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1 t (Postnatal Days [PD] 4-9) and treated with choline chloride (0, 10, 50, or 100 mg/kg) from PD 10-30
2 subcutaneous injections of saline vehicle or choline chloride (100 mg/kg/day) from PD 11-20, PD 21-30
4 inhibitory compounds, (1-pentylthiocarbonyl)choline chloride and (1-heptylthiocarbonyl)choline chlor
5 cantly inhibited by replacement of NaCl with choline chloride and by sulfobromophthalein-GSH, neither
7 p eutectic solvent (DES) formed by mixing of choline chloride and phenol was used as an extraction so
8 ceived, daily for 4 weeks, a diet containing choline chloride and UMP (a uridine source) and/or DHA b
9 ES for proposed extraction was performed and choline chloride-based DES containing oxalic acid as a h
11 ere measured in Na+-containing and Na+-free (choline chloride) buffers using cells grown on gelatin-c
13 ions [3H]-1-methyl-4-phenylpyridium and [3H]-choline chloride, but did not transport other classes of
14 Different combinations of DES consisting of choline chloride (ChCl) in various mixing ratios with su
16 , male Sprague-Dawley rats were exposed to a choline chloride deficient (DEF), sufficient (CON), or s
18 /kgH2O) for 48 h by replacement of NaCl with choline chloride did not prevent the up-regulation of th
19 ith the hypothesis that supplementation with choline chloride during early development leads to an in
21 )H]palmitic acid, [(3)H]oleic acid, or [(3)H]choline chloride from differentiated THP-1 monocytic cel
22 iet with adequate amounts of choline (1 g/kg choline chloride) from conception until weaning of offsp
25 ts with a choline supplemented diet (5 mg/kg choline chloride in AIN76A) prenatally on embryonic days
26 ods rats were fed a standard diet (1.1 mg/kg choline chloride in AIN76A); control rats consumed only
27 ular Na+ with either N-methyl-D-glucamine or choline chloride increased the ERK1/2 stimulation in res
28 ing solution was replaced isosmotically with choline chloride inward currents were abolished at all p
30 es in either NaCl medium (Na+-containing) or choline chloride medium (Na+-free) at 37 degrees C and 4
31 after 1 hour of incubation in NaCl medium or choline chloride (Na(+)-free) medium containing tracer G
33 ned on a choline-supplemented diet (5.1 g/kg choline chloride) or a control, unsupplemented diet with
34 diet supplemented with choline (SUP; 5 mg/kg choline chloride) or not supplemented (CON; 1.1 mg/kg ch
35 te buffer saline, sodium perchlorate, and in choline chloride plus oxalic acid, using analytical dete
36 09 and 1.02 +/- 0.06 in 0.3 M NaCl and 0.3 M choline chloride, respectively, at substrate concentrati
37 m tonicity with NaCl, sucrose, mannitol, and choline chloride stimulated S100A4 expression, whereas u
38 ibitory property, whereas the supernatant of choline chloride-treated R36A, containing CBPs, was mark
39 eously, the reaction could be carried out in choline chloride urea as a natural deep eutectic solvent
42 nce in a deep eutectic solvent (2:1 urea and choline chloride), utilizing various orthophosphate sour
43 l)choline chloride and (1-heptylthiocarbonyl)choline chloride, were calculated from kinetic data and
44 ts inhibitory activity, we incubated R36A in choline chloride, which selectively strips CBPs from its
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