ライフサイエンスコーパス: environmental exposure

1 column, making this a potentially realistic environmental exposure.

2 imization, which is a potentially modifiable environmental exposure.

3 and 10.5 years) was assessed as an index of environmental exposure.

4 are associated with cellular properties and environmental exposure.

5 fter absorption, with no studies on human or environmental exposure.

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

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

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

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

10 the gastrointestinal tract experimentally by environmental exposure.

11 e interactions, and contrasted situations of environmental exposure.

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

13 basophils at mucosal and cutaneous sites of environmental exposure.

14 the interplay between predisposing genes and environmental exposure.

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

16 arious neurodegenerative diseases, and toxic environmental exposure.

17 rent evolutionary properties shaped by prior environmental exposure.

18 sthmatic children and evaluate the impact of environmental exposures.

19 ost genetics, host immunity, microbiome, and environmental exposures.

20 ts for addressing Mn-associated disorders or environmental exposures.

21 Emerging research shows an association with environmental exposures.

22 ne environment is particularly vulnerable to environmental exposures.

23 hma trajectories and risk factors, including environmental exposures.

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

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

26 dual differences in genomic architecture and environmental exposures.

27 nconsistencies in observed associations with environmental exposures.

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

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

30 molecular signatures, diseases, pathways and environmental exposures.

31 influences, including relevant behaviors and environmental exposures.

32 tic background and variation in histories of environmental exposures.

33 n patterns by exploiting naturally occurring environmental exposures.

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

35 nderstanding of public health risks posed by environmental exposures.

36 ractions between multiple genes and multiple environmental exposures.

37 s, including the effects of both genetic and environmental exposures.

38 e barrier tissues to rapidly recall distinct environmental exposures.

39 sses that may reflect the body's response to environmental exposures.

40 ely related to abnormal immune responses and environmental exposures.

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

42 plicated in the protective effect of certain environmental exposures against asthma.

43 e expression programs that can be altered by environmental exposures, aging, and in pathogenesis.

44 erns, time scales, chromatin structures, and environmental exposures, all of which impact the resulti

45 roved mental well-being, and lowered harmful environmental exposures, all of which may affect human h

46 factor for COPD is tobacco smoke, but other environmental exposures also may contribute.

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

48 te valid associations between genetic and/or environmental exposure and disease development to scient

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

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

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

52 ecialized cells that have adapted to survive environmental exposure and perform the tasks necessary f

53 IT) is critical for evaluating the impact of environmental exposure and potential for nanoparticle dr

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

55 rces of these changes, including the role of environmental exposure and several cognitive mechanisms

56 etation for extended periods of time through environmental exposure and weathering.

57 The links between microbial environmental exposures and asthma are well documented,

58 rojected changes; poor spatial resolution in environmental exposures and behavioral assessments; few

59 sociation between a wide array of early-life environmental exposures and childhood obesity, using an

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

61 has been regarded as a biomarker for various environmental exposures and chronic diseases.

62 es in chromatin accessibility resulting from environmental exposures and chronic stress.

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

64 ncluding autism candidates are vulnerable to environmental exposures and common features may mediate

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

66 ion models examined the associations between environmental exposures and COPD prevalence adjusting fo

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

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

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

70 The differences in environmental exposures and genetic background between C

71 However, a combination of environmental exposures and genetic defects can result i

72 t in identifying epigenetic pathways between environmental exposures and health outcomes.

73 st decades, which is associated with altered environmental exposures and lifestyle practices.

74 a community-driven data model for describing environmental exposures and linking them to existing mod

75 ange of prenatal and postnatal lifestyle and environmental exposures and lung function in children.

76 CpG sites are subjected to the influences of environmental exposures and may regulate gene expression

77 vital signs), remote patient monitoring (eg, environmental exposures and medication adherence) as wel

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 Further analysis will describe and compare environmental exposures and other risk factors in this c

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

82 pG sites associated with asthma severity and environmental exposures and predictive of severe asthma

83 are altered by specific germline mutations, environmental exposures and related mechanisms that prom

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

85 It calls for providing a holistic view of environmental exposures and their effects on human healt

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

87 ith commensal and pathogenic microorganisms, environmental exposures, and cell age.

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

89 esult from generational differences in diet, environmental exposures, and lifestyle factors.

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

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

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

93 equires more samples and detailed measure of environmental exposures, and this limits the possible di

94 lar, for reviews of observational studies of environmental exposures, and we also comment more genera

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

96 As many environmental exposures are difficult to collect and qua

97 roportionate risk to rural communities where environmental exposures are high.

98 Chemical and nonchemical environmental exposures are increasingly suspected to in

99 1%; P < 0.0001).Conclusions: Rare and common environmental exposures are independent risk factors for

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

101 Environmental exposures are relevant for the development

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

103 A11 gene and show this is consistent with an environmental exposure, as opposed to medications or gen

104 It appears likely that environmental exposures, as opposed to major APOL1-secon

105 e focus on the interplay between advances in environmental exposure assessment and developments in po

106 us-based models are currently implemented in environmental exposure assessment to adapt biotransforma

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

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

109 Identifying environmental exposures associated with blood pressure i

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

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

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

113 Numerous environmental exposures (both positive and negative) can

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

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

116 Previous studies have suggested that environmental exposures can contribute to mania pathogen

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

118 a more comprehensive framework to define how environmental exposures can shape the gut microbiome and

119 In esophageal cancer, environmental exposures can trigger chronic inflammation

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

121 ation nasal allergen challenge (NAC) and the environmental exposure chamber (EEC) are 2 methods of co

122 An environmental exposure chamber (EEC) was used to reduce

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

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

125 Environmental exposure chambers are currently already us

126 Environmental exposure chambers, delivering a fixed amou

127 vor diagnostic criteria for ACO that include environmental exposures common to LMICs.

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

129 ngs provide new insights into how early life environmental exposures contribute to liver disease in a

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

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

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

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

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

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

136 Early life environmental exposures drive lasting changes to the fun

137 y the skin immune system and may explain how environmental exposures during life, and the microbiome,

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

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

140 Environmental exposures early in male life may alter spe

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

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

143 Environmental exposure, endogenous metabolism and cancer

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

145 , infectious diseases, NCD risk factors, and environmental exposure factors.

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

147 The exposome is defined as the totality of environmental exposures from conception onwards.

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

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

150 Environmental exposures, genetic factors, and structural

151 in neurons of people suffering from PD, and environmental exposure has also been linked with neurode

152 Various other environmental exposures have been implicated in the expl

153 d cancer incidence rates are increasing, and environmental exposures have been postulated to be playi

154 Environmental exposures have been recognized as critical

155 Environmental exposures have differential risk across et

156 Environmental exposures, health history, and clinical ou

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

158 l expresses, in parallel to the individual's environmental exposure history.

159 Despite shared environmental exposures, idiopathic pulmonary fibrosis (

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

161 To mimic environmental exposure in humans, naive BALB/c mice were

162 e systematic investigation of the effects of environmental exposure in neurologic disorders.

163 results suggest flaring may be a significant environmental exposure in parts of this region.

164 The role of environmental exposures in chronic obstructive pulmonary

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

166 Environmental exposures in early life appear to play an

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

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

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

170 that there is a need to broadly incorporate environmental exposures in psychiatric research, with th

171 rier defects, genetic locus alterations, and environmental exposures in the risk and sequence of occu

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

173 Self-reported occupational or environmental exposures, including aluminum smelting, le

174 associated with genetic mutations caused by environmental exposures, including occupational exposure

175 Early-life environmental exposures, including pathogens and commens

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

177 Recent studies indicate that environmental exposures, including urban and traffic-rel

178 We first show that environmental exposures (infection and disease) lead to

179 ssibility that parental life experiences and environmental exposures influence mental and physical he

180 Without environmental exposure information, our ability to reali

181 Environmental exposures interplay with human host factor

182 When the environmental exposure is a binary variable, analyses fr

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

184 etween genetic predisposition and early life environmental exposures is key in this regard.

185 cteristics of illness, and plausible food or environmental exposures leading to EAEC transmission wer

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

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

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

189 tematic exposome approach identified several environmental exposures, mainly chemicals, that might be

190 xploration of how genetic susceptibility and environmental exposure may interact to cause BA is warra

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

192 Other environmental exposures may contribute significantly.

193 genetic risk for type 1 diabetes (T1D) after environmental exposures may develop pancreatic islet aut

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

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

196 ich is modulated by both genetic factors and environmental exposures, may offer a unique opportunity

197 and effect are fundamental for understanding environmental exposures, mechanistic pathways of effect,

198 potheses for how modifiable risk factors and environmental exposures might be driving the worldwide i

199 l and targetable molecular mechanisms on how environmental exposures modify genetic effects.

200 Environmental exposures modulate the risk of developing

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

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

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

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

205 ly, the results from this study suggest that environmental exposure of humans to Sf-RV is likely to b

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

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

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

209 ) patient samples to evaluate the effects of environmental exposure on CNS inflammation.

210 atterns of immune development, the impact of environmental exposure on the severity of viral infectio

211 mental techniques interrogate the effects of environmental exposure on their bulk and surface propert

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

213 teraction between depression-PRS and adverse environmental exposures on mental health outcomes.

214 g suicidality) highlight the role of adverse environmental exposures on the presentation of bipolar d

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

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

221 Early life environmental exposure, particularly during perinatal pe

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

223 of POPs on ALS and supports the concept that environmental exposures play a role in disease pathogene

224 We examined the association between environmental exposures (PM(2.5), greenness, and urbanic

225 ties of hair can be impacted by internal and environmental exposures ranging from chemical stressors

226 of stress concentrators or degradation under environmental exposure, reducing strength and causing pr

227 During oxidative stress, inflammation, or environmental exposure, ribo- and deoxyribonucleotides a

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

229 sociated LUADs showed correlation with other environmental exposure signatures and a field effect in

230 fects on human health by evaluating multiple environmental exposures simultaneously during critical p

231 ing a unified view of inflammatory memory to environmental exposures (such as allergens, antigens, no

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

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

234 However, the role of potentially protective environmental exposures, such as pet ownership, is large

235 region have identified some local habits and environmental exposures that increase risk.

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

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

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

239 , these responses are strongly influenced by environmental exposures that stimulate innate immune pat

240 at although PE becomes more crystalline with environmental exposure, the lamellar order present in ne

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

242 Despite profound differences in environmental exposures, there might exist genuine patte

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

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

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

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

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

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

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

250 uestions about current methods for assessing environmental exposure to enteric pathogens.

251 Environmental exposure to food allergens may be a risk f

252 Environmental exposure to fungi is linked with acute sev

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

254 INTERPRETATION: Environmental exposure to higher concentrations of PM10,

255 humans and cercopithecines, perhaps through environmental exposure to microbes, diet, and/or associa

256 of allergic reactions such as asthma during environmental exposure to mite allergens, and therefore

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

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

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

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

261 Environmental exposure to polycyclic aromatic hydrocarbo

262 Environmental exposure to spores of pathogenic fungi can

263 Early-life environmental exposure to stress, depression, tobacco sm

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

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

266 Ancestral environmental exposures to a variety of factors and toxi

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

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

269 Environmental exposures to chemicals have been shown to

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

271 odel may be expanded to model a multitude of environmental exposures to elucidate the effect of vario

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

273 Ancestral environmental exposures to non-mutagenic agents can exer

274 f meat, animal products, produce, water, and environmental exposures to nontyphoidal Salmonella disea

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

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

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

278 and in vivo experiments in assessing risk of environmental exposures to semivolatile organic compound

279 idemiologic and mechanistic evidence linking environmental exposures to the development and exacerbat

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

281 mate change is having on major cancers, from environmental exposures to ultraviolet radiation, air po

282 4-day baseline challenge to rye grass in the environmental exposure unit (EEU), subjects were randomi

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

284 treatment challenge (PTC) to rye grass in an environmental exposure unit after 1 intervening grass po

285 PS2) and third (GPS3) intervening GPS in the environmental exposure unit.

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

287 unity and family socioeconomic variables and environmental exposure variables.

288 High physical-environmental exposure was significantly associated with

289 ary hypertension is strongly associated with environmental exposure, we hypothesize that CYPs play a

290 In addition, chemicals associated with environmental exposure were also detected from the skin,

291 Environmental exposures were abnormal, including light (

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

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

294 sociations between phenotypes and early-life environmental exposures were examined.

295 Environmental exposures were PM(2.5) derived from monito

296 Environmental exposures were recorded throughout.

297 s involve a combination of genetic and early environmental exposures, whereas late transient rhinitis

298 Our objective was to identify, from a set of environmental exposures, which exposure is associated wi

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

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