Division of Neurology, Saitama Children’s Medical Center, Saitama, Japan | Division of Neurology, Saitama Children's Medical Center, Saitama, Japan. | Division of Neurology, ...
KOL Resume for Shin‐ichiro Hamano
Division of Neurology, Saitama Children’s Medical Center, Saitama, Japan
Division of Neurology, Saitama Children's Medical Center, Saitama, Japan
Department for Child Health and Human Development, Saitama Children's Medical Center, Saitama, Japan
Division of Neurology, Saitama Children's Medical Center.
Department for Child Health and Human Development, Saitama Children's Medical Center, 2-1 Shin-toshin, Chuou-ku, Saitama-city, Saitama 330-8777, Japan.
Division of Neurology, Saitama Children's Medical Center, 1-2, Shintoshin, Chuo-ku, Saitama, Japan. Electronic address:
Division of Neurology, Saitama Children's Medical Center
From the Department of Pediatrics (Y.Y., H. Torisu, R.K., Y.I., Y.S., M.S., T.H.) and Department of Neurology, Neurological Institute (J.K.), Graduate School of Medical Sciences, Kyushu University, Fukuoka; Department of Pediatrics (H. Torisu), Fukuoka Dental College Medical and Dental Hospital, Fukuoka; Department of Pediatrics (T.I.), Yamaguchi University Graduate School of Medicine, Ube; Department of Pediatrics (A.O.), Kyorin University School of Medicine, Hachioji; Department of Pediatrics (T.K.), Tokyo Women's Medical University, Tokyo; Department of Child Development Pediatrics (S. Kimura), Kumamoto University Graduate School, Kumamoto; Division of Neurology (M.K.), National Center for Child Health and Development, Tokyo; Department of Pediatrics (J.T.), Kameda Medical Center, Kamogawa; National Epilepsy Center (Y.T.), Shizuoka Institute of Epilepsy and Neurological Disorders, Shizuoka; Department of Pediatrics (H. Tamai), Osaka Medical College, Takatsuki; Department of Pediatrics (J.N.), Nagoya University Graduate School of Medicine, Nagoya; Department of Neurology (S. Hamano), Saitama Children's Medical Center, Saitama; Department of Neurology (S. Hirabayashi), Nagano Children's Hospital, Azumino; Division of Child Neurology (Y.M.), Faculty of Medicine, Tottori University, Yonago; Department of Developmental Medical Sciences (M.M.), Graduate School of Medicine, The University of Tokyo; Department of Pediatrics (K.M.), Hokkaido Medical Center for Child Health and Rehabilitation, Sapporo; Department of Pediatric Neurology (H.Y.), Nagaoka Habilitation and Medical Center for Severely Handicapped Children, Nagaoka; and Department of Neurology (S. Kusunoki), Kinki University Faculty of Medicine, Osaka-Sayama, Japan.
Division of Neurology, Saitama Children's Medical Center, 2100, Magome, Iwatsuki-ku, Saitama-city, Saitama, 339-8551, Japan
Division of Neurology, Saitama Children's Medical Center, Saitama-city, Saitama, Japan
Division of Neurology, Saitama Children's Medical Center, Saitama 339-8551, Japan
Division of Neurology, Saitama Children's Medical Center, 2100 Magome, Iwatsuki-ku, Saitama, Japan
Division of Neurology, Saitama Children’s Medical Center, 2100, Magome, Iwatsuki-ku, 339-8551, Saitama, Saitama, Japan
Research Committee on Clinical Evidence of Medical Treatment for Status Epilepticus in Childhood, 8-1, Kawata-cho, Shinjuku-ku, Tokyo 162-8666, Japan
Division of Neurology, Saitama Children's Medical Center, 2100, Magome, Iwatsuki‐ku, Saitama‐city, Saitama, Japan
Division of Child Health and Human Development, Saitama Children's Medical Center
Divisions of Neurology, Saitama Children's Medical Center, Iwatsuki.
Division of Neurology, Saitama Children's Medical Center, Iwatsuki, Saitama.
Division of Neurology, Saitama Children’s Medical Center
Division of Neurology; Saitama Children’s Medical Center; Saitama, Japan
Division of Neurology, Saitama Children's Medical Center, Iwatsuki.
Division of Neurology, Saitama Children's Medical Center, 2100 Magome, Iwatsuki, Saitama 339, Japan
Division of Neurology, Saitama Children's Medical Center, 2100 Magome, Iwatsuki, Saitama 339,Japan
Division of Neurology; Saitama Children's Medical Center; Saitama, Japan
Division of Neurology, Saitama Childrens' Medical Center, Iwatsuki.
Division of Neurology, Saitama Children's Medical Centre, 2100 Magome, Iwatsuki, Saitama 339, Japan.
Division of Neurology, Saitama Children’s Medical Center, Iwatsuki, Saitama, Japan;, Department of Pediatrics, Jikei University School of Medicine, Tokyo, Japan;, Department of Neuroanatomy, Nihon University School of Medicine, Tokyo, Japan
Shin‐ichiro Hamano: Influence Statistics
|largesized neurons area||#1|
|gestational age diversity||#1|
|aetiologies unknown aetiology||#1|
|neuronal area neuropil||#1|
|pyridoxal therapy responders||#1|
|33 gw terms||#1|
|acth therapy regimen||#1|
|onset 65 months||#1|
|157 pediatric neurologists||#1|
|designated training facility||#1|
|1235 weeks gestation||#1|
|rcbf regional developmental||#1|
|computerassisted imageanalyser fetuses||#1|
|cryptogenic west syndrome||#1|
|lidocaine multivariate analysis||#1|
|large neurons total||#1|
|development human dorsal||#1|
|development 18 weeks||#1|
|safety 117 patients||#1|
|physicians retreatment spasms||#1|
|preschool colitis escherichia||#1|
|human fetal auditory||#1|
|1261 hz ase||#1|
Open the FULL List in Excel
Prominent publications by Shin‐ichiro Hamano
OBJECTIVE: To investigate the clinical spectrum caused by mutations in PIGA at Xp22.2, which is involved in the biosynthesis of the glycosylphosphatidylinositol (GPI) anchor, among patients with early-onset epileptic encephalopathies (EOEEs).
METHODS: Whole-exome sequencing was performed as a comprehensive genetic analysis for a cohort of 172 patients with EOEEs including early myoclonic encephalopathy, Ohtahara syndrome, and West syndrome, and PIGA mutations were carefully ...
|Known for Piga Mutations | Epileptic Encephalopathies | West Syndrome | Flow Cytometry | Gpianchored Proteins|
The axonal damage marker tau protein in the cerebrospinal fluid is increased in patients with acute encephalopathy with biphasic seizures and late reduced diffusion
[ PUBLICATION ]
Acute encephalopathy with biphasic seizures and late reduced diffusion (AESD) is a recently clinicoradiologically-established encephalopathy syndrome. In the present study, we examined the levels of cerebrospinal fluid (CSF) tau protein, a marker of axonal damage, in 11 patients with AESD. CSF tau levels were normal on day 1 and increased from day 3 of the disease between the initial and the secondary seizures. Magnetic resonance imaging (MRI) reveals reduced diffusion in the subcortical ...
|Known for Biphasic Seizures | Tau Protein | Axonal Damage | Acute Encephalopathy | Cerebrospinal Fluid|
Neurological manifestations of hemorrhagic colitis in the outbreak of Escherichia coli O157:H7 infection in Japan
[ PUBLICATION ]
An outbreak of hemorrhagic colitis associated with Escherichia coli O157:H7 occurred in a kindergarten in Saitama, Japan from September to November, 1990. Seven patients admitted to our hospital showed neurological manifestations: generalized seizures, impaired consciousness, urinary incontinence, gaze nystagmus, phrenic nerve palsy, action tremor and vertigo. Two patients died. On the basis of the clinical courses and laboratory findings of the seven patients and postmortem findings of ...
|Known for Escherichia Coli | H7 Infection | Neurological Manifestations | Generalized Seizures | Bacterial Toxins|
Measurement of pyridoxal 5′-phosphate, pyridoxal, and 4-pyridoxic acid in the cerebrospinal fluid of children
[ PUBLICATION ]
BACKGROUND: We quantified pyridoxal 5'-phosphate (PLP), pyridoxal (PL), and 4-pyridoxic acid (PA) in the cerebrospinal fluid (CSF) of children and to investigate the effect of age, sex, epilepsy, and anti-epileptic drug (AED) therapy on these vitamers.
METHODS: CSF samples prospectively collected from 116 pediatric patients were analyzed. PLP, PL, and PA were measured using high-performance liquid chromatography with fluorescence detection, using pre-column derivatization by ...
|Known for Cerebrospinal Fluid | Plp Pyridoxal | Pyridoxic Acid | Pa Concentrations | Fluorescence Detection|
The spectrum of ZEB2 mutations causing the Mowat–Wilson syndrome in Japanese populations
[ PUBLICATION ]
Mowat-Wilson syndrome (MWS) is a multiple congenital anomaly syndrome characterized by moderate or severe intellectual disability, a characteristic facial appearance, microcephaly, epilepsy, agenesis or hypoplasia of the corpus callosum, congenital heart defects, Hirschsprung disease, and urogenital/renal anomalies. It is caused by de novo heterozygous loss of function mutations including nonsense mutations, frameshift mutations, and deletions in ZEB2 at 2q22. ZEB2 encodes the zinc ...
|Known for Zeb2 Mutations | Mowat–wilson Syndrome | Hirschsprung Disease | Mws Microcephaly | Corpus Callosum|
OBJECTIVE: To investigate the clinical and epidemiologic features of pediatric acquired demyelinating syndromes (ADS) of the CNS in Japan.
METHODS: We conducted a nationwide survey and collected clinical data on children with ADS aged 15 years or younger, who visited hospitals between 2005 and 2007.
RESULTS: Among 977 hospitals enrolled, 723 (74.0%) responded to our inquiries and reported a total of 439 patients as follows: 244 with acute disseminated encephalomyelitis (ADEM), 117 with ...
|Known for Nationwide Survey | Acquired Demyelinating Syndromes | Pediatric Adem | Multiple Sclerosis | Neuromyelitis Optica|
New guidelines for management of febrile seizures in Japan
[ PUBLICATION ]
In 2015, the Japanese Society of Child Neurology released new guidelines for the management of febrile seizures, the first update of such guidelines since 1996. In 1988, the Conference on Febrile Convulsions in Japan published "Guidelines for the Treatment of Febrile Seizures." The Task Committee of the Conference proposed a revised version of the guidelines in 1996; that version released in 1996 was used for the next 19years in Japan for the clinical management of children with febrile ...
|Known for Febrile Seizures | Japanese Society | Child Neurology | Guidelines Management | Humans Japan|
Understanding of and misunderstandings regarding epilepsy: A survey of teachers in schools for special needs education in Japan
[ PUBLICATION ]
The present study surveyed the understanding of epilepsy and attitudes toward epilepsy among teachers in Japanese schools for special needs education. An adapted version of a self-reported questionnaire, consisting of 27 questions, was sent to 3474 teachers at all schools for special needs education in Saitama Prefecture. The response rate to the questionnaire was 62%, corresponding to 2109 valid responses. The responses to three basic questions were as follows: 99% had heard about ...
|Known for Attitudes Epilepsy | Correct Responses | Positive Attitude | Teachers Schools | Health Knowledge|
Novel mutations in Myoclonin1/EFHC1 in sporadic and familial juvenile myoclonic epilepsy
[ PUBLICATION ]
BACKGROUND: Juvenile myoclonic epilepsy (JME) accounts for 3 to 12% of all epilepsies. In 2004, the GENESS Consortium demonstrated four missense mutations in Myoclonin1/EFHC1 of chromosome 6p12.1 segregating in 20% of Hispanic families with JME.
OBJECTIVE: To examine what percentage of consecutive JME clinic cases have mutations in Myoclonin1/EFHC1.
METHODS: We screened 44 consecutive patients from Mexico and Honduras and 67 patients from Japan using heteroduplex analysis and direct ...
|Known for Myoclonic Epilepsy | Myoclonin1 Efhc1 | Missense Mutations | Calcium Binding | Dna Mutational|
Isolated cases of human herpesvirus 6 encephalopathy have recently been reported, although the pathophysiology remains largely unknown. To elucidate the changes specific to human herpesvirus 6 encephalopathy on diagnostic images, this study investigated magnetic resonance imaging findings in 10 patients with a diagnosis of human herpesvirus 6 encephalopathy including diffusion-weighted imaging in 6 of 10, and findings of cerebral blood flow imaging by single-photon emission computed ...
|Known for Human Herpesvirus | Frontal Lobes | Singlephoton Emission | Computed Tomography | Magnetic Resonance|
Epilepsies are common neurological disorders and genetic factors contribute to their pathogenesis. Copy number variations (CNVs) are increasingly recognized as an important etiology of many human diseases including epilepsy. Whole-exome sequencing (WES) is becoming a standard tool for detecting pathogenic mutations and has recently been applied to detecting CNVs. Here, we analyzed 294 families with epilepsy using WES, and focused on 168 families with no causative single nucleotide ...
|Known for Exome Data | Copy Variations | Cnvs Wes | Cnv Detection | Nucleotide Sequencing|
Predictive score for early diagnosis of acute encephalopathy with biphasic seizures and late reduced diffusion (AESD)
[ PUBLICATION ]
Acute encephalopathy with biphasic seizures and late reduced diffusion (AESD) at onset manifests an early seizure (ES) usually lasting more than 30 min. Following ES, some patients exhibit almost clear consciousness with no neurological symptoms, and no MRI abnormality for a few days, which may lead to an initial misdiagnosis of prolonged febrile seizures (PFS). To allow an early diagnosis of AESD, we retrospectively analyzed clinical manifestations, laboratory data, and radiologic and ...
|Known for Acute Encephalopathy | Late Reduced Diffusion | Patients Aesd | Biphasic Seizures | Preschool Diagnosis|
Therapeutic efficacy and adverse effects of adrenocorticotropic hormone therapy in west syndrome: Differences in dosage of adrenocorticotropic hormone, onset of age, and cause
[ PUBLICATION ]
OBJECTIVES: To determine the dosage and factors influencing efficacy of adrenocorticotropic hormone (ACTH) for West syndrome.
STUDY DESIGN: A retrospective study of 135 patients receiving ACTH therapy with a synthetic analogue for initial effect, seizure outcome 1 year after therapy, and adverse effects. Efficacy and adverse effects were compared among the groups divided by clinical factors: dosage, treatment lag, onset age, and cause.
RESULTS: One hundred thirteen patients had seizure ...
|Known for Adrenocorticotropic Hormone | West Syndrome | Acth Therapy | Efficacy Adverse Effects | Age Onset|
Mutations in the neuronal voltage-gated sodium channel alpha-subunit type I gene (SCN1A) were found responsible for severe myoclonic epilepsy in infancy (SMEI). The authors describe novel mutations of SCN1A in Japanese patients with SMEI. They screened 12 unrelated patients and a pair of monozygotic twins and detected 10 mutations that lead to truncation of the protein.
|Known for Myoclonic Epilepsy | Mutations Scn1a | Infancy Smei | Monozygotic Twins | Japanese Patients|
A retrospective multicenter study was conducted, designed to evaluate the efficacy and safety of midazolam for the treatment of status epilepticus. The subjects were 358 inpatients who received intravenous midazolam therapy for status epilepticus. The mean age was 48.6 +/- 46.5 months. The underlying disorder was epilepsy in 195 cases, and acute symptomatic diseases in 163 (encephalitis or encephalopathy in 88 cases). Midazolam was administered as a bolus dose (0.25 +/- 0.21 mg/kg), ...
|Known for Status Epilepticus | Intravenous Midazolam | Seizure Onset | Continuous Infusion | 10 Patients|
Key People For West Syndrome
Shin‐ichiro Hamano:Expert Impact
Concepts for whichShin‐ichiro Hamanohas direct influence:West syndrome, Status epilepticus, Febrile seizures, Tuberous sclerosis, Infantile spasms, Cryptogenic west syndrome, Acute encephalitis, Acute encephalopathy.
Shin‐ichiro Hamano:KOL impact
Concepts related to the work of other authors for whichfor which Shin‐ichiro Hamano has influence:Infantile spasms, Status epilepticus, Febrile seizures, Acute encephalopathy, Dravet syndrome, Severe myoclonic epilepsy, Sodium channel.
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