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1 ed based on their resistance to selection by ethionine.
2 uce S-adenosylethionine (SAE) from substrate ethionine.
4 in a manner similar to SAMe, confirming that ethionine also uses the same catalytic site to form the
8 rats exposed to a cyclic choline deficiency-ethionine (CDE) diet (2 weeks on, 1 week off) supports t
10 holine-deficient diet supplemented with 0.5% ethionine for 24 hrs and then challenging the animals wi
12 )), choline-deficient diet supplemented with ethionine, or 3,5-diethoxycarbonyl-1,4-dihydrocollidine
14 yzed livers of rats fed a choline-deficient, ethionine-supplemented (CDE) diet for phospho-Smad2.
15 hronic liver disease: the choline-deficient, ethionine-supplemented (CDE) diet versus thioacetamide (
17 e mice by placing them on choline-deficient, ethionine-supplemented (CDE) diets for 15 days; mice the
19 s isolated from rats fed a choline-deficient ethionine-supplemented diet (CDE diet, a regimen commonl
21 rimental models of AP (ie, choline-deficient-ethionine-supplemented diet and cerulein injections), ST
22 AP was induced by a choline-deficient and ethionine-supplemented diet for 4 days in normal C57BL/6
23 tes, respectively, in the choline-deficient, ethionine-supplemented diet model of liver injury and re
24 ung female mice were fed a choline-deficient/ethionine-supplemented diet to induce AP and were treate
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