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Apoptosis-necrosis paradox: Implica...

Medan, Djordje.

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Apoptosis-necrosis paradox: Implications to the pathogenesis of inflammatory disorders.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Apoptosis-necrosis paradox: Implications to the pathogenesis of inflammatory disorders./
作者:	Medan, Djordje.
面頁冊數:	75 p.
附註:	Source: Masters Abstracts International, Volume: 42-01, page: 0152.
Contained By:	Masters Abstracts International42-01.
標題:	Biology, Cell. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=1415055

Apoptosis-necrosis paradox: Implications to the pathogenesis of inflammatory disorders.
Medan, Djordje.

Apoptosis-necrosis paradox: Implications to the pathogenesis of inflammatory disorders. - 75 p.

Source: Masters Abstracts International, Volume: 42-01, page: 0152.

Thesis (M.S.)--West Virginia University, 2003.

The first section of this work addressed the relationship between apoptotic and necrotic cell death and their role in inflammatory lung injury induced by endotoxin.Subjects--Topical Terms:

1017686
Biology, Cell.

Apoptosis-necrosis paradox: Implications to the pathogenesis of inflammatory disorders.
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245 1 0 $a Apoptosis-necrosis paradox: Implications to the pathogenesis of inflammatory disorders.
300 $a 75 p.
500 $a Source: Masters Abstracts International, Volume: 42-01, page: 0152.
500 $a Chair: Yongyut Rojanasakul.
502 $a Thesis (M.S.)--West Virginia University, 2003.
520 $a The first section of this work addressed the relationship between apoptotic and necrotic cell death and their role in inflammatory lung injury induced by endotoxin.
520 $a In the second section, the focus shifted to the role of ROS in FasL-induced cell death. Given that Fas/FasL pathway has been implicated in the pathogenesis of numerous inflammatory disorders, potential therapeutic utility of antioxidants was investigated in an in vitro model.
520 $a Based on the findings presented within this work, excessive apoptosis and consequent inability of the tissues's phagocytes to promptly clear apoptotic bodies results in secondary necrosis and amplification of the overall tissue damage via release of the noxious cellular contents into the environment. Such relationship illustrates the apoptosis-necrosis paradox and suggests that strategies directed towards apoptosis inhibition and/or stimulation of the phagocyte system may show therapeutic utility in the treatment of inflammatory disorders. (Abstract shortened by UMI.)
590 $a School code: 0256.
650 4 $a Biology, Cell. $3 1017686
650 4 $a Health Sciences, Pathology. $3 1017854
690 $a 0379
690 $a 0571
710 2 0 $a West Virginia University. $3 1017532
773 0 $t Masters Abstracts International $g 42-01.
790 1 0 $a Rojanasakul, Yongyut, $e advisor
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792 $a 2003
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=1415055