The training of undergraduates, medical students, predoctoral and postdoctoral students, as well as the general public, organized by the Education and Training Core, is an integral part of this Wellstone Center proposal on "Biomarkers for Therapy of FSHD." The core's goal is to train the next generation of laboratory and clinician scientists in muscular dystrophy. By targeting students at multiple different levels of training from medical students through postdoctoral fellows, the core aims to increase the number of investigators in the field and to provide them with skills, through mentoring and assistance, to facilitate their transistion to productive, independent careers in muscular dystrophy research. During the previous grant award period, the Education Core has been a particular strength of our Wellstone having initiated a undergraduate student course in muscular dystrophy, trained predoctoral and postdoctoral laboratory students and a clinician scientist, several of whom have gone on to receive independent awards. The Core will continue to provide funding for 2 trainees for all projects involved in this proposal and will continue to involve 12 students from our Wellstone's participating insitutions funded by other mechanisms per year. It will be directed by Drs. Wagner (Core Director), Emerson (PI and Core Co-Director) and Brown (Core Co-Director) who with oversight by the Center Advisory Committee and NIH staff, will work with Center investigators to recruit, appoint, fund and mentor trainees. To enhance training of the students and to educate more broadly all FSHD investigators as well as FSHD patients, the Educational Core will include an annual internal Wellstone retreat, a biennial meeting with a FSH patient group, and an international research conference on FSHD.
FSHD research has gained considerable momentum in the past five years from the creation of this Wellstone as well as support of other collaborating groups. To maintain this momentum and to carry discoveries into the clinic, the number of both laboratory and clinical researchers trained in FSHD needs to grow. The Educational and Training Core of our Wellstone will address this need in the community.
|Zhang, Yuanfan; King, Oliver D; Rahimov, Fedik et al. (2014) Human skeletal muscle xenograft as a new preclinical model for muscle disorders. Hum Mol Genet 23:3180-8|
|Mitsuhashi, Hiroaki; Mitsuhashi, Satomi; Lynn-Jones, Taylor et al. (2013) Expression of DUX4 in zebrafish development recapitulates facioscapulohumeral muscular dystrophy. Hum Mol Genet 22:568-77|
|Rahimov, Fedik; Kunkel, Louis M (2013) The cell biology of disease: cellular and molecular mechanisms underlying muscular dystrophy. J Cell Biol 201:499-510|
|Homma, Sachiko; Chen, Jennifer C J; Rahimov, Fedik et al. (2012) A unique library of myogenic cells from facioscapulohumeral muscular dystrophy subjects and unaffected relatives: family, disease and cell function. Eur J Hum Genet 20:404-10|
|Homma, Sachiko; Beermann, Mary Lou; Miller, Jeffrey Boone (2011) Peripheral nerve pathology, including aberrant Schwann cell differentiation, is ameliorated by doxycycline in a laminin-?2-deficient mouse model of congenital muscular dystrophy. Hum Mol Genet 20:2662-72|
|Reed, Patrick W; Bloch, Robert J (2011) Crystallin-gazing: unveiling enzymatic activity. J Neurochem 118:315-6|
|Roche, Joseph A; Ford-Speelman, Diana L; Ru, Lisa W et al. (2011) Physiological and histological changes in skeletal muscle following in vivo gene transfer by electroporation. Am J Physiol Cell Physiol 301:C1239-50|
|Rahimov, Fedik; King, Oliver D; Warsing, Leigh C et al. (2011) Gene expression profiling of skeletal muscles treated with a soluble activin type IIB receptor. Physiol Genomics 43:398-407|
|Arashiro, Patricia; Eisenberg, Iris; Kho, Alvin T et al. (2009) Transcriptional regulation differs in affected facioscapulohumeral muscular dystrophy patients compared to asymptomatic related carriers. Proc Natl Acad Sci U S A 106:6220-5|
|Vishnudas, Vivek K; Miller, Jeffrey Boone (2009) Ku70 regulates Bax-mediated pathogenesis in laminin-alpha2-deficient human muscle cells and mouse models of congenital muscular dystrophy. Hum Mol Genet 18:4467-77|