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1 BPA and BPS altered the expression of an identical set o
2 BPA and BPS did not degrade (1 h; 100 degrees C) in wate
3 BPA and GEN exposed females had increased number of meta
4 BPA and phthalate metabolites were not associated with e
5 BPA and TBBPA both interfere with skeletal muscle functi
6 BPA bioaccessibility was evaluated in six positive sampl
7 BPA disrupts endocrine pathways in fish, but the long-te
8 BPA exposure down-regulated WNT2 expression, and elevate
9 BPA exposure impeded the interaction between the human c
10 BPA exposure increased Nrf2 binding to a putative antiox
11 BPA has been associated with numerous adverse health out
12 BPA increased Na(v)-mediated ramp currents elicited with
13 BPA may have toxic effects on the female reproductive sy
14 BPA or vehicle-treated rats from an FDA facility were us
15 BPA showed the lowest concentrations (8.3 pg/g f.w.), fa
16 BPA was detected in 17 out of 40 samples (42.5%); in som
17 BPA was not associated with most BASC-2 scales; however,
18 BPA was not associated with WPPSI-III scores; child sex
19 BPA was positively associated with the relationship prob
20 bited statistically significant (p < 0.0001) BPA removal (40% and 46%, respectively) over approximate
28 vide a definitive evaluation of bisphenol A (BPA) and explain disparities between traditional regulat
29 f serially assessed exposure to bisphenol A (BPA) and phthalates on measures of kidney function, tubu
33 nol S (BPS) as a substitute for bisphenol A (BPA) could actually increase the risk of endocrine disru
34 ealed that prenatal exposure to bisphenol A (BPA) disrupted the transcriptome profiles of genes in th
35 A positive association between Bisphenol A (BPA) exposure and coronary heart disease has been shown,
38 vironmental disrupting chemical bisphenol A (BPA) has estrogenic activity, but its implications in pa
40 Although prenatal exposure to bisphenol A (BPA) has recently been associated with the ASD risk, whe
41 on an innovative heterogeneous bisphenol A (BPA) immunoassay based on an electrolyte-gated organic f
46 vironmental endocrine disruptor bisphenol A (BPA) is ubiquitous and associated with the increased ris
48 Laboratory studies show that bisphenol A (BPA) leaches from bisphenol A-glycidyl methacrylate (bis
51 e endocrine disrupting chemical bisphenol A (BPA) while exerting estrogenic effects of comparable pot
53 gests that prenatal exposure to bisphenol A (BPA), a ubiquitous endocrine-disrupting chemical, is ass
54 increasingly used to substitute bisphenol A (BPA), a widespread environmental endocrine disruptor and
55 nol F diglycidyl ether (BFDGE), bisphenol A (BPA), bisphenol B (BPB), bisphenol F (BPF) and bisphenol
56 ignin-derivable alternatives to bisphenol A (BPA), but limited bioassay data are available on their e
57 in industrial chemicals, e.g., bisphenol A (BPA), present in plastics and other products that are pr
58 gers inhibited the oxidation of bisphenol A (BPA), suggesting the possible involvement of ROSs; howev
64 er of this family of compounds, bisphenol-A (BPA), when spiked (at 1 mug.g(-1) concentration) in the
68 ealth record-based "best practice advisory" (BPA) that prompted primary care providers to perform HCV
69 ectronic medical record best practice alert (BPA) based on procalcitonin and respiratory polymerase c
70 tigated the impact of a best practice alert (BPA) through the electronic health records on the rates
71 lectronic health record best practice alert [BPA], and patient solicitation), evaluated hepatitis C v
73 10 genes shared only between the BPA(25) and BPA(250) groups, with 115 of them predicted to be regula
75 significant differences between control and BPA dose groups at PND21, whereas at PND90 there were si
76 d among 80 pregnant women and 55 infants and BPA and phthalate concentrations in multiple maternal an
77 lysis, we reported that DEHP metabolites and BPA were significantly associated with an approximate 20
82 ed to the use of alternate chemicals such as BPA analogues bisphenol S (BPS) and bisphenol AF (BPAF)
84 used PA gel yielded higher SBS than the BCA/BPA etchants, it exhibited greater adhesive remnants wit
85 al variations of the benzylphenoxyacetamide (BPA) molecular skeleton were explored as a viable starti
87 expressed, although the association between BPA-responsive genes and AD-related genes has not been t
88 ed significant positive associations between BPA and fat weight [SMD=0.67 (95% CI: 0.53, 0.81)], trig
91 sure and 8-OHdG and 8-NO2Gua levels, between BPA and 8-isoPF2alpha levels, and between maternal CRP l
92 lorophyll (p > 0.19), and peroxidase between BPA-treated and untreated plants indicates substantial B
93 sing statistical models, 25 mug/kg BW/d BPA [BPA(25)], or 250 mug/kg BW/d BPA [BPA(250)] exerted effe
94 BW/d BPA [BPA(25)], or 250 mug/kg BW/d BPA [BPA(250)] exerted effects similar to that of EE2 at 0.5
95 f BPA from thermal paper receipts occurs but BPA pharmacokinetics following dermal exposure is not un
96 ves were primary sites for ERE activation by BPA and MBP, and transcriptomic analysis of microdissect
98 etween ERE activation in the heart valves by BPA's reactive metabolite MBP and the development of val
101 Regulatory Insights on Bisphenol-A (CLARITY-BPA) is a rare collaboration of guideline-compliant (cor
102 ulatory Insights on Toxicity of BPA (CLARITY-BPA; henceforth CLARITY), was launched by three US agenc
104 tors, and urinary creatinine concentrations, BPA, but not BPF or BPS, was significantly associated wi
106 on, using statistical models, 25 mug/kg BW/d BPA [BPA(25)], or 250 mug/kg BW/d BPA [BPA(250)] exerted
107 ug/kg BW/d BPA [BPA(25)], or 250 mug/kg BW/d BPA [BPA(250)] exerted effects similar to that of EE2 at
108 CD-1 mice exposed to 4 to 40,000 mug/kg/day BPA or 0.02 to 2 mug/kg/day EE from conception until 12-
110 s, relative to BPA and one petroleum-derived BPA analogue (bisphenol F, BPF), and the incorporation o
111 e the pharmacokinetics of dermal and dietary BPA exposure, six male participants handled simulated re
118 d dental materials and that chronic low-dose BPA exposure may adversely affect child health, strategi
119 to carcinoma in rats given neonatal low-dose BPA with adult T+E but not in rats given adult T+E alone
120 he exposure also disrupted a unique low-dose BPA-gene signature with predictive value for survival ou
121 tions of 6 chemical exposure measures (i.e., BPA, PA, and 4 phthalate metabolite groups) and clinical
122 rved evidence of sexually dimorphic effects; BPA concentrations were associated with increased odds o
123 To satisfy the increasing need to ensure "BPA-free" articles, a liquid chromatography-tandem mass
127 orst-case (10x ) maximum fetal exposures for BPA, or equivalent concentrations of its metabolite MBP,
131 nol S (BPS), which have been substituted for BPA in some consumer products, have also shown endocrine
132 s on average about 250 times higher than for BPA for an equal oral molar dose of the two compounds.
141 t migration pattern groups were highlighted: BPA and Zn (and Pb to a lesser extent) showed similar mi
146 inants in different food matrices, including BPA, BPS, bis(2-ethylhexyl) adipate, dibutyl adipate, he
147 ning relevant levels of BPA (isotope-labeled BPA-d16) for 5 min, followed by hand-washing 2 h later.
148 d BPAP (1.6 ng L(-1)), while bottles leached BPA (<222 ng L(-1)) and BPF, BPE, BPB and BPZ (1.1-4.6 n
151 t differences between control and the lowest BPA dose and between control and the lowest EE2 dose in
154 ndings from this study suggest that maternal BPA exposure may increase AD risk in offspring by dysreg
155 in the hippocampus and suggest that maternal BPA exposure may increase ASD susceptibility by dysregul
158 ffect child health, strategies that minimize BPA exposure could potentially improve child health.
159 sal root ganglia (DRG) nociceptors with 1 nM BPA increases the frequency of action potential firing.
162 ronic PND21 specimens displayed nonmonotonic BPA effects, with a breaking point between the 25 and 25
165 o dietary BPA exposure, dermal absorption of BPA leads to prolonged exposure and may lead to higher p
167 nd urine after intravenous administration of BPA, BPS, and BPS glucuronide (BPSG) and gavage administ
168 ereas there were significant associations of BPA exposure with general and abdominal obesity, BPF or
172 th percentiles) of urinary concentrations of BPA, BPF, and BPS were 1.40 (0.19-3.85), 0.65 (0.34-1.39
176 ndard deviation [SD] 1.6), concentrations of BPA, phthalic acid (PA), and phthalate metabolites were
178 determined, which will inform the design of BPA removal phytotechnologies for a variety of soil cond
181 based TK model describing the disposition of BPA and BPS and their glucuronides was built from these
183 In contrast, only 77% of the oral dose of BPA was absorbed and underwent an extensive first-pass g
184 rague-Dawley rats were exposed to 5 doses of BPA [0, 25, 250, 2,500, or 25,000 mug/kg body weight (BW
185 ther lifelong exposure to different doses of BPA induced uterine abnormalities and molecular changes
189 ucted in piglets to evaluate the kinetics of BPA, BPS, and their glucuronoconjugated metabolites in p
191 lated receipts containing relevant levels of BPA (isotope-labeled BPA-d16) for 5 min, followed by han
197 We compared efficacy and safety outcomes of BPA with or without pulmonary vasodilators to pulmonary
202 r was also applied for the quantification of BPA present drinking water stored in the plastic bottles
203 omparing the highest with lowest quartile of BPA, 1.02 (0.70-1.47) for BPF, and 1.22 (0.81-1.83) for
205 line was mainly caused by the replacement of BPA by BPS in thermal paper and the lower dermal uptake
210 demic and Regulatory Insights on Toxicity of BPA (CLARITY-BPA; henceforth CLARITY), was launched by t
215 ernal diet to GEN (250 mg/kg feed weight) or BPA (5 mg/kg feed weight, low dose- LD or 50 mg/kg, uppe
216 We recently demonstrated that perinatal BPA exposure is associated with higher body fat, impaire
218 e estimated the association between prenatal BPA exposure and child neurobehavior at 3 y of age in a
220 dings from this study indicate that prenatal BPA exposure alters the expression of ASD-linked genes i
221 iling data from several previously published BPA studies consistently showed that BPA-responsive gene
222 ome profiling data from previously published BPA studies consistently showed that BPA-responsive gene
223 hly sensitive methods are needed to quantify BPA in various matrices including water, serum, and food
225 n of 476 human orthologous genes in this rat BPA signature robustly predicted the overall survival (p
226 d humans, our results suggest that replacing BPA with BPS will likely lead to increased internal expo
228 er but with different kind of sauces, showed BPA levels ranging from <1microgkg(-1) (limit of quantif
230 The automated antimicrobial stewardship BPA effectively reduced antibiotic use and discharge pre
231 The automated antimicrobial stewardship BPA effectively reduced antibiotic use and discharge pre
236 mportantly, with significantly lower EA than BPA over an environmentally relevant range of 10(-10)-10
237 cts to BPA and that BPAF is more potent than BPA, further highlighting health concerns regarding the
239 Taken together, these data demonstrate that BPA exposure alters trophoblast cell invasion and causes
241 blished BPA studies consistently showed that BPA-responsive genes were significantly associated with
242 blished BPA studies consistently showed that BPA-responsive genes were significantly associated with
245 ly shorter AGD in daughters, suggesting that BPA may alter the hormonal environment of the female fet
251 d a set of 710 genes shared only between the BPA(25) and BPA(250) groups, with 115 of them predicted
252 he pseudo-second-order rate constant for the BPA pollutant is 182.3 g mg(-1) min(-1), which is the hi
254 fraction were managed by 93 providers in the BPA (n=997 patients) and 102 providers in the no BPA (n=
258 xhibit significant inhibitory effects on the BPA metabolism, especially the sulfate conjugation.
259 t demonstrates significant inhibition on the BPA metabolism, indicating the possible natural existenc
262 DRG from ERbeta(-/-) mice indicate that this BPA effect involves ERalpha and phosphoinositide 3-kinas
266 duce similar toxic and estrogenic effects to BPA and that BPAF is more potent than BPA, further highl
267 the extent to which children are exposed to BPA from dental treatment with bisGMA materials, by amou
269 ted from neonatal pups prenatally exposed to BPA was conducted and revealed a list of differentially
271 ernal and/or ancestral embryonic exposure to BPA affects liver metabolism leading to development-dist
274 c review suggest that early-life exposure to BPA may increase adiposity and circulating lipid levels
275 e for concern that developmental exposure to BPA or GEN might affect the microbiome-gut-brain axis.
279 valuate the relationship between exposure to BPA, ClxBPA and the occurrence of myocardial infarction
281 nt reduction in EA in all cases, relative to BPA and one petroleum-derived BPA analogue (bisphenol F,
283 and estradiol, also occurring in response to BPA/BPS exposure, likely affect the placental-brain axis
289 We hypothesized that posttreatment urinary BPA (uBPA) concentrations would be higher among patients
290 f MI was significantly associated with urine BPA detection: adjusted OR = 1.97 (1.05-3.70), p = 0.04.
296 y been associated with the ASD risk, whether BPA dysregulates ASD-related genes in the developing bra
298 emic availability of BPS, in comparison with BPA, and its lower plasma clearance (3.5 times lower), t
299 (71.0 meters, 95% CI: 47.4-94.5 meters with BPA versus 47.8 meters, 95% CI: 34.5-61.2 meters with pu
300 ere we show that treatment of male mice with BPA (50 ug/kg/day) during 8 days, decreases the latency
301 the PMS decomposition tests with and without BPA and the comparison with a (1)O(2)-generation system