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1 ic differences controlling susceptibility to autoimmune myocarditis.
2 myocarditogenic peptide-induced experimental autoimmune myocarditis.
3 and cardiac function in murine experimental autoimmune myocarditis.
4 ce results in the spontaneous development of autoimmune myocarditis.
5 nd modulation of immune responses to prevent autoimmune myocarditis.
6 cell effector cells in a new mouse model of autoimmune myocarditis.
7 urified myosin, which normally causes severe autoimmune myocarditis.
8 of captopril on myosin-induced experimental autoimmune myocarditis.
9 of IL-10 in the induction and suppression of autoimmune myocarditis.
10 ity in mice with myosin-induced experimental autoimmune myocarditis.
11 myosin antibodies and their ability to cause autoimmune myocarditis.
12 cells are a critical APC in the induction of autoimmune myocarditis.
13 cTnI values were first measured in mice with autoimmune myocarditis.
14 elevant mathematical models as they apply to autoimmune myocarditis.
16 portantly, CM is the autoantigen that causes autoimmune myocarditis, a heart autoimmune disease whose
17 ctivity is associated with cardiac damage in autoimmune myocarditis, an inflammatory heart disease ch
18 otoxic T lymphocytes contribute to viral and autoimmune myocarditis and cardiac allograft rejection.
19 vel therapeutic strategy in the treatment of autoimmune myocarditis and inflammatory cardiomyopathy.
20 cate that captopril ameliorates experimental autoimmune myocarditis and may act, at least in part, by
21 oped severe coxsackievirus B3 (CVB3)-induced autoimmune myocarditis and myocarditogenic peptide-induc
22 1(-/-);MRL-Fas(lpr) mice died as a result of autoimmune myocarditis and pneumonitis before developing
24 ults suggest that apoJ limits progression of autoimmune myocarditis and protects the heart from posti
25 use antimyosin autoantibodies are present in autoimmune myocarditis and rheumatic carditis, the purpo
26 tion receptors promotes CD4+ T-cell-mediated autoimmune myocarditis and subsequent inflammatory cardi
27 s critical for the induction of experimental autoimmune myocarditis and that it acts through compleme
28 on specifically and robustly in experimental autoimmune myocarditis, and thus allowed for an unpreced
29 ght mice were studied after the induction of autoimmune myocarditis by immunization with alpha-myosin
30 irect experimental evidence that spontaneous autoimmune myocarditis can occur in the absence of infec
32 n, a heart autoantigen, induced experimental autoimmune myocarditis (EAM) in susceptible animals.
33 ng in the development of murine experimental autoimmune myocarditis (EAM) induced by cardiac myosin i
37 deficient mice developed severe experimental autoimmune myocarditis (EAM), in which mice are immunize
38 stablished model of TnI-induced experimental autoimmune myocarditis (EAM), we demonstrated that both
41 riety of cardiomyopathies, but its effect on autoimmune myocarditis has not been addressed experiment
42 Herein, we demonstrate that ANT1 can induce autoimmune myocarditis in A/J mice by generating autorea
44 e found that the acute phase of experimental autoimmune myocarditis in IFN-gamma-KO mice was characte
47 al hearts should result in a T cell-mediated autoimmune myocarditis in the healthy syngeneic rats.
49 We conclude that IFN-gamma deficiency in autoimmune myocarditis is associated with preferential e
51 and 'molecular mimicry' in the CB-3-induced autoimmune myocarditis model, and instead favors the ide
53 i-CM sera and mAbs derived from experimental autoimmune myocarditis targeted the heart cell surface a
58 To test its ability to modify myosin-induced autoimmune myocarditis, we generated apoJ-deficient mice
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