ライフサイエンスコーパス: environmental exposure

1 basophils at mucosal and cutaneous sites of environmental exposure.

2 o oxidative stress, aberrant metabolism, and environmental exposure.

3 arious neurodegenerative diseases, and toxic environmental exposure.

4 havioral vulnerability induced by early-life environmental exposure.

5 still occur despite substantial reduction in environmental exposure.

6 r adverse effects to occur following chronic environmental exposure.

7 substances (PFASs) are sources of human and environmental exposure.

8 nstrate that Td-WTe2 is readily oxidized via environmental exposure.

9 age, suggesting the cumulative influence of environmental exposure.

10 igh penetrance of mesothelioma requires such environmental exposure.

11 even for samples subject to degradation from environmental exposure.

12 are associated with cellular properties and environmental exposure.

13 bolites as biomarkers/indicators of in utero environmental exposure.

14 kidney, and lung, often occurs secondary to environmental exposure.

15 d, built, and sociodemographic) to represent environmental exposure.

16 the gastrointestinal tract experimentally by environmental exposure.

17 e interactions, and contrasted situations of environmental exposure.

18 and convenient tool to screen for human and environmental exposure.

19 molecular signatures, diseases, pathways and environmental exposures.

20 influences, including relevant behaviors and environmental exposures.

21 tic background and variation in histories of environmental exposures.

22 n patterns by exploiting naturally occurring environmental exposures.

23 ability, both inherently, and in response to environmental exposures.

24 nderstanding of public health risks posed by environmental exposures.

25 ractions between multiple genes and multiple environmental exposures.

26 ne environment is particularly vulnerable to environmental exposures.

27 OR, 4.41; 95% CI, 2.24-8.67) despite similar environmental exposures.

28 obtained and analyzed for mercury and other environmental exposures.

29 spatiotemporal assessment of human risks to environmental exposures.

30 ation, employment, housing, and physical and environmental exposures.

31 me by DNA sequence variation and by lifetime environmental exposures.

32 estionnaire that assessed various early life environmental exposures.

33 sorders are associated with occupational and environmental exposures.

34 L) in surrogate tissues may be influenced by environmental exposures.

35 ationship between genetic predisposition and environmental exposures.

36 between generations in the absence of direct environmental exposures.

37 r transgenerational disease and/or ancestral environmental exposures.

38 olic pathways related to diet, microbiome or environmental exposures.

39 therapeutic and prevention regimens based on environmental exposures.

40 hma trajectories and risk factors, including environmental exposures.

41 nts, unlinked genes, epigenetic factors, and environmental exposures.

42 omprising an individual's genetic burden and environmental exposures.

43 dual differences in genomic architecture and environmental exposures.

44 nconsistencies in observed associations with environmental exposures.

45 dulthood from early-life episodes of adverse environmental exposures.

46 re diverse in genetic ancestry, culture, and environmental exposures.

47 data: geographic proximity, community type, environmental exposures, access to resources and service

48 tification of the effects of all deleterious environmental exposures according to duration of exposur

49 Environmental exposures affect gamete function and ferti

50 trait resulting from the interaction between environmental exposure and a susceptible polygenic backg

51 st study of associations between this common environmental exposure and autoimmune diseases in humans

52 menting and analyzing community discovery of environmental exposure and consequential processes.

53 as the best fit for DHOS exposure: physical-environmental exposure and economic exposure.

54 s are exposed to N-nitroso compounds through environmental exposure and endogenous metabolism.

55 e of air-surface exchange helps to interpret environmental exposure and evaluate the effectiveness of

56 of multiple sclerosis is believed to involve environmental exposure and genetic susceptibility.

57 heimer's disease (AD) is believed to involve environmental exposure and genetic susceptibility.

58 In a study of environmental exposure and health in Taiwan, we measured

59 hcare providers must be knowledgeable of the environmental exposure and its effects on physiologic fu

60 g individuals because of differences in both environmental exposure and metabolism.

61 onomic and structural challenges to changing environmental exposure and offered recommendations for c

62 l and need to be taken into consideration in environmental exposure and risk analyses of these compou

63 of effluent dynamics and retransformation on environmental exposure and risk prediction.

64 the risk assessment framework for evaluating environmental exposure and the corresponding development

65 Environmental exposures and ancestry-related factors may

66 dies assessing miRNAs as markers of in-utero environmental exposures and as candidates for the molecu

67 variation also captured covariation between environmental exposures and children's inattention/hyper

68 gain a deeper understanding of the impact of environmental exposures and combinatory toxic effects on

69 e concept of the exposome, which encompasses environmental exposures and concomitant biological respo

70 aluating the potential relationships between environmental exposures and disease risk.

71 ved to be active and thus more accessible to environmental exposures and events related to gene trans

72 found relationships between specific indoor environmental exposures and exacerbation of asthma.

73 n reported, including studies of other early environmental exposures and female subjects.

74 pigenome provides a mechanistic link between environmental exposures and gene expression profiles ult

75 populations provide an opportunity to model environmental exposures and gene-environment interaction

76 The differences in environmental exposures and genetic background between C

77 There is clear evidence that environmental exposures and genetic predisposition contr

78 organophosphates, phenols, metals, and other environmental exposures and metabolites measured in part

79 reverse causation, confounded by unmeasured environmental exposures and might miss time points for w

80 tcomes and be a source of new biomarkers for environmental exposures and of novel prognostic and diag

81 s, immunology, asthma, environmental health, environmental exposures and pollutants, epidemiology, pu

82 rum disorder (ASD), but evidence of specific environmental exposures and susceptibility windows is li

83 Susceptibility to allergen exposure, other environmental exposures and their interactions may also

84 ic outcomes often consider interactions with environmental exposures and, in particular, apply tests

85 he product of (high genetic loading+moderate environmental exposure) and male cases of (high environm

86 vironment interaction with a higher level of environmental exposure) and threshold interactions (e.g.

87 Melioidosis is typically acquired through environmental exposure, and case clusters are rare, even

88 iator of the long-term programming effect of environmental exposure, and multiple lines of evidence p

89 Endogenous metabolism, environmental exposure, and treatment with some chemothe

90 , including race/ethnicity, genetic factors, environmental exposures, and alterations in the gut micr

91 n humans for susceptibility or resistance to environmental exposures, and identifying gene variants t

92 lyses by adjusting for socioeconomic status, environmental exposures, and intensity of therapy.

93 her molecular measurements, medical history, environmental exposures, and lifestyle.

94 mmatory and allergy markers, family history, environmental exposures, and medications.

95 Tobacco smoke, air pollution, environmental exposures, and occupational hazards affect

96 m incorporating measures of lifestyle, diet, environmental exposures, and other risk factors from ear

97 igenome is profiled over time, over changing environmental exposures, and over generations to better

98 index, harmful alcohol use, some dietary and environmental exposures, and physical inactivity.

99 to obtain information on lifestyle factors, environmental exposures, and symptoms of allergic diseas

100 With its coordinated longitudinal biologic, environmental-exposure, and phenotypic data and samples,

101 lasticity (AD-A), presumably due to previous environmental exposures; another subset of AD LCLs demon

102 tools to study the health impacts of complex environmental exposures are lacking.

103 Environmental exposures are relevant for the development

104 on, and bee products, but the risks posed by environmental exposures are still not well understood.

105 ntuberculous mycobacteria (NTMs), suggesting environmental exposure as an underlying cause of differe

106 and Pu in their initial formation and after environmental exposure as well as occasions of unexpecte

107 children in this study in which we utilized environmental exposure assessment (surface wipe and indo

108 luding the improved data analytical methods, environmental exposure assessment, and incorporation of

109 suggest that higher blood pressure--or some environmental exposure associated with higher blood pres

110 Air particulate matter (PM) is a ubiquitous environmental exposure associated with oxidation, inflam

111 Identifying environmental exposures associated with blood pressure i

112 of genetic predisposition, epigenetics, and environmental exposures, avoiding pitfalls, such as reca

113 dow' for Treg-mediated asthma protection via environmental exposure before age 6 years.

114 ided by study of the exposome (or collective environmental exposures beginning during the prenatal pe

115 an examination of macro-level differences in environmental exposures between high- and low-incidence

116 Numerous environmental exposures (both positive and negative) can

117 Food is an important environmental exposure, but the role of food diversity i

118 othesized to affect immunologic responses to environmental exposures by supporting healthy gut microb

119 rk represents an example of how chemical and environmental exposures can be evaluated to better under

120 Rodent experiments indicate that environmental exposures can have effects on subsequent g

121 In esophageal cancer, environmental exposures can trigger chronic inflammation

122 in outcome that differs by the value of the environmental exposure) can invalidate traditional joint

123 etic processes can be induced in response to environmental exposures, can influence disease risk, and

124 itis symptoms caused by ragweed pollen in an environmental exposure chamber (EEC) 3 weeks after treat

125 subjects were exposed to cat allergen in an environmental exposure chamber (EEC) before and after tr

126 nasal symptom scores (TNSSs) over the 8-hour environmental exposure chamber exposure period.

127 l-group clinical trial, subjects attended an environmental exposure chamber in which they were expose

128 l HDM immunotherapy was demonstrated in this environmental exposure chamber study, supporting further

129 ficacy and safety of 3 doses of STG320 in an environmental exposure chamber.

130 On the contrary, environmental exposure chambers (EECs) aim to operate wi

131 Environmental exposure chambers are currently already us

132 Environmental exposure chambers, delivering a fixed amou

133 ization against profiles defined in terms of environmental exposure combined with monitoring and stud

134 metal-containing nanoparticles at realistic environmental exposure concentrations.

135 t metal content of human islets under normal environmental exposure conditions has not been described

136 characterizing nanoparticles under realistic environmental exposure conditions.

137 ide association studies (GWASs) and specific environmental exposures, controlling for overall genetic

138 ise and progress, and 3) how various adverse environmental exposures could contribute to developmenta

139 al data, and unmeasured variables related to environmental exposures could not be accounted for.

140 statistics, applied them to the genetic and environmental exposure data for esophageal adenocarcinom

141 ta that are obtained in the patient history: environmental exposures, diet, social data, etc.

142 d that despite the many possible genetic and environmental exposure differences in infants across 4 c

143 ntical constitutional genetic background and environmental exposure, different lung cancers in the sa

144 ity to define mutational processes driven by environmental exposures, DNA repair abnormalities, and m

145 d adult risk for type 2 diabetes may reflect environmental exposures during developmental plasticity

146 vestigate whether BAFF levels are related to environmental exposures during pregnancy and early child

147 Emerging science also suggests that environmental exposures during the prenatal period and e

148 natural environments may ameliorate adverse environmental exposures (e.g., air pollution, noise, and

149 Environmental exposures early in male life may alter spe

150 d by a complex interaction between genes and environmental exposures; early-life exposures in particu

151 s, personal risk factors (eg, genetics), and environmental exposures (eg, airway microbiome) promote

152 Environmental exposure, endogenous metabolism and cancer

153 ts of inherited DNA variation and a range of environmental exposures experienced throughout the life

154 ve questionnaire of illnesses, symptoms, and environmental exposures for 80 sequential patients with

155 The developing human brain is shaped by environmental exposures--for better or worse.

156 posome" is defined as "the totality of human environmental exposures from conception onward, compleme

157 in biomarker levels, arising from changes in environmental exposures from conception onwards, leads t

158 some is defined as the totality of all human environmental exposures from conception to death.

159 ctors, such as antibiotic treatment, diet or environmental exposure, further modulate the development

160 We studied environmental exposures, genetic ancestry, and immune pr

161 Environmental exposures, genetic factors, and structural

162 Various other environmental exposures have been implicated in the expl

163 Environmental exposures have been recognized as critical

164 able to healthy term infants despite limited environmental exposures, high levels of antibiotic admin

165 rofiles, lifestyle patterns, dietary habits, environmental exposure history and long-term health outc

166 By examining environmental exposure history in cervical dystonia pati

167 Despite shared environmental exposures, idiopathic pulmonary fibrosis (

168 regulatory measures against occupational or environmental exposures (ie, the preventive effort does

169 ata and continual improvement in measures of environmental exposures implicated in complex disease ou

170 and stone polishing, supporting the role of environmental exposure in disease pathogenesis.

171 heterogeneous and is affected by genetic and environmental exposures in addition to interactions betw

172 ylation varies in populations with different environmental exposures in different parts of the world.

173 Environmental exposures in early life appear to play an

174 We sought to determine whether environmental exposures in early life influence cytokine

175 y 15, 2010) triggered a need to characterize environmental exposures in four dimensions through sampl

176 ts, and whether it is modulated by the first environmental exposures in infancy.

177 pression modulate cellular susceptibility to environmental exposures in PD patients.

178 Prompted case report forms including environmental exposures in prospective registries will l

179 and asthma, but little is known about indoor environmental exposures in relation to childhood eczema.

180 s we aimed to determine the role of previous environmental exposures in relation to disease penetranc

181 Prior research has reported disparities in environmental exposures in the United States, but, to ou

182 nes, indicating that they may be affected by environmental exposures, in either mother or offspring,

183 Environmental exposures including maternal inflammation,

184 s increasing evidence that the same or other environmental exposures, including those that occur duri

185 expression profiles due to various in-utero environmental exposures, including xenochemicals, endoge

186 ons of variants across gene categories, plus environmental exposures, increase susceptibility to the

187 atic inflation across different outcomes and environmental exposures (inflation-factor estimates rang

188 ity in the extent and nature of responses to environmental exposures is a critical aspect of human he

189 netic modifications that result from complex environmental exposures is a major challenge for current

190 Used in epidemiologic studies of environmental exposure, it offers the promise to causall

191 In a population with environmental exposure levels similar to the U.S. genera

192 -wide association studies (GWAS) account for environmental exposures, like smoking, potentially impac

193 There are numerous examples of how environmental exposures, like tobacco, chronic stress, o

194 nts disparate from the health outcome or the environmental exposure may be confounded by intervening

195 in young adulthood indicating that pediatric environmental exposures may be important in the etiology

196 iations observed in this study indicate that environmental exposures may be overlooked contributors t

197 nufacturing, there is concern that human and environmental exposures may lead to adverse immune outco

198 health outcomes and their temporal links to environmental exposures may lead to improvements in pros

199 ironmental exposure) and male cases of (high environmental exposure+moderate genetic loading), (2) on

200 national asthma guidelines to target indoor environmental exposures, most insurers generally have no

201 extrapolated to lower doses more relevant to environmental exposures, mouse population-derived variab

202 To mimic environmental exposure, naive mice were exposed to peanu

203 urce outbreak following a meal was caused by environmental exposures, not food.

204 Major changes in environmental exposure occur right after birth, upon wea

205 val of Me(O)NPs, thus allowing for long-term environmental exposure of diverse biological communities

206 range, which makes the determination of the environmental exposure of PAHs originating from biochars

207 f the reproductive system as a surrogate for environmental exposure of parents to unmeasured developm

208 Our data suggest the environmental exposure of ruminants to a broad range of

209 ro-migratory tissue signals as a function of environmental exposure of the inside of the tissue.

210 Consideration of these environmental exposures of both humans and mice can pote

211 Estimates on 81 environmental exposures of current health concern were o

212 s related to distinct prenatal and postnatal environmental exposures of mother and child, such as con

213 l advance understanding about the impacts of environmental exposures on human disease.

214 cohort study examining the health effects of environmental exposures on pregnant women and their chil

215 rlying regulatory mechanisms under different environmental exposure or disease states.

216 s of DNA methylation patterns in relation to environmental exposures or clinical outcomes.

217 ding consequences: facilitating tolerance to environmental exposures or contributing to the developme

218 between people may reflect disease-relevant environmental exposures or genetic variation.

219 tions is dependent on other factors, such as environmental exposures or host factors.

220 may be indicative of genetic differences and environmental exposures or their interactions that relat

221 A plausible hypothesis is that 1 or more environmental exposures, or lack thereof, induce epigene

222 ated with other strains and after continuous environmental exposure, our work highlights the importan

223 ted sites amongst loci previously associated environmental exposures, particularly maternal smoking d

224 ene-environment interaction occurs only when environmental exposure reaches a certain threshold level

225 Environmental exposures represent a group of understudie

226 Environmental exposure science is now embarking on a new

227 The use of metabolite data as a proxy for environmental exposures should be carefully considered i

228 Environmental exposures should be considered even in rou

229 utero bisphenol A (BPA) exposure as a model environmental exposure shown to disrupt neurodevelopment

230 ota taxonomic alpha diversity increases with environmental exposures, such as air particulates, resid

231 This highlights the influence of environmental exposures, such as allergens, air pollutio

232 Environmental exposures that affect accumulation of poly

233 rance to beta cells can be broken by several environmental exposures that induce generation of hybrid

234 presentation of these patients and highlight environmental exposures that may affect disease risk, pa

235 the mid-20th century initiated a search for environmental exposures that may explain these phenomena

236 and multigenerational implications of total environmental exposures, the exposome, require coordinat

237 cause genetic variants are not influenced by environmental exposures, these results provide new suppo

238 s are thought to reflect enduring effects of environmental exposures, they may be useful in distingui

239 The ability to characterize environmental exposures through biomonitoring is key to

240 ng information about the impact of modifying environmental exposures through regulation or behavior c

241 Understanding the effect of the summation of environmental exposures throughout a child's development

242 One challenge in linking environmental exposure to accumulation is determining va

243 It has previously been shown that environmental exposure to aeroallergens in household dus

244 gies and policies aiming at the reduction of environmental exposure to air pollution requires the ass

245 creen population-wide cumulative dietary and environmental exposure to authorized, unauthorized and b

246 kemia may be associated with traffic-related environmental exposure to benzene, and additional data a

247 Environmental exposure to bisphenol A (BPA) affects mamm

248 of effective early diagnosis and increasing environmental exposure to cancer-causing agents.

249 Environmental exposure to food allergens may be a risk f

250 childhood leukemia have been associated with environmental exposure to gasoline; aromatic hydrocarbon

251 INTERPRETATION: Environmental exposure to higher concentrations of PM10,

252 The role of environmental exposure to lead as a risk factor for chro

253 y the TLR4 genotype of the individual and by environmental exposure to LPS.

254 Information about environmental exposure to melamine and renal injury in a

255 result in increased potential for human and environmental exposure to MNs during manufacturing, use,

256 Occupational and/or environmental exposure to nickel has been implicated in

257 vestigated endometriosis risk in relation to environmental exposure to OCPs.

258 This study supports the hypothesis that environmental exposure to organic pollutants may play a

259 from different risk factors such as prenatal environmental exposure to organochlorines and metals, so

260 ensitization and the current evidence on how environmental exposure to peanut affects the development

261 It has been hypothesized that high environmental exposure to peanut allergens may be a pote

262 We have shown that an infant's environmental exposure to peanut is most likely to be du

263 dence is mounting to support the theory that environmental exposure to peanut, such as in house dust,

264 ide suggestive evidence of the potential for environmental exposure to phthalates and/or BPA to disru

265 Environmental exposure to polycyclic aromatic hydrocarbo

266 re, some patients have pre-existing Abs from environmental exposure to Pseudomonas exotoxin, the comp

267 Environmental exposure to spores of pathogenic fungi can

268 per-billion levels, suggesting a low endemic environmental exposure to the three chemicals that could

269 , and bioavailability, determining potential environmental exposure to these materials requires an in

270 yet no current epidemic is evident, despite environmental exposure to viruses that infect human cell

271 Occupational and environmental exposures to airborne asbestos and silica

272 in relation to personal characteristics and environmental exposures to allergens and endotoxin and t

273 g mechanism that translates the influence of environmental exposures to changes in gene expression, r

274 Environmental exposures to chemicals have been shown to

275 lifestyle, there is increasing evidence that environmental exposures to chemicals known as obesogens

276 We examined the association between environmental exposures to lead, mercury, and cadmium an

277 Ancestral environmental exposures to non-mutagenic agents can exer

278 We evaluated the potential effects of low environmental exposures to perchlorate on thyroid functi

279 human populations may be useful for linking environmental exposures to potential health effects.

280 lar environments simplify the organism-level environmental exposures to provide a tractable influence

281 ity of blood-based omic profiles for linking environmental exposures to their potential health effect

282 y of birth and (ii) contribution of measured environmental exposures to these differences.

283 4-day baseline challenge to rye grass in the environmental exposure unit (EEU), subjects were randomi

284 induced by controlled pollen exposure in the environmental exposure unit (EEU).

285 A recently reported small, out-of-season environmental exposure unit study found nasal filters to

286 re identified to mitigate possible human and environmental exposures upon industrial implementation.

287 ing are modeled as multivariate responses to environmental exposure using a generalized estimating eq

288 ide genotyping of participants and collected environmental exposures using the Childhood Trauma Quest

289 High physical-environmental exposure was significantly associated with

290 Past environmental exposures were assessed using a detailed 1

291 Environmental exposures were assigned to each member of

292 events, infant feeding, and nutritional and environmental exposures were collected at 15 weeks' gest

293 Data on wheeze and environmental exposures were collected with standardized

294 Symptoms of wheeze, rhinitis, fever, and environmental exposures were documented with weekly diar

295 Environmental exposures were preliminarily examined.

296 ergen function is one of the determinants of environmental exposure, which is essential for IgE sensi

297 ylation markers may mediate pathways linking environmental exposures with health outcomes.

298 resilient individuals are able to withstand environmental exposures with minimal effects to their he

299 links childhood and adolescent lifestyle and environmental exposures with subsequent risk of cancers

300 unities the tools needed to understand their environmental exposures with these data individual and c