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The inflammatory response to acute m...

O'Fallon, Kevin S.

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The inflammatory response to acute muscle injury.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	The inflammatory response to acute muscle injury./
作者:	O'Fallon, Kevin S.
面頁冊數:	139 p.
附註:	Source: Dissertation Abstracts International, Volume: 75-07(E), Section: B.
Contained By:	Dissertation Abstracts International75-07B(E).
標題:	Biology, Physiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3615438
ISBN:	9781303814389

The inflammatory response to acute muscle injury.
O'Fallon, Kevin S.

The inflammatory response to acute muscle injury. - 139 p.

Source: Dissertation Abstracts International, Volume: 75-07(E), Section: B.

Thesis (Ph.D.)--University of Massachusetts Amherst, 2014.

The overall goal of this dissertation was to examine inflammatory and regenerative responses to acute skeletal muscle damage and to define molecular mediators of repair. Study I examined the effects of an oral anti-inflammatory supplement on exercise-induced muscle damage (EIMD) and systemic inflammation in a human model. Quercetin has been shown in animal and in vitro models to downregulate nuclear factor-kappa beta (NF-kappaB) nuclear transactivation and monocyte chemoattractant protein 1 (MCP-1) secretion, which regulate muscle regeneration and inflammatory signaling between muscle and immune cells after injury. Subjects ingested quercetin (N=15) or placebo (N=15) before and after performing 24 eccentric contractions of the elbow flexors. Subjects experienced moderate strength losses and delayed onset muscle soreness, indicating damage, but no supplementation effect was observed. The null effect of quercetin in the human model (with its complex inflammatory response) encouraged us to explore basic injury-induced inflammation in a controlled in vitro model, to better understand the post-injury roles of NF-kappaB and MCP-1.

ISBN: 9781303814389Subjects--Topical Terms:

1017816
Biology, Physiology.

The inflammatory response to acute muscle injury.
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500 $a Adviser: Lawrence M. Schwartz.
502 $a Thesis (Ph.D.)--University of Massachusetts Amherst, 2014.
520 $a The overall goal of this dissertation was to examine inflammatory and regenerative responses to acute skeletal muscle damage and to define molecular mediators of repair. Study I examined the effects of an oral anti-inflammatory supplement on exercise-induced muscle damage (EIMD) and systemic inflammation in a human model. Quercetin has been shown in animal and in vitro models to downregulate nuclear factor-kappa beta (NF-kappaB) nuclear transactivation and monocyte chemoattractant protein 1 (MCP-1) secretion, which regulate muscle regeneration and inflammatory signaling between muscle and immune cells after injury. Subjects ingested quercetin (N=15) or placebo (N=15) before and after performing 24 eccentric contractions of the elbow flexors. Subjects experienced moderate strength losses and delayed onset muscle soreness, indicating damage, but no supplementation effect was observed. The null effect of quercetin in the human model (with its complex inflammatory response) encouraged us to explore basic injury-induced inflammation in a controlled in vitro model, to better understand the post-injury roles of NF-kappaB and MCP-1.
520 $a Study II used an in vitro injury model (scratch of C 2C12 myotubes) to identify the roles and interplay of NF-kappaB and MCP-1 in muscle regeneration and inflammation following acute injury.
520 $a Protein expression changes of NF-kappaB and MCP-1, and morphological changes in regenerating muscle cultures were monitored for 24-72 hours (h) post-injury (3-6 replicates per experiment). NF-kappaB activation was significantly downregulated (-30+/-1.4% to -44+/-1.1%) at 6-12h post-injury. Pharmacological blockade of NF-kappaB downregulated satellite cell proliferation by 19+/-9% after 19h and 72h, evidence for a role of NF-kappaB signaling in post-injury regeneration. Furthermore, NF-kappaB activation strongly correlated (R=0.69) with MCP-1 secretion from injured muscle cultures, and blockade of NF-kappaB reduced MCP-1 secretion at 1-24h (-33+/-0.1%) and strongly correlated (R=0.74) with NF-kappaB activation. These data support recent in vivo findings to demonstrate that NF-kappaB and MCP-1 signaling are critical regulators of inflammatory and regenerative responses following muscle injury. Moreover, this work provides the first kinetic profile of early (<24 hours) molecular responses of NF-kappaB and MCP-1 to acute muscle injury, and introduces novel evidence that NF-kappaB regulates MCP-1 protein secretion, indicating an indispensible role of NF-kappaB signaling in muscle inflammation in vitro.
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