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1 d hydrolyze the CoA thioester to release the free acid.
2  also cleaved the thioester bond to give the free acid.
3 2)-G and PGE(2)-EA less efficiently than the free acid.
4 ence for the alcohols and aldehydes over the free acids.
5              It has low activity against the free acids.
6 s the dramatic difference in potency between free acid 17 and its methyl ester 21 (IC50 > 200 microM)
7   Both synthetic LXA(4) and 15-epi-LXA(4) as free acids activate recombinant human LXA(4) receptor (A
8 over a 3-wk period, both misoprostol and its free acid-active metabolite 5C-30695 significantly reduc
9 tector signal as a function of micrograms of free acid added were demonstrated in the presence of the
10                 The method allows the use of free acid and dextran-conjugated dyes.
11               In contrast, 10 nM latanoprost free acid and fluprostenol caused membrane depolarizatio
12  leukotriene A4 methyl ester, leukotriene A4 free acid and GSH were 7.6 microM, 3.6 microM and 1.6 mM
13 ve inhibitor for ibuprofen oxidation in both free acid and ibuprofen ester form.
14 ansferase (COMT; EC 2.1.1.68) methylates the free acids and caffeoyl CoA 3-O-methyltransferase (CCoAO
15 ons and low-abundance acyl neutral losses as free acids and ketenes.
16  -selective (ONO-AE1-259, AH13205, butaprost-free acid) and EP4 -selective (L-902,688, TCS251) agonis
17 M1, trans-unoprostone isopropyl, latanoprost free acid, and fluprostenol were studied on Ca(2+)-activ
18 es which include combinations of monoesters, free acids, and amines, some of which are inhibitors of
19 vity, serum liver enzymes, adipokines, fatty free acids, and high-sensitivity C-reactive protein (hsC
20                              Cytoplasmic ATP free-acid ([ATP](i)), but not the MgATP complex, activat
21 hough the native CTL epitope terminates as a free acid, both tetrasubstituted peptides only function
22  The two regimens were ceftiofur crystalline-free acid (CCFA) administered to either one or all steer
23  effects of injectable ceftiofur crystalline-free acid (CCFA) versus in-feed chlortetracycline on the
24 indicate that this lipid, in contrast to its free-acid counterpart, acts as a peroxisome proliferator
25 atives bound significantly better than their free acid counterparts, suggesting that the state of met
26 process readily delivered the Fmoc-protected free acid derivatives of AHMOD ((2S)-amino-(6R)-hydroxy-
27 allows selective quantitation of the desired free acid drug forms without significant interferences f
28 thout decomposition, avoid the production of free acid during acylation reactions, and can be used un
29  between common cationic peptides and low Mw free acid end-group poly(lactic-co-glycolic acids) (PLGA
30 reasing masses were detected and assigned to free acids, esters and polyesters with up to eight units
31  has been successful in remineralizing resin-free, acid-etched dentin, with evidence of intrafibrilla
32                       Orally consumed 3.42 g free-acid (FA-HMB) HMB (providing 2.42 g of pure HMB) ex
33 ifferentiated using this method; the salt-to-free acid form conversion ranged between less than the l
34 fter the dye ester has been converted to the free acid form in the cytoplasm.
35 ause the volatility of a drug present in its free acid form is typically much higher than that of its
36 s linked to active efflux of the hydrophilic free acid form of BCECF from the MRP-overexpressing cell
37                       ESI/QMS studies of the free acid form of low molecular weight poly(carboxylic a
38  slices gave indications that Zinquin in its free acid form was able to diffuse across the plasma and
39 onding dimethyl ester suggests that only the free-acid form of glutamine effectively inhibits ANR act
40 (TDMS) for the detection and quantitation of free acid forms in pharmaceutical drug products formulat
41 with control (0.015% ethanol in DMEM) or the free acid forms of bimatoprost (0.01 or 0.1 microg/mL),
42 ng the concentration of both the anionic and free acid forms of the Meldrum's adduct 6 in real time.
43 d with 5-6-fold higher affinities than their free acid forms.
44 ll four substrates with a preference for the free acid forms.
45  the acid binding almost completely depletes free acid from the deblocking solution.
46 ond the unit cell parameters to positions of free acid groups and included water molecules.
47  substrates are transported as CoA esters or free acids has been a matter of debate.
48  show that inhibition is competitive for the free acid ibuprofen substrate, no doubt because this sub
49 erally been supposed that pABA exists as the free acid in plant cells and that it moves between organ
50 s may be deprotected in one step to give the free acids in quantitative yields.
51 s of bimatoprost, latanoprost, and their C-1 free acids indicate that latanoprost, but not bimatopros
52 ensitivity of the method was demonstrated at free acid levels of 0.6% w/w (6 microg absolute mass).
53                                  Latanoprost-free acid (LFA)-treated NTM cells were analyzed for OPN
54 leic (LA) acids in different chemical forms (free acids, methyl esters and homogeneous triacylglycero
55 ng with PGE2, PGE2 methyl ester, misoprostol-free acid, misoprostol, and sulprostone suggested that a
56      The hydrolysis of dehydrodiferulates to free acids occurs in two discrete steps, one involving d
57                                          The free acid of acetic acid and the imidazolium ion showed
58                                          The free acids of these compounds also served as the best ac
59 ly occur via two parallel pathways involving free acids or their coenzyme A (CoA) esters.
60 ays with 10 microg/mL of either latanoprost (free acid) or prostaglandin F(2alpha) ethanolamide and c
61 sugar, sucrose, water insoluble solids, ash, free acid, pH, HMF contents, electrical conductivity and
62 all polymers but does not always release the free acid product.
63 e energy of formation of this complex from a free acid, pyridine, and a carboxylic acid dimer to be a
64  much more potent PPARalpha ligands than the free acids, resulting in altered PPARalpha conformation
65 -chain alpha-keto acids to the corresponding free acids results in the formation of ATP via substrate
66 ion; A0 = absorbance of the sensor in a salt-free acid solution) was found, and the current approach
67 e of the formulations (low molecular weight, free acid terminated) exhibited the same mechanism in vi
68 ycerols or acyl-CoA esters to the respective free acids that are required for GLUT4 transport vesicle
69 ods not only in their bound form but also as free acids that can be extracted from non-hydrolyzed sam
70 d on the concentration of ceramide; only the free acid was formed if the truncated ceramide was absen
71                                          The free acids were analyzed in a negative-ion mode, whereas
72 s of bimatoprost, latanoprost, and their C-1 free acids were determined by liquid chromatography and
73                                              Free acids were obtained by acid hydrolysis of the amide
74 ostone isopropyl ester, and their respective free acids were shown to be FP agonists in the h-TM cell

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