scholarly journals Growth hormone inhibition causes increased selenium levels in Duchenne muscular dystrophy: a possible new approach to therapy.

1984 ◽  
Vol 21 (4) ◽  
pp. 254-256 ◽  
Author(s):  
P J Collipp ◽  
J Kelemen ◽  
S Y Chen ◽  
M Castro-Magana ◽  
M Angulo ◽  
...  
2010 ◽  
pp. OR35-6-OR35-6 ◽  
Author(s):  
MM Rutter ◽  
J Collins ◽  
JG Woo ◽  
SR Rose ◽  
H Sawnani ◽  
...  

2010 ◽  
Vol 20 (9-10) ◽  
pp. 662
Author(s):  
J.J. Collins ◽  
M.M. Rutter ◽  
J. Woo ◽  
S. Rose ◽  
H. Sawnani ◽  
...  

1986 ◽  
Vol 24 (3) ◽  
pp. 549-566 ◽  
Author(s):  
Mayana Zatz ◽  
Roberto T. B. Betti ◽  
Oswaldo Frota-Pessoa ◽  
John M. Opitz ◽  
James F. Reynolds

1988 ◽  
Vol 31 (4) ◽  
pp. 821-833 ◽  
Author(s):  
Mayana Zatz ◽  
Debora Rapaport ◽  
Mariz Vainzof ◽  
Rita de Cassia M. Pavanello ◽  
Jane M. L. Rocha ◽  
...  

Author(s):  
Yoshitsugu Aoki ◽  
◽  
Tetsuya Nagata ◽  
Shin’ichi Takeda

Duchenne Muscular Dystrophy (DMD) is a lethalmuscle disorder characterized by mutations in the DMD gene. These mutations primarily disrupt the reading frame, resulting in the absence of functional dystrophin protein. Exon skipping, which involves the use of antisense oligonucleotides is a promising therapeutic approach for DMD, and clinical trials on exon skipping are currently underway in DMD patients. Recently, stable and less-toxic antisense oligonucleotides with higher efficacy have been developed in mouse and dog models of DMD. This review highlights a new approach for antisense oligonucleotide-based therapeutics for DMD, particularly for exon skipping-based methods.


1972 ◽  
Vol 51 (5) ◽  
pp. 1118-1124 ◽  
Author(s):  
Daniel Rudman ◽  
Samuel B. Chyatte ◽  
Joseph H. Patterson ◽  
Glynda G. Gerron ◽  
Irma O'Beirne ◽  
...  

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