ライフサイエンスコーパス: gene-environment interaction

1 mplex Human Diseases (multiple gene-gene and gene-environment interactions).

2 nmental (human exposome) factors through the gene-environment interaction.

3 gene-environment independence in estimating gene-environment interaction.

4 rather than the main effect in a model with gene-environment interaction.

5 at this robustness extends to assessments of gene-environment interaction.

6 also plagues other methods of assessment of gene-environment interaction.

7 th an altered gene-expression network due to gene-environment interaction.

8 omparisons yielded significant evidence of a gene-environment interaction.

9 significant heterogeneity and gene-gene and gene-environment interaction.

10 ase-only designs for tests of association in gene-environment interaction.

11 ng untested rare variants, and gene-gene and gene-environment interaction.

12 otype, reflecting a molecular consequence of gene-environment interaction.

13 NTDs among Sp(2)(H) embryos, demonstrating a gene-environment interaction.

14 ata aimed at identifying genes involved in a gene-environment interaction.

15 among Asian/Pacific Islanders likely due to gene-environment interaction.

16 this study, which is suggestive of possible gene-environment interaction.

17 eptibility to acidosis-induced arrhythmia, a gene-environment interaction.

18 re and structural variation, and the role of gene-environment interaction.

19 confirming a sentinel finding in research on gene-environment interaction.

20 validate traditional joint tests of gene and gene-environment interaction.

21 re living in Costa Rica to examine potential gene-environment interactions.

22 ts, environmental effects and the effects of gene-environment interactions.

23 Ls, environmental effects and the effects of gene-environment interactions.

24 inconsistent, possibly because of unexplored gene-environment interactions.

25 role of this genetic variant on behavior and gene-environment interactions.

26 ociated pathways, epigenetic mechanisms, and gene-environment interactions.

27 ent, as once again are studies investigating gene-environment interactions.

28 ects, and combinations of factors, including gene-environment interactions.

29 and geographic differences suggest important gene-environment interactions.

30 n permits assessment of exposure effects and gene-environment interactions.

31 rom the existing literature on gene-gene and gene-environment interactions.

32 with complex diseases and with gene-gene and gene-environment interactions.

33 e propose avenues for future studies to find gene-environment interactions.

34 rait loci (QTL) by considering epistatic and gene-environment interactions.

35 netic process with the capacity to integrate gene-environment interactions.

36 model of such growth that takes into account gene-environment interactions.

37 d to consider genetic epistasis in assessing gene-environment interactions.

38 ; this indicates a need for more research on gene-environment interactions.

39 cts complex genetic effects and multifaceted gene-environment interactions.

40 or the most complex human diseases that have gene-environment interactions.

41 crosses to include environmental effects and gene-environment interactions.

42 of QTL, their main and epistatic effects and gene-environment interactions.

43 remains difficult to identify gene-gene and gene-environment interactions.

44 Oral sensation varies with genetics and gene-environment interactions.

45 rgent pathogenic mechanisms and/or different gene-environment interactions.

46 s and may be particularly useful for testing gene-environment interactions.

47 of cigarette smoke, to look for evidence of gene-environment interactions.

48 and may provide a useful tool to investigate gene-environment interactions.

49 dependently as well as through gene-gene and gene-environment interactions.

50 ow for genetic analysis and interrogation of gene-environment interactions.

51 ream evaluation of exposure associations and gene-environment interactions.

52 enced by synthesis, protein degradation, and gene-environment interactions.

53 pharmacogenetic purposes, and gene-gene and gene-environment interactions.

54 This provides a potential mechanism for gene-environment interactions.

55 ergies and asthma, are the result of complex gene-environment interactions.

56 Growth and development are dominated by gene-environment interactions.

57 s exist to facilitate an unbiased search for gene-environment interactions?

58 ciations (86%); fewer evaluated gene-gene or gene-environment interactions (17%), the prevalence of g

59 To detect gene-environment interactions, a logistic regression mod

60 The strongest statistical evidence for a gene-environment interaction across studies was for vege

61 First, is it likely that gene-environment interactions actually exist?

62 Gene-environment interaction adds another layer of compl

63 n, demonstrating the potential for important gene-environment interactions affecting mitochondrial he

64 development, increasing understanding of how gene-environment interaction affects variation in stress

65 there was evidence of a protective effect of gene-environment interaction against atopy in children,

66 This study also highlights the value of gene-environment interaction analyses in evaluating gene

67 Gene-environment interaction analyses suggested addition

68 With the use of gene-environment interaction analyses, we sought to clar

69 is a useful tool for exploring gene*gene or gene*environment interactions and identifying a small nu

70 sed depends on the strength and direction of gene-environment interaction and association, the level

71 actorial conditions that are associated with gene-environment interaction and immune function.

72 ene interaction) and other phenomena such as gene-environment interaction and locus heterogeneity.

73 We examine the reasons for investigating gene-environment interactions and address recent reports

74 dow of opportunity for research on genes and gene-environment interactions and also to investigate ho

75 o pathogenesis include discoveries regarding gene-environment interactions and an increasing understa

76 In this opinion piece, we critically discuss gene-environment interactions and attempt to answer thre

77 Therefore, to generate new insights into gene-environment interactions and complex behaviour, we

78 We also accounted for gene-environment interactions and conditionally dependen

79 pproaches can empower the discovery of novel gene-environment interactions and discuss specific metho

80 pportunities to advance our understanding of gene-environment interactions and fundamental processes

81 ay-based approach may identify gene-gene and gene-environment interactions and increase predictive po

82 ript supports the idea that ASD results from gene-environment interactions and that in the presence o

83 opment and severity has brought the focus on gene-environment interactions and the identification of

84 greater detail (including any gene-gene and gene-environment interactions) and to determine any impl

85 le of multiple gestation in pathogenesis, of gene environment interaction, and how to influence brain

86 ntal origins even if it is associated with a gene-environment interaction, and implies that a large p

87 olicies for infectious disease surveillance, gene-environment interactions, and health disparities gl

88 Pharmacogenetics is one example of how gene-environment interactions are already being taken in

89 Gene-environment interactions are being explored, primar

90 Our results indicated that gene-environment interactions are important for asthma d

91 s migrating from other countries, suggesting gene-environment interactions are important.

92 Gene-environment interactions are of interest in genetic

93 pregnancy outcome or developmental disease, gene-environment interactions are responsible for the ma

94 ikelihood estimators for genetic effects and gene-environment interactions are unbiased and statistic

95 cestors with nonhuman primates involved many gene-environment interactions at the population level, a

96 ing strategies are proposed for multivariate gene-environment interactions at two levels: interaction

97 us on asthma as a model disease for studying gene-environment interactions because of relatively larg

98 We tested for gene-environment interaction between EoE-predisposing po

99 We observed what appears to be a gene-environment interaction between MBL-2 variants and

100 Evidence of a gene-environment interaction between previously reported

101 analysis suggested a possible multiplicative gene-environment interaction between rs238406 genotypes

102 In this study, we show a significant gene-environment interaction between SHBG D356N polymorp

103 Weak evidence of gene-environment interaction between smoking and shared

104 The authors investigated whether the gene-environment interaction between the genotype for th

105 We detected gene-environment interactions between 25-OHD concentrati

106 tional studies of gene expression identified gene-environment interactions between progestin use and

107 Significant gene-environment interactions between the GSTT1-null pol

108 triglycerides and glucose, suggest possible gene-environment interactions, but do not provide eviden

109 have been applied to identify gene-gene and gene-environment interactions, but future efforts should

110 A systematic approach to studying gene-environment interaction can have immediate impact o

111 t, we have demonstrated the power with which gene-environment interactions can be investigated using

112 onal analyses, and analyses of gene-gene and gene-environment interactions can be performed.

113 mouse is an optimal model organism in which gene-environment interactions can be used to study the p

114 Gene-environment interactions can have important implica

115 gene expression in changing environments and gene-environment interactions causing developmental diff

116 In a seminal study of gene-environment interaction, childhood maltreatment pre

117 shift of focus from early life to pregnancy, gene-environment interactions, cohort effects, and time

118 ction analyses can identify genes exhibiting gene-environment interactions critical for unraveling di

119 sents a powerful teaching tool, showing that gene-environment interactions depend on route-of-adminis

120 Gene-environment interactions determine the biological o

121 Gene-environment interactions driven by early life xenoe

122 evealing mechanisms of genetic variation and gene environment interactions during fetal heart develop

123 , apply tests that jointly consider gene and gene-environment interaction effects for analysis.

124 eraged to increase efficiency for estimating gene-environment interaction effects in comparison with

125 To identify gene-environment interaction effects on childhood asthma

126 d on a linear mixed model with epistasis and gene-environment interaction effects, were conducted, us

127 nmental confounder is nonzero, then there is gene-environment interaction either between the genetic

128 ltered innate and adaptive immune responses, gene-environment interactions, epigenetic regulation, an

129 helps to understand the mechanistic base of gene-environment interactions essential for organismic d

130 ic mechanisms are believed to integrate such gene-environment interactions, fine-tuning gene expressi

131 We also found a gene-environment interaction for 4 nonexonic SNPs and ir

132 the EIRA data, we could not confirm a major gene-environment interaction for anti-CCP formation betw

133 des one of the first examples of a potential gene-environment interaction for NHL.

134 ion interrogation approaches and to evaluate gene-environment interaction for the magnesium-associate

135 ssian adolescent boys (n = 392), we assessed gene-environment interactions for 337 tagging single-nuc

136 on test scores, suggesting that articulating gene-environment interactions for cognition is more comp

137 c actions of molecular systems and to assess gene-environment interactions for elucidating the behavi

138 Two other studies investigating gene-environment interactions found that effects of stre

139 Investigating and understanding gene-environment interaction (G x E) in a neurodevelopme

140 polar disorder, may be ascribed to a complex gene-environment interaction (G x E) model, linking the

141 Few gene-environment interactions (G x E) have been discover

142 ve variables involved in gene-gene (GGI) and gene-environment interactions (GEI) that are associated

143 onsidered to be multi-factorial, with likely gene-environment interactions (GEI).

144 heuristics for visualizing and interpreting gene-environment interactions (GEIs) and to assess the d

145 and behavior, yet little is known about the gene-environment interactions (GEIs) that underlie these

146 d on relevant exposures that are involved in gene-environment interactions (GEIs), such as rhinovirus

147 Furthermore, the role of gene-environment interaction, gene-gene interaction, and

148 netic, neurobiological, pharmacological, and gene-environment interaction (GxE) approaches.

149 Therefore, the study of gene-environment interaction (GxE) has been a focus of r

150 The analysis of gene-environment interaction (GxE) may hold the key for

151 Large-scale gene-lifestyle or more generally gene-environment interaction (GxE) meta-analysis studies

152 Reports of gene-environment interactions (GxE) between the serotoni

153 n psychiatry, the identification of measured gene-environment interactions (GxE) has promoted a heate

154 analytical methods have emerged for studying gene-environment interactions (GxEs) in large-scale stud

155 Evidence for gene-environment interactions has been found between HLA

156 Several methods for screening gene-environment interaction have recently been proposed

157 Although gene-environment interactions have been investigated for

158 Gene-environment interactions have been scrutinized sinc

159 Gene-environment interactions have the potential to shed

160 We examined this gene-environment interaction hypothesis in a sample of 3

161 provide tantalizing evidence suggesting that gene-environment interactions, i.e., the modulation by a

162 Gene-environment interactions impact the development of

163 underlying neurobiological mechanism of this gene-environment interaction in ADHD is unknown.

164 eatment interaction in a randomized trial or gene-environment interaction in an observational study.

165 On the test of gene-environment interaction in ARIC EA participants, th

166 risk factors, highlighting the importance of gene-environment interaction in esophageal carcinogenesi

167 for the powerful ability of BAP1 to regulate gene-environment interaction in human carcinogenesis.

168 erations may provide important insights into gene-environment interaction in inflammatory bowel disea

169 s could introduce a new mechanistic model of gene-environment interaction in RA.

170 The data were collected in the gene-environment interaction in respiratory disease surv

171 ogramming is defined as the process by which gene-environment interaction in the developing organism

172 We confirmed this gene-environment interaction in two birth cohorts, and w

173 We tested gene-environment interactions in 7610 women who develope

174 We suggest that studying gene-environment interactions in animal models, although

175 provide key insights into developmental and gene-environment interactions in autoimmunity.

176 ral approach to testing for sufficient-cause gene-environment interactions in case-control studies.

177 These results shed some new light on gene-environment interactions in decision making, which

178 This study provides evidence for possible gene-environment interactions in glioma development.

179 etics of TLRs provides important insights in gene-environment interactions in health and disease, and

180 nse to Salmonella infection, (ii) uncovering gene-environment interactions in host response to bacter

181 rtunity to model environmental exposures and gene-environment interactions in human disease and to in

182 des a neurobiologically consistent model for gene-environment interactions in impulsive aggression.

183 with LPS, revealing the high significance of gene-environment interactions in preterm birth.

184 These observations strongly implicate gene-environment interactions in susceptibility and more

185 egression modeling to test for gene-gene and gene-environment interactions in the case-control data s

186 avioral abnormalities, suggesting a role for gene-environment interactions in the determination of co

187 ariance, indicating a need to better explore gene-environment interactions in the development of IBD.

188 Our findings provide evidence for specific gene-environment interactions in the emergence of enduri

189 underlining the importance of understanding gene-environment interactions in the pathogenesis of ast

190 g the role of genetics, the environment, and gene-environment interactions in these common lung disea

191 These data suggest complex gene-environment interactions in which genetic susceptib

192 tribution of inherited genetic variation and gene/environment interactions in relation to disease.

193 It is likely that a gene-environment interaction, in which genetically susce

194 actors, including genetic susceptibility and gene/environment interaction, in relation to disease and

195 Analysis of gene-environment interactions, included in only a small

196 Furthermore, there was some evidence for gene-environment interactions, including physical activi

197 wide association study era is characterizing gene-environment interactions, including scanning for in

198 Our investigation of the gene-environment interaction involved in AMD revealed a

199 tudinally across ages 7-15 years, along with gene-environment interactions involving the major enviro

200 We propose that gene-environment interaction is a major contributor to p

201 DCM is applicable, and each attribute or the gene-environment interaction is associated with outcome.

202 associations with childhood asthma risk, and gene-environment interaction is one possible explanation

203 The concept of gene-environment interaction is receiving support from e

204 er, mapping genes with epistatic effects and gene-environment interactions is a difficult problem bec

205 The study of gene-environment interactions is an active and much need

206 and their interactions with other genes, and gene-environment interactions is compiled to provide the

207 ure-based meta-analysis conducted to examine gene-environment interactions is unlikely to provide a m

208 flected by a rising sex ratio, influenced by gene-environment interaction, is the most likely.

209 tional and experimental approach uncovered a gene-environment interaction linking Mg(2+) deficiency t

210 r understanding some of the confusion in the gene-environment interaction literature on stress, 5-HTT

211 clude that, for future genome-wide scans for gene-environment interactions, major power gain is possi

212 This gene-environment interaction may contribute to the compl

213 Emerging evidence has suggested that the gene-environment interaction may partly explain such var

214 These gene-environment interactions may occur in the father, m

215 Further investigations into gene-gene and gene-environment interactions may prove enlightening.

216 and systemic mechanisms underlying specific gene-environment interactions may provide insights into

217 Gene-environment interactions mediated at the epigenetic

218 large-scale association scans where the true gene-environment interaction model is unknown.

219 In our gene-environment interaction model, we demonstrate that

220 ion over the past two decades has focused on gene-environment interaction models to explain the relat

221 x of 12 variants showed significant additive gene-environment interactions, most notably NAT2 (P = 7

222 exposure) and threshold interactions (e.g., gene-environment interaction occurs only when environmen

223 ich brain regions mediate the effect of this gene-environment interaction on ADHD severity.

224 The present study aimed to reveal possible gene-environment interactions on decision making in a la

225 th transregulation, demonstrating effects of gene-environment interactions on disease.

226 urons and illustrate the profound effects of gene-environment interactions on the translational profi

227 er smokers (OR=1.2, P=0.66), demonstrating a gene-environment interaction (P=0.03).

228 nce, but it still persists if estimating the gene-environment interaction parameter itself is of inte

229 ronmental confounding will bias estimates of gene-environment interaction parameters even under gene-

230 Gene-environment interaction patterns differ between pat

231 ELF4 gene passed the significance cutoff for gene-environment interaction (Pge = 1.14 x 10(-5)).

232 eas of interest and investigation--including gene-environment interaction, pharmacogenetics, and gene

233 ns, environment-wide association studies and gene-environment interactions, phenome-wide association

234 Gene-environment interactions play a crucial role in the

235 understanding of the role that genetics and gene-environment interactions play in the development of

236 ly linear regression approach to testing for gene-environment interaction recently considered by Clar

237 of these approaches has uncovered effects of gene-environment interactions relevant to drug response

238 osure modification, which characterizes most gene-environment interactions reported to date, is intro

239 lopmental windows, is the optimal design for gene-environment interaction research.

240 rature elucidates significant gene--diet and gene--environment interactions resulting in altered lipi

241 Thus, this gene-environment interaction reveals two faces of 17q21:

242 Our understanding of gene-environment interactions should lead to a better us

243 Recent association and gene-environment interaction studies have increased our

244 Current Challenges and New Opportunities for Gene-Environment Interaction Studies of Complex Diseases

245 Gene-environment interaction studies offer the prospect

246 The ability to conduct gene-environment interaction studies remotely would redu

247 Gene-environment interaction studies suggest that the ef

248 Nonetheless, continued investment in gene-environment interaction studies through large colla

249 Gene-environment interaction studies using genome-wide a

250 on and re-sequencing projects, together with gene-environment interaction studies, are expected to fu

251 ications of these results for the conduct of gene-environment interaction studies.

252 develop a platform for the remote conduct of gene-environment interaction studies.

253 mote methods are suitable for the conduct of gene-environment interaction studies.

254 rtunity to increase capacity for large-scale gene-environment interaction studies.

255 s are involved in the design and analysis of gene-environment interaction studies.

256 ells in asthma exacerbation in a genome-wide gene-environment interaction study that has been replica

257 controlled by natural genetic variation and gene-environment interactions, suggesting that the compl

258 The observed gene-environment interaction suggests a role of early-li

259 signs including family-based association and gene-environment interaction testing.

260 The findings highlight an important gene-environment interaction that elucidates the role of

261 This may suggest a possible underlying gene-environment interaction that warrants further study

262 Risk of PTB is affected by complex gene-environment interactions that are not well understo

263 autonomous effects modulated by sex-specific gene-environment interactions that could still include p

264 ty of PDAC results from complex, progressive gene-environment interactions that currently fall outsid

265 inheritance of risk, providing the focus for gene-environment interactions that determine susceptibil

266 exposure; however, well-conducted studies of gene-environment interactions that draw on data from mor

267 to systematically decipher the gene-gene and gene-environment interactions that influence complex mul

268 Our findings provide new insight into gene-environment interactions that influence individual

269 ated inflammatory disease and is a model for gene-environment interactions that may be relevant to ot

270 Thus, Nrf2 could be a critical factor for gene-environment interactions that may determine suscept

271 eates a context permissive for gene-gene and gene-environment interactions that modulate PFC function

272 dysregulation in the airways by translating gene-environment interactions that underpin disease path

273 The conventional method of detecting gene-environment interactions, the case-control analysis

274 ns important for cognitive control link this gene-environment interaction to ADHD severity.

275 ly test for marginal genetic association and gene-environment interaction to discover single nucleoti

276 method for mediation analysis, allowing for gene-environment interaction, to a lung cancer case-cont

277 A significant result is indicative of a gene-environment interaction under a multiplicative mode

278 py, and confounding, and several examples of gene-environment interaction under gene-environment depe

279 NA editing in human brains may shed light on gene-environment interactions underlying complex behavio

280 However, meta-analysis of gene-environment interactions using published literature

281 Here I discuss the testing and estimation of gene-environment interactions via the case/pseudocontrol

282 This gene-environment interaction was successfully replicated

283 This gene-environment interaction was successfully replicated

284 No evidence of gene-environment interactions was observed.

285 To test for evidence of gene-environment interactions, we compared genotypic rel

286 To identify the role of 5hmC in gene-environment interactions, we exposed both young (6-

287 To illustrate one way to estimate such gene-environment interactions, we used prospective data

288 Gene-environment interactions were observed with cigaret

289 ber of potentially interesting gene-gene and gene-environment interactions were reported, but these w

290 ncept that late-onset ADHR is the product of gene-environment interactions whereby the combined prese

291 the pathogenesis of CD requires gene-gene or gene-environment interactions which are absent in Asian

292 or the presence of a main genetic effect and gene-environment interaction will be biased if the genet

293 sis, and considerable evidence suggests that gene-environment interactions will be important.

294 Gene-environment interactions will be missed in genome-w

295 so detect trend interactions (e.g., a larger gene-environment interaction with a higher level of envi

296 The association of this gene-environment interaction with ADHD symptom count was

297 enetic variation in ARMS2, and a significant gene-environment interaction with cigarette smoking was

298 detect a particular type of sufficient-cause gene-environment interaction with greater sensitivity.

299 use of relatively large numbers of candidate gene-environment interactions with asthma risk in the li

300 Asthma is a consequence of complex gene-environment interactions, with heterogeneity in cli