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The pathogenesis of coxsackievirus B...

Hill, Susan Lynnett.

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The pathogenesis of coxsackievirus B3-induced autoimmune myocarditis.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	The pathogenesis of coxsackievirus B3-induced autoimmune myocarditis./
作者:	Hill, Susan Lynnett.
面頁冊數:	247 p.
附註:	Advisers: Noel R. Rose; Diane E. Griffin; Marsha Wills-Karp; Charles J. Lowenstein.
Contained By:	Dissertation Abstracts International61-10B.
標題:	Biology, Microbiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9993121
ISBN:	0493005668

The pathogenesis of coxsackievirus B3-induced autoimmune myocarditis.
Hill, Susan Lynnett.

The pathogenesis of coxsackievirus B3-induced autoimmune myocarditis. - 247 p.

Advisers: Noel R. Rose; Diane E. Griffin; Marsha Wills-Karp; Charles J. Lowenstein.

Thesis (Ph.D.)--The Johns Hopkins University, 2001.

Coxsackievirus B3 (CB3), shown to induce intracardiac interferon-gamma (IFN-γ) and nitric oxide (NO) production, causes heart lesions ranging from viral myocarditis to autoimmune myocarditis in susceptible mouse strains. We hypothesized that IFN-γ-induced NO production is important in disease pathogenesis: initially it prevents viral myocarditis whereas later it induces autoimmune myocarditis through its antiviral activity and immune modulating capability, respectively.

ISBN: 0493005668Subjects--Topical Terms:

1017734
Biology, Microbiology.

The pathogenesis of coxsackievirus B3-induced autoimmune myocarditis.
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100 1 $a Hill, Susan Lynnett. $3 1256415
245 1 0 $a The pathogenesis of coxsackievirus B3-induced autoimmune myocarditis.
300 $a 247 p.
500 $a Advisers: Noel R. Rose; Diane E. Griffin; Marsha Wills-Karp; Charles J. Lowenstein.
500 $a Source: Dissertation Abstracts International, Volume: 61-10, Section: B, page: 5226.
502 $a Thesis (Ph.D.)--The Johns Hopkins University, 2001.
520 $a Coxsackievirus B3 (CB3), shown to induce intracardiac interferon-gamma (IFN-γ) and nitric oxide (NO) production, causes heart lesions ranging from viral myocarditis to autoimmune myocarditis in susceptible mouse strains. We hypothesized that IFN-γ-induced NO production is important in disease pathogenesis: initially it prevents viral myocarditis whereas later it induces autoimmune myocarditis through its antiviral activity and immune modulating capability, respectively.
520 $a First, we examined B 10.M mice (H-2<super>f</super>) for gender-specific susceptibility to the development of autoimmune myocarditis. Using the CB3- and myosin-induced disease models, female mice developed autoimmune myocarditis, based on cardiac interstitial infiltrates and murine cardiac myosin (MCM)-specific splenocyte proliferation, whereas male mice did not, Successful transfer of disease with splenocytes in female mice further supported their susceptibility to autoimmune disease.
520 $a Second, we proposed that NO exerts both antiviral and autoimmune disease promoting effects in CB3-infection. Aminoguanidine (AG) blockage of inducible-nitric oxide synthase enzyme (I-NOS) early (days 0–7) after virus-inoculation enhanced cardiac necrotizing (viral) lesions in B 10.M male and female mice without affecting the cardiac viral titers. Late (days 10–20) blockage of I-NOS reduced the severity of cardiac interstitial (autoimmune) lesions in susceptible female B 10.M mice independent of MCM-specific severity. We concluded that NO plays a protective role in the viral disease and a detrimental role during the autoimmune disease.
520 $a Third, we hypothesized that IFN-γ-dependent NO production is important in CB3-induced disease. Blocking circulating IFN-γ in A.CA mice (H-2<super> f</super>) using a monoclonal rat anti-mouse IFN-γ antibody early (days -1 + 3) in infection reduced the severity of cardiac lesions and decreased urinary NO levels on day 8 after CB3-inoculation. Late (days 7 + 11) anti-IFN-γ treatment failed to alter the disease severity on day 21 after virus-inoculation. Early IFN-γ production contributes to the development of cardiac histopathologic lesions through a NO-independent mechanism during viral disease, but may be important in NO-dependent cardiac lesions during the autoimmune disease.
520 $a NO plays a dichotomous role in CB3-infection by preventing cardiac viral lesions while concurrently enhancing cardiac autoimmune lesions in susceptible B 10.M female mice. IFN-γ contributes to disease pathogenesis through NO-dependent and NO-independent effector functions.
590 $a School code: 0098.
650 4 $a Biology, Microbiology. $3 1017734
650 4 $a Health Sciences, Immunology. $3 1017716
690 $a 0410
690 $a 0982
710 2 0 $a The Johns Hopkins University. $3 1017431
773 0 $t Dissertation Abstracts International $g 61-10B.
790 $a 0098
790 1 0 $a Griffin, Diane E., $e advisor
790 1 0 $a Lowenstein, Charles J., $e advisor
790 1 0 $a Rose, Noel R., $e advisor
790 1 0 $a Wills-Karp, Marsha, $e advisor
791 $a Ph.D.
792 $a 2001
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9993121