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The effects of deflazacort and nitri...

Archer, Jonathan David.

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The effects of deflazacort and nitric oxide manipulation on mdx mouse dystrophy.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	The effects of deflazacort and nitric oxide manipulation on mdx mouse dystrophy./
作者:	Archer, Jonathan David.
面頁冊數:	128 p.
附註:	Source: Masters Abstracts International, Volume: 42-06, page: 2080.
Contained By:	Masters Abstracts International42-06.
標題:	Biology, Anatomy. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=MQ89436
ISBN:	0612894363

The effects of deflazacort and nitric oxide manipulation on mdx mouse dystrophy.
Archer, Jonathan David.

The effects of deflazacort and nitric oxide manipulation on mdx mouse dystrophy. - 128 p.

Source: Masters Abstracts International, Volume: 42-06, page: 2080.

Thesis (M.Sc.)--University of Manitoba (Canada), 2004.

The effects of the glucocorticoid deflazacort and nitric oxide (NO) manipulation on muscle function and regeneration were studied using the mdx mouse, the genetic model of the lethal Duchenne muscular dystrophy (DMD). Using the mdx mouse, 'clinical trials' were created using the beneficial glucocorticoid deflazacort, in conjunction with manipulation of NO levels. Deflazacort reduces the progression of dystrophy whilst improving muscle regeneration. Nitric Oxide Synthase (NOS) produces NO from the substrate L-arginine and is inhibited by N-Nitro-L-arginine-methyl-ester (L-NAME). The muscle specific isoform of NOS, NOS-1mu, is detached from the dystroglycan complex (DGC) and dispensed in the cytoplasm of dystrophic muscle. Satellite cell (muscle precursor cell) activation is dependent on NO and therefore is affected by the lack of NOS in muscular dystrophy. It was hypothesized that NO manipulation would improve the already known benefits of deflazacort treatment. (Abstract shortened by UMI.)

ISBN: 0612894363Subjects--Topical Terms:

1021727
Biology, Anatomy.

The effects of deflazacort and nitric oxide manipulation on mdx mouse dystrophy.
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520 $a The effects of the glucocorticoid deflazacort and nitric oxide (NO) manipulation on muscle function and regeneration were studied using the mdx mouse, the genetic model of the lethal Duchenne muscular dystrophy (DMD). Using the mdx mouse, 'clinical trials' were created using the beneficial glucocorticoid deflazacort, in conjunction with manipulation of NO levels. Deflazacort reduces the progression of dystrophy whilst improving muscle regeneration. Nitric Oxide Synthase (NOS) produces NO from the substrate L-arginine and is inhibited by N-Nitro-L-arginine-methyl-ester (L-NAME). The muscle specific isoform of NOS, NOS-1mu, is detached from the dystroglycan complex (DGC) and dispensed in the cytoplasm of dystrophic muscle. Satellite cell (muscle precursor cell) activation is dependent on NO and therefore is affected by the lack of NOS in muscular dystrophy. It was hypothesized that NO manipulation would improve the already known benefits of deflazacort treatment. (Abstract shortened by UMI.)
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