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 tions was significantly higher, suggesting a gene-environment interaction.

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

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

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

6 genetic studies is the limited knowledge of gene-environment interaction.

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

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

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

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

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

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

13 nal summary statistics from a joint model of gene-environment interaction.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

34 Many diseases are driven by gene-environment interactions.

35 and geographic differences suggest important gene-environment interactions.

36 ogenic pathways, and elucidate gene-gene and gene-environment interactions.

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

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

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

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

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

42 n birth defects resulting from gene-gene and gene-environment interactions.

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

44 -female differences in heritability and some gene-environment interactions.

45 founding (gene-environment correlations) and gene-environment interactions.

46 evere thunderstorm asthma may be enhanced by gene-environment interactions.

47 ized to be mediated by TP53 mutation-related gene-environment interactions.

48 ameworks are required to capture the complex gene-environment interactions.

49 trients, which suggests a potential role for gene-environment interactions.

50 rain and face thought to result from complex gene-environment interactions.

51 -origin and maternal effects, as well as for gene-environment interactions.

52 and CHD in humans could be caused by similar gene-environment interactions.

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

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

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

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

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

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

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

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

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

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

63 Gene-environment interaction adds another layer of compl

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

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

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

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

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

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

70 different forms of interplay among the two (gene-environment interaction and correlation).

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

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

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

76 d in a separate testing set (70%) to examine gene-environment interactions and compare predictive mod

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

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

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

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

85 life-time outcomes, which represent complex gene-environment interactions, and prioritizes potential

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

87 Gene-environment interactions are being explored, primar

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

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

90 ive roles epigenetic factors play in shaping gene-environment interactions are now well recognized.

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

92 regulation of the genome may mediate dynamic gene-environment interactions at the molecular level by

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

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

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

96 These data demonstrate a gene-environment interaction between APOE and obesogenic

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

98 No evidence for gene-environment interaction between genetic risk and ad

99 Evidence of a gene-environment interaction between previously reported

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

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

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

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

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

105 Gene-environment interactions, by means of abnormal macr

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

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

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

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

110 Gene-environment interactions can have important implica

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

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

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

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

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

116 Gene-environment interactions determine the biological o

117 Gene-environment interactions driven by early life xenoe

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

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

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

121 To identify gene-environment interaction effects on childhood asthma

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

123 on test and a joint test of genetic main and gene-environment interaction effects.

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

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

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

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

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

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

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

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

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

133 genetic variants, environmental factors, and gene-environment interaction (G x E) effects.

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

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

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

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

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

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

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

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

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

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

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

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

146 Gene-environment interactions (GxE) can be fundamental i

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

148 ion studies has facilitated the discovery of gene-environment interactions (GxE).

149 ying a complex disease hinges on discovering gene-environment interactions (GXE).

150 e propose a simple, unifying mixed model for gene-environment interaction (GxEMM).

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

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

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

154 Gene-environment interactions have a pivotal role in ASD

155 Although gene-environment interactions have been implicated in th

156 Although gene-environment interactions have been investigated for

157 sion, both gene-environment correlations and gene-environment interactions have been observed.

158 Gene-environment interactions have been scrutinized sinc

159 Gene-environment interactions have long been theorized t

160 Gene-environment interactions have the potential to shed

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

162 Gene-environment interactions impact the development of

163 These results illuminate mechanisms of gene-environment interaction in a multifactorial model o

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

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

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

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

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

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

170 Finally, we demonstrate a gene-environment interaction in mouse embryos between No

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

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

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 Overlooking gene-environment interactions in birth defect etiology l

177 tance of and current challenges in resolving gene-environment interactions in birth defects.

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

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

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

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

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

183 Recent studies have implicated gene-environment interactions in PD susceptibility.

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

185 nt exposures and highlight the importance of gene-environment interactions in shaping the premalignan

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 and can serve as a converging point for many gene-environment interactions in the pathogenesis of ASD

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

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

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

193 ility (miR-QTLs) and the lower occurrence of gene-environment interactions, in stark contrast with eQ

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

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

196 provide a unique opportunity to examine how gene-environment interactions influence cancer risk when

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

198 Reported gene-environment interactions involving adiposity and LE

199 Here, we report on gene-environment interactions involving genetic mutation

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

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

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

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

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

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

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

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

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

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

210 This gene-environment interaction may contribute to the compl

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

212 Detecting gene-environment interactions may allow us to elucidate

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

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

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

216 E epsilon4 status, which elucidated possible gene-environment interaction mechanisms in which residen

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 ach and sufficient sample size for analyzing gene-environment interactions on brain structure and fun

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

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

227 However, the impact of gene-environment interactions on phenotypic traits mostl

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

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

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

231 Gene-environment interaction patterns differ between pat

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

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 enetic interactions (including gene-gene and gene-environment interactions) play important roles beyo

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

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

239 their greater adiposity, and explains other gene-environment interactions, remains to be determined.

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

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

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

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

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

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

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

247 Gene-environment interaction studies offer the prospect

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

249 Gene-environment interaction studies suggest that the ef

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

251 Gene-environment interaction studies using genome-wide a

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

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

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

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

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

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

258 were aggregated by genes and evaluated by a gene-environment interaction test and a joint test of ge

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

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

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

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

266 ant tissue, thus placing greater emphasis on gene-environment interactions that enable disease phenot

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

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

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

270 gic disease is rising as a result of complex gene-environment interactions that shape the immune syst

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

272 sensitive mechanism of action and examining gene-environment interactions, this study defined a lowe

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

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

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

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

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

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

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

280 This gene-environment interaction was successfully replicated

281 This gene-environment interaction was successfully replicated

282 No evidence of gene-environment interactions was observed.

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

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

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

286 In addition, sixty-five purported gene-environment interactions were found to be potential

287 Gene-environment interactions were investigated using Sh

288 Gene-environment interactions were observed with cigaret

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

290 validity of a PRS and to demonstrate a novel gene-environment interaction, whereby the effect of diab

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