Research Interests
degenerative disorders
,
genetics/genome
,
neurosciences/behavior
Recent Publications
Willard SL, Register TC, Bennett AJ, Pierre PJ, Laudenslager ML, Kitzman DW, Childers MK, Grange RW, Kritschevsky SB [sic] [Kritchevsky SB], Shively CA.
Developing models of aging and physical function in three species of old world monkeys [abstract]. Am J Primatol.
2011;
73(Suppl 1):81.
Markert CD, Meaney MP, Voelker KA, Grange RW, Dalley HW, Cann JK, Ahmed M, Bishwokarma B, Walker SJ, Childers MK, et al.
Functional muscle analysis of the Tcap knockout mouse. Hum Mol Genet.
2010;
19(11):2268-2283.
Beggs AH, Bohm J, Snead E, Kozlowski M, Maurer M, Minor K, Childers MK, Taylor SM, Hitte C, Mickelson JR, et al.
MTM1 mutation associated with X-linked myotubular myopathy in Labrador Retrievers. Proc Natl Acad Sci U S A.
2010;
107(33):14697-702.
Shelton GD, Bohm J, Snead E, Kozlowski M, Minor K, Tiret L, Childers MK, Taylor SM, Mickelson JR, Guo LT, et al.
A missense variant in the MTM1 gene associated with X-linked myotubular myopathy in Labrador retrievers [abstract]. Neuromuscul Disord.
2009;
19(8-9):636.
Cheng C-P, Cheng H-J, Zhou P, Markert CD, Cross M, Kornegay JN, Stedman H, Childers MK.
Cardiomyopathy in a canine model of Duchenne muscular dystrophy: effects of left ventricle and myocyte systolic and diastolic functional performance, L-type calcium current response and beta-adrenergic modulation [abstract]. Circulation.
2009;
120(18 Suppl):S667.
Childers MK, Feldman JB, Guo HM.
Myofascial pain syndrome. In: Frontera WR, Silver JK, Rizzo TD, eds. Essentials of physical medicine and rehabilitation: musculoskeletal disorders, pain, and rehabilitation. 2nd ed.
Phildelphia: Saunders/Elsevier;
2008:
529-537.
Naumann M, So Y, Argoff CE, Childers MK, Dykstra DD, Gronseth GS, Jabbari B, Kaufmann HC, Schurch B, Silberstein SD, et al.
Assessment: botulinum neurotoxin in the treatment of autonomic disorders and pain (an evidence-based review): report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology.
2008;
70(19):1707-1714.
Childers M.
Trochanteric bursitis. In: Waldman SD, ed. Pain management, vol 2.
Philadelphia: Saunders/Elsevier;
2007:
859-863.
Childers MK, Markert C.
Cervical dystonia. In: Waldman SD, ed. Pain management, vol 1.
Philadelphia: Saunders/Elsevier;
2007:
591-597.
All Publications
For a listing of recent publications, refer to PubMed, a service provided by the National Library of Medicine.
For a list of earlier publications, visit the Carpenter Library Publication Search.
Dr. Childers studied music as an undergraduate at Seattle Pacific University. His graduate studies were completed at Western University, College of Osteopathic Medicine (DO) and at the University of Missouri, Dept. of Physical Medicine & Rehabilitation, and Dept. of Physiology (PhD).
SYNOPSIS OF AREA OF INTEREST
Stem cell therapy on the effects of protein deficiencies that cause degenerative muscle diseases (muscular dystrophies) is the primary focus. We use cultured muscle cells, single fiber and whole muscle functional assays in rodent and canine models. The canine model of dystrophin deficiency allows for function assessment of muscle strength and response to cellular, gene or pharmacologic agents potentially useful in the treatment of humans with muscular dystrophy.
DETAILED AREA OF INTEREST
Duchenne muscular dystrophy (DMD) afflicts 1 in 3300 males born each year in the US causing devastating weakness, contractures and early death. Despite over a century of research there is no cure for this inherited disease stemming, in part, from the lack of animal models that reflect both the genotype and phenotype of the human condition. Recently, we and others have described the golden retriever muscular dystrophy (GRMD) dog model. Affected dogs display progressive clinical deterioration and death by 1-2 years of age reflective of humans with DMD. Although effective treatment does not yet exist, novel therapeutic strategies, particularly stem cell therapy, hold great promise. Recently, an Italian group made world-wide headlines when they reported that intra-arterial delivery of perivascular stem cells in GRMD dogs ameliorated dystrophic muscle pathology. Enthusiasm for this discovery has been tempered by the fact that the perivascular stem cells were derived from neonatal muscle tissue – a non-renewable problematic resource. In addition, such cells have only a limited number of cell divisions limiting their capability to produce long-term benefit without repeated infusions. Coincident with the Italian report came the remarkable finding by A. Atala and colleagues at the WFIRM of stem-like properties from cells derived from amniotic fluid. Stem cells derived from the amniotic membrane hold similar promise. We are currently evaluating the therapeutic potential of stem cells derived from canine amniotic membrane by measuring their migration and engraftment abilities in immunodeficient mice.