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1 ounterpart Na-exposed rats (pair-fed 216 ppm sodium acetate).
2 cetonitrile, followed by a cleanup step with sodium acetate.
3 fiber diet, or normal chow supplemented with sodium acetate.
4 ophoresis in solutions containing 0.01-1.0 M sodium acetate.
5 thanebis(diazene-N-oxide-N'-hydroxylate) and sodium acetate.
6 degrees C to produce methane by pyrolysis of sodium acetate.
7 thanebis(diazene-N-oxide-N'-hydroxylate) and sodium acetate.
8 es from 9:1 DMF/water mixtures buffered with sodium acetate.
9 ses for both Whatman 1PS paper and 30% TlNO3/sodium acetate.
10 s concentrations of potassium, rubidium, and sodium acetate.
11 ot to a normal meal or one supplemented with sodium acetate.
12 in calli supplemented with [U-(13)C]glucose, sodium acetate (1,2-(13)C2) and sodium octanoate (1,2,3,
14 ere administered lead acetate, 100 mg/kg, or sodium acetate, 36 mg/kg (control), by i.p. for 7 days.
15 urbit[6]uril analogue (1) in aqueous buffer (sodium acetate, 50 mM, pH 4.74, 25 degrees C) toward a v
18 the literature conditions (acetic anhydride/sodium acetate) affords both the indole 6 and the indoli
19 phaE328A was sensitive to chemical rescue by sodium acetate, an effect that was not reproduced by pho
20 product at 100 degrees C in the presence of sodium acetate and 1% sodium dodecyl sulfate generates f
23 tified via intravenous infusion of [1-(13)C] sodium acetate and mass isotopomer distribution analysis
24 of eicosanoids were poorly resolved by IMS, sodium acetate and metal adducts (e.g., Li, Na, Ag, Ba,
25 creased levels of select components, notably sodium acetate and sodium bicarbonate, restored the leve
26 l cellulose (MC) core with anthocyanidin and sodium acetate, and chitosan/gallotannin-based shell.
27 l cellulose (MC) core with anthocyanidin and sodium acetate, and chitosan/gallotannin-based shell.
29 dium formate, [1-(13)C]glycine, and [2-(13)C]sodium acetate, and our technique is immediately extenda
30 r of salts (sodium sulfate, sodium fluoride, sodium acetate, and sodium chloride) on the thermodynami
32 ent, 3.5% (wt%) DCl in D(2)O as the solvent, sodium acetate as an internal standard, and heating at 9
34 in was inhibited by acetylsalicylic acid and sodium acetate as well as by N-acetylated glucosamine an
35 situ from partial transformation of aqueous sodium acetate at 300 degrees C and 2.4-3.5 GPa and that
36 , potassium phosphate, potassium acetate and sodium acetate) at varying concentrations (0.8 to 1.6 M)
40 al and electrochemical parameters used were: sodium acetate buffer (pH = 4.3), an accumulation potent
41 u were labeled with DOTATATE by heating in a sodium acetate buffer and 4-(2-hydroxyethyl)-1-piperazin
46 A solution of AlCl(3).6H(2)O in a pH 4.0 sodium-acetate buffer was mixed with an aqueous solution
47 acidified 5 M NaCl solution directly into a sodium acetate-buffered solution containing a DOTA (1,4,
48 experiments, different acids or acetic acid/sodium acetate buffers at different pHs were used to evo
49 he vast majority of studies rely on standard sodium acetate buffers or commercially sourced reagents
51 on the observations of different patterns of sodium acetate clusters that are characteristic for each
52 ensity, are quantified as functions of salt (sodium acetate) concentration for the interactions of th
59 ling the fast, exothermic crystallization of sodium acetate from a metastable aqueous solution into t
60 matography using sodium hydroxide (NaOH) and sodium acetate gradients, coupled with integrated pulsed
61 ication was carried out using supersaturated sodium acetate heat packs and results compared to those
62 e phase modifiers (i.e., ammonium formate or sodium acetate); however, these ESI adduct signals are l
64 deprotected and cyclized in the presence of sodium acetate in refluxing ethanol to afford (+/-)-abys
66 ion of aqueous solvents sodium hydroxide and sodium acetate, in contrast to conventional isocratic el
68 is is associated with changes of glucose and sodium acetate metabolism, demonstrating HRMAS NMR as a
69 by a high-fiber diet or supplementation with sodium acetate modified alloimmunity in a kidney transpl
70 broader (+13 to +42) in solutions containing sodium acetate (NaAc), ammonium chloride (AmmCl), potass
72 ve to 500 mM concentrations of NaCl, Na2SO4, sodium acetate (NaAc), KCl, K2SO4, potassium acetate (KA
73 ylbutyrate (PBA), sodium butyrate (NaB), and sodium acetate (NaAC), on ZIKV replication and associate
74 0 mM histidine/240 mM sucrose buffer, 0.25 M sodium acetate (NaOAc) buffer containing 5 mg.mL(-1) n-a
75 ute application of SCFAs (sodium propionate, sodium acetate or butyric acid) dose-dependently (0.5-30
76 In contrast, the replacement of NaCl with sodium acetate, or pretreatment of cells with the Cl- ch
78 ution conditions used (3.8 mM protein, 50 mM sodium acetate, pH 4.5, 20 degreesC), and that it tumble
80 solution containing guanidinium thiocyanate, sodium acetate, phenol and chloroform, followed by centr
81 m-proton antiporter genes also contribute to sodium acetate, potassium acetate, and ammonium acetate
82 370) potassium chloride (PubChem CID: 4873), sodium acetate (PubChem CID: 517045), loganic acid (PubC
83 s, replacement of 300 mosmol/kgH2O NaCl with sodium acetate resulted in down-regulation of the gamma
84 ly from microbial membranes using an aqueous sodium acetate (SA) buffer that can be used to identify
87 its for sodium chloride, potassium chloride, sodium acetate, sodium fluoride, sodium dodecyl sulfate
88 ure for up to 1 month in the ethylene glycol-sodium acetate solvent system without the requirement fo
91 under 300 nm irradiation in the presence of sodium acetate to afford 5,6-bis(methylthio)-5-hexenol i
93 Zymomonas mobilis mutant (AcR) demonstrating sodium acetate tolerance that has potential importance i
95 itter was incubated with 100 mM of [2-(13)C] sodium acetate under thermophilic anaerobic conditions.
96 ocks, including chromium, iron, nitrate, and sodium acetate, were selected to represent the shocks of
97 romatic C-H activation was first promoted by sodium acetate with [Cp*MCl2]2 (M = Rh, Ir) at room temp