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Yu Ming
yu.ming@neuro.ki.se
Curriculum Vitae
Thesis Project
Abstracts
Publications
Curriculum Vitae
Place of Birth: Jinan, China
Nationality: P.R. of China
Current Status: PhD student, Dept. of Neuroscience, Karolinska
Institutet, Stockholm, Sweden
Education
1981-1987: Shandong Medical University, Jinan, Shandong, P.R.China.
Major: Medicine. In 1987, degree received: M.D.
1995-1996: Postgraduate study, Shandong Medical University, Jinan,
Shandong, P.R.China. Graduate course for Master of Science. Major: Immunology
Training
Oct.1996-Sept.1997: Japanese Sasakawa Medical Scholarship, Visiting
scientist,
Growth Factor Division, National Cancer Center Research Institute,
Tokyo, Japan
Sept.1991-Dec.1991: Fellowship of Japan International Cooperation Agency,
Trainiging in Adoptive Immunotherapy of Cancer at Division of Medical
Oncology, National Cancer Center Hospital, Tokyo, Japan
Professional Position
Jan.1998-present: Guest researcher and then PhD student, Dept. of Neuroscience,
Karolinska
Institutet, Stockholm, Sweden ,Wenner-Grenska Samfundet, Konung
Gustaf
V:s och Drotting Victorias Stiftelse
Jan.1989-Sept.1996: Researcher, Shandong Tumor Biotherapy Center,
Shandong Academy of Medical Sciences, Shandong, China
Jul.1987-Dec.1988: Resident physician, Shandong Provincial Hospital,
Shandong, China
Thesis Project
Studies on ageing-related changes in cytokine signaling
in central and peripheral neurons, supportive cells and target tissues
Aging is closely associated with sensorimotor impairment, which seriously
compromises the daily behavioral activities of the elderly. Impairment
of sensorimotor functions in senescence is not associated with any significant
loss of either sensory or motoneurons. Instead, aging is manifested by
loss of neuronal connections, axon dystrophy, myelin aberrations, phenotypic
changes in gene expression pattern, and neuron atrophy in certain cell
populations. Thus, a key issues is: if the neurons are still there, why
don’t they remain connected? Is it due to processes intrinsic to the neurons?
What is the role of the target cell(s) in this process? Are inflammatory
mechanisms of significance? What changes occur in the supportive cell lines?
The project is an attempt to clarify if [changes in] cytokine
signaling (including neurotrophins, neuropoietins, growth factors, interferons,
tumour necrosis factors and interleukins) is involved in aging processes
of neurons, target(s) and supportive cells.
Abstracts
Changed expression of neurotrophins and neurotrophin
receptors in peripheral sensory pathways during aging.
Bergman, E., Fundin, B.T., Ming, Y., Edström, E. and B.
Ulfhake.
Society for neuroscience, 1999. Abstract.
Evidence for decreased neurotrophin-trk
signaling in aged motoneurons.
Edström, E., Johnson, H., Ming, Y., Bergman, E. and B.
Ulfhake.
Society for neuroscience, 1999. Abstract.
Evidence for increased GDNF-GFR?-1/RET signaling
in aged sensory and motor neurons.
Ming, Y., Bergman, E., Edström, E., Kullberg, S. and B.
Ulfhake.
Society for neuroscience, 1999. Abstract.
Publications
Regulation
of neurotrophin signaling in aging sensory and motoneurons. Dissipation of
target support?
Ulfhake B, Bergman E, Edstrom E, Fundin BT, Johnson H, Kullberg S,
Ming Y.
Mol Neurobiol 2000 Jun;21(3):109-35. PubMed
Reciprocal
changes in the expression of neurotrophin mRNAs in target tissues and peripheral
nerves of aged rats.
Ming Y, Bergman E, Edstrom E, Ulfhake B
Neurosci Lett. 1999 Oct 8;273(3):187-90. PubMed
Upregulation
of GFRalpha-1 and c-ret in primary sensory neurons and spinal motoneurons
of aged rats.
Bergman E, Kullberg S, Ming Y, Ulfhake B
J Neurosci Res 1999 Jul 15;57(2):153-65. PubMed,
InterScience
Evidence
for increased GDNF signaling in aged sensory and motor neurons.
Ming Y, Bergman E, Edstrom E, Ulfhake B
Neuroreport 1999 May 14;10(7):1529-35. PubMed
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