Genomes and Genes


Nobuhiro Yuki



  1. Rodella U, Negro S, Scorzeto M, Bergamin E, Jalink K, Montecucco C, et al. Schwann cells are activated by ATP released from neurons in an in vitro cellular model of Miller Fisher syndrome. Dis Model Mech. 2017;10:597-603 pubmed publisher
  2. Chan Y, Therimadasamy A, Sainuddin N, Wilder Smith E, Yuki N. Serial electrophysiological studies in a Guillain-Barré subtype with bilateral facial neuropathy. Clin Neurophysiol. 2016;127:1694-1699 pubmed publisher
    ..Serial NCS suggests that the bifacial GBS subtype is demyelinating in nature. This study provides further evidence for a bifacial subtype of GBS with a demyelinating pathophysiology. ..
  3. Miyaji K, Paul F, Shahrizaila N, Umapathi T, Yuki N. Autoantibodies to tetraspanins (CD9, CD81 and CD82) in demyelinating diseases. J Neuroimmunol. 2016;291:78-81 pubmed publisher
    ..It is unlikely that these autoantibodies are pathogenic or serve as potential biomarkers in demyelinating diseases. ..
  4. Ishii J, Yuki N, Kawamoto M, Yoshimura H, Kusunoki S, Kohara N. Recurrent Guillain-Barré syndrome, Miller Fisher syndrome and Bickerstaff brainstem encephalitis. J Neurol Sci. 2016;364:59-64 pubmed publisher
    ..Recurrences occurred more frequently in patients with MFS or BBE compared with those with GBS. Patients with recurrent MFS might be younger than those with non-recurrent MFS. ..
  5. Sudo M, Miyaji K, Späth P, Morita Matsumoto K, Yamaguchi Y, Yuki N. Polyclonal IgM and IgA block in vitro complement deposition mediated by anti-ganglioside antibodies in autoimmune neuropathies. Int Immunopharmacol. 2016;40:11-15 pubmed publisher
    ..Although the safety concerns about the use of IgM and IgA for an immunotherapy still remain, IgM and IgA may serve as an alternative immunotherapy in those anti-ganglioside antibody-mediated neuropathies. ..
  6. Wang Q, Xing C, Hao Y, Shi Q, Qi Z, Lv Z, et al. Memory B cells in Guillain-Barré syndrome. J Neuroimmunol. 2017;305:1-4 pubmed publisher
    ..Our study provides the evidences that memory B cells may be involved in mechanism of GBS. ..
  7. Devaux J, Miura Y, Fukami Y, Inoue T, Manso C, Belghazi M, et al. Neurofascin-155 IgG4 in chronic inflammatory demyelinating polyneuropathy. Neurology. 2016;86:800-7 pubmed publisher
    ..The autoantibodies may serve as a biomarker to improve patients' diagnosis and guide treatments. ..
  8. Miyaji K, Furukawa J, Suzuki Y, Yamamoto N, Shinohara Y, Yuki N. Altered gene expression of glycosyltransferases and sialyltransferases and total amount of glycosphingolipids following herpes simplex virus infection. Carbohydr Res. 2016;434:37-43 pubmed publisher
    ..HSV-1 and HSV-2 infections resulted in changes in the total amount of gangliosides depending on the cell lines used and type of virus. Qualitative changes caused by each infection of HSV-1 and HSV-2 were almost negligible. ..
  9. Wakerley B, Kokubun N, Funakoshi K, Nagashima T, Hirata K, Yuki N. Clinical classification of 103 Japanese patients with Guillain-Barré syndrome. J Neurol Sci. 2016;369:43-47 pubmed publisher
    ..Application of the new clinical diagnostic criteria allowed accurate retrospective diagnosis and classification of GBS and MFS subtypes. ..

More Information


  1. Wang Y, Shi Q, Lv H, Hu M, Wang W, Wang Q, et al. IgG-degrading enzyme of Streptococcus pyogenes (IdeS) prevents disease progression and facilitates improvement in a rabbit model of Guillain-Barré syndrome. Exp Neurol. 2017;291:134-140 pubmed publisher
    ..Our data support that IdeS treatment is a promising therapeutic strategy for GBS. ..