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2 omarkers that include arachidonic acid (AA), prostaglandin G(2) (PGG(2)), and cyclooxygenase 2 (COX-2
3 peroxide product of the PGHS-cyclooxygenase, prostaglandin G(2) (PGG(2)), by elevating the concentrat
5 mandates for arachidonic acid conversion to prostaglandin G(2) within the cyclooxygenase (COX) activ
6 lished the conversion of arachidonic acid to prostaglandin G(2), presumably because of a steric clash
10 induced prostaglandin endoperoxide synthase, prostaglandin G/H synthase (PGHS)-2 mRNA expression and
14 egans prostaglandins are synthesized without prostaglandin G/H synthase homologs, the targets of nons
16 igated the mechanisms by which inhibitors of prostaglandin G/H synthase-2 (PGHS-2; known colloquially
18 electively elevated induction of hippocampal prostaglandin G/H synthase-2 by kainic acid correlates w
20 vated, and that kainic acid up-regulation of prostaglandin G/H synthase-2 mRNA expression in hippocam
21 ar in both seizure models, peak induction of prostaglandin G/H synthase-2 mRNA is 7-fold greater in t
23 produces a variety of prostaglandin-EA's and prostaglandin-G's nearly as diverse as those derived fro
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