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1  against developmental toxicity from certain environmental chemicals.
2 ts obesity and diabetes, as does exposure to environmental chemicals.
3 ism of a wide variety of important drugs and environmental chemicals.
4  and experimental animals exposed to certain environmental chemicals.
5 PK) of nutrients, drugs, phytochemicals, and environmental chemicals.
6 end against sensitization by highly reactive environmental chemicals.
7 e associated with physiological responses to environmental chemicals.
8 he adverse effects of DNA lesions induced by environmental chemicals.
9 diseases including cancers induced by common environmental chemicals.
10 y reaction in microbial metabolism of varied environmental chemicals.
11 ing prominence in the toxicity evaluation of environmental chemicals.
12 f departure for risk-based prioritization of environmental chemicals.
13 % of clinically prescribed drugs and various environmental chemicals.
14 nt of potential nephrotoxic therapeutics and environmental chemicals.
15 ods to evaluate the endocrine bioactivity of environmental chemicals.
16 a persistent challenge in risk assessment of environmental chemicals.
17 ws forecasting of average exposure intake of environmental chemicals.
18 rocarbons (PAHs) are abundant and widespread environmental chemicals.
19 lication to human health risk assessments of environmental chemicals.
20  assess internal dose (i.e., body burden) to environmental chemicals.
21              Nephrotoxicity due to drugs and environmental chemicals accounts for significant patient
22  and provide a mechanism whereby exposure to environmental chemical activators of PPAR can suppress e
23 own about the mechanistic processes by which environmental chemicals alter brain development.
24 were generated in eight cell systems for 641 environmental chemicals and 135 reference pharmaceutical
25   Glutathione S-transferases (GSTs) detoxify environmental chemicals and are involved in oxidative st
26 time required for toxicological screening of environmental chemicals and can also reduce the need for
27              Understanding whether different environmental chemicals and druglike molecules impact mi
28 ened a library of approximately 10,000 (10K) environmental chemicals and drugs in three independent r
29 tudinal study designed to assess exposure to environmental chemicals and fecundity in couples who wer
30 vides information about interactions between environmental chemicals and gene products and their rela
31 o identifying possible relationships between environmental chemicals and health impacts, but sparse d
32 pha, a nuclear receptor activated by diverse environmental chemicals and hypolipidemic drugs classifi
33  to efficiently screen a large collection of environmental chemicals and identify compounds that indu
34 natural log urine concentrations of selected environmental chemicals and metabolites found in at leas
35              We examined the interplay among environmental chemicals and NKT cells in the regulation
36 th current etiologic theories that implicate environmental chemicals and oxidative stress in the path
37 ry study investigated exposure to individual environmental chemicals and selected mixtures in relatio
38              The relation between persistent environmental chemicals and semen quality is evolving, a
39 blic resource that promotes understanding of environmental chemicals and their effects on human healt
40  detection of the potential toxic effects of environmental chemicals and to understand their risks to
41 atic circulation, altered bioavailability of environmental chemicals and/or antioxidants from food, a
42  with population exposures to tobacco, diet, environmental chemicals, and other exogenous factors.
43 n enzymes that metabolize therapeutic drugs, environmental chemicals, and physiologically important e
44 tegrated 'FRET on Fiber' sensors for on-line environmental, chemical, and biomedical detection, with
45 e, and control through biological, cultural, environmental, chemical, and regulatory means.
46  a nociceptive channel important for sensing environmental chemicals; and a distinct subtype labeled
47 tate of the art of the PP-LFER approaches in environmental chemical applications.
48                     In the olfactory system, environmental chemicals are deconstructed into neural si
49                                              Environmental chemicals are known to induce a high degre
50                                 Thousands of environmental chemicals are subject to regulatory review
51 e metabolic bioactivation of drugs and other environmental chemicals, are capable of binding to a var
52 arch agenda to better understand the role of environmental chemicals as potential risk factors for ob
53 ant role in providing relief from both toxic environmental chemicals as well as physiological oxidati
54  is regarded as a classical model system for environmental chemical biology.
55 says and animal toxicity studies of drug and environmental chemical candidates fail to reveal toxicit
56 de (B[c] PhDE) is well known as an important environmental chemical carcinogen that preferentially mo
57                  DNA damage from exposure to environmental chemical carcinogens and failure of repair
58 RPs are the receptors of a growing number of environmental chemicals (chemesthesis).
59 utadiene (BD) is an important industrial and environmental chemical classified as a human carcinogen
60  support a link between prenatal exposure to environmental chemical contaminants and childhood asthma
61 ions of prenatal exposures to a large set of environmental chemical contaminants with asthma and ecze
62 iates biological responses to endogenous and environmental chemical cues.
63                        Prolonged exposure to environmental chemicals (ECs) can perturb this process w
64 nfants have been associated with exposure to environmental chemicals (ECs) during development.
65   Alkylative damage to DNA can be induced by environmental chemicals, endogenous metabolites and some
66 signed to investigate the effect of low-dose environmental chemical exposure on normal mammary gland
67    When iJRF is applied to the data from the environmental chemical exposure study, we detected a few
68                                              Environmental chemicals exposure is one of the primary f
69    Potential associations between background environmental chemical exposures and autoimmunity are un
70                                  Research on environmental chemical exposures and type 1 diabetes was
71 vention studies should evaluate the suite of environmental chemical exposures as candidates in the co
72                   Emerging evidence suggests environmental chemical exposures during critical windows
73             The associations between NHL and environmental chemical exposures have typically been eva
74 important role in quantifying how early life environmental chemical exposures influence the risk of c
75 ths and weaknesses of studies evaluating how environmental chemical exposures may affect obesity and
76 matic hydrocarbons in the mammary gland when environmental chemical exposures minimally induce CYP1A1
77 for investigating the potential influence of environmental chemical exposures on EED development, inc
78          A comprehensive characterization of environmental chemical exposures prenatally and occurrin
79  this type play an important role in testing environmental chemicals for carcinogenic activity.
80                                 Prioritizing environmental chemicals for obesity and diabetes outcome
81 r Screening Program (EDSP) screens and tests environmental chemicals for potential effects in estroge
82                                  Exposure to environmental chemicals has also been shown to promote s
83   Addressing the safety aspects of drugs and environmental chemicals has historically been undertaken
84 catalyze the oxidation of numerous drugs and environmental chemicals in human liver, remains largely
85 ut microbe variability on the disposition of environmental chemicals in humans.
86 g population biomonitoring data for multiple environmental chemicals in the context of the risk asses
87                    Understanding the role of environmental chemicals in the development or progressio
88                    Understanding the role of environmental chemicals in the development or progressio
89 tabolism of drugs, steroids, fatty acids and environmental chemicals, including cytochromes P450 (P45
90                                  Exposure to environmental chemicals, including phthalates and phenol
91 wn about their role in the toxicodynamics of environmental chemicals, including those recently found
92              The widely held hypothesis that environmental chemicals induce a substantial fraction of
93 ndogenous 15d-PGJ(2)-mediated enhancement of environmental chemical-induced apoptosis represents acti
94 eptor (AhR) has been studied for its role in environmental chemical-induced toxicity.
95 ue in numerous respects: curation focuses on environmental chemicals; interactions are manually curat
96 res that can be formed from the thousands of environmental chemicals is enormous, and testing all of
97 fluences, the contribution of pollutants and environmental chemicals is less clear.
98 enous compounds and the majority of ingested environmental chemicals, leading to their elimination an
99   The hormone-disrupting properties of these environmental chemicals may adversely affect human repro
100  Evidence suggests that paternal exposure to environmental chemicals may adversely affect reproductiv
101 ng interest in the concept that exposures to environmental chemicals may be contributing factors to t
102 overy of biological mechanisms through which environmental chemicals may contribute to obesity, ather
103 se and gestational diabetes, and exposure to environmental chemicals may contribute to risk, although
104 pport the concept that antibiotics and other environmental chemicals may exert neurobehavioral effect
105         An emerging literature suggests that environmental chemicals may play a role in the developme
106              These findings demonstrate that environmental chemicals may sex-dependently accumulate i
107  modalities for cancer treatment and because environmental chemicals may trigger DNA alkylation.
108 ausal scenarios for epidemiologic studies of environmental chemicals measured in urine or serum.
109 r the analysis were available for only three environmental chemicals (methylmercury, organophosphate
110 t pairs from the Maternal Infant Research on Environmental Chemicals (MIREC) Study, a trans-Canada bi
111 t pairs from the Maternal-Infant Research on Environmental Chemicals (MIREC) Study, conducted in Cana
112 est in determining the impact of exposure to environmental chemical mixtures on human health.
113 city of polyaromatic halogenated hydrocarbon environmental chemicals, most notably dioxin.
114  in the National Report on Human Exposure to Environmental Chemicals [NER; Centers for Disease Contro
115 Our aim was to develop new hypotheses around environmental chemicals of potential interest for diabet
116  compile the phenotypic effects of drugs and environmental chemicals offer the opportunity to adopt a
117                                The impact of environmental chemicals on children's neurodevelopment i
118  promotes understanding about the effects of environmental chemicals on human health.
119  hypotheses for understanding the effects of environmental chemicals on human health.
120 aluating the potential harm from exposure to environmental chemicals or the safety of drugs prior to
121 res, because of sunlight exposure as well as environmental chemicals present in food and drinking wat
122 d after controlling for creatinine and other environmental chemicals previously linked to altered neu
123 sorption on mineral surfaces is an important environmental chemical process, but the structures and r
124  sulfate adsorption and its effects on other environmental chemical processes and have important impl
125 posures to a mixture of commonly encountered environmental chemicals produce effects in concert that
126 atial and temporal differentiation of marine environmental chemical profiles using SPATTs, and we pro
127  in the National Report on Human Exposure to Environmental Chemicals provide information on the prese
128 e ice-air interface is an important locus of environmental chemical reactions.
129 erstanding of human variation in toxicity to environmental chemicals remains limited, so human health
130    The findings demonstrate that exposure to environmental chemicals results in new, structurally div
131 e an enormous protein family that translates environmental chemical signals into neuronal electrical
132  of insects, as they recognize and transport environmental chemical signals to receptors.
133      Humans are exposed to a large number of environmental chemicals: Some of these may be toxic, and
134  to humans, orient themselves in response to environmental chemical stimuli, but the contribution of
135 ans, and its susceptibility to disruption by environmental chemicals, stress and pregnancy hormones c
136 ed in the MIREC (Maternal-Infant Research on Environmental Chemicals) study.Breast-milk tetrahydrofol
137                                    These two environmental chemical substrates (TCB and B[a]P) as wel
138 ple are often exposed to complex mixtures of environmental chemicals such as gasoline, tobacco smoke,
139 ts for EED, and should now expand to include environmental chemicals such as pesticides and heavy met
140 ting exposure to nonpersistent, semivolatile environmental chemicals such as phthalates and phenols (
141                             Exposure to many environmental chemicals, such as phthalates, has been sh
142     Polyaromatic hydrocarbons are ubiquitous environmental chemicals that are important mutagens and
143 at this receptor is hepatoprotective against environmental chemicals that are metabolized in this tis
144 alian olfactory system detects a plethora of environmental chemicals that are perceived as odors or s
145                                   Persistent environmental chemicals that exhibit hormonal properties
146 st 20 years, an increased focus on detecting environmental chemicals that pose a risk of adverse effe
147 c aromatic hydrocarbons (PAH) are ubiquitous environmental chemicals that suppress the immune system
148 ovides an approach to prospectively identify environmental chemicals that transcriptionally mimic aut
149 ected SK-BR-3 cells could also be induced by environmental chemicals that were known to have an estro
150 f the nervous system, and the target of many environmental chemicals, these results have wide-reachin
151 -level analysis suggest that the spectrum of environmental chemicals to consider in research related
152 nce that independently links gut ecology and environmental chemicals to obesity and diabetes, providi
153 mes detoxify metabolites, drugs, toxins, and environmental chemicals via conjugation to glucuronic ac
154 ers, we observed that a subset of persistent environmental chemicals were associated with reduced fec
155 ow gut ecology may affect the disposition of environmental chemicals were identified.
156 metabolites and a vast number of dietary and environmental chemicals, which reduces the risk of toxic
157 etermination of the physical interactions of environmental chemicals with cellular proteins is import
158 motes understanding about the interaction of environmental chemicals with gene products, and their ef
159 s from this exercise suggest the spectrum of environmental chemicals with potential endocrine activit
160      Phenolic compounds represent a class of environmental chemicals with potentially endocrine-disru
161 onstrate the feasibility of qHTS to identify environmental chemicals with the potential to interact w
162 central roles in protecting the body against environmental chemicals (xenobiotics).

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