Faculty Profiles - TAKASHIMA Hiroshi

Papers - TAKASHIMA Hiroshi

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Matsuura E, Enose-Akahata Y, Yao K, Oh U, Tanaka Y, Takashima H, Jacobson S. . Dynamic acquisition of HTLV-1 tax protein by mononuclear phagocytes: Role in neurologic disease. . Journal of Neuroimmunology304 43 - 50 2017.3Dynamic acquisition of HTLV-1 tax protein by mononuclear phagocytes: Role in neurologic disease.Reviewed

Eiji Matsuura, Yoshimi Enose-Akahata, Karen Yao, Unsong Oh, Yuetsu Tanaka, Hiroshi Takashima, Steven Jacobson . Dynamic acquisition of HTLV-1 tax protein by mononuclear phagocytes: Role in neurologic disease . JOURNAL OF NEUROIMMUNOLOGY304 43 - 50 2017.3Reviewed International journal

Language：English Publisher：ELSEVIER SCIENCE BV

Pathology of HTLV-1 associated myelopathy/Tropical spastic paraparesis (HAM/rsp) is believed to be the result of "bystander damage" involving effector CD8 (+) T lymphocytes (CTLs) killing of virus infected cells. But the specific cellular events leading up to tissue injury are still unclear. Here, we developed the Microscopy Imaging of Cytotoxic T lymphocyte assay with Fluorescence emission (MI-CaFe), an optimized visualization analysis to explore the interactions between CTLs and virus infected or viral antigen presenting target cells. Various cell-to -cell formations can be observed and our results demonstrate elevated frequencies of CTL-target cell conjugates in HAM/TSP patient PBMCs compared to control PBMCs. Furthermore, HTLV-1 Tax protein expression can be localized at the cell -cell junctions and also tracked moving from an infected cell to a CD14 (+) mononuclear phagocyte (MP). Activation of CD14 (+) MPs in HAM/TSP patient PBMCs and antigenic presentation of HTLV-1 Tax by MPs can be inferred by their spontaneous cytotoxicity after 18 h of in vitro culture. Given that CD4 (+) T lymphocytes are the primary reservoirs of HTLV-1 and MPs are scavenger cells responsible for pathogen clearance, spontaneous cytotoxicity against MPs in HAM/TSP PBMCs suggests a mechanism of chronic inflammation, secondary to low level of persistent virus infection within the central nervous system. Published by Elsevier B.V.

DOI： 10.1016/j.jneuroim.2016.09.014

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Yu Hiramatsu, Michiyoshi Yoshimura, Ryuji Saigo, Hitoshi Arata, Yuji Okamoto, Eiji Matsuura, Haruhiko Maruyama, Hiroshi Takashima . Toxocara canis myelitis involving the lumbosacral region: a case report . JOURNAL OF SPINAL CORD MEDICINE40 ( 2 ) 241 - 245 2017.3Reviewed International journal

Authorship：Last author Language：English Publishing type：Research paper (scientific journal) Publisher：TAYLOR & FRANCIS LTD

Context: Toxocara canis is a parasite known to cause visceral larva migrans. The infection rarely affects the central nervous system but there have been several reports of myelitis caused by visceral larva migrans due to Toxocara canis. In previous reported cases, the lesions were located in the thoracic or cervical spinal cord. To the best of our knowledge, this is the first report of a lesion involving the lumbosacral region.
Findings: A 60-year-old man developed weakness and dysesthesia in the lower limbs. The symptoms resolved spontaneously, but recurred after five months. One month later, the patient developed pollakiuria and constipation. He was a dog owner and frequently ate raw chicken meat and beef liver. Sagittal T2-weighted image (T2WI) showed swelling and hyperintensity in the spinal cord from T10 to the lumbosacral region and focal nodular enhancement on the posterior segment of the lumbar spinal cord. Blood cell counts showed slight eosinophilia and elevated serum immunoglobulin E level. Cerebrospinal fluid examination showed slight pleocytosis with eosinophilia. Enzyme-linked immunosorbent assay showed high levels of anti-Toxocara antibodies in the serum and cerebrospinal fluid. In addition, confirmatory test by Western blot was positive. The patient was initially treated with intravenous methylprednisolone with slight improvement in muscle weakness. Albendazole was added with a second course of intravenous methylprednisolone. The muscle weakness in the lower limbs improved considerably, and swelling and hyperintensity on T2WI almost disappeared.
Conclusion: Our results suggest that Toxocara canis myelitis cannot be discounted even if the myelitis involves the lumbosacral region.

DOI： 10.1080/10790268.2015.1114230

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Yoshimura A, Yuan JH, Hashiguchi A, Hiramatsu Y, Ando M, Higuchi Y, Nakamura T, Okamoto Y, Matsumura K, Hamano T, Sawaura N, Shimatani Y, Kumada S, Okumura Y, Miyahara J, Yamaguchi Y, Kitamura S, Haginoya K, Mitsui J, Ishiura H, Tsuji S, Takashima H. . Clinical and mutational spectrum of Japanese patients with Charcot-Marie-Tooth disease caused by GDAP1 variants. . Clinical Genetics 2017.2Clinical and mutational spectrum of Japanese patients with Charcot-Marie-Tooth disease caused by GDAP1 variants.Reviewed

Yuan JH, Hashiguchi A, Yoshimura A, Yaguchi H, Tsuzaki K, Ikeda A, Wada-Isoe K, Ando M, Nakamura T, Higuchi Y, Hiramatsu Y, Okamoto Y, Takashima H. . Clinical diversity caused by novel IGHMBP2 variants. . Journal of Human Genetics 2017.2Clinical diversity caused by novel IGHMBP2 variants.Reviewed

Emi Motokura, Toru Yamashita, Yoshiaki Takahashi, Keiichiro Tsunoda, Kota Sato, Mami Takemoto, Nozomi Hishikawa, Yasuyuki Ohta, Akihiro Hashiguchi, Hiroshi Takashima, Koji Abe . An AOA2 patient with a novel compound heterozygous SETX frame shift mutations . JOURNAL OF THE NEUROLOGICAL SCIENCES372 294 - 296 2017.1Reviewed

Arata Hitoshi, Takashima Hiroshi . I. Neurological Findings to Identify Autoimmune Encephalopathy . Nihon Naika Gakkai Zasshi106 ( 8 ) 1542 - 1549 2017

Taniguchi Takaki, Hokezu Youichi, Okada Takashi, Ishibashi Masato, Hashiguchi Akihiro, Matsuura Eiji, Takashima Hiroshi . A amyotrophic lateral sclerosis (ALS) 4 family misdiagnosed as hereditary spastic paraplegia―a case report― . Rinsho Shinkeigaku57 ( 11 ) 685 - 690 2017Reviewed

Authorship：Last author Publisher：Societas Neurologica Japonica

We report a 44 years old man with slowly progressive muscular atrophy of the extremities for over 30 years. He experienced difficulty in walking in his 10's and was diagnosed as hereditary spastic paraplegia (HSP) in his 20's. And then, muscle atrophy of the extremities slowly progressed especially in his distal muscles. Sensory axonal neuropathy was detected with sural nerve biopsy. His father and uncle have been diagnosed as HSP in their early days. His father noticed weakness of his leg in his 20's. He lost motor function of the leg in his 60's. In addition, marked disturbance of thermal sensation, vibration, and sense of position were found by physical examination. Our genetic study detected senataxin (SETX) gene mutation (c.8C>T,p.T3I) in the blood of those two patients, and they had been identified as family cases of amyotrophic lateral sclerosis (ALS) 4. As clinical symptoms of ALS4 would be similar to those of HSP at the onset, we suggest considering ALS4 in seeing patients with HSP without gene diagnosis.

DOI： 10.5692/clinicalneurol.cn-000996

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Fujisawa Miwako, Sano Yasuteru, Omoto Masatoshi, Ogasawara Jyun-ichi, Koga Michiaki, Takashima Hiroshi, Kanda Takashi . Charcot-Marie-Tooth disease type 2 caused by homozygous MME gene mutation superimposed by chronic inflammatory demyelinating polyneuropathy . Rinsho Shinkeigaku57 ( 9 ) 515 - 520 2017Reviewed

Language：Japanese Publisher：Societas Neurologica Japonica

We report a 59-year-old Japanese male who developed gradually worsening weakness and numbness of distal four extremities since age 50. His parents were first cousins, and blood and cerebral spinal examinations were unremarkable. Homozygous mutation of MME gene was detected and thus he was diagnosed as autosomal-recessive Charcot-Marie-Tooth disease 2T (AR-CMT2T); however, electrophysiological examinations revealed scattered demyelinative changes including elongated terminal latency in several peripheral nerve trunks. Sural nerve biopsy showed endoneurial edema and a lot of thinly myelinated nerve fibers with uneven distribution of remnant myelinated fibers within and between fascicles. Immunoglobulin treatment was initiated considering the possibility of superimposed inflammation and demyelination, and immediate clinical as well as electrophysiological improvements were noted. Our findings indicate that AR-CMT2T caused by MME mutation predisposes to a superimposed inflammatory demyelinating neuropathy. This is the first report which documented the co-existence of CMT2 and chronic inflammatory demyelinating polyneuropathy (CIDP); however, in the peripheral nervous system, neprilysin, a product of MME gene, is more abundant in myelin sheath than in axonal component. The fragility of myelin sheath due to mutated neprilysin may trigger the detrimental immune response against peripheral myelin in this patient.

DOI： 10.5692/clinicalneurol.cn-001036

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Yamamoto Yuki, Matsui Naoko, Hiramatsu Yu, Miyazaki Yoshimichi, Nodera Hiroyuki, Izumi Yuishin, Takashima Hiroshi, Kaji Ryuji . Mitochondrial trifunctional protein deficiency: an adult patient with similar progress to Charcot-Marie-Tooth disease . Rinsho Shinkeigaku57 ( 2 ) 82 - 87 2017Reviewed

Language：Japanese Publisher：Societas Neurologica Japonica

A 45-year-old man presented to us due to slowly progressive muscle weakness and sensory disturbances in his lower limbs since his 40's. He reported multiple episodes of exercise-induced severe muscle fatigue and brown urine in his childhood, which disappeared by age 20. A nerve conduction study showed peripheral axonal neuropathy and then Charcot-Marie-Tooth disease (CMT) was considered as the most likely diagnosis; however, exome sequencing failed to identify a mutation in the known genes of CMTs. Since age 55, he recurrently developed severe rhabdomyolysis that required hospitalization. On suspicion of lipid metabolism disorders, we performed serum acylcarnitine analysis, and which revealed mildly elevated long-chain fatty acids. We re-examined variants obtained via exome sequencing and found a mutation in HADHB. Mitochondrial trifunctional protein (MTP) deficiency is a rare autosomal recessive disorder of mitochondrial fatty acid beta-oxidation caused by HADHA or HADHB mutation. It can be a life-threatening multiorgan disorder with early infantile onset, but it can also present in childhood or adolescence with peripheral neuropathy and recurrent rhabdomyolysis. This case of adult-diagnosed MTP deficiency was characterized by slowly progressive peripheral neuropathy masquerading CMT in addition to muscular symptoms. MTP deficiency should be considered in patients with the combination of peripheral neuropathy and recurrent rhabdomyolysis.

DOI： 10.5692/clinicalneurol.cn-000976

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Matsuura E, Nozuma S, Tashiro Y, Kubota R, Izumo S, Takashima H. . HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP): A comparative study to identify factors that influence disease progression. . Journal of Neurological Sciences 371 112 - 116 2016.12HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP): A comparative study to identify factors that influence disease progression.Reviewed

ｈｉｒａｎｏ M, Oka N, Hashiguchi A, Ueno S, Sakamoto H, Takashima H, Higuchi Y, Kusunoki S, Nakamura Y. . Histopathological features of a patient with Charcot-Marie-Tooth disease type 2U/AD-CMTax-MARS. . Journal of Peripheral Nervous System21 ( 4 ) 370 - 374 2016.12Histopathological features of a patient with Charcot-Marie-Tooth disease type 2U/AD-CMTax-MARS.Reviewed

Sone J, Mori K, Inagaki T, Katsumata R, Takagi S, Yokoi S, Araki K, Kato T, Nakamura T, Koike H, Takashima H, Hashiguchi A, Kohno Y, Kurashige T, Kuriyama M, Takiyama Y, Tsuchiya M, Kitagawa N, Kawamoto M, Yoshimura H, Suto Y, Nakayasu H, Uehara N, Sugiyama H, Takahashi M, Kokubun N, Konno T, Katsuno M, Tanaka F, Iwasaki Y, Yoshida M, Sobue G. . Clinicopathological features of adult-onset neuronal intranuclear inclusion disease. . Brain139 3170 - 3186 2016.12Clinicopathological features of adult-onset neuronal intranuclear inclusion disease.Reviewed

Kawarai T, Yamasaki K, Mori A, Takamatsu N, Osaki Y, Banzrai C, Miyamoto R, Oki R, Pedace L, Orlacchio A, Nodera H, Hashiguchi A, Higuchi Y, Takashima H, Nishida Y, Izumi Y, Kaji R. . MFN2 transcripts escaping from nonsense-mediated mRNA decay pathway cause Charcot-Marie-Tooth disease type 2A2. . Journal of Neurology, Neurosurgery and Psychiatry87 ( 11 ) 1263 - 1265 2016.11MFN2 transcripts escaping from nonsense-mediated mRNA decay pathway cause Charcot-Marie-Tooth disease type 2A2.

Ichikawa K, Numasawa K, Takeshita S, Hashiguchi A, Takashima H. . Novel mutations in SH3TC2 in a young Japanese girl with Charcot-Marie-Tooth disease type 4C. . Pediatrics International58 ( 11 ) 1252 - 1254 2016.11Novel mutations in SH3TC2 in a young Japanese girl with Charcot-Marie-Tooth disease type 4C.Reviewed

Misawa S, Sato Y, Katayama K, Nagashima K, Aoyagi R, Sekiguchi Y, Sobue G, Koike H, Yabe I, Sasaki H, Watanabe O, Takashima H, Nishizawa M, Kawachi I, Kusunoki S, Mitsui Y, Kikuchi S, Nakashima I, Ikeda S, Kohara N, Kanda T, Kira J, Hanaoka H, Kuwabara S; Japanese POEMS Syndrome for Thalidomide (J-POST) Trial Study Group. . Safety and efficacy of thalidomide in patients with POEMS syndrome: a multicentre, randomised, double-blind, placebo-controlled trial. Misawa S, Sato Y, Katayama K, Nagashima K, Aoyagi R, Sekiguchi Y, Sobue G, Koike H, Yabe I, Sasaki H, Watanabe O, Takashima H, Nishizawa M, Kawachi I, Kusunoki S, Mitsui Y, Kikuchi S, Nakashima I, Ikeda S, Kohara N, Kanda T, Kira J, Hanaoka H, Kuwabara S; Japanese POEMS Syndrome for Thalidomide (J-POST) Trial Study Group. . The Lancet, Neurology15 ( 11 ) 1129 - 1137 2016.11Safety and efficacy of thalidomide in patients with POEMS syndrome: a multicentre, randomised, double-blind, placebo-controlled trial. Misawa S, Sato Y, Katayama K, Nagashima K, Aoyagi R, Sekiguchi Y, Sobue G, Koike H, Yabe I, Sasaki H, Watanabe O, Takashima H, Nishizawa M, Kawachi I, Kusunoki S, Mitsui Y, Kikuchi S, Nakashima I, Ikeda S, Kohara N, Kanda T, Kira J, Hanaoka H, Kuwabara S; Japanese POEMS Syndrome for Thalidomide (J-POST) Trial Study Group.Reviewed

Maruyama K, Ogaya S, Kurahashi N, Umemura A, Yamada K, Hashiguchi A, Takashima H, Torres RJ, Aso K. . Arts syndrome with a novel missense mutation in the PRPS1 gene: A case report. . Brain and Development38 ( 10 ) 954 - 958 2016.11 Arts syndrome with a novel missense mutation in the PRPS1 gene: A case report.Reviewed

Yamada K, Yuan J, Mano T, Takashima H, Shibata M. . Arthropathy-related pain in a patient with congenital impairment of pain sensation due to hereditary sensory and autonomic neuropathy type II with a rare mutation in the WNK1/HSN2 gene: a case report. . BMC Neurology16 ( 1 ) 201 - 201 2016.10Arthropathy-related pain in a patient with congenital impairment of pain sensation due to hereditary sensory and autonomic neuropathy type II with a rare mutation in the WNK1/HSN2 gene: a case report.Reviewed

Maki Y, Takashima H . [Clinical Features and Treatment of Hashimoto Encephalopathy . Brain and Nerve68 ( 9 ) 1025 - 1033 2016.9[Clinical Features and Treatment of Hashimoto Encephalopathy

Shiohama Y, Naito T, Matsuzaki T, Tanaka R, Tomoyose T Takashima H, Fukushima T, Tanaka Y, Saito M7. . Absolute quantification of HTLV-1 basic leucine zipper factor (HBZ) protein and its plasma antibody in HTLV-1 infected individuals with different clinical status. . Retrovirology13 ( 29 ) 2016.4Absolute quantification of HTLV-1 basic leucine zipper factor (HBZ) protein and its plasma antibody in HTLV-1 infected individuals with different clinical status.Reviewed

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Papers - TAKASHIMA Hiroshi