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The etiology and pathogenesis of gre...
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Herbst, Lawrence Henry.
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The etiology and pathogenesis of green turtle fibropapillomatosis.
紀錄類型:
書目-語言資料,印刷品 : Monograph/item
正題名/作者:
The etiology and pathogenesis of green turtle fibropapillomatosis./
作者:
Herbst, Lawrence Henry.
面頁冊數:
284 p.
附註:
Chairperson: Paul A. Klein.
Contained By:
Dissertation Abstracts International57-02B.
標題:
Agriculture, Animal Pathology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9618703
The etiology and pathogenesis of green turtle fibropapillomatosis.
Herbst, Lawrence Henry.
The etiology and pathogenesis of green turtle fibropapillomatosis.
- 284 p.
Chairperson: Paul A. Klein.
Thesis (Ph.D.)--University of Florida, 1995.
Green turtle fibropapillomatosis (GTFP) is a threat to populations of Chelonia mydas worldwide. This project attempted to characterize the etiology and to describe the pathogenesis of GTFP. Transmission studies showed that tumors could be induced in recipient turtles by inoculation with twice frozen and thawed cell-free homogenates prepared from spontaneous tumors. Tumors were not induced by inoculation with intact spirorchid ova nor were spirorchid ova found in any experimentally induced tumors. Oncogenicity of tumor homogenates passed through 0.45 $\muSubjects--Topical Terms:
1021764
Agriculture, Animal Pathology.
The etiology and pathogenesis of green turtle fibropapillomatosis.
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The etiology and pathogenesis of green turtle fibropapillomatosis.
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Source: Dissertation Abstracts International, Volume: 57-02, Section: B, page: 0784.
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Green turtle fibropapillomatosis (GTFP) is a threat to populations of Chelonia mydas worldwide. This project attempted to characterize the etiology and to describe the pathogenesis of GTFP. Transmission studies showed that tumors could be induced in recipient turtles by inoculation with twice frozen and thawed cell-free homogenates prepared from spontaneous tumors. Tumors were not induced by inoculation with intact spirorchid ova nor were spirorchid ova found in any experimentally induced tumors. Oncogenicity of tumor homogenates passed through 0.45 $\mu
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but not 0.2 $\mu
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filters, and was destroyed by chloroform. Some spontaneous and experimentally induced tumors had epidermal eosinophilic intranuclear inclusions, which contained herpesvirus-like particles. Attempts to culture this virus on 2 reptilian cell lines were unsuccessful. Particles resembling herpesvirus were found in pooled isopycnic gradient fractions of one transmission-positive tumor preparation, but were not tumorigenic. Green turtle antibody class-specific monoclonal antibodies, developed for the detection of turtle antibody responses to putative GTFP agents, were used with a proven herpesvirus-specific turtle antiserum, to demonstrate herpesvirus antigens in spontaneous and induced tumors. Tissue sections containing herpesvirus were also used to screen plasma samples for antibody reactivity to herpesvirus antigens by immunohistochemistry. Antibody reactivities to herpesvirus developed in all experimental transmission-positive turtles, but not in controls or transmission-negatives. A strong association between antibody reactivity to herpesvirus and clinical GTFP was also found in free-ranging turtles. In contrast, antibody reactivity to spirorchid trematodes was not associated with clinical GTFP. The transformed phenotype of GTFP-derived fibroblast cultures was demonstrated using tumorigenicity assays and preliminary studies showed differences in mRNA expression between matched pairs of normal skin- and GTFP-derived cell lines. Although the pathogenesis of GTFP can be explained by herpesvirus, proof that herpesvirus causes GTFP will require reproduction of the disease in turtles with purified virus, or demonstration of herpesviral gene sequences among these differentially expressed messages in GTFP cell lines and in transmission positive tumor homogenates, that can transform normal fibroblasts to the tumorigenic phenotype.
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http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9618703
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