ライフサイエンスコーパス: environmental chemical

1 lication to human health risk assessments of environmental chemicals.

2 assess internal dose (i.e., body burden) to environmental chemicals.

3 ts obesity and diabetes, as does exposure to environmental chemicals.

4 ism of a wide variety of important drugs and environmental chemicals.

5 and experimental animals exposed to certain environmental chemicals.

6 PK) of nutrients, drugs, phytochemicals, and environmental chemicals.

7 end against sensitization by highly reactive environmental chemicals.

8 e associated with physiological responses to environmental chemicals.

9 he adverse effects of DNA lesions induced by environmental chemicals.

10 diseases including cancers induced by common environmental chemicals.

11 y reaction in microbial metabolism of varied environmental chemicals.

12 against developmental toxicity from certain environmental chemicals.

13 loration of metabolic alterations induced by environmental chemicals.

14 bryos to survey the toxicological effects of environmental chemicals.

15 r with drugs and natural products as well as environmental chemicals.

16 l alternative approach in risk assessment of environmental chemicals.

17 environmental stimuli, including exposure to environmental chemicals.

18 rtant matrix in biomonitoring of exposure to environmental chemicals.

19 lack experimental reference spectra, such as environmental chemicals.

20 study endocrine and metabolism disruption by environmental chemicals.

21 e potential risk factors for the toxicity of environmental chemicals.

22 robiota in evaluating the toxic potential of environmental chemicals.

23 ing prominence in the toxicity evaluation of environmental chemicals.

24 consider for this class of widely occurring environmental chemicals.

25 f departure for risk-based prioritization of environmental chemicals.

26 e effects of pharmaceutical, industrial, and environmental chemicals.

27 % of clinically prescribed drugs and various environmental chemicals.

28 nt of potential nephrotoxic therapeutics and environmental chemicals.

29 ods to evaluate the endocrine bioactivity of environmental chemicals.

30 a persistent challenge in risk assessment of environmental chemicals.

31 ws forecasting of average exposure intake of environmental chemicals.

32 rocarbons (PAHs) are abundant and widespread environmental chemicals.

33 Nephrotoxicity due to drugs and environmental chemicals accounts for significant patient

34 and provide a mechanism whereby exposure to environmental chemical activators of PPAR can suppress e

35 erature-based curated content describing how environmental chemicals affect human health.

36 own about the mechanistic processes by which environmental chemicals alter brain development.

37 are used in commerce, yet cost for targeted environmental chemical analysis limits surveillance to a

38 were generated in eight cell systems for 641 environmental chemicals and 135 reference pharmaceutical

39 Glutathione S-transferases (GSTs) detoxify environmental chemicals and are involved in oxidative st

40 time required for toxicological screening of environmental chemicals and can also reduce the need for

41 Understanding whether different environmental chemicals and druglike molecules impact mi

42 ened a library of approximately 10,000 (10K) environmental chemicals and drugs in three independent r

43 cted a study to explore associations between environmental chemicals and endogenous molecules using G

44 tudinal study designed to assess exposure to environmental chemicals and fecundity in couples who wer

45 vides information about interactions between environmental chemicals and gene products and their rela

46 o identifying possible relationships between environmental chemicals and health impacts, but sparse d

47 pha, a nuclear receptor activated by diverse environmental chemicals and hypolipidemic drugs classifi

48 to efficiently screen a large collection of environmental chemicals and identify compounds that indu

49 eminal plasma, including both known priority environmental chemicals and less studied chemicals, to i

50 of enzyme-nanomaterial hybrids for degrading environmental chemicals and may unlock new potential for

51 natural log urine concentrations of selected environmental chemicals and metabolites found in at leas

52 We examined the interplay among environmental chemicals and NKT cells in the regulation

53 th current etiologic theories that implicate environmental chemicals and oxidative stress in the path

54 ry study investigated exposure to individual environmental chemicals and selected mixtures in relatio

55 The relation between persistent environmental chemicals and semen quality is evolving, a

56 een prenatal and early postnatal exposure to environmental chemicals and the development of autism in

57 blic resource that promotes understanding of environmental chemicals and their effects on human healt

58 cell-based mitochondrial toxicity assay for environmental chemicals and their mixtures extracted fro

59 detection of the potential toxic effects of environmental chemicals and to understand their risks to

60 atic circulation, altered bioavailability of environmental chemicals and/or antioxidants from food, a

61 ctive oxygen species, atmospheric radiation, environmental chemicals, and chemotherapeutics.

62 with population exposures to tobacco, diet, environmental chemicals, and other exogenous factors.

63 n enzymes that metabolize therapeutic drugs, environmental chemicals, and physiologically important e

64 ow was applied to predict the spectra of 367 environmental chemicals, and the accuracy was evaluated

65 tegrated 'FRET on Fiber' sensors for on-line environmental, chemical, and biomedical detection, with

66 However, environmental, chemical, and genetic insults often lead

67 e, and control through biological, cultural, environmental, chemical, and regulatory means.

68 a nociceptive channel important for sensing environmental chemicals; and a distinct subtype labeled

69 tate of the art of the PP-LFER approaches in environmental chemical applications.

70 In the olfactory system, environmental chemicals are deconstructed into neural si

71 Environmental chemicals are known to induce a high degre

72 Thousands of environmental chemicals are subject to regulatory review

73 e metabolic bioactivation of drugs and other environmental chemicals, are capable of binding to a var

74 arch agenda to better understand the role of environmental chemicals as potential risk factors for ob

75 ant role in providing relief from both toxic environmental chemicals as well as physiological oxidati

76 is regarded as a classical model system for environmental chemical biology.

77 lly confers various health benefits, whereas environmental chemicals can affect its constitution and

78 ntal and theoretical studies have shown that environmental chemicals can change the fitness cost asso

79 Exposure to environmental chemicals can impair neurodevelopment, and

80 Prenatal and early life exposure to environmental chemicals can increase the risk of multipl

81 says and animal toxicity studies of drug and environmental chemical candidates fail to reveal toxicit

82 de (B[c] PhDE) is well known as an important environmental chemical carcinogen that preferentially mo

83 DNA damage from exposure to environmental chemical carcinogens and failure of repair

84 RPs are the receptors of a growing number of environmental chemicals (chemesthesis).

85 rom the Canadian Maternal-Infant Research on Environmental Chemicals-Child Development study.

86 utadiene (BD) is an important industrial and environmental chemical classified as a human carcinogen

87 support a link between prenatal exposure to environmental chemical contaminants and childhood asthma

88 ions of prenatal exposures to a large set of environmental chemical contaminants with asthma and ecze

89 response of major transport determinants to environmental chemical cues.

90 iates biological responses to endogenous and environmental chemical cues.

91 ing the significance of microbial impacts on environmental chemical cycling.

92 Prolonged exposure to environmental chemicals (ECs) can perturb this process w

93 nfants have been associated with exposure to environmental chemicals (ECs) during development.

94 mental exposure to individual or mixtures of environmental chemicals (ECs) is associated with autism

95 Alkylative damage to DNA can be induced by environmental chemicals, endogenous metabolites and some

96 tion is an important pathway for exposure to environmental chemicals, especially for children.

97 signed to investigate the effect of low-dose environmental chemical exposure on normal mammary gland

98 When iJRF is applied to the data from the environmental chemical exposure study, we detected a few

99 e association of neuropsychiatric illness to environmental chemical exposure, and their potential int

100 Environmental chemicals exposure is one of the primary f

101 Potential associations between background environmental chemical exposures and autoimmunity are un

102 Research on environmental chemical exposures and type 1 diabetes was

103 vention studies should evaluate the suite of environmental chemical exposures as candidates in the co

104 Emerging evidence suggests environmental chemical exposures during critical windows

105 The associations between NHL and environmental chemical exposures have typically been eva

106 We assessed environmental chemical exposures in a case-control study

107 important role in quantifying how early life environmental chemical exposures influence the risk of c

108 ths and weaknesses of studies evaluating how environmental chemical exposures may affect obesity and

109 matic hydrocarbons in the mammary gland when environmental chemical exposures minimally induce CYP1A1

110 for investigating the potential influence of environmental chemical exposures on EED development, inc

111 A comprehensive characterization of environmental chemical exposures prenatally and occurrin

112 archers have explored links between CTCL and environmental chemical exposures, such as aromatic hydro

113 this type play an important role in testing environmental chemicals for carcinogenic activity.

114 Prioritizing environmental chemicals for obesity and diabetes outcome

115 r Screening Program (EDSP) screens and tests environmental chemicals for potential effects in estroge

116 Exposure to synthetic environmental chemicals found in plastics and personal c

117 in fibroblasts were exposed to four priority environmental chemicals found in the Antarctic sea-ice e

118 Over the past few decades, numerous environmental chemicals from solvents to pesticides have

119 Exposure to environmental chemicals has also been shown to promote s

120 Addressing the safety aspects of drugs and environmental chemicals has historically been undertaken

121 valuations for drugs, consumer products, and environmental chemicals have a critical impact on human

122 However, few environmental chemicals have been assessed for potential

123 catalyze the oxidation of numerous drugs and environmental chemicals in human liver, remains largely

124 that the workflow supports quantification of environmental chemicals in human plasma (200 uL) and tis

125 ut microbe variability on the disposition of environmental chemicals in humans.

126 g population biomonitoring data for multiple environmental chemicals in the context of the risk asses

127 Understanding the role of environmental chemicals in the development or progressio

128 ntal screen in cultured cells, we identified environmental chemicals in two classes that disrupt olig

129 ts, have been prenatally exposed to multiple environmental chemicals, in part due to an older housing

130 tabolism of drugs, steroids, fatty acids and environmental chemicals, including cytochromes P450 (P45

131 Exposure to environmental chemicals, including phthalates and phenol

132 wn about their role in the toxicodynamics of environmental chemicals, including those recently found

133 The widely held hypothesis that environmental chemicals induce a substantial fraction of

134 ndogenous 15d-PGJ(2)-mediated enhancement of environmental chemical-induced apoptosis represents acti

135 eptor (AhR) has been studied for its role in environmental chemical-induced toxicity.

136 ue in numerous respects: curation focuses on environmental chemicals; interactions are manually curat

137 res that can be formed from the thousands of environmental chemicals is enormous, and testing all of

138 fluences, the contribution of pollutants and environmental chemicals is less clear.

139 enous compounds and the majority of ingested environmental chemicals, leading to their elimination an

140 The hormone-disrupting properties of these environmental chemicals may adversely affect human repro

141 Evidence suggests that paternal exposure to environmental chemicals may adversely affect reproductiv

142 Exposure to environmental chemicals may be a modifiable risk factor

143 udies suggest that differential exposures to environmental chemicals may be associated with geographi

144 ng interest in the concept that exposures to environmental chemicals may be contributing factors to t

145 overy of biological mechanisms through which environmental chemicals may contribute to obesity, ather

146 se and gestational diabetes, and exposure to environmental chemicals may contribute to risk, although

147 pport the concept that antibiotics and other environmental chemicals may exert neurobehavioral effect

148 An emerging literature suggests that environmental chemicals may play a role in the developme

149 These findings demonstrate that environmental chemicals may sex-dependently accumulate i

150 modalities for cancer treatment and because environmental chemicals may trigger DNA alkylation.

151 ausal scenarios for epidemiologic studies of environmental chemicals measured in urine or serum.

152 Our results provide unique insights into environmental chemical mechanisms of action on cellular

153 r the analysis were available for only three environmental chemicals (methylmercury, organophosphate

154 The Maternal-Infant Research on Environmental Chemicals (MIREC) study recruited particip

155 ng data from the Maternal-Infant Research on Environmental Chemicals (MIREC) Study, a cohort exposed

156 t pairs from the Maternal Infant Research on Environmental Chemicals (MIREC) Study, a trans-Canada bi

157 t pairs from the Maternal-Infant Research on Environmental Chemicals (MIREC) Study, conducted in Cana

158 enrolled in the Maternal-Infant Research on Environmental Chemicals (MIREC) study.

159 est in determining the impact of exposure to environmental chemical mixtures on human health.

160 city of polyaromatic halogenated hydrocarbon environmental chemicals, most notably dioxin.

161 in the National Report on Human Exposure to Environmental Chemicals [NER; Centers for Disease Contro

162 Our aim was to develop new hypotheses around environmental chemicals of potential interest for diabet

163 compile the phenotypic effects of drugs and environmental chemicals offer the opportunity to adopt a

164 The impact of environmental chemicals on children's neurodevelopment i

165 promotes understanding about the effects of environmental chemicals on human health.

166 hypotheses for understanding the effects of environmental chemicals on human health.

167 human health effects of exposure to a given environmental chemical or chemicals.

168 However, environmental chemicals or physiologically active metabo

169 aluating the potential harm from exposure to environmental chemicals or the safety of drugs prior to

170 this context, the presence of the widespread environmental chemical phthalic anhydride and its impact

171 res, because of sunlight exposure as well as environmental chemicals present in food and drinking wat

172 d after controlling for creatinine and other environmental chemicals previously linked to altered neu

173 Included studies assessed exposure to environmental chemicals prior to 2 months of age in huma

174 sorption on mineral surfaces is an important environmental chemical process, but the structures and r

175 sulfate adsorption and its effects on other environmental chemical processes and have important impl

176 posures to a mixture of commonly encountered environmental chemicals produce effects in concert that

177 atial and temporal differentiation of marine environmental chemical profiles using SPATTs, and we pro

178 , we further proposed a framework, i.e., the environmental Chemical-Protein Interaction Network (eCPI

179 in the National Report on Human Exposure to Environmental Chemicals provide information on the prese

180 e ice-air interface is an important locus of environmental chemical reactions.

181 , we investigated a possible link between an environmental chemical receptor implicated in lung cance

182 igated a novel role for an immunosuppressive environmental chemical receptor, previously implicated i

183 erstanding of human variation in toxicity to environmental chemicals remains limited, so human health

184 The findings demonstrate that exposure to environmental chemicals results in new, structurally div

185 n this work, blow flies were investigated as environmental chemical sample collectors following a che

186 hat the detoxification of plant material and environmental chemicals seem to be performed by SI micro

187 e an enormous protein family that translates environmental chemical signals into neuronal electrical

188 of insects, as they recognize and transport environmental chemical signals to receptors.

189 Humans are exposed to a large number of environmental chemicals: Some of these may be toxic, and

190 to humans, orient themselves in response to environmental chemical stimuli, but the contribution of

191 ans, and its susceptibility to disruption by environmental chemicals, stress and pregnancy hormones c

192 ed data from the Maternal-Infant Research on Environmental Chemicals study, a pan-Canadian cohort.

193 ed in the MIREC (Maternal-Infant Research on Environmental Chemicals) study.Breast-milk tetrahydrofol

194 These two environmental chemical substrates (TCB and B[a]P) as wel

195 ple are often exposed to complex mixtures of environmental chemicals such as gasoline, tobacco smoke,

196 Exposure to environmental chemicals such as lead (Pb) during vulnera

197 ts for EED, and should now expand to include environmental chemicals such as pesticides and heavy met

198 ting exposure to nonpersistent, semivolatile environmental chemicals such as phthalates and phenols (

199 Exposure to environmental chemicals such as phthalates has been link

200 ceptibility remains poorly characterized for environmental chemicals such as tetrachloroethylene (PER

201 Exposure to many environmental chemicals, such as phthalates, has been sh

202 ty and promise of computationally predicting environmental chemical-target interactions to efficientl

203 Polyaromatic hydrocarbons are ubiquitous environmental chemicals that are important mutagens and

204 at this receptor is hepatoprotective against environmental chemicals that are metabolized in this tis

205 alian olfactory system detects a plethora of environmental chemicals that are perceived as odors or s

206 aracterizing complex phenotypic responses to environmental chemicals that can be used for determining

207 pitulated in wild-type (WT) cells exposed to environmental chemicals that cause hyperpolarization.

208 Persistent environmental chemicals that exhibit hormonal properties

209 s (ACD) is a pruritic skin disease caused by environmental chemicals that induce cell-mediated skin i

210 st 20 years, an increased focus on detecting environmental chemicals that pose a risk of adverse effe

211 ng approaches to evaluate the vast number of environmental chemicals that require assessment are hamp

212 c aromatic hydrocarbons (PAH) are ubiquitous environmental chemicals that suppress the immune system

213 ovides an approach to prospectively identify environmental chemicals that transcriptionally mimic aut

214 ected SK-BR-3 cells could also be induced by environmental chemicals that were known to have an estro

215 When communities are exposed to environmental chemicals, the federal government's respon

216 f the nervous system, and the target of many environmental chemicals, these results have wide-reachin

217 -level analysis suggest that the spectrum of environmental chemicals to consider in research related

218 nce that independently links gut ecology and environmental chemicals to obesity and diabetes, providi

219 mes detoxify metabolites, drugs, toxins, and environmental chemicals via conjugation to glucuronic ac

220 ers, we observed that a subset of persistent environmental chemicals were associated with reduced fec

221 ow gut ecology may affect the disposition of environmental chemicals were identified.

222 metabolites and a vast number of dietary and environmental chemicals, which reduces the risk of toxic

223 chemical, and whether coexposure of multiple environmental chemicals will affect each other's fate in

224 etermination of the physical interactions of environmental chemicals with cellular proteins is import

225 motes understanding about the interaction of environmental chemicals with gene products, and their ef

226 s from this exercise suggest the spectrum of environmental chemicals with potential endocrine activit

227 Phenolic compounds represent a class of environmental chemicals with potentially endocrine-disru

228 onstrate the feasibility of qHTS to identify environmental chemicals with the potential to interact w

229 Arsenic is one of these environmental chemicals, with multiple epidemiology stud

230 central roles in protecting the body against environmental chemicals (xenobiotics).