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Modulation of HSV-induced angiogenes...

Lee, Sujin.

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Modulation of HSV-induced angiogenesis in HSK pathogenesis.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Modulation of HSV-induced angiogenesis in HSK pathogenesis./
作者:	Lee, Sujin.
面頁冊數:	108 p.
附註:	Major Professor: Barry T. Rouse.
Contained By:	Dissertation Abstracts International63-07B.
標題:	Health Sciences, Immunology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3059750
ISBN:	0493754423

Modulation of HSV-induced angiogenesis in HSK pathogenesis.
Lee, Sujin.

Modulation of HSV-induced angiogenesis in HSK pathogenesis. - 108 p.

Major Professor: Barry T. Rouse.

Thesis (Ph.D.)--The University of Tennessee, 2002.

Herpes simplex virus (HSV) infection of the eye can result in a blinding immunoinflammatory lesion in the corneal stroma. In humans, this is an important cause of vision impairment. The murine lesions resemble the human counterpart both clinically and histopathologically especially in susceptible mouse strains such as BALB/c mice infected with the RE strain of HSV-1. HSV-1 ocular infection of BALB/c mice leads to transient mild epithelial lesions caused by virus replication and destruction of epithelial cells. These lesions quickly heal with little or no scarring and the cornea appears normal until around day 5–8 post infection. Subsequently, most infected animals develop progressive corneal opacity, edema, neovascularization, necrosis and ulceration, all of which become evident in a span of 2–3 weeks after infection. Studies on experimental herpetic stromal keratitis (HSK) in animal models have revealed that the pathogenesis involves numerous cellular and molecular participants. One early essential event appears to be neovascularization of the normally avascular corneal stroma. This event is assumed to be necessary to assist corneal access of some of the cellular orchestrators of HSK. In line with this notion, inhibition of new blood vessel development serves to moderate the severity of HSK lesions.

ISBN: 0493754423Subjects--Topical Terms:

1017716
Health Sciences, Immunology.

Modulation of HSV-induced angiogenesis in HSK pathogenesis.
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245 1 0 $a Modulation of HSV-induced angiogenesis in HSK pathogenesis.
300 $a 108 p.
500 $a Major Professor: Barry T. Rouse.
500 $a Source: Dissertation Abstracts International, Volume: 63-07, Section: B, page: 3218.
502 $a Thesis (Ph.D.)--The University of Tennessee, 2002.
520 $a Herpes simplex virus (HSV) infection of the eye can result in a blinding immunoinflammatory lesion in the corneal stroma. In humans, this is an important cause of vision impairment. The murine lesions resemble the human counterpart both clinically and histopathologically especially in susceptible mouse strains such as BALB/c mice infected with the RE strain of HSV-1. HSV-1 ocular infection of BALB/c mice leads to transient mild epithelial lesions caused by virus replication and destruction of epithelial cells. These lesions quickly heal with little or no scarring and the cornea appears normal until around day 5–8 post infection. Subsequently, most infected animals develop progressive corneal opacity, edema, neovascularization, necrosis and ulceration, all of which become evident in a span of 2–3 weeks after infection. Studies on experimental herpetic stromal keratitis (HSK) in animal models have revealed that the pathogenesis involves numerous cellular and molecular participants. One early essential event appears to be neovascularization of the normally avascular corneal stroma. This event is assumed to be necessary to assist corneal access of some of the cellular orchestrators of HSK. In line with this notion, inhibition of new blood vessel development serves to moderate the severity of HSK lesions.
520 $a In the present study, an attempt was made to define and understand the molecular and cellular mechanisms in the HSV ocular infection induced angiogenesis. Experiments were designed to address the role of angiogenesis in HSK lesion development. Part I is a general introduction of the mechanism of angiogenesis and its role in HSK pathogenesis. Part II is that IL-12 inhibits angiogenesis in HSK pathogenesis. The inhibitory effect of IL-12 turned out to be an effect on angiogenesis mediated by at least two intermediate proteins: interferon gamma and IP-10 chemokine. Part III consists of the role of stromal matrix degrading enzymes, such as MMP-9 produced by neutrophils in HSK angiogenesis. These results suggest that angiogenesis is an essential step in HSK pathogenesis and inhibition of angiogenesis using plasmid DNA administration is reflected in the reduced severity of subsequent HSK lesions.
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