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1 d out by isothermal titration calorimeter in dimethylsulfoxide.
2 rom the framework under acidic conditions in dimethylsulfoxide.
3 thylacetamide approximately propionic acid < dimethylsulfoxide.
4 benign solvents such as water, formamide, or dimethylsulfoxide.
5 ogues (3, 18, 19, and 21) was carried out in dimethylsulfoxide.
6 ed with CLT compared with those treated with dimethylsulfoxide.
7 the antioxidant agents Desferal, Tempol, and dimethylsulfoxide.
8 ed air or were injected with the NNK solvent dimethylsulfoxide.
9 eal delivery of 50 mg/kg AG1296 or AG1478 in dimethylsulfoxide 1 hour before V2O5 instillation and ag
11 the same substrate, changing the solvent to dimethylsulfoxide, 3-methyl-2-alkynyl-benzofurans were s
15 ignal-to-noise ratio, excellent tolerance of dimethylsulfoxide and detergent, and the ability to dete
16 he prototypical inducers of differentiation, dimethylsulfoxide and hexamethylene bisacetamide (HMBA),
18 c acid or an acidic ion-exchange resin) with dimethylsulfoxide and/or poly(1-vinyl-2-pyrrolidinone) a
19 lar concentration of a cryoprotectant agent (dimethylsulfoxide), and the distribution of organic mate
20 nal-to-noise ratio, substantial tolerance of dimethylsulfoxide, and excellent ability to detect compe
22 fiers (DMF, thiodiglycol, dimethylacetamide, dimethylsulfoxide, and N-methylpyrrolidone) can signific
23 t differentiating agents, dimethylformamide, dimethylsulfoxide, and retinoic acid, total NEU activity
24 The 3D NMR structures of the analogues in dimethylsulfoxide are consistent with the observed bindi
26 we show superior preparations of antigens in dimethylsulfoxide, avoiding their rapid decomposition in
28 highly denaturing PCR conditions (i.e., with dimethylsulfoxide), both low- and high-stability paralog
29 been measured in solution (acetonitrile and dimethylsulfoxide) by using the EPR radical equilibratio
30 with our studies designed to understand why dimethylsulfoxide causes terminal differentiation of the
31 hloride, dimethylformamide, tetrahydrofuran, dimethylsulfoxide, chloroform, and hexamethylphosphorami
32 ing (1 degrees C/min); and 2), intracellular dimethylsulfoxide concentration is lower (by as much as
34 ring solution ionic strength in concert with dimethylsulfoxide content is sufficient to disrupt the p
35 lower polarity water-miscible solvents like dimethylsulfoxide, controls the homopolymer assembly int
36 methyl sulfoxides, dibenzyl sulfoxides, and dimethylsulfoxide could be utilized to generate diaryl s
37 udy, we showed that hepatocytes in long-term dimethylsulfoxide culture have definite advantages over
39 oxidase caused recognition and ingestion of dimethylsulfoxide-differentiated HL-60 cells by J774A.1
43 material at room temperature are described: dimethylsulfoxide (DMSO) and tetrabutylammonium fluoride
45 er systems were performed in the presence of dimethylsulfoxide (DMSO) at 2, 5, 10, and 100 mol % DMSO
46 emically-defined medium supplemented with 2% dimethylsulfoxide (DMSO) can be maintained in a well-dif
47 eviously shown that hepatocytes in long-term dimethylsulfoxide (DMSO) culture, fed a chemically defin
50 f these reactions reveal the key role of the dimethylsulfoxide (DMSO) ligand in controlling this chem
52 ), washed, and cultured (3 days) with either dimethylsulfoxide (DMSO) or hexamethylene bisacetamide (
53 Using the microperfusion chamber, water and dimethylsulfoxide (DMSO) permeability coefficients of mo
55 form of the cofactor that is required by the dimethylsulfoxide (DMSO) reductase family of enzymes, wh
57 ons on dipalmitoylphosphatidylcholine (DPPC)/dimethylsulfoxide (DMSO) system that has the same lipid:
58 s: the control group (group 1) received only dimethylsulfoxide (DMSO) which is the solvent for CMX-13
59 meation of the mixture was enhanced with 15% dimethylsulfoxide (DMSO), 1% limonene, and rosemary oil.
60 olic acidosis and liver and kidney toxicity; dimethylsulfoxide (DMSO), a free radical-scavenging solv
61 ulation, we tested the effects of capsaicin, dimethylsulfoxide (DMSO), and morphine on withdrawal lat
62 ia (MEL) cells induced to differentiate with dimethylsulfoxide (DMSO), and p300 and Tal1 were observe
63 tities of certain organic chemicals, such as dimethylsulfoxide (DMSO), betaine, polyethylene glycol a
64 based solutions to which either no additive, dimethylsulfoxide (DMSO), or N-methylpyrrolidine-2-thion
65 er mobility than the backbone labels, and in dimethylsulfoxide (DMSO), the backbone end labels were s
66 In a more polar solvent, for example, in dimethylsulfoxide (DMSO), the two isomers interconvert t
67 amine N-oxide (TMAO) and the organic solvent dimethylsulfoxide (DMSO), which we refer to as 'chemical
72 fatigue trial; (2) a group given intravenous dimethylsulfoxide (DMSO, 0.5 ml/kg of a 50% solution) be
73 were treated with sophorolipids or vehicle (dimethylsulfoxide [DMSO]/physiologic saline) by intraven
75 urine erythroleukemia (MEL) cells induced by dimethylsulfoxide, expression of TfR1 increased, whereas
76 t with antioxidants, N-ACETYL-L-CYSTEINE, or dimethylsulfoxide, failed to attenuate plasma endotoxin
77 xarotene or 9-cis retinoic acid) or vehicle (dimethylsulfoxide) for 24 hours before stimulation with
79 on, whereas a scavenger of hydroxyl radical (dimethylsulfoxide), hydrogen peroxide (catalase), and su
81 y the hydroxyl radical scavengers, including dimethylsulfoxide, mannitol, and 5,5-dimethyl-1-pyrrolin
83 ion (mDP) and different solvents (ethanol or dimethylsulfoxide)] on this interaction by fluorescence
84 in organic solvents, such as isopropanol and dimethylsulfoxide or by enzymatic cleavage of the pyroph
85 In a Sla1(-) background, [PSI] curing by dimethylsulfoxide or excess Hsp104 is increased, while t
89 oups were studied: phosphate-buffered saline/dimethylsulfoxide (PBS/DMSO) (vehicles), PBS/ANTU, and K
93 ductase (PcrAB), a specialized member of the dimethylsulfoxide reductase superfamily, catalyzes the f
94 tein-bound sites of DMSOR and TMAOR (DMSOR = dimethylsulfoxide reductase, TMAOR = trimethylamine N-ox
100 mation of POBN-CH3 adduct in the presence of dimethylsulfoxide, suggesting the production of hydroxyl
101 ed from 20 to 72 wt% with the addition of 2% dimethylsulfoxide to distilled water used as a medium.
102 enes, we discovered the capacity of HMBA and dimethylsulfoxide to enhance the expression of transient
103 upplemented with epidermal growth factor and dimethylsulfoxide to maintain rat hepatocytes in a highl
106 eutic window: STAZN (0.6 mg/kg) dissolved in dimethylsulfoxide was given intra-peritoneally at 2 and
109 ron generation, an organogel was obtained in dimethylsulfoxide, while nanorods and micellar aggregate
111 ation of the dimsyl anion by the reaction of dimethylsulfoxide with potassium tert-butoxide was cruci