878-884, 2019.04.
14. Yamashita K, Hatae R, Hiwatashi A, Togao O, Kikuchi K, Momosaka D, Yamashita Y, Kuga D, Hata N, Yoshimoto K, Suzuki SO, Iwaki T, Iihara K, Honda H., Predicting TERT promoter mutation using MR images in patients with wild-type IDH1 glioblastoma., Diagn Interv Imaging. , 10.1016/j.diii.2019.02.010, in press, 2019.04.
15. Hamasaki H, Honda H, Suzuki SO, Shijo M, Ohara T, Hatabe Y, Okamoto T, Ninomiya T, Iwaki T., Tauopathy in basal ganglia involvement is exacerbated in a subset of patients with Alzheimer's disease: The Hisayama study., Alzheimers Dement (Amst)., 10.1016/j.dadm.2019.04.008. eCollection 2019 Dec, 11, 415-423, 2019.06.
16. Mukae N, Morioka T, Torio M, Sakata A, Suzuki SO, Iihara K., Continuous ictal discharges with high frequency oscillations confined to the non-sclerotic hippocampus in an epileptic patient with radiation-induced cavernoma in the lateral temporal lobe., Epilepsy Behav Case Rep., 10.1016/j.ebcr.2019.01.003. eCollection 2019, 11, 87-91, 2019.01.
17. Sarukawa M, Morioka T, Murakami N, Shimogawa T, Mukae N, Kuga N, Suzuki SO, Iihara K., Human tail-like cutaneous appendage with a contiguous stalk of limited dorsal myeloschisis., Childs Nerv Syst., 10.1007/s00381-019-04071-w, 35, 6, 973-978, 2018.08.
18. Tomita Y, Morioka T, Murakami N, Noguchi Y, Sato Y, Suzuki SO., Slender Stalk with Combined Features of Saccular Limited Dorsal Myeloschisis and Congenital Dermal Sinus in a Neonate., Pediatr Neurosurgery., 10.1159/000495810, 54, 2, 125-131, 2019.01.
19. Lee S, Morioka T, Chong PF, Suzuki SO, Imagi T, Murakami N, Baba H, Kira R., Subcortical axonal loss with glial reactions following partial status epilepticus with neuroradiological findings of reduced subcortical diffusion., Neurol Sci., 10.1007/s10072-018-3635-4, 40, 4, 851-855, 2019.11.
20. Murakami N, Morioka T, Shimogawa T, Mukae N, Inoha S, Sasaguri T, Suzuki SO, Iihara K., Ependyma-Lined Canal with Surrounding Neuroglial Tissues in Lumbosacral Lipomatous Malformations: Relationship with Retained Medullary Cord., Pediatr Neurosurgery., 10.1159/000494029, 53, 6, 387-394, 2018.11.
21. Shen C, Honda H, Suzuki SO, Maeda N, Shijo M, Hamasaki H, Sasagasako N, Fujii N, Iwaki T., Dynactin is involved in Lewy body pathology., Neuropathology., 10.1111/neup.12512, 38, 6, 583-590, 2018.09.
22. Hiraoka A, Morioka T, Murakami N, Suzuki SO, Mizoguchi M., Limited dorsal myeloschisis with no extradural stalk linking to a flat skin lesion: a case report., Childs Nerv Syst., 10.1007/s00381-018-3938-z, 34, 12, 2497-2501, 2018.08.
23. Shimogawa T, Morioka T, Murakami N, Mukae N, Hashiguchi K, Suzuki SO, Iihara K., Bony and Cartilaginous Tissues in Lumbosacral Lipomas., Pediatr Neurosurgery., 10.1159/000490391, 53, 5, 305-310, 2018.07.
24. Maeda N, Honda H, Suzuki SO, Fujii N, Kira JI, Iwaki T., Mitochondrial dysfunction and altered ribostasis in hippocampal neurons with cytoplasmic inclusions of multiple system atrophy., Neuropathology., 10.1111/neup.12482, in press, 2018.07.
25. Morioka T, Suzuki SO, Murakami N, Mukae N, Shimogawa T, Haruyama H, Kira R, Iihara K., Surgical histopathology of limited dorsal myeloschisis with flat skin lesion., Childs Nerv Syst., 10.1007/s00381-018-3870-2, 35, 1, 119-128, 2018.07.
26. Yuhei Sangatsuda, Nobuhiro Hata, Satoshi O. Suzuki, Yojiro Akagi, Ryusuke Hatae, Daisuke Kuga, Koji Yoshimoto, Seiya Momosaki, Toru Iwaki, Koji Iihara, An elderly case of malignant small cell glioma with hemorrhage coexistent with a calcified pilocytic astrocytoma component in the cerebellar hemisphere, Neuropathology. , 10.1111/neup.12478, in press, 2018.05.
27. Tomohiro Okuda, Nobuhiro Hata, Satoshi O. Suzuki, Koji Yoshimoto, Koichi Arimura, Takeo Amemiya, Yojiro Akagi, Daisuke Kuga, Utako Oba, Yuhki Koga, Shouichi Ohga, Toru Iwaki, Koji Iihara, Pediatric ganglioglioma with an H3 K27M mutation arising from the cervical spinal cord, Neuropathology. , 10.1111/neup.12471, in press, 2018.04.
28. Kazufumi Kikuchi, Akio Hiwatashi, Osamu Togao, Koji Yamashita, Ryotaro Kamei, Koji Yoshimoto, Koji Iihara, Satoshi O. Suzuki, Toru Iwaki, Yuriko Suzuki, Hiroshi Honda, Arterial spin-labeling is useful for the diagnosis of residual or recurrent meningiomas., Eur Radiol. , 10.1007/s00330-018-5404-4, in press, 2018.04.
29. Reiji Hommyo, Satoshi O. Suzuki, Nona Abolhassani, Hideomi Hamasaki, Masahiro Shijo, Norihisa Maeda, Hiroyuki Honda, Yusaku Nakabeppu, Toru Iwaki, Expression of CRYM in different rat organs during development and its decreased expression in degenerating pyramidal tracts in amyotrophic lateral sclerosis., Neuropathology. , 10.1111/neup.12466, 38, 3, 247-259, 2018.01.
30. Yojiro Akagi, Koji Yoshimoto, Nobuhiro Hata, Daisuke Kuga, Ryusuke Hatae, Takeo Amemiya, Yuhei Sangatsuda, Satoshi O. Suzuki, Toru Iwaki, Masahiro Mizoguchi, Koji Iihara, Reclassification of 400 consecutive glioma cases based on the revised 2016WHO classification., Brain Tumor Pathol., 10.1007/s10014-018-0313-4, 35, 2, 81-89, 2018.04.
31. Ryota Kurogi, Akira Nakamizo, Satoshi O. Suzuki, Masahiro Mizoguchi, Koji Yoshimoto, Toshiyuki Amano, Takeo Amemiya, So Takagishi, Koji Iihara, Inhibition of glioblastoma cell invasion by hsa-miR-145-5p and hsa-miR-31-5p co-overexpression in human mesenchymal stem cells., J Neurosurg. , 10.3171/2017.8.JNS1788, in press, 2018.03.
32. Hiroyuki Honda, Naokazu Sasagasako, Chang Shen, Masahiro Shijo, Hideomi Hamasaki, Satoshi O.Suzuki, Yoshio Tsuboi, Naoki Fujii, Toru Iwaki, DCTN1 F52L mutation case of Perry syndrome with progressive supranuclear palsy-like tauopathy., Parkinsonism Relat Disord., 10.1016/j.parkreldis.2018.02.038, S1353-8020(18)30090-7, 2018.02.
33. Osamu Togao, Akio Hiwatashi, Koji Yamashita, Kazufumi Kikuchi, Daichi Momosaka, Koji Yoshimoto, Daisuke Kuga, Masahiro Mizoguchi, Satoshi O Suzuki, Toru Iwaki, Marc Van Cauteren, Koji Iihara, Hiroshi Honda, Measurement of the perfusion fraction in brain tumors with intravoxel incoherent motion MR imaging: validation with histopathological vascular density in meningiomas., Br J Radiol. , 10.1259/bjr.20170912, 91(1085):20170912. , 2018.05.
34. Nobuya Murakami, Takato Morioka, Takafumi Shimogawa, Kimiaki Hashiguchi, Nobutaka Mukae, Kazuyoshi Uchihashi, Satoshi O. Suzuki, Koji Iihara, Retained medullary cord extending to a sacral subcutaneous meningocele., Childs Nerv Syst., 10.1007/s00381-017-3644-2, 34, 3, 527-533, 2018.03.
35. Takato Morioka, Satoshi O Suzuki, Nobuya Murakami, Takafumi Shimogawa, Nobutaka Mukae, Satoshi Inoha, Takakazu Sasaguri, Koji Iihara, Neurosurgical pathology of limited dorsal myeloschisis., Childs Nerv Syst., 10.1007/s00381-017-3625-5, 34, 2, 293-303, 2018.02.
36. Hiroyuki Honda, Kensuke Sasaki, Hiroshi Takashima, Daisuke Mori, Sachiko Koyama, Satoshi O Suzuki, Toru Iwaki, Different Complicated Brain Pathologies in Monozygotic Twins With Gerstmann-Sträussler-Scheinker Disease., J Neuropathol Exp Neurol. , 10.1093/jnen/nlx068, 76, 10, 854-863, 2017.10.
37. Mihori Ryorin, Takato Morioka, Nobuya Murakami, Satoshi O Suzuki, Nobuko Kawamura, Dynamic morphological changes of thrombosed lateral sinus pericranii revealed by serial magnetic resonance images., Childs Nerv Syst., 10.1007/s00381-017-3592-x, 34, 1, 143-148, 2018.01.
38. Kazufumi Kikuchi, Hiwatashi Akio, Osamu Togao, Koji Yamashita, Koji Yoshimoto, Masahiro Mizoguchi, Satoshi O Suzuki, Yuriko Suzuki, Toru Iwaki, Hiroshi Honda, Correlation between arterial spin-labeling perfusion and histopathological vascular density of pediatric intracranial tumors., J Neurooncol., 0.1007/s11060-017-2604-8, 135, 3, 561-569, 2017.12.
39. Koji Yoshimoto, Ryusuke Hatae, Satoshi O Suzuki, Nobuhiro Hata, Daisuke Kuga, Yojiro Akagi, Takeo Amamiya, Yuhei Sangetsuda, Nobutaka Mukae, Masahiro Mizoguchi, Toru Iwaki, Koji Iihara, High-resolution melting and immunohistochemical analysis efficiently detects mutually exclusive genetic alterations of adamantinomatous and papillary craniopharyngiomas., Neuropathology., doi: 10.1111/neup.12408., 38, 1, 3-10, 2018.02.
40. Kenji Miki, Koji Yoshimoto, Ataru Nishimura, Satoshi O Suzuki, Hiwatashi Akio, Koji Iihara, A case of ecchordosis physaliphora in the prepontine cistern: a rare entity in the differential diagnosis of an epidermoid cyst., World Neurosurg., doi: 10.1016/j.wneu.2017.06.003, in press, 2017.06.
41. Koji Yoshimoto, Ryusuke Hatae, Yuhei Sangetsuda, Satoshi O Suzuki, Nobuhiro Hata, Yojiro Akagi, DAISUKE KUGA, Hideki Murata, Koji Yamashita, Osamu Togao, Hiwatashi Akio, Toru Iwaki, Masahiro Mizoguchi, Koji Iihara, Prevalence and clinicopathological features of H3.3 G34-mutant high-grade gliomas: a retrospective study of 411 consecutive glioma cases in a single institution., Brain Tumor Pathol., doi: 10.1007/s10014-017-0287-7, in press, 2017.04.
42. Takato Morioka, Nobuya Murakami, Takafumi Shimogawa, Mukae Nobutaka, KIMIAKI HASHIGUCHI, Satoshi O Suzuki, Koji Iihara, Neurosurgical management and pathology of lumbosacral lipomas with tethered cord., Neuropathology, doi: 10.1111/neup.12382, in press, 2017.04.
43. Iwao Takeshita, Satoshi O Suzuki, Toru Iwaki, [Idiopathic Intracranial Hypotension]., Brain Nerve., doi: 10.11477/mf.1416200654, 69, 2, 143-150, 2017.02.
44. Nobuhiro Hata, Koji Yoshimoto, Ryusuke Hatae, DAISUKE KUGA, Yojiro Akagi, Yuhei Sangetsuda, Satoshi O Suzuki, Tadahisa Shono, Masahiro Mizoguchi, Koji Iihara, Add-on bevacizumab can prevent early clinical deterioration and prolong survival in newly diagnosed partially resected glioblastoma patients with a poor performance status., Onco Targets Ther, doi: 10.2147/OTT.S125587, 18, 10, 429-437, 2017.01.
45. Nobuhiro Hata, Ryusuke Hatae, Koji Yoshimoto, Hideki Murata, DAISUKE KUGA, Yojiro Akagi, Yuhei Sangetsuda, Satoshi O Suzuki, Toru Iwaki, Masahiro Mizoguchi, Koji Iihara, Insular primary glioblastomas with IDH mutations: Clinical and biological specificities., Neuropathology, doi: 10.1111/neup.12362, 37, 3, 200-206, 2017.01.
46. Masahiro Shijo, Hiroyuki Honda, Satoshi O Suzuki, Hideomi Hamasaki, Masao Hokama, Abolhassani Nona, Yusaku Nakabeppu, Toshiharu Ninomiya, Kitazono T, Toru Iwaki, Association of adipocyte enhancer-binding protein 1 with Alzheimer's disease pathology in human hippocampi., Brain Pathol., doi: 10.1111/bpa, in press, 2016.12.
47. Nobuhiro Hata, Koji Yoshimoto, Ryusuke Hatae, DAISUKE KUGA, Yojiro Akagi, Satoshi O Suzuki, Toru Iwaki, Tadahisa Shono, Masahiro Mizoguchi, Koji Iihara, Deferred radiotherapy and upfront procarbazine-ACNU-vincristine administration for 1p19q codeleted oligodendroglial tumors are associated with favorable outcome without compromising patient performance, regardless of WHO grade., Onco Targets Ther, DOI: 10.2147/OTT.S115911, 17, 9, 7123-7131, 2016.11.
48. Ryusuke Hatae, Nobuhiro Hata, Satoshi O Suzuki, Koji Yoshimoto, DAISUKE KUGA, Hideki Murata, Yojiro Akagi, Yuhei Sangetsuda, Toru Iwaki, Masahiro Mizoguchi, Koji Iihara, A comprehensive analysis identifies BRAF hotspot mutations associated with gliomas with peculiar epithelial morphology., Neuropathology, 10.1111/neup.12347, 37, 3, 191-199, 2017.06.
49. Hideomi Hamasaki, Hiroyuki Honda, Tsuyoshi Okamoto, Sachiko Koyama, Satoshi O Suzuki, Tomoyuki Ohara, Toshiharu Ninomiya, Yutaka Kiyohara, Toru Iwaki, Recent Increases in Hippocampal Tau Pathology in the Aging Japanese Population: The Hisayama Study., J Alzheimers Dis., 10.3233/JAD-160521, in press, 2016.02.
50. Nobuya Murakami, Takato Morioka, Satoshi O Suzuki, Mukae Nobutaka, KIMIAKI HASHIGUCHI, Koji Iihara, Tadpole-shaped lateralized parietal atretic cephalocele associated with an ipsilateral lacrimal gland fistula and schizencephalic clefts., Childs Nerv Syst., 10.1007/s00381-016-3254-4, in press, 2016.10.
51. Hiroyuki Honda, Kosuke Matsuzono, Soichiro Fushimi, Kota Sato, Satoshi O Suzuki, Koji Abe, Toru Iwaki, C-Terminal-Deleted Prion Protein Fragment Is a Major Accumulated Component of Systemic PrP Deposits in Hereditary Prion Disease With a 2-Bp (CT) Deletion in PRNP Codon 178., J Neuropathol Exp Neurol, in press, in press, 2016.09.
52. Ryosuke Hatae, Nobuhiro Hata, Koji Yoshimoto, DAISUKE KUGA, Yojiro Akagi, Hideki Murata, Satoshi O Suzuki, Masahiro Mizoguchi, Koji Iihara, Precise Detection of IDH1/2 and BRAF Hotspot Mutations in Clinical Glioma Tissues by a Differential Calculus Analysis of High-Resolution Melting Data., PLos One, 10.1371/journal.pone.0160489, 11, 8, e0160489, 11(8):e0160489, 2016.08.
53. Takafumi Shimogawa, Takato Morioka, Hisasuke Onozawa, Satoshi O Suzuki, Ryutaro Kira, Nasal Dermal Sinus Associated with a Dumbbell-Shaped Dermoid: A Case Report., J Neurol Surg Rep., 10.1055/s-0036-1584525, in press, 2016.07.
54. Nobuya Murakami, Takato Morioka, Nobuko Kawamura, Satoshi O Suzuki, Ryutaro Kira, Venous anomaly analogous to vertical embryonic positioning of the straight sinus associated with atretic cephalocele at the suboccipital region., Childs Nerv Syst., 10.1007/s00381-016-3134-y, in press, 2016.07.
55. Yamashita Koji, Hiwatashi Akio, Osamu Togao, Kazufumi Kikuchi, Yoshiyuki Kitamura, Masahiro Mizoguchi, Koji Yoshimoto, DAISUKE KUGA, Satoshi O Suzuki, Shingo Baba, Takuro Isoda, Toru Iwaki, Koji Iihara, Hiroshi Honda, Diagnostic utility of intravoxel incoherent motion mr imaging in differentiating primary central nervous system lymphoma from glioblastoma multiforme., J Magn Reson Imaging, 10.1002/jmri.25261, in press, 2016.04.
56. Shotaro Hayashida, Masaki Katsuhisa, Tomomi Yonekawa, Satoshi O Suzuki, Hiwatashi Akio, Takuya Matsushita, Mitsuru Watanabe, Ryo Yamasaki, Toshihiko Suenaga, Toru Iwaki, Hiroyuki Murai, Jun-ichi Kira, Early and Extensive Spinal White Matter Involvement in Neuromyelitis Optica., Brain Pathol, 10.1111/bpa.12386, in press, 2016.04.
57. Osamu Togao, Hiwatashi Akio, Yamashita Koji, Kazufumi Kikuchi, Jochen Keupp, Koji Yoshimoto, DAISUKE KUGA, Masami Yoneyama, Satoshi O Suzuki, Toru Iwaki, Masaya Takahashi, Koji Iihara, Hiroshi Honda, Grading diffuse gliomas without intense contrast enhancement by amide proton transfer MR imaging: comparisons with diffusion- and perfusion-weighted imaging., Eur Radiol, in press, 2016.03.
58. Hiroyuki Honda, Kensuke Sasaki, Hideomi Hamasaki, Masahiro Shijo, Sachiko Koyama, Tomoyuki Ohara, Toshiharu Ninomiya, Yutaka Kiyohara, Satoshi O Suzuki, Toru Iwaki, Trends in autopsy-verified dementia prevalence over 29 years of the Hisayama study., Neuropathology, 10.1111/neup.12298, in press, 2016.02.
59. Hiwatashi Akio, Osamu Togao, Yamashita Koji, Kazufumi Kikuchi, Koji Yoshimoto, Masahiro Mizoguchi, Satoshi O Suzuki, Takashi Yoshiura, Hiroshi Honda, Evaluation of glioblastomas and lymphomas with whole-brain CT perfusion: Comparison between a delay-invariant singular-value decomposition algorithm and a Patlak plot., J Neuroradiol, 10.1016/j.neurad.2016.01.147. , in press, 2016.03.
60. NISHIO MIKI, Keishi Sugimachi, Hiroki Goto, Jia Wang, Takumi Morikawa, Yosuke Miyachi, Yusuke Takano, Hiroki Hikasa, Tohru Itoh, Satoshi O Suzuki, Hiroki Kurihara, Shinichi Aishima, Andrew Leask, Takehiko Sasaki, Toru Nakano, Hiroshi Nishina, Yuji Nishikawa, Yoshitaka Sekido, Kazuwa Nakao, Kazuo Shin-ya, Dysregulated YAP1/TAZ and TGF-β signaling mediate hepatocarcinogenesis in Mob1a/1b-deficient mice., Proc Natl Acad Sci U S A, 0.1073/pnas.1517188113., 113, 1, E71-E80, 2016.01.
61. Yamashita Koji, Hiwatashi Akio, Osamu Togao, Kazufumi Kikuchi, Ryusuke Hatae, Koji Yoshimoto, Masahiro Mizoguchi, Satoshi O Suzuki, Takashi Yoshiura, Hiroshi Honda, MR Imaging-Based Analysis of Glioblastoma Multiforme: Estimation of IDH1 Mutation Status., Am J Neuroradiol, in press, 2015.09.
62. Osamu Togao, Hiwatashi Akio, Yamashita Koji, Kazufumi Kikuchi, Masahiro Mizoguchi, Koji Yoshimoto, Satoshi O Suzuki, Toru Iwaki, Makoto Obara, Marc van Cauteren, Hiroshi Honda, Differentiation of high-grade and low-grade diffuse gliomas by intravoxel incoherent motion MR imaging., Neuro Oncol, in press, 2015.08.
63. Shumpei Watanabe, Ohno Shinji, Yuta Shirogane, Satoshi O Suzuki, Ritsuko Koga, Yusuke Yanagi, Measles Virus Mutants Possessing the Fusion Protein with Enhanced Fusion Activity Spread Effectively in Neuronal Cells, but Not in Other Cells, without Causing Strong Cytopathology., Journal of Virology, 89, 5, 2710-2717, 2015.03, Subacute sclerosing panencephalitis (SSPE) is caused by persistent measles virus (MV) infection in the central nervous system (CNS). Since human neurons, its main target cells, do not express known MV receptors (signaling lymphocyte activation molecule [SLAM] and nectin 4), it remains to be understood how MV infects and spreads in them. We have recently reported that fusion-enhancing substitutions in the extracellular domain of the MV fusion (F) protein (T461I and S103I/N462S/N465S), which are found in multiple SSPE virus isolates, promote MV spread in human neuroblastoma cell lines and brains of suckling hamsters. In this study, we show that hyperfusogenic viruses with these substitutions also spread efficiently in human primary neuron cultures without inducing syncytia. These substitutions were found to destabilize the prefusion conformation of the F protein trimer, thereby enhancing fusion activity. However, these hyperfusogenic viruses exhibited stronger cytopathology and produced lower titers at later time points in SLAM- or nectin 4-expressing cells compared to the wild-type MV. Although these viruses spread efficiently in the brains of SLAM knock-in mice, they did not in the spleens. Taken together, the results suggest that enhanced fusion activity is beneficial for MV to spread in neuronal cells where no cytopathology occurs, but detrimental to other types of cells due to strong cytopathology. Acquisition of enhanced fusion activity through substitutions in the extracellular domain of the F protein may be crucial for MV's extensive spread in the CNS and development of SSPE.
Subacute sclerosing panencephalitis (SSPE) is a fatal disease caused by persistent measles virus (MV) infection in the central nervous system (CNS). Its cause is not well understood, and no effective therapy is currently available. Recently, we have reported that enhanced fusion activity of MV through the mutations in its fusion protein is a major determinant of efficient virus spread in human neuronal cells and brains of suckling hamsters. In this study, we show that those mutations render the conformation of the fusion protein less stable, thereby making it hyperfusogenic. Our results also show that enhanced fusion activity is beneficial for MV to spread in the CNS but detrimental to other types of cells in peripheral tissues, which are strongly damaged by the virus. Our findings provide important insight into the mechanism for the development of SSPE after MV infection..
64. Mukae Nobutaka, Satoshi O Suzuki, Takato Morioka, Nobuya Murakami, KIMIAKI HASHIGUCHI, Hiroshi Shigeto, Ayumi Sakata, Koji Iihara, ILAE focal cortical dysplasia type IIIc in the ictal onset zone in epileptic patients with solitary meningioangiomatosis, Epileptic Disord, 10.1684/epd.2014.0695, 2014.11.
65. Nobuhiro Hata, Satoshi O Suzuki, Hideki Murata, Ryusuke Hatae, Yojiro Akagi, Yuhei Sangatsuda, TOSHIYUKI AMANO, Koji Yoshimoto, Tomoko Tahira, Masahiro Mizoguchi, Genetic Analysis of a Case of Glioblastoma with Oligodendroglial Component Arising During the Progression of Diffuse Astrocytoma, Pathol Oncol Res, 10.1007/s12253-014-9850-2, 2014.10.
66. Hiroyuki Honda, Hideomi Hamasaki, Tomihiro Wakamiya, Sachiko Koyama, Satoshi O Suzuki, Naoki Fujii, Toru Iwaki, Loss of hnRNPA1 in ALS spinal cord motor neurons with TDP-43-positive inclusions, Neuropathology, 10.1111/neup.12153, 2014.10.
67. Tomihiro Wakamiya, Satoshi O Suzuki, Hideomi Hamasaki, Hiroyuki Honda, Masahiro Mizoguchi, Koji Yoshimoto, Toru Iwaki, Elevated expression of fatty acid synthase and nuclear localization of carnitine palmitoyltransferase 1C are common among human gliomas., Neuropathology, in press, 2014.07, Fatty acid synthase (FASN) and carnitine palmitoyltransferase 1C (CPT1C), a brain-specific isoform of the CPT1 family, are upregulated in certain types of cancers, including gliomas. Acetyl-CoA carboxylase (ACC) catalyzes the carboxylation of acetyl-CoA to malonyl-CoA, the rate-limiting step in fatty acid synthesis, and its phosphorylated form inhibits lipid synthesis. We examined the expression and subcellular localization of these fatty acid metabolism-related molecules in human gliomas. We performed immunostaining of two glioma cell lines (U373MG and U87MG) and 41 surgical specimens of diffuse gliomas with various histological grades (21 with the isocitrate dehydrogenase 1(IDH1) R132H mutation and 20 without the mutation). In the cultured glioma cells, CPT1C and phosphorylated ACC (p-ACC) were mainly localized to the nuclei, whereas FASN localized to the cytoplasm. In the surgical specimens, most glioma tissues showed nuclear staining for CPT1C and p-ACC, and cytoplasmic staining for FASN, regardless of the genetic status of IDH1 and the histological grade. Therefore, elevated cytoplasmic expression of FASN and nuclear localization of CPT1C are common among human diffuse gliomas, which may be regulated by the differential phosphorylation status of ACC in the cellular compartment..
68. Shingo Tanaka, Mitsutoshi Nakada, Sumihito Nobusawa, Satoshi O Suzuki, Hemragul Sabit, Katsuyoshi Miyashita, Yutaka Hayashi, Epithelioid glioblastoma arising from pleomorphic xanthoastrocytoma with the BRAF V600E mutation., Brain Tumor Pathology, 31, 172-176, 2014.06, Pleomorphic xanthoastrocytoma (PXA) is classified by the World Health Organization as a grade II astrocytic tumor with relatively favorable prognosis among gliomas. A valine-to-glutamic acid substitution at position 600 of the serine/threonine-protein kinase BRAF (BRAF V600E) mutation, which is commonly found in PXA, has recently been detected in approximately 50 % of all epithelioid glioblastoma (GBM) cases. We herein report a case of epithelioid GBM developing at the site of a left temporal PXA 13 years after the treatment of the primary tumor. The BRAF V600E mutation was detected in both tumors. These findings suggest that epithelioid GBM may arise from a PXA with a BRAF V600E mutation.
69. Koji Shinoda, Hideaki Asahara, Taira Uehara, Katsue Miyoshi, Satoshi O Suzuki, Toru Iwaki, Jun-ichi Kira, Multiphasic acute disseminated encephalomyelitis associated with atypical rubella virus infection., Multiple Sclerosis, 2014.05.
70. Yiwen Cui, Masaki Katsuhisa, Ryo Yamasaki, Shihoko Imamura, Satoshi O Suzuki, HAYASHI SHINTARO, Sinya Sato, Yuko Nagara, Mami F Kawamura, Jun-ichi Kira, Extensive dysregulations of oligodendrocytic and astrocytic connexins are associated with disease progression in an amyotrophic lateral sclerosis mouse model., Journal of Neuroinflammation, 10.1186/1742-2094-11-42, 2014.03, BACKGROUND:
Non-cell-autonomous motor neuronal death is suggested in a mutant Cu/Zn superoxide dismutase 1 (mSOD1)-mediated amyotrophic lateral sclerosis (ALS) model, in which glial cells play significant roles in disease progression. Connexins (Cxs) form homotypic or heterotypic gap junctions (GJs) and allow direct intercellular communications among nervous tissue cells. The role of Cxs in motor neuron disease has never been investigated; therefore, we aimed to evaluate alterations of Cxs in mSOD1-transgenic (mSOD1-Tg) mice in comparison with their non-transgenic (non-Tg) littermates at the same ages.
We pathologically evaluated temporal changes to astrocytic Cx43/Cx30 and oligodendrocytic Cx47/Cx32 immunoreactivities at presymptomatic, disease-progressive, and end stages, relative to aquaporin-4 (AQP4), glial fibrillary acidic protein (GFAP), excitatory amino acid transporter-2 (EAAT2), myelin-oligodendrocyte glycoprotein (MOG), and Nogo-A immunoreactivities, and observed neuronal loss by NeuN and neurofilament immunostaining, and microglial response by Iba-1 immunostaining. We also performed quantitative immunoblotting and real-time PCR analyses for Cxs.
The mSOD1-Tg mice showed neuronal and axonal loss in the anterior horns of the lumbar spinal cord accompanied by increased activation of microglia compared with non-Tg mice at the disease-progressive and end stages. Expression patterns of Cxs were not different between mSOD1-Tg and non-Tg mice at the presymptomatic stage, but immunoreactivities for GFAP, Cx43, Cx30 and AQP4 were increased in the anterior horns of mSOD1-Tg mice at the disease-progressive and end stages. By contrast, Cx47 and Cx32 immunoreactivities were markedly diminished in Nogo-A-positive oligodendrocytes in the anterior horns of mSOD1-Tg mice at the disease-progressive and end stages, especially in oligodendrocytes showing SOD1 accumulation. EAAT2 immunoreactivity was also diminished in the anterior horns of mSOD1-Tg mice at the disease-progressive and end stages. Quantitative immunoblotting revealed a significant reduction in Cx47 and Cx32 protein levels in mSOD1-Tg mice at the disease-progressive and end stages. The levels of Cx47 and Cx32 mRNAs were also decreased at these stages.
Our findings indicate that oligodendrocytic and astrocytic GJ proteins in the anterior horns of spinal cord in mSOD1-Tg mice are profoundly affected at the disease-progressive and end stages, where disruption of GJs among glial cells may exacerbate motor neuronal death..
71. Hideomi Hamasaki, Hiroyuki Honda, Satoshi O Suzuki, Masaaki Hokama, Yutaka Kiyohara, Yusaku Nakabeppu, Toru Iwaki, Down-regulation of MET in hippocampal neurons of Alzheimer's disease brains., Neuropathology, 10.1111/neup.12095, 2014.01, We found that mRNA of MET, the receptor of hepatocyte growth factor (HGF), is significantly decreased in the hippocampus of Alzheimer's disease (AD) patients. Therefore, we tried to determine the cellular component-dependent changes of MET expressions. In this study, we examined cellular distribution of MET in the cerebral neocortices and hippocampi of 12 AD and 11 normal controls without brain diseases. In normal brains, MET immunoreactivity was observed in the neuronal perikarya and a subpopulation of astrocytes mainly in the subpial layer and white matter. In AD brains, we found marked decline of MET in hippocampal pyramidal neurons and granule cells of dentate gyrus. The decline was more obvious in the pyramidal neurons of the hippocampi than that in the neocortical neurons. In addition, we found strong MET immunostaining in reactive astrocytes, including those near senile plaques. Given the neurotrophic effects of the HGF/MET pathway, this decline may adversely affect neuronal survival in AD cases. Because it has been reported that HGF is also up-regulated around senile plaques, β-amyloid deposition might be associated with astrocytosis through the HGF signaling pathway.
72. Osamu Togao, Takashi Yoshiura, Jochen Keupp, Hiwatashi Akio, Yamashita Koji, Kazufumi Kikuchi, Yuriko Suzuki, Satoshi O Suzuki, Toru Iwaki, Nobuhiro Hata, Masahiro Mizoguchi, Koji Yoshimoto, Koji Sagiyama, Masaya Takahashi, Hiroshi Honda, Amide proton transfer imaging of adult diffuse gliomas: correlation with histopathological grades, NEURO-ONCOLOGY, 10.1093/neuonc/not158, 16, 3, 441-448, 2014.03.
73. Masaki Katsuhisa, Satoshi O Suzuki, Takuya Matsushita, Takeshi Matsuoka, Shihoko Imamura, Ryo Yamasaki, Makiko Suzuki, Toshihiko Suenaga, Toru Iwaki, Jun-ichi Kira, Connexin 43 astrocytopathy linked to rapidly progressive multiple sclerosis and neuromyelitis optica., PLoS One, 10.1371/journal.pone.0072919, 8, 8, e72919, 2013.08, BACKGROUND:
Multiple sclerosis (MS) and neuromyelitis optica (NMO) occasionally have an extremely aggressive and debilitating disease course; however, its molecular basis is unknown. This study aimed to determine a relationship between connexin (Cx) pathology and disease aggressiveness in Asian patients with MS and NMO.
Samples included 11 autopsied cases with NMO and NMO spectrum disorder (NMOSD), six with MS, and 20 with other neurological diseases (OND). Methods of analysis included immunohistochemical expression of astrocytic Cx43/Cx30, oligodendrocytic Cx47/Cx32 relative to AQP4 and other astrocytic and oligodendrocytic proteins, extent of demyelination, the vasculocentric deposition of complement and immunoglobulin, and lesion staging by CD68 staining for macrophages. Lesions were classified as actively demyelinating (n=59), chronic active (n=58) and chronic inactive (n=23). Sera from 120 subjects including 30 MS, 30 NMO, 40 OND and 20 healthy controls were examined for anti-Cx43 antibody by cell-based assay. Six NMO/NMOSD and three MS cases showed preferential loss of astrocytic Cx43 beyond the demyelinated areas in actively demyelinating and chronic active lesions, where heterotypic Cx43/Cx47 astrocyte oligodendrocyte gap junctions were extensively lost. Cx43 loss was significantly associated with a rapidly progressive disease course as six of nine cases with Cx43 loss, but none of eight cases without Cx43 loss regardless of disease phenotype, died within two years after disease onset (66.7% vs. 0%, P=0.0090). Overall, five of nine cases with Cx43 loss and none of eight cases without Cx43 loss had distal oligodendrogliopathy characterized by selective myelin associated glycoprotein loss (55.6% vs. 0.0%, P=0.0296). Loss of oligodendrocytic Cx32 and Cx47 expression was observed in most active and chronic lesions from all MS and NMO/NMOSD cases. Cx43-specific antibodies were absent in NMO/NMOSD and MS patients.
These findings suggest that autoantibody-independent astrocytic Cx43 loss may relate to disease aggressiveness and distal oligodendrogliopathy in both MS and NMO..
74. Makiko Suzuki, Hideya Kawasaki, Masaki Katsuhisa, Satoshi O Suzuki, Tatsuhiro Terada, Takashi Tsuchida, Tsutomu Tokuyama, Satoshi Kono, Takashi Komori, Satoshi Baba, Jun-ichi Kira, Hiroaki Miyajima, An autopsy case of the Marburg variant of multiple sclerosis (acute multiple sclerosis)., Internal Medicine, 10.2169/internalmedicine.52.0425, 52, 16, 1825-1832, 52: 1825-1832, 2013, 2012.03, We herein report an autopsy case of the Marburg variant of multiple sclerosis (MS). A 29-year-old woman developed acute and progressive neurological symptoms. A diagnosis of MS was suspected based on the patient's clinical background and brain MRI findings and the lack of evidence of malignancy on a brain biopsy. Despite the administration of typical treatment for MS, a fatal outcome occurred three months after disease onset. The autopsy revealed multiple inflammatory demyelinating lesions in the central nervous system. In addition, two noteworthy histopathological features were observed compared with prototypical MS. We evaluate the pathogenic differences between the Marburg type and prototypical MS by discussing the neuropathology and cerebrospinal fluid (CSF) findings of our case..
75. Nobuya Murakami, Takato Morioka, KIMIAKI HASHIGUCHI, Takashi Yoshiura, Hiwatashi Akio, Satoshi O Suzuki, Akira Nakamizo, TOSHIYUKI AMANO, Nobuhiro Hata, Tomio Sasaki, Usefulness of three-dimensional T1-weighted spoiled gradient-recalled echo and three-dimensional heavily T2-weighted images in preoperative evaluation of spinal dysraphism., Childs Nerv Syst, 2013.05.
76. Kamada T, Sun W, Takase K, Hiroshi Shigeto, Satoshi O Suzuki, Ohyagi Y, Jun-ichi Kira, Spontaneous seizures in a rat model of multiple prenatal freeze lesioning., Epilepsy Res, pii: S0920-1211(13)00088-0. 10.1016/j.eplepsyres.2013.03.003., 2013.04.
77. Yuichiro Kikkawa, Satoshi O Suzuki, Akira Nakamizo, Tsuchimochi R, Murakami N, Yoshitake T, Shinichi Aishima, Okubo F, Nobuhiro Hata, TOSHIYUKI AMANO, Koji Yoshimoto, Masahiro Mizoguchi, Toru Iwaki, Tomio Sasaki, Radiation-induced spinal cord glioblastoma with cerebrospinal fluid dissemination subsequent to treatment of lymphoblastic lymphoma., Surg Neurol Int., 10.4103/2152-7806, 2013.02.
78. Hiroyuki Honda, Ishii R, Hamano A, Itoh K, Satoshi O Suzuki, Fushiki S, Nakagawa M, Toru Iwaki, Microsphere formation in a subtype of Creutzfeldt-Jakob disease with a V180I mutation and codon 129 MM polymorphism., Neuropathol Appl Neurobiol, 10.1111/nan.12047., 2013.03.
79. Masahiro Mizoguchi, Nobuhiro Hata, Satoshi O Suzuki, Fujioka Y, Murata H, TOSHIYUKI AMANO, Akira Nakamizo, Koji Yoshimoto, Toru Iwaki, Tomio Sasaki, Pediatric glioblastoma with oligodendroglioma component: Aggressive clinical phenotype with distinct molecular characteristics., Neuropathology, doi: 10.1111/neup.12029. , 2013.03.
80. Amran, Muhammad Yunus, Fujii, Jun, Satoshi O Suzuki, Kolling, Glynis L., Villanueva, Sharon Y. A. M., Kainuma, Mosaburo, Kobayashi, Hideyuki, Kameyama, Hideko, Yoshida, Shin-ichi, Investigation of Encephalopathy Caused by Shiga Toxin 2c-Producing Escherichia coli Infection in Mice, PLOS ONE, 10.1371/journal.pone.0058959, 8, 3, e58959, 2013.03.
81. Tsujimoto S, Ishida T, Onomura Y, Tsukimori K, Takechi S, Yamaguchi T, Uchi H, Satoshi O Suzuki, Yamamoto M, Himeno M, Furue M, Yamada H, Selenium-binding protein 1: Its physiological function, dependence on aryl hydrocarbon receptors, and role in wasting syndrome by 2,3,7,8-tetrachlorodibenzo-p-dioxin., Biochim Biophys Acta, 10.1016/j.bbagen.2013.03.008., 1830, 6, 3616-3624, 2013.03.
82. Kikkawa Y, Suzuki SO, Nakamizo A, Tsuchimochi R, Murakami N, Yoshitake T, Aishima S, Okubo F, Hata N, Amano T, Yoshimoto K, Mizoguchi M, Iwaki T, Sasaki T, Radiation-induced spinal cord glioblastoma with cerebrospinal fluid dissemination subsequent to treatment of lymphoblastic lymphoma, Surgical Neurology International, 2013;4:27, 2013.02, [URL].
83. Watanabe S, Shirogane Y, Suzuki SO, Ikegame S, Koga R, Yanagi Y., Mutant fusion proteins with enhanced fusion activity promote measles virus spread in human neuronal cells and brains of suckling hamsters., J Virol, 87, 5, 2648-59, 2013.03.
84. Nishio M, Hamada K, Kawahara K, Sasaki M, Noguchi F, Chiba S, Mizuno K, Suzuki SO, Dong Y, Tokuda M, Morikawa T, Hikasa H, Eggenschwiler J, Yabuta N, Nojima H, Nakagawa K, Hata Y, Nishina H, Mimori K, Mori M, Sasaki T, Mak TW, Nakano T, Itami S, Suzuki A., Cancer susceptibility and embryonic lethality in Mob1a/1b double-mutant mice., J Clin Invest, 122, 12, 4505-18, 2012.12.
85. Yamashita K, Yoshiura T, Hiwatashi A, Togao O, Yoshimoto K, Suzuki SO, Abe K, Kikuchi K, Maruoka Y, Mizoguchi M, Iwaki T, Honda H., Differentiating primary CNS lymphoma from glioblastoma multiforme: assessment using arterial spin labeling, diffusion-weighted imaging, and (18)F-fluorodeoxyglucose positron emission tomography., Neuroradiology, in press, 2012.09.
86. Kikkawa Y, Nakamizo A, Suzuki SO, Tanaka S, Tsuchimochi R, Amano T, Yoshimoto K, Mizoguchi M, Iwaki T, Sasaki T , Spinal endodermal cyst resembling an arachnoid cyst in appearance: Pitfalls in intraoperative diagnosis of cystic lesions , Surg Neurol Int, 3, 1, 78, Available FREE in open access from:
, 2012.07.
87. Nobuya Murakami, Takato Morioka, Kimiaki Hashiguchi, Satoshi O Suzuki, Takayuki Amano, Ayumi Sakata, Toru Iwaki, Tomio Sasaki, Focal cortical dysplasia of Palmini type IIA as an epileptogenesis in patients with epilepsy associated with Sturge-Weber syndrome

, Epilepsia, in press, 2012.07.
88. Kanata A, Morioka T, Tsukamoto H, Katsuta T, Suzuki SO., A Patient with a Dysembryoplastic Neuroepithelial Tumor Who Underwent Epilepsy Surgery after Initial Seizure., Pediatr Neurosurg. , 47, 6, 436-441, 2012.07.
89. Mizoguchi M, Yoshimoto K, Ma X, Guan Y, Hata N, Amano T, Nakamizo A, Suzuki SO, Iwaki T, Sasaki T., Molecular characteristics of glioblastoma with 1p/19q co-deletion., Brain Tumor Pathol. , in press, 2012.06.
90. Amano T, Suzuki SO, Mizoguchi M, Yoshimoto K, Nakamizo A, Murata H, Iwaki T, Sasaki T., A fibrotic nodule arising from the cerebellopontine angle., Brain Tumor Pathol., in press, 2012.06.
91. Masaki K, Suzuki SO, Matsushita T, Yonekawa T, Matsuoka T, Isobe N, Motomura K, Wu XM, Tabira T, Iwaki T, Kira J., Extensive loss of connexins in Baló's disease: evidence for an auto-antibody-independent astrocytopathy via impaired astrocyte-oligodendrocyte/myelin interaction., Acta Neuropathol., 123, 6, 887-900, 2012.06.
92. Horiguchi M, Koyanagi S, Okamoto A, Suzuki SO, Matsunaga N, Ohdo S., Stress-Regulated Transcription Factor ATF4 Promotes Neoplastic Transformation by Suppressing Expression of the INK4a/ARF Cell Senescence Factors.
, Cancer Res., 72, 2, 395-401, 2012.01.
93. Satoshi O. Suzuki, Toru Iwaki, Kenji Arakawa, Hirokazu Furuya,, Naoki Fujii, Akiko Iwaki, An autopsy case of adult-onset hereditary spastic paraplegia type 2 with a novel mutation in exon 7 of the proteolipid protein 1 gene, Acta Neuropathol , 22, 6, 775-81, 2011.12.
94. Harada S, Suzuki SO, Seki Y, Nakamura S, Iwaki T. , Differential activation of proapoptotic molecules between mouse and rat models of distal motor trigeminal denervation. , J Oral Pathol Med. in press., 41, 4, 354-60, 2011.10.
95. Yamashita K, Yoshiura T, Hiwatashi A, Togao O, Yoshimoto K, Suzuki SO, Kikuchi K, Mizoguchi M, Iwaki T, Honda H., Arterial spin labeling of hemangioblastoma: differentiation from metastatic brain tumors based on quantitative blood flow measurement.

Neuroradiology. , Neuroradiology. in press, 2011.11.
96. Matsuzaki T, Sasaki K, Hata J, Hirakawa Y, Fujimi K, Ninomiya T, Suzuki SO, Kanba S, Kiyohara Y, Iwaki T., Association of Alzheimer disease pathology with abnormal lipid metabolism: The Hisayama Study., Neurology , 77, 11, 1068-75, Neurology. 2011 Sep 13;77(11):1068-75., 2011.09.
97. Honda H, Sasaki K, Minaki H, Masui K, Suzuki SO, Doh-Ura K, Iwaki T., Protease-resistant PrP and PrP oligomers in the brain in human prion diseases after intraventricular pentosan polysulfate infusion., Neuropathology, in press, in press, 2011.09.
98. Nakamizo A, Suzuki SO, Shimogawa T, Amano T, Mizoguchi M, Yoshimoto K, Sasaki T., Concurrent spinal nerve root schwannoma and meningioma mimicking single-component schwannoma, Neuropathology, in press, 2011.07.
99. Hata N, Hisada K, Torisu R, Suzuki SO, Kameda K, Sasaki T., Foreign body granuloma associated with dura-cranioplasty after resection of convexity meningioma with extracranial extension: case report., Neurol Med Chir (Tokyo). 2011;51(3):236-8., 51, 3, 236-8, 2011.03.
100. Nakamizo A, Akagi Y, Amano T, Suzuki SO, Otsuka R, Abe Y, Yoshimoto K, Iwaki T, Sasaki T., Donor-derived adult T-cell leukaemia., Lancet. , 377, 9771, 1124, 2011.03.
101. Araki Y, Mizoguchi M, Yoshimoto K, Shono T, Amano T, Nakamizo A, Suzuki SO, Iwaki T, Sasaki T., Quantitative digital assessment of MGMT immunohistochemical expression in glioblastoma tissue., Brain Tumor Pathol. 2011 Feb;28(1):25-31., 28, 1, 25-31, 2011.02.
102. Matsuoka T, Suzuki SO, Toshihiko Suenaga, Iwaki T, Kira JI., Reappraisal of Aquaporin-4 Astrocytopathy in Asian Neuromyelitis
Optica and Multiple Sclerosis Patients, Brain Pathology, in press, 2010.12.
103. Rina Torisu, Satoshi O. Suzuki, Kenta Masui, Koji Yoshimoto, Masahiro Mizoguchi, Makoto Hashizume, Peter Canoll, James E. Goldman, Tomio Sasaki, Toru Iwaki, Persistent roles of signal transduction of platelet-derived growth factor B in genesis, growth and anaplastic transformation of gliomas in an in vivo serial transplantation model, Brain Tumor Pathology, 28, 1, 33-42, 28(1):33-42., 2011.02.
104. Masui K, Suzuki SO, Hashiguchi K, Morioka T, Yoshiura T, Sasaki T, Iwaki T., Focal cortical dysplasia coexisting with diffuse astrocytoma in childhood: A case report and reappraisal of the glial component in archival FCD cases., Neuropathology, in press, 2010.12.
105. Seki Y, Suzuki SO, Masui K, Harada S, Nakamura S, Kanba S, Iwaki T., A simple and high-yield method for preparation of rat microglial cultures utilizing Aclar plastic film., Neuropathology, 31, 3, 215-22, 31(3):215-22, 2011.01.
106. Matsuoka T, Fujii N, Kondo A, Iwaki A, Hokonohara T, Honda H, Sasaki K, Suzuki SO, Iwaki T., An autopsied case of sporadic adult-onset amyotrophic lateral sclerosis with FUS-positive basophilic inclusions., Neuropathology, 31, 1, 71-6, 2011 Feb;31(1):71-6, 2011.02.
107. Nakamizo A, Suzuki SO, Saito N, Shono T, Matsumoto K, Onaka S, Mizoguchi M, Sasaki T., Clinicopathological study on chronic encapsulated expanding hematoma associated with incompletely obliterated AVM after stereotactic radiosurgery., Acta Neurochir (Wien), 153, 4, 883-93, 153(4):883-93., 2011.04.
108. Matsuzaki T, Sasaki K, Tanizaki Y, Hata J, Fujimi K, Matsui Y, Sekita A, Suzuki SO, Kanba S, Kiyohara Y, Iwaki T., Insulin resistance is associated with the pathology of Alzheimer disease: the Hisayama study., Neurology , 75, 9, 764-70, 2010.08.
109. Hashiguchi K, Morioka T, Murakami N, Suzuki SO, Hiwatashi A, Yoshiura T, Sasaki T., Utility of 3-T FLAIR and 3D short tau inversion recovery MR imaging in the preoperative diagnosis of hippocampal sclerosis: direct comparison with 1.5-T FLAIR MR imaging., Epilepsia, 51, 9, 1820-8, 2010.09.
110. Matsuoka T, Suzuki SO, Iwaki T, Tabira T, Ordinario AT, Kira JI., Aquaporin-4 astrocytopathy in Baló's disease., Acta Neuropathol, 120, 5, 651-60, 2010 Nov;120(5):651-60, 2010.11.
111. Guan Y, Mizoguchi M, Yoshimoto K, Hata N, Shono T, Suzuki SO, Araki Y, Kuga D, Nakamizo A, Amano T, Ma X, Hayashi K, Sasaki T., MiRNA-196 Is Up-Regulated in Glioblastoma but not in Anaplastic Astrocytoma and has Prognostic Significance., Clin Cancer Res, 16, 16, 4289-97, 2010 Aug 15;16(16):4289-97, 2010.08.
112. Kenta Masui, Satoshi O. Suzuki, Rina Torisu, James E. Goldman, Peter Canoll, Toru Iwaki, Glial progenitors in the brainstem give rise to malignant gliomas by platelet-derived growth factor stimulation , Glia , 58, 9, 1050-1065, 2010.07.
113. Yamaguchi S, Suzuki SO, Matsuo Y, Uesaka T, Matsukado K, Masui K, Iwaki T., Large hypothalamic hamartoma with calcification and cystic components in an adult--case report., Neurol Med Chir (Tokyo). 2010;50(6):495-8., 50, 6, 495-8, 2010.06.
114. Midori Yamamoto M, Satoshi O Suzuki, Masaru Himeno, Resveratrol-induced autophagy in human U373 glioma cells, Oncol Lett, 1, 3, 489-493, 2010.05.
115. Yamamoto M, Suzuki SO, Himeno M., The effects of dynein inhibition on the autophagic pathway in glioma cells., Neuropathology. , 30, 1, 1-6, 2010.02.
116. Masui K, Suzuki SO, Kondo A, Iwaki T., A 6-YEAR-OLD GIRL WITH AN EXTRA-AXIAL MASS IN THE MIDDLE CRANIAL FOSSA, Brain Pathol., 20, 269–272, 2010.01.
117. Hidaka N, Yamamoto N, Tsukimori K, Hojo S, Suzuki SO, Wake N., Prenatal diagnosis of trisomy 16 mosaicism manifested as pulmonary artery stenosis., J Clin Ultrasound. , 37, 2, 107-111, 2009.02.
118. Mizoguchi Y, Monji A, Kato T, Seki Y, Gotoh L, Horikawa H, Suzuki SO, Iwaki T, Yonaha M, Hashioka S, Kanba S., Brain-Derived Neurotrophic Factor (BDNF) Induces Sustained Elevation of Intracellular Ca2+ in Rodent Microglia., J Immunol. 2009 , Advanced online publication, 2009.11.
119. Ishihara N, Nomura M, Jofuku A, Kato H, Suzuki SO, Masuda K, Otera H, Nakanishi Y, Nonaka I, Goto Y, Taguchi N, Morinaga H, Maeda M, Takayanagi R, Yokota S, Mihara K., Mitochondrial fission factor Drp1 is essential for embryonic development and synapse formation in mice., Nat Cell Biol. , 11, 8, 958-966, 2009.08.
120. Assanah MC, Bruce JN, Suzuki SO, Chen A, Goldman JE, Canoll P., PDGF stimulates the massive expansion of glial progenitors in the neonatal forebrain., Glia, 57, 16, 1835-1847, 2009.12.
121. Seki Y, Suzuki SO, Nakamura S, Iwaki T., Degenerative and protective reactions of the rat trigeminal motor nucleus after removal of the masseter and temporal muscles., J Oral Pathol Med. , 38, 10, 777-784, 2009.11.
122. Samura K, Morioka T, Hashiguchi K, Yoshida F, Miyagi Y, Yoshiura T, Suzuki SO, Sasaki T., Coexistence of a human tail and congenital dermal sinus associated with lumbosacral lipoma., Childs Nerv Syst, 25:137-41, 2009.01.
123. Takase K, Shigeto H, Suzuki SO, Kikuchi H, Ohyagi Y, Kira J., Cortical kindling in a focal freeze lesion rat model. , J Clin Neurosci, 16:94-8., 2009.01.
124. Sasaki T, Shono T, Hashiguchi K, Yoshida F, Suzuki SO., Histological considerations of the cleavage plane for preservation of facial and cochlear nerve functions in vestibular schwannoma surgery. , J Neurosurg, 110, 4, 648-655, 2009.04.
125. Kuga D, Mizoguchi M, Guan Y, Hata N, Yoshimoto K, Shono T, Suzuki SO, Kukita Y, Tahira T, Nagata S, Sasaki T, Hayashi K., Prevalence of copy number neutral LOH in glioblastomas revealed by genome-wide analysis of laser-microdissected tissues. , Neuro Oncol, 10:995-1003, 2008.08.
126. Shono T, Yokoyama N, Uesaka T, Kuroda J, Takeya R, Yamasaki T, Amano T, Mizoguchi M, Suzuki SO, Niiro H, Miyamoto K, Akashi K, Iwaki T, Sumimoto H, Sasaki T. , Enhanced expression of NADPH oxidase Nox4 in human gliomas and its roles in cell proliferation and survival. , Int J Cancer. 2008;123:787-92., 123:787-92., 2008.08.
127. Samura K, Morioka T, Yoshida F, Hashiguchi K, Miyagi Y, Mizoguchi M, Shono T, Nagata S, Suzuki SO, Sasaki T, Focal cortical dysplasia with calcification: a case report. , Childs Nerv Syst , 24(5):619-22, 2008.05.
128. Samura K, Morioka T, Hashiguchi K, Yoshida F, Hokama M, Yamaguchi S, Nagata S, Suzuki SO, Yoshiura K, Sasaki T, Bursal cyst (bursitis) of the coccygeal region clinically mimics sacrococcygeal meningocele. , Childs Nerv Syst , 24:533-535, 2008.04.
129. Kato T, Mizoguchi Y, Monji A, Horikawa H, Suzuki SO, Seki Y, Iwaki T, Hashioka S, Kanba S., Inhibitory Effects of Aripiprazole on Interferon-gamma-Induced Microglial Activation via Intracellular Ca(2+) Regulation in Vitro., J Neurochem, 電子版, 2008.04.
130. Masui K, Mawatari SY, Suzuki SO, Iwaki T., Evaluation of sensitivity and specificity of doublecortin immunostatining for the detection of infiltrating glioma cells., Brain Tumor Pathol., 25(1):1-7, 2008.04.
131. Noguchi T, Yoshiura T, Hiwatashi A, Togao O, Yamashita K, Nagao E, Shono T, Mizoguchi M, Nagata S, Sasaki T, Suzuki SO, Iwaki T, Kobayashi K, Mihara F, Honda H., Perfusion imaging of brain tumors using arterial spin-labeling: correlation with histopathologic vascular density., Am J Neuroradiol, 29(4):688-93, 2008.04.
132. Guan Y, Hata N, Kuga D, Yoshimoto K, Mizoguchi M, Shono T, Suzuki SO, Tahira T, Kukita Y, Higasa K, Yokoyama N, Nagata S, Iwaki T, Sasaki T, Hayashi K., Narrowing of the regions of allelic losses of chromosome 1p36 in meningioma tissues by an improved SSCP analysis., Int J Cancer., 122(8):1820-6., 2008.04.
133. Takase KI, Shigeto H, Suzuki SO, Kikuchi H, Ohyagi Y, Kira JI., Prenatal freeze lesioning produces epileptogenic focal cortical dysplasia., Epilepsia, 49, 6, 997-1010, 2008.03.
134. Yotsumoto F, Yagi H, Suzuki SO, Oki E, Tsujioka H, Hachisuga T, Sonoda K, Kawarabayashi T, Mekada E, Miyamoto S, Validation of HB-EGF and amphiregulin as targets for human cancer therapy. , Biochem Biophys Res Commun , 365:555-561, 2008.01.
135. Maeda Y, Hirano K, Kai Y, Hirano M, Suzuki SO, Sasaki T, Kanaide H., Up-regulation of proteinase-activated receptor 1 and increased contractile responses to thrombin after subarachnoid haemorrhage., Br J Pharmacol, 152(7):1131-9., 2007.12.
136. Shono T, Natori Y, Morioka T, Torisu R, Mizoguchi M, Nagata S, Suzuki SO, Iwaki T, Inamura T, Fukui M, Oka K, Sasaki T., Results of a long-term follow-up after neuroendoscopic biopsy procedure and third ventriculostomy in patients with intracranial germinomas., J Neurosurg., 107(3 Suppl):193-8., 2007.09.
137. Uesaka T, Shono T, Kuga D, Suzuki SO, Niiro H, Miyamoto K, Matsumoto K, Mizoguchi M, Ohta M, Iwaki T, Sasaki T., Enhanced expression of DNA topoisomerase II genes in human medulloblastoma and its possible association with etoposi, J Neurooncol. , 84(2):119-29, 2007.09.
138. Uesaka T, Shono T, Suzuki SO, Nakamizo A, Niiro H, Mizoguchi M, Iwaki T, Sasaki T., Expression of VEGF and its receptor genes in intracranial schwannomas., J Neurooncol. , 83(3):259-66., 2007.07.
139. Suzuki SO, McKenney RJ, Mawatari SY, Mizuguchi M, Mikami A, Iwaki T, Goldman JE, Canoll P,Vallee RB. , Expression patterns of LIS1, dynein and their interaction partners dynactin, NudE, NudEL and NudC in human gliomas suggest roles in invasion and proliferation., Acta Neuropatholgica, 113(5):591-9, 2007.05.
140. Farin A, Suzuki SO, Weiker M, Goldman JE, Bruce JN, Canoll P, Transplanted glioma cells migrate and proliferate on host brain vasculature: a dynamic analysis., Glia, 2006;53:799-808, 2006.06.
141. Tanaka Y, Miyamoto S, Suzuki SO, Oki E, Yagi H, Sonoda K, Yamazaki A, Mizushima H, Maehara Y, Mekada E, Nakano H:., Clinical significance of heparin-binding epidermal growth factor-like growth factor and a disintegrin and metalloprotease 17 expression in human ovarian cancer., Clin. Cancer. Res., 10.1158/1078-0432.CCR-04-1426, 11, 13, 4783-4792, 11: 4783-4789, 2005, 2005.01.
142. Suzuki SO and Iwaki T, Dynamic analysis of glioma cells: looking into "movement phenotypes"., Neuropathology, 10.1111/j.1440-1789.2005.00626.x, 25, 3, 254-262, 25:254-62, 2005, 2005.01.
143. Matsumoto K, Suzuki SO, Fukui M, Iwaki T, Accumulation of MDM2 in pleomorphic xanthoastrocytomas., Pathol. Int., 10.1111/j.1440-1827.2004.01637.x, 54, 6, 387-391, 54:387-391, 2004, 2004.01.
144. Furuta A, Noda M, Suzuki SO, Goto Y, Kanahori Y, Rothstein J.D., Iwaki T., Translocation of glutamate transporter subtype excitatory amino acid carrier 1 protein in Kainic acid-induced rat epilepsy, American Journal of Pathology, 10.1016/S0002-9440(10)63705-4, 163, 2, 779-787, 163(2):779-787, 2003.08.
145. Suzuki SO, Goldman JE., Multiple cell populations in the early postnatal subventricular zone take distinct migratory pathways: a dynamic study of glial and neuronal progenitor migration., J Neurosci, 23, 10, 4240-4250, 23(10):4240-50., 2003.05.
146. Kikuchi H, Furuta A, Nishioka K, Suzuki SO, Nakabeppu Y, Iwaki T., Impairment of mitochondrial DNA repair enzymes against accumulation of 8-oxo-guanine in the spinal motor neurons of amyotrophic lateral sclerosis, Acta Neuropathol, 10.1007/s00404-001-0480-x, 103, 4, 408-414, 408:408-414, 2002.01.
147. Suzuki OS, Kitai R, Llena J, Lee CS, Goldman EJ, Shafit-Zagardo B., MAP-2e, a novel MAP-2 isoform, is expressed in Gliomas and delineates tumor architecture and patterns of infiltration., J Nuropath and Exp Neurol, 61(5):403-412, 2002, 2002.05.
148. Miyagi, Y., Suzuki, S.O., Iwaki, T., Shima, F., Ishido, K., Araki, T. and Kamikaseda, K., Pleomorphic xanthoastrocytoma with predominantly exophytic growth: case report, Surg Neurol, 10.1016/S0090-3019(01)00565-1, 56, 5, 330-332, 56(5):330-2., 2001.11.
149. Shono, T., Inamura, T., Morioka, T., Matsumoto, K., Suzuki, S.O., Ikezaki, K., Iwaki, T.and Fukui, M., Vascular endothelial growth factor in chronic subdural haematomas., J Clin Neurosci, 10.1054/jocn.2000.0951, 8, 5, 411-415, 8(5):411-5., 2001.09.
150. Nakayama H, Suzuki S, Hikino S, Tezuka J, Hara T., Multiple cerebral arteriovenous fistulas and malformations in the neonate., Pediatr Neurol, 10.1016/S0887-8994(01)00308-3, 25, 3, 236-238, 25(3):236-8, 2001.09.
151. Kawashima, M., Suzuki, S.O., Yamashima, T., Fukui, M. and Iwaki, T., Prostaglandin D synthase(b-trace) in meningeal hemangiopericytoma, Mod Pathol, 10.1038/modpathol.3880285, 14, 3, 197-201, 14(3):197-201., 2001.03.
152. Kawashima M, Suzuki SO, Ikezaki K, Matsushima T, Fukui M, Iwaki T., Different responses of benign and atypical meningiomas to gamma-knife radiosurgery: report of two cases with immunohistochemical analysis., Brain Tumor Pathol, 18(2):61-6., 2001.02.
153. Suzuki, S.O. and Iwaki T., Amplification and overexpression of mdm2 gene in ependymomas,, Mod Pathol, 10.1038/modpathol.3880095, 13, 5, 548-553, 13(5):548-53., 2000.05.
154. Kawashima, M., Suzuki S. O., Doh-ura K. and Iwaki T., α-Synuclein is expressed in a variety of brain tumors showing neuronal differentiation, Acta Neuropathol, 99, 2, 154-160, 99(2):154-60., 2000.02.
155. Miyagi, Y., Suzuki S.O., Iwaki T., Ishido K., Araki T. and Kamikaseda K., Magnetic resonance appearance of multiple intracranial epidermoid cysts: intrathecal seeding of the cysts?, J Neurosurg, 92(4):711-4., 2000.04.