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Effects of chronic wound fluid on ce...

Seah, Ching Ching.

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Effects of chronic wound fluid on cell cycle-regulatory proteins in human newborn dermal fibroblasts.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Effects of chronic wound fluid on cell cycle-regulatory proteins in human newborn dermal fibroblasts./
作者:	Seah, Ching Ching.
面頁冊數:	168 p.
附註:	Major Adviser: Hee-Young Park.
Contained By:	Dissertation Abstracts International62-07B.
標題:	Biology, Cell. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3021062
ISBN:	0493318623

Effects of chronic wound fluid on cell cycle-regulatory proteins in human newborn dermal fibroblasts.
Seah, Ching Ching.

Effects of chronic wound fluid on cell cycle-regulatory proteins in human newborn dermal fibroblasts. - 168 p.

Major Adviser: Hee-Young Park.

Thesis (Ph.D.)--Boston University, 2002.

Chronic venous ulcers, a type of chronic wound, constitute a major health problem among the elderly in the industrialized world. The lack of effective therapies for, and the frequent recurrence of, chronic leg ulcers impose an annual medical cost of over a billion dollars. Understanding the underlying molecular mechanisms responsible for the impaired healing of chronic ulcers would lead to the development of more effective therapies, thereby improving the quality of life among the elderly and reducing healthcare costs.

ISBN: 0493318623Subjects--Topical Terms:

1017686
Biology, Cell.

Effects of chronic wound fluid on cell cycle-regulatory proteins in human newborn dermal fibroblasts.
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245 1 0 $a Effects of chronic wound fluid on cell cycle-regulatory proteins in human newborn dermal fibroblasts.
300 $a 168 p.
500 $a Major Adviser: Hee-Young Park.
500 $a Source: Dissertation Abstracts International, Volume: 62-07, Section: B, page: 3037.
502 $a Thesis (Ph.D.)--Boston University, 2002.
520 $a Chronic venous ulcers, a type of chronic wound, constitute a major health problem among the elderly in the industrialized world. The lack of effective therapies for, and the frequent recurrence of, chronic leg ulcers impose an annual medical cost of over a billion dollars. Understanding the underlying molecular mechanisms responsible for the impaired healing of chronic ulcers would lead to the development of more effective therapies, thereby improving the quality of life among the elderly and reducing healthcare costs.
520 $a It has been suggested that chronic wound fluid (CWF) may contain molecules that adversely affect wound repair. CWF inhibits the growth of dermal fibroblasts by arresting cells mostly in the G1/G0 phase, and prevents DNA synthesis. In this thesis, the molecular mechanisms affected by CWF were determined. Specifically, the effects of CWF on levels of the cell cycle regulatory proteins c-Fos, c-Jun, retinoblastoma, protein (Rb), cyclin D1, CDK4 and p21<super> Cip1/Waf1</super>, were examined. CWF from five separate patients, when added to dermal fibroblasts (250μg/ml) consistently downregulated the otherwise induced protein levels of c-Fos, c-Jun, hyperphosphorylated Rb, cyclin D1 and active Ras-GTP. In contrast, CWF elevated the level of the cell cycle inhibitory protein p21<super>Cip1/Waf1</super>. The level of CDK4 was unaffected by CWF. Transient transfection of dermal fibroblasts with the constitutively active Ras38V mutant abrogated the effects of CWF on cyclin D1 and Rb hyperphosphorylation. Furthermore, treatment with the MEK inhibitor PD 98059, mimicked effects of CWF on cyclin D1 and Rb hyperphosphorylation, and concurrent treatment with PD 98059 and CWF produced additive effects.
520 $a Taken together, these results suggest that CWF suppresses the growth of dermal fibroblasts at least in part by modulating levels of G1 cell cycle-regulatory proteins such that dermal fibroblasts are prevented from initiating DNA synthesis. Moreover, a Ras-dependent signaling pathway may be the key pathway affected by CWF as reconstitution of Ras activity overcomes the inhibitory effects of CWF on cell cycle-regulatory proteins.
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