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   1 e production in RAW264.7 cells (a measure of anti-inflammation).                                     
     2 possible regulatory pathways of MC1-R beyond anti-inflammation.                                      
     3  applied to antimutation, antityrosinase and anti-inflammation.                                      
     4 compounds i.e. anti-cancer, anti-allergy and anti-inflammation.                                      
     5  for its pharmacological functions including anti-inflammation.                                      
     6 anced cellular DNA repair, antioxidation and anti-inflammation.                                      
     7 f miR-33 that mediates simvastatin-triggered anti-inflammation.                                      
     8 nnexin A1 (AnxA1), an effector of endogenous anti-inflammation.                                      
     9 ects in vasodilation, anti-angiogenesis, and anti-inflammation.                                      
    10 Progesterone treatment showed no significant anti-inflammation action on cytokine concentrations.    
  
  
  
    14 ovel cyclooxygenase inhibitors, may serve as anti-inflammation and anticancer agents, and may contrib
  
    16 nt of green tea extract, exhibits effects of anti-inflammation and antioxidation on periodontal infla
  
  
    19 ontributing to the development of a state of anti-inflammation and dichotomy of immunologic polarizat
  
    21 sal antimicrobial responses demonstrate that anti-inflammation and proresolution are different respon
    22    There is an important distinction between anti-inflammation and resolution; anti-inflammation is p
  
    24 ced KLF2 and eNOS expression as well as flow anti-inflammation, and suggest that HDAC5 could be a pot
    25  signaling, cell migration, tissue survival, anti-inflammation, and T-cell-mediated cellular immunity
    26 tiatherogenic effects of HDL (antioxidation, anti-inflammation, antithrombotic effects, endothelial s
    27 acid-stimulated neutrophils, consistent with anti-inflammation but not COX inhibition (IC50s = 1-8 mM
    28 pha transcription and suggest a mechanism of anti-inflammation by the antioxidants through control of
    29 efficacy in lung function, QOL, and possibly anti-inflammation compared with BUD plus Tulo treatment.
    30 ic functions for this effector of endogenous anti-inflammation could be unveiled by studying collagen
    31 haracterize the balance of systemic pro- and anti-inflammation early after burn and inhalation injury
    32 2-nHP66 scaffold exerts potent antibacterial/anti-inflammation effects in vivo and promotes bone form
    33 )-induced metabolic diseases due to enhanced anti-inflammation engineered by lowering receptor intera
    34 ranscriptional regulator for antioxidant and anti-inflammation enzymes that binds to its endogenous i
    35 ta has been shown to play a critical role in anti-inflammation; however, the signaling mechanisms of 
  
    37 10 was a critical mediator for PGRN-mediated anti-inflammation in collagen-induced arthritis by using
    38 s model to explore the importance of dynamic anti-inflammation in promoting resolution of infection a
    39 on between anti-inflammation and resolution; anti-inflammation is pharmacologic intervention in infla
  
  
    42 sting that these terpenoid compounds have an anti-inflammation potential through the inhibition of T-
    43 in the 1980s demonstrated that pharmacologic anti-inflammation prevented and slowed the progression o
  
    45 ein A-I mimetic peptide with antioxidant and anti-inflammation properties on a high-fat or normal cho
  
  
  
  
  
    51    To investigate the molecular mechanism of anti-inflammation, we analyzed the regulation of tumor n
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