|1.||Chamberlain, Jeffrey S: 44 articles (01/2015 - 03/2002)|
|2.||Duan, Dongsheng: 37 articles (12/2015 - 03/2002)|
|3.||Takeda, Shin'ichi: 37 articles (05/2015 - 03/2002)|
|4.||Matsuo, Masafumi: 36 articles (01/2016 - 01/2002)|
|5.||Takeshima, Yasuhiro: 32 articles (01/2016 - 01/2002)|
|6.||Aartsma-Rus, Annemieke: 29 articles (01/2015 - 10/2002)|
|7.||Muntoni, Francesco: 28 articles (11/2014 - 07/2002)|
|8.||Davies, Kay E: 27 articles (12/2015 - 04/2002)|
|9.||Yagi, Mariko: 27 articles (01/2015 - 01/2002)|
|10.||Dickson, George: 24 articles (08/2015 - 04/2002)|
|1.||Duchenne Muscular Dystrophy (Muscular Dystrophy, Becker)
02/01/2014 - "When transplanted into mdx mice models for Duchenne muscular dystrophy (DMD), the proposed muscle patches led to the formation of a significantly greater number of dystrophin-positive muscle fibers, indicating that dystrophin replacement and myogenesis is achievable in vivo with this approach. "
07/01/1997 - "Hopes ran high that a cure for Duchenne muscular dystrophy (DMD) would quickly follow the discovery of dystrophin by Lou Kunkel and his group in the 1980's. "
01/01/2007 - "Duchenne muscular dystrophy (DMD) is an X-linked recessive disease caused by mutations of dystrophin gene, there is no effective treatment for this disorder at present. "
03/01/2004 - "Despite a wealth of recent information about the molecular basis of Duchenne muscular dystrophy (DMD), there is no effective treatment for this condition because the mechanism how dystrophin deficiency produces the muscle fiber degradation is unknown. "
07/01/2012 - "Antisense oligonucleotide (AON)-mediated exon skipping to restore dystrophin expression in Duchenne muscular dystrophy (DMD) therapy shown promise in a number of human clinical trials. "
|2.||Muscular Dystrophies (Muscular Dystrophy)
07/15/2014 - "The dnOrai1 transgene also significantly reduced the severity of muscular dystrophy in both mdx (dystrophin mutant mice) and δ-sarcoglycan-deficient (Sgcd(-/-)) mouse models of disease. "
11/03/2008 - "We show that sarcospan (SSPN), a unique tetraspanin-like component of the DGC, ameliorates muscular dystrophy in dystrophin-deficient mdx mice. "
01/04/2008 - "A cure for dystrophin-deficient muscular dystrophy requires treating both skeletal muscle and the heart. "
07/01/2003 - "Expression of dystrophin driven by the 1.35-kb MCK promoter ameliorates muscular dystrophy in fast, but not in slow muscles of transgenic mdx mice."
02/01/1998 - "Elucidating the mechanisms leading to cell death may help to explain the variabilities in disease expression that are seen as a function of age, among different muscles, and across species in animals with muscular dystrophy due to dystrophin deficiency."
04/01/2001 - "However, the exact functions of dystrophin are still not fully understood and the complex process leading to subsequent muscle fiber necrosis has not been clearly described; hence there has not yet been any marked improvement in patient treatment. "
04/01/2002 - "These results suggest that a combination of promoting muscle regenerative capacity and preventing muscle necrosis could be an effective treatment for the secondary symptoms caused by the primary loss of dystrophin."
04/15/2006 - "To explore the mechanisms of myofiber necrosis in dystrophin-deficient muscle, we tested the hypothesis that restoration of this complex without a link to the cytoskeleton ameliorates dystrophic pathology. "
03/01/1999 - "This study shows that limb immobilization prevents the occurrence of the first round of myofiber necrosis in mdx mice and suggests that muscle contractions play a role in the skeletal muscle degeneration of dystrophin-deficient mdx mouse muscles."
11/01/1995 - "This review discusses critically the results of these studies and their relevance to understanding the mechanisms by which dystrophin-deficiency leads to muscle necrosis."
|4.||Muscular Diseases (Myopathy)
05/26/1988 - "The biochemical assay for dystrophin should prove helpful in delineating myopathies that overlap clinically with Duchenne's and Becker's dystrophies, and it shows promise as an accurate diagnostic tool."
09/01/2011 - "Previous studies have shown that MMP-9 exacerbates myopathy in dystrophin-deficient mdx mice. "
10/01/2005 - "This study brings a new insight in the pathophysiology of dystrophin-related myopathies. "
12/13/2002 - "This study suggests that blood flow regulation might be disturbed in dystrophin-related myopathies, possibly increasing organ damage."
11/01/1995 - "A large number of recent studies have used the mdx mouse model to examine the potential role of dystrophy in normal muscle and the mechanisms by which dystrophin-deficiency leads to myopathy. "
07/01/2015 - "CtermDys gene titration and dystrophin replacement studies further established a target threshold of 50% membrane-bound intact dystrophin necessary to prevent mice from CtermDys cardiomyopathy. "
04/01/2014 - "Our study aimed to elucidate which dystrophin levels in the heart are required to prevent or delay cardiomyopathy in mice. "
12/15/1996 - "Contrary to previous reports, which indicated the involvement of 5'-end mutations in cardiomyopathies as a result of dystrophin gene alterations, this study shows that despite the apparent concentration of deletions in two regions (5'-end and exons 47 through 49), no general conclusions can be drawn regarding the involvement of specific gene mutations in the development of cardiomyopathy. "
01/15/2016 - "A de-novo deletion of dystrophin provoking severe 'peri-partum cardiomyopathy': The importance of genetic testing in peripartum cardiomyopathy to uncover female carriers."
07/01/2015 - "Thus, CtermDys must be localized to the sarcolemma, with intact dystrophin <50% of normal levels, to exert dominant-negative peptide-dependent cardiomyopathy. "
|4.||Complementary DNA (cDNA)
|6.||Carrier Proteins (Binding Protein)
|7.||Proteins (Proteins, Gene)
|8.||Protein Isoforms (Isoforms)
|9.||RNA Precursors (Precursor, mRNA)
|2.||Transplantation (Transplant Recipients)
|4.||Bone Marrow Transplantation (Transplantation, Bone Marrow)
|5.||Low-Level Laser Therapy (LLLT)