S Hirose

Summary

Affiliation: Fukuoka University
Country: Japan

Publications

  1. pmc The kick-in system: a novel rapid knock-in strategy
    Yuko Tomonoh
    Department of Pediatrics, School of Medicine, Fukuoka University, Fukuoka, Japan
    PLoS ONE 9:e88549. 2014
  2. pmc Novel HCN2 mutation contributes to febrile seizures by shifting the channel's kinetics in a temperature-dependent manner
    Yuki Nakamura
    Department of Pediatrics, Faculty of Medicine, Fukuoka University, Fukuoka, Japan The Research Institute for the Molecular Pathomechanisms of Epilepsy, Fukuoka University, Fukuoka, Japan
    PLoS ONE 8:e80376. 2013
  3. pmc Identification of ATP1A3 mutations by exome sequencing as the cause of alternating hemiplegia of childhood in Japanese patients
    Atsushi Ishii
    Department of Pediatrics, School of Medicine, Fukuoka University, Fukuoka, Japan
    PLoS ONE 8:e56120. 2013
  4. pmc A human Dravet syndrome model from patient induced pluripotent stem cells
    Norimichi Higurashi
    Department of Pediatrics, School of Medicine, Fukuoka University, 45 1, 7 chome, Nanakuma, Jonan ku, Fukuoka 814 0180, Japan
    Mol Brain 6:19. 2013
  5. doi request reprint SCN1A testing for epilepsy: application in clinical practice
    Shinichi Hirose
    Department of Pediatrics and Research Institute for the Molecular Pathomechanisms of Epilepsy, Fukuoka University, Fukuoka, Japan
    Epilepsia 54:946-52. 2013
  6. ncbi request reprint Molecular genetics of human familial epilepsy syndromes
    Shinichi Hirose
    Department of Pediatrics, School of Medicine, Fukuoka University, Fukuoka, and Department of Neuropsychiatry, School of Medicine, Hirosaki University, Hirosaki, Japan
    Epilepsia 43:21-5. 2002
  7. ncbi request reprint X-linked mental retardation and epilepsy: pathogenetic significance of ARX mutations
    Shinichi Hirose
    Department of Pediatrics, School of Medicine, Fukuoka University, 45 1, 7 chome Nanakuma, Jonan ku, Fukuoka 814 0180, Japan
    Brain Dev 25:161-5. 2003
  8. ncbi request reprint Genetic abnormalities underlying familial epilepsy syndromes
    Shinichi Hirose
    Department of Pediatrics, School of Medicine, Fukuoka University, 45 1, 7 chome Nanakuma, Jonan ku, Japan
    Brain Dev 24:211-22. 2002
  9. ncbi request reprint The genetics of febrile seizures and related epilepsy syndromes
    Shinichi Hirose
    Department of Pediatrics, School of Medicine, Fukuoka University, 45 1, 7 chome Nanakuma, Jonan ku, Fukuoka 814 0180, Japan
    Brain Dev 25:304-12. 2003
  10. ncbi request reprint Genetics of idiopathic epilepsies
    Shinichi Hirose
    Department of Pediatrics, School of Medicine, Fukuoka University, Fukuoka, Japan
    Epilepsia 46:38-43. 2005

Collaborators

Detail Information

Publications58

  1. pmc The kick-in system: a novel rapid knock-in strategy
    Yuko Tomonoh
    Department of Pediatrics, School of Medicine, Fukuoka University, Fukuoka, Japan
    PLoS ONE 9:e88549. 2014
    ....
  2. pmc Novel HCN2 mutation contributes to febrile seizures by shifting the channel's kinetics in a temperature-dependent manner
    Yuki Nakamura
    Department of Pediatrics, Faculty of Medicine, Fukuoka University, Fukuoka, Japan The Research Institute for the Molecular Pathomechanisms of Epilepsy, Fukuoka University, Fukuoka, Japan
    PLoS ONE 8:e80376. 2013
    ..Thus, mutant HCN2 channels cause significant cAMP-independent enhanced availability of I h during high temperatures, which may contribute to hyperthermia-induced neuronal hyperexcitability in some individuals with FS. ..
  3. pmc Identification of ATP1A3 mutations by exome sequencing as the cause of alternating hemiplegia of childhood in Japanese patients
    Atsushi Ishii
    Department of Pediatrics, School of Medicine, Fukuoka University, Fukuoka, Japan
    PLoS ONE 8:e56120. 2013
    ..S. and Europe have described ATP1A3 mutations in AHC. However, the genotype-phenotype relationship remains unclear. The purpose of this study was to identify the genetic abnormality in a Japanese cohort of AHC using exome analysis...
  4. pmc A human Dravet syndrome model from patient induced pluripotent stem cells
    Norimichi Higurashi
    Department of Pediatrics, School of Medicine, Fukuoka University, 45 1, 7 chome, Nanakuma, Jonan ku, Fukuoka 814 0180, Japan
    Mol Brain 6:19. 2013
    ..However, no such effort has been reported to date. We here report a cellular model for DS that utilizes patient-derived iPSCs...
  5. doi request reprint SCN1A testing for epilepsy: application in clinical practice
    Shinichi Hirose
    Department of Pediatrics and Research Institute for the Molecular Pathomechanisms of Epilepsy, Fukuoka University, Fukuoka, Japan
    Epilepsia 54:946-52. 2013
    ..Obtaining written informed consent and genetic counseling should be considered prior to molecular testing, depending on the clinical situation and local regulations...
  6. ncbi request reprint Molecular genetics of human familial epilepsy syndromes
    Shinichi Hirose
    Department of Pediatrics, School of Medicine, Fukuoka University, Fukuoka, and Department of Neuropsychiatry, School of Medicine, Hirosaki University, Hirosaki, Japan
    Epilepsia 43:21-5. 2002
    ..Our working hypothesis is to view certain idiopathic epilepsies as disorders of ion channels (i.e., "channelopathies"). Such a hypothesis should provide a new insight into our understanding of the genetic background of epilepsy...
  7. ncbi request reprint X-linked mental retardation and epilepsy: pathogenetic significance of ARX mutations
    Shinichi Hirose
    Department of Pediatrics, School of Medicine, Fukuoka University, 45 1, 7 chome Nanakuma, Jonan ku, Fukuoka 814 0180, Japan
    Brain Dev 25:161-5. 2003
    ..These findings provide solid evidence for the relationship between MR and epilepsy at a molecular level, opening a new avenue for understanding the pathogeneses of MR associated with epilepsy...
  8. ncbi request reprint Genetic abnormalities underlying familial epilepsy syndromes
    Shinichi Hirose
    Department of Pediatrics, School of Medicine, Fukuoka University, 45 1, 7 chome Nanakuma, Jonan ku, Japan
    Brain Dev 24:211-22. 2002
    ..Our working hypothesis is to view certain idiopathic epilepsies as disorders of ion channels, i.e. 'channelopathies'. Such hypothesis should provide a new insight to our understanding of the genetic background of epilepsy...
  9. ncbi request reprint The genetics of febrile seizures and related epilepsy syndromes
    Shinichi Hirose
    Department of Pediatrics, School of Medicine, Fukuoka University, 45 1, 7 chome Nanakuma, Jonan ku, Fukuoka 814 0180, Japan
    Brain Dev 25:304-12. 2003
    ..This hypothesis may facilitate our understanding of the genetic background of FS...
  10. ncbi request reprint Genetics of idiopathic epilepsies
    Shinichi Hirose
    Department of Pediatrics, School of Medicine, Fukuoka University, Fukuoka, Japan
    Epilepsia 46:38-43. 2005
    ..Genetic defects have been identified recently in certain inherited epilepsy syndromes in which the phenotypes are similar to those of common idiopathic epilepsies...
  11. ncbi request reprint Are some idiopathic epilepsies disorders of ion channels?: A working hypothesis
    S Hirose
    Department of Pediatrics, School of Medicine, Fukuoka University, 45 1, 7 chome Nanakuma, Jonan ku, 814 0180, Fukuoka, Japan
    Epilepsy Res 41:191-204. 2000
    ..A working hypothesis to view certain idiopathic epilepsies as disorders of ion channels should provide a new insight to our understanding of epilepsy and allow the design of novel therapies...
  12. ncbi request reprint [Child neurology in Asia]
    S Hirose
    No To Hattatsu 36:141-2. 2004
  13. ncbi request reprint A new paradigm of channelopathy in epilepsy syndromes: intracellular trafficking abnormality of channel molecules
    Shinichi Hirose
    Department of Pediatrics, Fukuoka University, 45 1, 7 chome Nanakuma, Jonan ku, Fukuoka 814 0180, Japan
    Epilepsy Res 70:S206-17. 2006
    ....
  14. ncbi request reprint Phenotypes and genotypes in epilepsy with febrile seizures plus
    M Ito
    Department of Pediatrics, Shiga Medical Center for Children, 5 7 30 Moriyama, Moriyama 524 0022, Japan
    Epilepsy Res 70:S199-205. 2006
    ..There is a possibility of simultaneous involvement of multiple genes for seizure phenotypes...
  15. ncbi request reprint Effect of localization of missense mutations in SCN1A on epilepsy phenotype severity
    K Kanai
    Department of Neuropsychiatry, Hirosaki University School of Medicine, 5 Zaifu cho, Hirosaki, Aomori 036 8562, Japan
    Neurology 63:329-34. 2004
    ..The authors analyzed the localization of missense mutations in SCN1A identified in patients with GEFS+ and SMEI to clarify the phenotype-genotype relationships...
  16. ncbi request reprint Electroclinical picture of autosomal dominant nocturnal frontal lobe epilepsy in a Japanese family
    M Ito
    Department of Pediatrics, Shiga Medical Center for Children, Moriyama, Japan
    Epilepsia 41:52-8. 2000
    ..The aim of this report is precisely to describe the electroclinical manifestations of ADNFLE in this family and to compare these findings with those of other families reported previously in the literature...
  17. ncbi request reprint Gene expression of human squamous cell carcinoma antigens 1 and 2 in human cell lines
    K Hamada
    Department of Obstetrics and Gynecology, School of Medicine, Ehime University, Shitsukawa, Ehime 791 0295, Japan
    Oncol Rep 8:347-54. 2001
    ....
  18. ncbi request reprint Autosomal dominant epilepsy with febrile seizures plus with missense mutations of the (Na+)-channel alpha 1 subunit gene, SCN1A
    M Ito
    Department of Pediatrics, Shiga Medical Center for Children, 5 7 30 Moriyama, Moriyama 524 0022, Japan
    Epilepsy Res 48:15-23. 2002
    ..The spectrum of GEFS+ should be expanded to include partial epilepsies and better to be termed autosomal dominant epilepsy with febrile seizures plus (ADEFS+)...
  19. doi request reprint Focal epilepsy resulting from a de novo SCN1A mutation
    A Okumura
    Department of Pediatrics, Juntendo University School of Medicine, Tokyo, Japan
    Neuropediatrics 38:253-6. 2007
    ..Genetic analysis showed a heterozygous missense mutation (c.5311A>T: I1771F) in the patient, which was not detected in her parents...
  20. ncbi request reprint A novel mutation of KCNQ3 (c.925T-->C) in a Japanese family with benign familial neonatal convulsions
    S Hirose
    Department of Pediatrics, School of Medicine, Fukuoka University, Japan
    Ann Neurol 47:822-6. 2000
    ..925T-->C replaced Trp309, a conserved residue within the P-loop of the KCNQ potassium channel family that holds the channel pore open, with an Arg (W309R). We report c.925T-->C as the second mutation of KCNQ3 responsible for BFNC2...
  21. doi request reprint Novel de novo splice-site mutation of SCN1A in a patient with partial epilepsy with febrile seizures plus
    Akira Kumakura
    Department of Pediatrics, Kitano Hospital, The Tazuke Kofukai Medical Institute, Ohgimachi, Kita ku, Osaka 530 8480, Japan
    Brain Dev 31:179-82. 2009
    ..We present the first case report of partial epilepsy with FS+ associated with a truncation mutation of SCN1A. The possibility exists for concomitant involvement of multiple genes other than SCN1A for seizure phenotypes...
  22. ncbi request reprint A novel mutation of CHRNA4 responsible for autosomal dominant nocturnal frontal lobe epilepsy
    S Hirose
    Department of Pediatrics, School of Medicine, Fukuoka University, Japan
    Neurology 53:1749-53. 1999
    ..To identify the mutation responsible for autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) in a nonwhite family...
  23. ncbi request reprint Mutations of neuronal voltage-gated Na+ channel alpha 1 subunit gene SCN1A in core severe myoclonic epilepsy in infancy (SMEI) and in borderline SMEI (SMEB)
    Goryu Fukuma
    Department of Pediatrics, Fukuoka University, Japan
    Epilepsia 45:140-8. 2004
    ..The aim of this study was to delineate the genetic correlation between core SMEI and SMEB and to estimate the frequency of mutations in both phenotypes...
  24. ncbi request reprint Deletions involving both KCNQ2 and CHRNA4 present with benign familial neonatal seizures
    H Kurahashi
    Department of Pediatrics, School of Medicine, Fukuoka University, Japan
    Neurology 73:1214-7. 2009
    ..This study set out to determine the frequency of microchromosomal deletions of KCNQ2 or KCNQ3 associated with BFNS...
  25. doi request reprint Developmental changes in KCNQ2 and KCNQ3 expression in human brain: possible contribution to the age-dependent etiology of benign familial neonatal convulsions
    Takeshi Kanaumi
    Department of Pediatrics, School of Medicine, Fukuoka University, 45 1, 7 chome Nanakuma, Jonan ku, Fukuoka 814 0180, Japan
    Brain Dev 30:362-9. 2008
    ..Simultaneous and high expressions of KCNQ2 and KCNQ3 were observed in each region from late fetal life to early infancy, coinciding with the time when BFNC occurs. Such coexpression may contribute to the pathogenesis of BFNC...
  26. ncbi request reprint [Sympathetic skin response in patients with severe motor and intellectual disabilities]
    Atsushi Ogawa
    Department of Pediatrics, School of Medicine, Fukuoka University, Fukuoka
    No To Hattatsu 39:347-50. 2007
    ....
  27. ncbi request reprint Carnitine palmitoyltransferase II deficiency due to a novel gene variant in a patient with rhabdomyolysis and ARF
    Hidetoshi Kaneoka
    Department of Internal Medicine, Division of Nephrology and Rheumatology, Fukuoka University School of Medicine, Fukuoka, Japan
    Am J Kidney Dis 45:596-602. 2005
    ..Genetic analysis of the patient identified a novel variant of the CPT II gene...
  28. doi request reprint Altered KCNQ3 potassium channel function caused by the W309R pore-helix mutation found in human epilepsy
    Akira Uehara
    Department of Physiology, School of Medicine, Fukuoka University, 45 1, 7 chome Nanakuma, Jonan ku, Fukuoka 814 0180, Japan
    J Membr Biol 222:55-63. 2008
    ..This pore-helix mutation, if occurs in the brain M channels, could thus lead to a channel dysfunction sufficient to trigger epileptic hyperexcitability...
  29. ncbi request reprint Neuropathology of methylmalonic acidemia in a child
    Takeshi Kanaumi
    Department of Pediatrics, School of Medicine, Fukuoka University, Fukuoka, Japan
    Pediatr Neurol 34:156-9. 2006
    ....
  30. ncbi request reprint Age-dependent modulation of hippocampal excitability by KCNQ-channels
    Motohiro Okada
    Department of Neuropsychiatry, Hirosaki University, 036 8562, Hirosaki, Japan
    Epilepsy Res 53:81-94. 2003
    ....
  31. ncbi request reprint Developmental changes in the expression of GABAA receptor alpha 1 and gamma 2 subunits in human temporal lobe, hippocampus and basal ganglia: an implication for consideration on age-related epilepsy
    Takeshi Kanaumi
    Department of Pediatrics, School of Medicine, Fukuoka University, Jonan ku, Fukuoka 814 0180, Japan
    Epilepsy Res 71:47-53. 2006
    ..These developmental changes in the expression of these subunits may contribute to the age dependency in some epilepsy syndromes where deficiency of GABARA1 and GABARG2 is involved...
  32. ncbi request reprint Biphasic actions of topiramate on monoamine exocytosis associated with both soluble N-ethylmaleimide-sensitive factor attachment protein receptors and Ca(2+)-induced Ca(2+)-releasing systems
    M Okada
    Department of Neuropsychiatry, School of Medicine, Hirosaki University, Hirosaki 036 8562, Japan
    Neuroscience 134:233-46. 2005
    ....
  33. doi request reprint Missense mutation of the sodium channel gene SCN2A causes Dravet syndrome
    Xiuyu Shi
    Department of Pediatrics, School of Medicine, Fukuoka University, Fukuoka 814 0180, Japan
    Brain Dev 31:758-62. 2009
    ..This finding suggests that both nonsense mutations and missense SCN2A mutations cause Dravet syndrome...
  34. doi request reprint Microchromosomal deletions involving SCN1A and adjacent genes in severe myoclonic epilepsy in infancy
    Ji Wen Wang
    Department of Pediatrics, School of Medicine, Fukuoka University, Fukuoka, Japan
    Epilepsia 49:1528-34. 2008
    ..Microchromosomal deletions have been recently reported as additional causes of SMEI. This study examines whether such microdeletions are associated with SMEI as well as with SMEB...
  35. ncbi request reprint Seizure phenotypes of a family with missense mutations in SCN2A
    Masatoshi Ito
    Department of Pediatrics, Shiga Medical Center for Children, Moriyama, Japan
    Pediatr Neurol 31:150-2. 2004
    ..However, it is suggested that the penetrance rate of this pedigree is extremely low, or that other genes may have modified the phenotype of the proband...
  36. ncbi request reprint Severe myoclonic epilepsy in infancy: clinical analysis and relation to SCN1A mutations in a Japanese cohort
    Hirokazu Oguni
    Department of Pediatrics, Tokyo Women s Medical University, Tokyo, Japan
    Adv Neurol 95:103-17. 2005
  37. ncbi request reprint Genetics of epilepsy: current status and perspectives
    Sunao Kaneko
    Department of Neuropsychiatry, Hirosaki University, Hirosaki 036 8562, Japan
    Neurosci Res 44:11-30. 2002
    ..Based upon these findings, pathogenesis of epilepsy as a channelopathy and perspectives of molecular study of epilepsy are discussed...
  38. ncbi request reprint [Genetic approach to the pathogeneses of epilepsy]
    Shinichi Hirose
    Department of Pediatrics, School of Medicine, Fukuoka University
    Rinsho Shinkeigaku 44:975-8. 2004
    ..However, the similarities in symptomatology between such familial epilepsies and common idiopathic epilepsy may provide us with clues to the genetics of common idiopathic epilepsies...
  39. doi request reprint A de novo KCNQ2 mutation detected in non-familial benign neonatal convulsions
    Atsushi Ishii
    Department of Pediatrics, School of Medicine, Fukuoka University, 45 1, 7 chome Nanakuma, Jonan ku, Fukuoka 814 0180, Japan
    Brain Dev 31:27-33. 2009
    ..Yet, few genetic abnormalities have been reported for commoner epilepsy, i.e., sporadic idiopathic epilepsy, which share a phenotype similar to those of familial epilepsy...
  40. ncbi request reprint Mutation (Ser284Leu) of neuronal nicotinic acetylcholine receptor alpha 4 subunit associated with frontal lobe epilepsy causes faster desensitization of the rat receptor expressed in oocytes
    Nobuaki Matsushima
    Department of Biology, Faculty of Science, Kyushu University, 10 1, 6 chome Hakozaki Higashi ku, 812 8581, Fukuoka, Japan
    Epilepsy Res 48:181-6. 2002
    ....
  41. doi request reprint Positive association between benign familial infantile convulsions and LGI4
    Atsushi Ishii
    Department of Pediatrics, School of Medicine, Fukuoka University, Jonanku, Fukuoka, Japan
    Brain Dev 32:538-43. 2010
    ..LGI4 belongs to a family of proteins with the epilepsy-associated repeat (EAR) domain and is associated with various epilepsies. We investigated whether LGI4 is a candidate gene for BFIC...
  42. ncbi request reprint Molecular cloning of human squamous cell carcinoma antigen 1 gene and characterization of its promoter
    K Hamada
    Department of Obstetrics and Gynecology, School of Medicine, Ehime University, Shitsukawa, Shigenobu, Osen gun, Ehime 791 0295, Japan
    Biochim Biophys Acta 1518:124-31. 2001
    ....
  43. ncbi request reprint Proximal symphalangism with "coarse" facial appearance, mixed hearing loss, and chronic renal failure: new malformation syndrome?
    J Morimoto
    Fukuoka University Hospital Kidney Center, Fukuoka University School of Medicine, Fukuoka, Japan
    Am J Med Genet 98:269-72. 2001
    ..These clinical manifestations indicate a hitherto undescribed combination of manifestations and nephropathy...
  44. ncbi request reprint Effect of growth hormone on high plasma levels of glucagon-like peptide-1 (GLP-1) in hypophysectomized rats
    K Tateishi
    Department of Biochemistry, Fukuoka University School of Medicine, Fukuoka, Japan
    Exp Clin Endocrinol Diabetes 110:361-3. 2002
    ..These results suggested that secretion of GLP-1 might be influenced by the function of GH...
  45. doi request reprint Rats harboring S284L Chrna4 mutation show attenuation of synaptic and extrasynaptic GABAergic transmission and exhibit the nocturnal frontal lobe epilepsy phenotype
    Gang Zhu
    Department of Neuropsychiatry, Institute of Brain Science, Graduate School of Medicine, Hirosaki University, Hirosaki 036 8562, Japan
    J Neurosci 28:12465-76. 2008
    ..The currently available genetically engineered animal models of epilepsy are limited to mice; thus, our transgenic rats offer another dimension to the epilepsy research field...
  46. ncbi request reprint Lack of potassium current in W309R mutant KCNQ3 channel causing benign familial neonatal convulsions (BFNC)
    Yoshihiro Sugiura
    Department of Neurology, Fukushima Medical University, School of Medicine, Fukushima, Japan
    Epilepsy Res 84:82-5. 2009
    ..We found a lack of potassium current in W309R mutant KCNQ3 and KCNQ2 channels, which can explain the hyper-excitability of CNS in patients with BFNC...
  47. ncbi request reprint Identification and characterization of temperature-sensitive mild mutations in three Japanese patients with nonsevere forms of very-long-chain acyl-CoA dehydrogenase deficiency
    Yuichi Takusa
    Department of Pediatrics, Shimane Medical University, Izumo, Shimane 693 8501, Japan
    Mol Genet Metab 75:227-34. 2002
    ..Expression analysis at 30 degrees C may be more useful for evaluating these missense mutations, compared with that at 37 degrees C...
  48. doi request reprint Mutational analysis of GABRG2 in a Japanese cohort with childhood epilepsies
    Xiuyu Shi
    Department of Pediatrics, School of Medicine, Fukuoka University, Fukuoka, Japan
    J Hum Genet 55:375-8. 2010
    ..This mutation in such an important position may hamper the function of the channel and contribute to the case's pathogenesis of GTCS...
  49. ncbi request reprint Protein kinase associated with gating and closing transmission mechanisms in temporoammonic pathway
    Motohiro Okada
    Department of Neuropsychiatry, Hirosaki University, Zaifu cho 5, Hirosaki 036 8562, Japan
    Neuropharmacology 47:485-504. 2004
    ..Thus, GABAergic inhibition, which is regulated by PKC activity, in the temporoammonic pathway is more significant than that in the trisynaptic pathway...
  50. ncbi request reprint [Criteria for differential diagnosis of epilepsy and long QT syndrome presenting with seizures and EEG abnormalities]
    Ayumi Yamamoto
    Department of Pediatrics, Fukuoka Tokusyukai Medical Center, Fukuoka
    No To Hattatsu 41:442-6. 2009
    ....
  51. ncbi request reprint An infant with a mitochondrial A3243G mutation demonstrating the MELAS phenotype
    Takeshi Kanaumi
    Department of Pediatrics, School of Medicine, Fukuoka University, Fukuoka, Japan
    Pediatr Neurol 34:235-8. 2006
    ..This case suggests that MELAS can develop in early infancy with its typical clinical presentation. The high percentage of A3243G may contribute to the early onset of the MELAS phenotype in this patient...
  52. doi request reprint Phenotype for activated tissue macrophages in histiocytic necrotizing lymphadenitis
    Yuko Nomura
    Department of Pathology, School of Medicine, Kurume University, Kurume 830 0011, Japan
    Pathol Int 59:631-5. 2009
    ..It is suggested that these characteristic tissue macrophages may be associated with the pathogenesis of HNL and that M2 macrophages may infiltrate to repair the lymphoid tissue injured by cytotoxic T cells in HNL...
  53. ncbi request reprint Both 3,4-dihydroxyphenylalanine and dopamine releases are regulated by Ca2+-induced Ca2+ releasing system in rat striatum
    Gang Zhu
    Department of Neuropsychiatry, Hirosaki University, Hirosaki 036 8562, Japan
    Neurosci Lett 362:244-8. 2004
    ....
  54. ncbi request reprint Late-onset ornithine transcarbamylase deficiency in male patients: prognostic factors and characteristics of plasma amino acid profile
    Eimei Harada
    Department of Pediatrics and Child Health, Kurume University School of Medicine, Asahi machi, Kurume, Japan
    Pediatr Int 48:105-11. 2006
    ..The aim of this study was to determine the prognostic factors that affect the prognosis of life, to explore a basis for therapeutic strategy...
  55. ncbi request reprint Mutations in the NHLRC1 gene are the common cause for Lafora disease in the Japanese population
    Shweta Singh
    Department of Biological Sciences and Bioengineering, Indian Institute of Technology, Kanpur, India
    J Hum Genet 50:347-52. 2005
    ..Our study, in addition to documenting the genetic and molecular heterogeneity observed for LD, suggests that mutations in the NHLRC1 gene may be a common cause of LD in the Japanese population...
  56. ncbi request reprint Involvement of Ca(2+)-induced Ca2+ releasing system in interleukin-1beta-associated adenosine release
    Gang Zhu
    Department of Neuropsychiatry, Hirosaki University School of Medicine, Hirosaki 036 8562, Japan
    Eur J Pharmacol 532:246-52. 2006
    ....
  57. ncbi request reprint Development of highly functional long-term culture method of liver slice embedded in agarose gel for bioartificial liver
    Hideki Nonaka
    Department of Functional Polymer Science, Faculty of Textile Science and Technology, Shinshu University 3 15 1 Tokida, Ueda 386 8567, Japan
    Cell Transplant 12:491-8. 2003
    ..In the future, it is possible that this method could be used to develop a highly functional bioartificial liver...
  58. ncbi request reprint Mutation screening of AP3M2 in Japanese epilepsy patients
    Ming Chih Huang
    Comparative Systems Biology Team, Genomic Sciences Center, RIKEN, 1 7 22 Suehiro cho, Tsurumi ku, Yokohama 230 0045, Japan
    Brain Dev 29:462-7. 2007
    ....