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1 ither impromidine (10 microM) nor R(-)-alpha-methylhistamine (10 microM), selective H2 or H3 agonists
2 th bsT and the urinary histamine metabolites methylhistamine and methylimidazole acetic acid (MIMA) w
3 thus inhibited acid secretion, and (r)-alpha-methylhistamine attenuated somatostatin and increased ac
5 study was to evaluate urinary histamine and methylhistamine excretion in patients with food allergy
6 icantly higher levels of urine histamine and methylhistamine excretion were found under unrestricted
9 f 36% to 47% at a bsT level of 28.0 mug/L, a methylhistamine level of 231.0 mumol/mol creatinine, and
12 The influence of these factors on urinary methylhistamine (MH) and methylimidazole acetic acid (MI
13 lites methylimidazole acetic acid (MIMA) and methylhistamine (MH) to select patients for bone marrow
14 ptase and the urinary histamine metabolites, methylhistamine (MH), and methylimidazole acetic acid.
16 lite of prostaglandin D2 (r = 0.98) and Ntau-methylhistamine (r = 0.91), suggesting that the cellular
17 ptors, the effects of the H3 agonist R-alpha-methylhistamine (RAMH) and the H3 antagonist thioperamid
19 H3R activation with the agonist R-(-)-alpha-methylhistamine to produce a unique time- and cell type-
21 tor; the major difference was that (R)-alpha-methylhistamine was a low potency agonist of the AXOR35
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