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1 inflammation and outcome in a mouse model of viral myocarditis.
2 To review how autoimmunity is induced in viral myocarditis.
3 M were observed in the subgroup (n=130) with viral myocarditis.
4 is a characteristic of both human and mouse viral myocarditis.
5 t, and is a potential therapeutic target for viral myocarditis.
6 specific T cell responses during subclinical viral myocarditis.
7 CVB3 is a primary cause of viral myocarditis.
8 ces in IFN antagonism to the pathogenesis of viral myocarditis.
9 Four patients had probable viral myocarditis.
10 +) T regulatory cells, which protect against viral myocarditis.
11 he myocardial inflammatory response in acute viral myocarditis.
12 response during the initial phases of acute viral myocarditis.
13 nvestigate non-immune-mediated mechanisms of viral myocarditis.
14 re inflammation and injury, also occurred in viral myocarditis.
15 lymphoid cell compartment, are protective in viral myocarditis.
18 8-52] years) with a history of biopsy-proven viral myocarditis and drug-refractory VT; 5 patients pre
19 n mediating cardiac injury in the setting of viral myocarditis and is the first demonstration that ca
21 ew insights into the innate host response to viral myocarditis and the various therapeutic strategies
22 thogenic processes of coxsackievirus-induced viral myocarditis and to screen antiviral therapeutics f
23 subanalysis in 130 adult patients with acute viral myocarditis and viral prodrome within 2 weeks from
25 f sepsis, seven patients with a diagnosis of viral myocarditis, and five control patients without cli
27 ate the long-term mortality in patients with viral myocarditis, and to establish the prognostic value
29 n only rarely develop life-threatening acute viral myocarditis (AVM), given that the causal viral inf
33 ong been considered the most common cause of viral myocarditis; however, we previously demonstrated b
36 been speculated that ARVD/C is a sequela of viral myocarditis in some patients, and the role of the
38 endocardial fibroelastosis is a sequela of a viral myocarditis, in particular of that due to mumps vi
39 V-1 model will enable fundamental studies of viral myocarditis, including IFN-gamma modulation as a t
47 de range of clinical symptoms, biopsy-proven viral myocarditis is associated with a long-term mortali
48 esis of chronic dilated cardiomyopathy after viral myocarditis is complex and determined by host and
53 ackievirus B3 (CVB3) is a causative agent of viral myocarditis, pancreatitis, and meningitis in human
54 ), an important human causative pathogen for viral myocarditis, pancreatitis, and meningitis, has evo
57 sclerosis, acute coronary syndromes, stroke, viral myocarditis, sepsis, ischemia/reperfusion injury,
58 immunity signal transducer IRAK4 exacerbates viral myocarditis through inhibition of interferon produ
60 The benefits of TIMP-1 blockade in treating viral myocarditis were confirmed by administering, to wi
61 unction, we treated a patient with fulminant viral myocarditis with the interleukin-1 receptor blocki
62 s modulate heart failure pathogenesis during viral myocarditis, yet their identities and functions re
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