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1 LR ligands in the presence and/or absence of triclosan.
2 DEET, carbamazepine, dilantin, naproxen, and triclosan.
3 55, which is abrogated by pre-treatment with triclosan.
4 and exposure history alter the influence of triclosan.
5 nd identified sociodemographic predictors of triclosan.
6 rnal concentrations followed by tonalide and triclosan.
7 CI: 0.97, 1.4) per log(10) unit increase in triclosan.
8 phthalate, and 8,000-24,000 ppm (range) for triclosan.
9 thpaste with polymer and fluoride containing triclosan.
10 to those achieved with toothpaste containing triclosan.
11 nol, ibuprofen, diclofenac, bisphenol A, and triclosan.
12 containing chlorophenol side-chains such as triclosan.
13 , ketorolac, and Total toothpaste containing triclosan.
14 e oxidation of either mono- or dichlorinated triclosan.
15 is the target of the antibacterial compound, triclosan.
16 , ethionamide, ofloxacin, thiolactomycin and triclosan.
17 enzyme has the requisite amino acids to bind triclosan.
18 ifference in affinities of FabI and InhA for triclosan.
19 cobacterial enoyl reductases are targets for triclosan.
20 san, show significantly reduced affinity for triclosan.
21 ficiently inhibited by low concentrations of triclosan.
22 was also NADH dependent but not inhibited by triclosan.
23 nd propyl parabens), 2,5-dichlorophenol, and triclosan.
24 children was also positively associated with triclosan.
25 als treated with the lowest doses of MPB and triclosan.
26 combination of rifampicin, sparfloxacin and triclosan.
27 on balloons were inflated with a solution of triclosan (10 g/L), the catheters drained freely for at
28 none-3 (2-hydroxy-4-metoxybenzophenone); and triclosan (2,4,4'-trichloro-2'-hydroxyphenyl ether).
29 analytes studied (gemfibrozil, nonylphenol, triclosan, 2,4,6-trichlorophenol, and naphthenic acids),
32 ct concentrations (LOAECs) were 1.04 muM for triclosan, 3.17 muM for triclocarban, 0.372 muM for bis-
33 at were amended with lower concentrations of triclosan (5 mg/kg and 50 mg/kg) initially diverged and
35 inary inhibition studies, we have shown that triclosan, 5-ethyl-2-phenoxyphenol (EPP), and 5-chloro-2
38 s chlorination experiments were performed on triclosan, a previously studied environmental contaminan
40 rophenol, pyraclostrobin, sulfasalazine, and triclosan, achieving detection limits of 0.07, 0.24, 10.
41 R with triclosan and NAD(+) which reveal how triclosan acts as a site-directed, picomolar inhibitor o
42 eplacement of A197 with Met has no impact on triclosan affinity, indicating that differences in the s
43 ased concomitantly with the disappearance of triclosan after a 15 min reaction, the sustained toxicit
46 ficantly increased with the level of urinary triclosan among male subjects (odds ratio for third vs f
47 ies indicate that the antibacterial compound triclosan, an additive in many personal care products, i
52 hod to calculate the affinity of a series of triclosan analogues for the E. coli enoyl reductase FabI
53 ly reduce the teratogenicity of bisphenol A, triclosan and 17alpha-ethinyl estradiol without generati
55 eactions with free chlorine alone, while for triclosan and bisphenol A the free iodine mediated trans
58 ing one between the ubiquitous antimicrobial triclosan and erm(X), a 23S rRNA methyltransferase impli
59 A nonmonotonic association was observed for triclosan and girls' adiposity; however, it was due to e
60 dren and exposure to the antibacterial agent triclosan and having filaggrin (FLG) loss-of-function mu
63 persive SPE cleanup procedure for extracting triclosan and methyltriclosan from fish roe and surimi s
64 TiO(2), precursor-complex formation between triclosan and MnO(2) was much slower and likely became t
65 lexes of E. coli and Brassica napus ENR with triclosan and NAD(+) which reveal how triclosan acts as
66 ry complex with NADH, a ternary complex with triclosan and NAD(+), and as ternary complexes bound to
67 trend toward an inverse association between triclosan and paraben exposure and allergic sensitizatio
68 association between prenatal and early-life triclosan and paraben exposure and childhood allergic di
69 However, levels of the antimicrobial EDCs triclosan and parabens were significantly associated wit
73 sed with the level of the antimicrobial EDCs triclosan and propyl and butyl parabens (P </= .04).
74 mechanism for the antibacterial activity of triclosan and substantiate the hypothesis that its activ
76 nhA, Y156F FabI has a decreased affinity for triclosan and the inhibitor binds to both E.NAD(+) and E
77 results in markedly increased resistance to triclosan and the purified enzyme is much more resistant
78 ewed research, this statement concludes that triclosan and triclocarban are environmentally persisten
79 The polychlorinated aromatic antimicrobials triclosan and triclocarban are in widespread use for kil
81 other hazards to humans and ecosystems from triclosan and triclocarban is presented along with recom
86 urinary chemical concentrations of parabens, triclosan and triclorcarban in relation to TTP; chemical
88 nols (e.g., bisphenol A, benzophenone-3, and triclosan) and parabens is widespread in the population.
89 ting chemicals such as phthalates, parabens, triclosan, and benzophenone-3 (BP-3) for adolescent girl
90 f the phenolic compounds 2,4-dichlorophenol, triclosan, and bisphenol A in chlorinated waters contain
91 nalyzed for phthalate metabolites, parabens, triclosan, and BP-3 using high-performance liquid chroma
92 labeled to be free of phthalates, parabens, triclosan, and BP-3, can reduce personal exposure to pos
93 g10 concentrations of widely monitored HHCB, triclosan, and carbamazepine explained 71-82% of the var
95 m of the bacteriostatic agents triclocarban, triclosan, and its transformation product methyl triclos
98 e class of antibacterial agents, the biocide triclosan, and one of the targets for the front-line ant
99 ons and urinary bisphenol A, benzophenone-3, triclosan, and paraben levels in male and female childre
100 scopy results indicate that phenol, aniline, triclosan, and related byproducts are associated with th
101 ), bisphenols, benzophenone-type UV filters, triclosan, and triclocarban are used in a variety of con
102 l phthalate (DEP), methyl paraben (MPB), and triclosan] and urine and serum concentrations of their r
103 n urinary concentrations of triclocarban and triclosan, another commonly used antibacterial agent.
104 n northern MN, the four dioxins derived from triclosan are present prior to the patent of triclosan,
105 e" complex accounts for the effectiveness of triclosan as a FabI inhibitor and illustrates that mutat
108 ther exposures (total parabens, bisphenol A, triclosan, benzophenone-3, total phthalates, and 2,4-DCP
109 ination Survey in which urinary bisphenol A; triclosan; benzophenone-3; propyl, methyl, butyl, and et
110 These data define the structural basis of triclosan binding to PfENR and will facilitate structure
112 ly, the Y158 hydroxyl group is important for triclosan binding, suggesting that triclosan binds in si
113 rtant for triclosan binding, suggesting that triclosan binds in similar ways to both InhA and EnvM.
115 scence binding experiments, we conclude that triclosan binds to the enzyme-NAD(+) product complex whi
116 strate specificity that encompasses not only triclosan but the detergent SDS, which are often used to
118 0156-PA0157-PA0158 pump, which only effluxed triclosan, but not closely related compounds, antibiotic
119 The replacement of the ether linkage in triclosan by a carbon bridge in hexachlorophene prevente
120 explain the observed adsorption behavior of triclosan by the binary oxide mixtures and single oxides
121 to strong adsorption and slow desorption of triclosan by TiO(2), precursor-complex formation between
122 red to the wild-type enzyme, indicating that triclosan can stimulate the emergence of isoniazid-resis
126 h percentile, and 4-fold higher than maximum triclosan concentration that has been detected in U.S. b
127 zation among those in the fourth quartile of triclosan concentration was 2.0 [95% confidence interval
128 JK) Delta(mexXY) strain PAO509 to increasing triclosan concentrations and derived a resistant strain,
131 erns, variability, and predictors of urinary triclosan concentrations in 389 mother-child pairs enrol
136 frice in reducing gingivitis compared to the triclosan/copolymer control in this partially supervised
137 L and root caries versus the sodium fluoride/triclosan/copolymer control in xerostomic patients.
139 the limits of the present study, the use of triclosan/copolymer dentifrice promoted additional clini
142 ve control dentifrice (sodium fluoride/0.30% triclosan/copolymer) in 440 medication-induced xerostomi
143 es were amended with 5, 50, and 500 mg/kg of triclosan, corresponding to the median, 95th percentile,
145 he accumulation rates and temporal trends of triclosan, CTDs, and dioxins in aquatic sediments were f
146 ources recorded increasing concentrations of triclosan, CTDs, and their derived dioxins since the pat
147 of waters to these compounds, the levels of triclosan, CTDs, and their derived dioxins were determin
149 2) dentifrice relative to a positive control triclosan dentifrice for prevention of clinical attachme
150 icrobial agent in handsoaps, and chlorinated triclosan derivatives (CTDs, formed during disinfection
151 positive bacteria are naturally resistant to triclosan due to the presence of the triclosan-resistant
153 may function as a two-component RND pump for triclosan efflux but must associate with OprM to form a
156 he function, composition and assembly of the triclosan efflux transporter TriABC-OpmH from Pseudomona
157 ded parabens, phthalates, bisphenol A (BPA), triclosan, ethanolamines, alkylphenols, fragrances, glyc
160 e residue, with Phe, reduces the affinity of triclosan for the enzyme and results in noncompetitive i
161 netic selection experiments, the affinity of triclosan for the FabI mutants G93V, M159T, and F203L is
162 e) and one personal care product ingredient (triclosan) for the oligochaete Lumbriculus variegatus.
164 y methylparaben, propylparaben, bisphenol A, triclosan, galaxolide, and 4- methylbenzilidene camphor
165 stic actions, and the personal care products triclosan, galaxolide, and nonylphenol are representativ
167 te than either patients with diabetes in the triclosan group or patients without diabetes in each gro
171 analysis of the inhibition of the enzyme by triclosan has been conducted showing that triclosan is a
172 crobial agents such as stannous fluoride and triclosan have been incorporated into dentifrice formula
173 expressing FabI(Y147H) was also resistant to triclosan; however, the strain expressing FabI(M99T) was
174 very little information, however, about how triclosan impacts microbial communities in anaerobic dig
177 : 0.21-5.43; P = 0.93; I = 44%) CONCLUSIONS: Triclosan-impregnated sutures do not decrease the rate o
183 se oxide [MnOx(s)] with phenol, aniline, and triclosan in batch experiments using X-ray photoelectron
184 elates with resistance to the common biocide triclosan in Mycobacterium smegmatis, binding to form th
188 yl paraben, benzophenone-3, bisphenol A, and triclosan in urine collected during 1997-2006 from 50 pa
189 of alkyl esters of p-hydroxybenzoic acid and triclosan in vitro on the basis of steady-state fluoresc
190 s, benzophenone-3, BPA, two dichlorophenols, triclosan) in spot urine samples collected during pregna
191 by triclosan has been conducted showing that triclosan is a competitive inhibitor with respect to NAD
192 t with previous studies, we report here that triclosan is a slow, reversible, tight binding inhibitor
196 phthalates and phenols such as parabens and triclosan, is ubiquitous within the U.S. general populat
198 unexposed communities were exposed to 500 mg triclosan/kg, function was maintained, but the abundance
200 as a significant interaction between sex and triclosan level, with male subjects being more likely to
201 trogenic activity of CPC, BAK, rotenone, and triclosan may be related to their mitochondrial inhibito
202 Mass ratios of DCC-to-TCC and of methyl-triclosan (MeTCS)-to-TCS, serving as indicators of trans
205 y where the enzyme contained either a single triclosan molecule, in a configuration typical of other
207 tal, Brisbane, Australia, were randomized to triclosan (n = 193) or placebo (n = 190) groups and asse
208 rmine effects of the anti-inflammatory agent triclosan on the TLR-hyper-inflammatory phenotype, prima
209 Whereas cyperin was much less potent than triclosan on this target site, their ability to cause li
211 association between prenatal and early-life triclosan or paraben concentrations and childhood asthma
212 sociations of maternal plasma or child urine triclosan or paraben concentrations with asthma or recur
214 her organic chemicals (i.e., benzophenone-3, triclosan, parabens) in human urine, milk, and serum to
217 but only the association in males exposed to triclosan remained statistically significant after corre
218 ss correlation coefficients (ICCs) to assess triclosan reproducibility and identified sociodemographi
221 aeruginosa achieves high-level (MIC>1 mg/ml) triclosan resistance either by constitutive expression o
222 haracterization of a DNA fragment conferring triclosan resistance from one of these mutants revealed
223 tation in the chromosomal safabI gene led to triclosan resistance in S. aureus; however, these strain
227 tant to triclosan due to the presence of the triclosan-resistant enoyl-ACP reductase isoforms, FabK a
229 cide triclosan as a selective agent, several triclosan-resistant mutants of a susceptible Pseudomonas
232 f InhA with the broad spectrum antimicrobial triclosan revealed a unique stoichiometry where the enzy
234 ents of our optimization program to decouple triclosan's specific FabI effect from its nonspecific cy
236 the increased tetracycline, penicillin, and triclosan sensitivities resulted from repression of the
237 in resistance of Mycobacterium smegmatis to triclosan, show significantly reduced affinity for tricl
238 e ability to improve the in vitro potency of triclosan significantly by replacing the suboptimal 5-ch
240 configuration typical of other bacterial ENR:triclosan structures, or harbored two triclosan molecule
242 tional calculations of the excited states of triclosan support the involvement of a radical intermedi
243 in P. aeruginosa shown to efficiently efflux triclosan, supporting the notion that efflux is the prim
244 ic domains, and its inhibition by drugs like triclosan (TCL) can increase cytotoxicity and decrease d
255 of bisphenol A (BPA), benzophenone-3 (BP-3), triclosan (TCS), and parabens with serum total testoster
256 ), benzophenone-3 (BP-3), bisphenol A (BPA), triclosan (TCS), butyl paraben (B-PB), methyl paraben (M
258 LISA) for the detection of the antimicrobial triclosan (TCS; 2,4,4'-trichloro-2'-hydroxydiphenyl ethe
260 ere with the formation of a stable FabI-NAD+-triclosan ternary complex acquire resistance to the drug
263 nto surface waters via wastewater effluents, triclosan, the antimicrobial agent in handsoaps, and chl
264 activity was NADH dependent and inhibited by triclosan; the residual activity in the fabI mutant was
265 ver weeks to months; children are exposed to triclosan through the use of some personal-care products
266 n of the slow-onset, tight-binding inhibitor triclosan to explore the interactions between the type I
267 tants to compare and contrast the binding of triclosan to InhA, the homologous enoyl reductase from M
273 two inhibitors having well-defined targets: triclosan (TRC), which inhibits InhA; and thiolactomycin
274 dations intended to prevent future harm from triclosan, triclocarban, and antimicrobial substances wi
275 stance genes and the antimicrobial chemicals triclosan, triclocarban, and methyl-, ethyl-, propyl-, a
276 of BASL4 overpredicted the concentrations of triclosan, triclocarban, and miconazole in root and shoo
279 trends were directly attributed to increased triclosan use, local improvements in treatment, and chan
280 ure to the synthetic antimicrobial chemical, triclosan, used in personal care products, has been hypo
286 l in the MnOx(s) surface after reaction with triclosan was detected by XPS survey scans, while no Cl
287 losan, and its transformation product methyl triclosan was investigated after their uptake into carro
293 a phenolic ring (parabens, bisphenol A, and triclosan) were completely transformed on this anode at
294 and 5-chloro-2-(2,4-dichlorophenoxy)phenol (triclosan)) were measured for 15 sorbents: fresh and car
295 is was associated with the highest levels of triclosan, whereas no association was seen for current a
296 was as sensitive as the wild-type strain to triclosan, whereas the ygaA knockout was 250-fold more s
297 berculosis drug isoniazid and the antiseptic triclosan, which are inhibitors of fatty acid biosynthes
299 rd to the structure-activity relationship of triclosan while affording gains against cultured parasit
300 tuberculosis, show unimpaired inhibition by triclosan, with uncompetitive inhibition constants (K(i)
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