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English Journal

Recombinant murine calreticulin fragment 39-272 expands CD1d(hi)CD5+ IL-10-secreting B cells that modulate experimental autoimmune encephalomyelitis in C57BL/6 mice.

Hong C, Zhang T, Gao XM.SourceInstitute of Biology and Medical Sciences, Soochow University, Suzhou, China.
Molecular immunology.Mol Immunol.2013 Oct;55(3-4):237-46. doi: 10.1016/j.molimm.2013.02.003. Epub 2013 Mar 21.
Calreticulin (CRT) is a Ca²⁺ binding molecular chaperone in the endoplasmic reticulum, but can also accumulate in soluble form in serum and/or synovial fluid of patients with rheumatic disorders. We have recently shown that a prokaryotically expressed recombinant CRT fragment 39-272 (rCRT/39-272)
PMID 23523122

Prominent fatigue in spinal muscular atrophy and spinal and bulbar muscular atrophy: Evidence of activity-dependent conduction block.

Noto Y, Misawa S, Mori M, Kawaguchi N, Kanai K, Shibuya K, Isose S, Nasu S, Sekiguchi Y, Beppu M, Ohmori S, Nakagawa M, Kuwabara S.SourceDepartment of Neurology, Graduate School of Medicine, Chiba University, Chiba, Japan; Department of Neurology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan. Electronic address: y-noto@koto.kpu-m.ac.jp.
Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology.Clin Neurophysiol.2013 Sep;124(9):1893-8. doi: 10.1016/j.clinph.2012.12.053. Epub 2013 Apr 30.
OBJECTIVES: To clarify whether patients with spinal muscular atrophy (SMA) or spinal and bulbar muscular atrophy (SBMA) suffer disabling muscle fatigue, and whether activity-dependent conduction block (ADCB) contributes to their fatigue. ADCB is usually caused by reduced safety factor for impulse tr
PMID 23643309

FGF2 and FGFR1 signaling regulate functional recovery following cuprizone demyelination.

Mierzwa AJ, Zhou YX, Hibbits N, Vana AC, Armstrong RC.SourceDepartment of Anatomy, Physiology and Genetics, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814, United States; Center for Neuroscience and Regenerative Medicine, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814, United States.
Neuroscience letters.Neurosci Lett.2013 Aug 26;548:280-5. doi: 10.1016/j.neulet.2013.05.010. Epub 2013 May 14.
In demyelinating diseases, such as multiple sclerosis, remyelination offers the potential to recover function of viable denuded axons by restoring saltatory conduction and/or protecting from further damage. Mice with genetic reduction of fibroblast growth factor 2 (Fgf2) or Fgf receptor 1 (Fgfr1) ex
PMID 23684572