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1 e in S. equi pathogenicity by stimulating an overzealous and inappropriate Th1 response that may inte
4 is viewpoint will help temper enthusiasm for overzealous conversion of guidelines into performance me
6 tion (AT2 AT1) was critical for mounting the overzealous host immune response in fatal disease; ALO m
7 of N. aromaticivorans, and the promotion of overzealous IFN-gamma- and IL-17-dominated T cell respon
8 ion, suggesting that intestinal damage or an overzealous immune response is not the primary mediator
9 ead damage in the lungs in the setting of an overzealous immune response whose origin remains unclear
12 or disease susceptibility due to a muted or overzealous immune system, with a primary focus on the c
13 o respond to injury with what is arguably an overzealous immunological response; thus setting the sta
14 that the response the TLR triggers might be overzealous in its attempt to counter the attack by the
15 The immunopathophysiology of sepsis entails overzealous inflammation causing acute organ dysfunction
16 s an inflammatory condition characterized by overzealous inflammation that leads to joint damage and
18 dwide, involves concomitant expression of an overzealous inflammatory response and inefficient bacter
21 We also emphasized overt complications of overzealous needling of such a vascular lesion for histo
25 Acute myocardial infarction (MI) results in overzealous production and infiltration of neutrophils t
26 ng inflammatory responses via suppression of overzealous production of inflammatory cytokines/chemoki
28 erapy was associated with suppression of the overzealous production of tumor necrosis factor alpha, i
29 umoniae pulmonary infection by preventing an overzealous proinflammatory response mediated by TNF-alp
30 cytokines are known to promote fibrosis, an overzealous repair response, but their contribution to h