ライフサイエンスコーパス: adolescence

1 d parental death or divorce during childhood/adolescence.

2 istent influence on brain development during adolescence.

3 enhanced memory formation from childhood to adolescence.

4 d developing chronic or relapsing disease by adolescence.

5 t fear-associated memories emerging later in adolescence.

6 ss pollen allergy during childhood and up to adolescence.

7 navigation of the social environment during adolescence.

8 in linking social stress with depression in adolescence.

9 in early childhood and peaks in onset during adolescence.

10 irments that manifest later in childhood and adolescence.

11 erienced better well-being in early and late adolescence.

12 tients develop clinically silent fibrosis by adolescence.

13 iagnostic criteria for the first time during adolescence.

14 isorder (ADHD) run a variable course through adolescence.

15 e and use of psychotropic medications during adolescence.

16 d the greatest conditioned fear responses in adolescence.

17 lnerable to altered brain development during adolescence.

18 tic plasticity and circuit refinement during adolescence.

19 ifferences in cognitive functioning in early adolescence.

20 ialization of the striatal DA system through adolescence.

21 diatric patients from the neonatal period to adolescence.

22 ures of emotion regulation and depression in adolescence.

23 1 y was related to metabolic health through adolescence.

24 Schizophrenia typically onsets after adolescence.

25 at immigration, and myopia occurrence during adolescence.

26 spite the high prevalence rates of co-use in adolescence.

27 ing interneurons by excitatory inputs during adolescence.

28 dministering a second dose of vaccine during adolescence.

29 operative behaviour improves markedly across adolescence.

30 lnerability for diagnosed psychopathology in adolescence.

31 ildhood neglect on externalizing problems in adolescence.

32 ng children in foster care were mitigated by adolescence.

33 me budgets of children from early infancy to adolescence.

34 elates of prosocial development during early adolescence.

35 ties during the transition from childhood to adolescence.

36 d with an escalating Meth regime during late adolescence.

37 and a "depression/mood" type, with onset in adolescence.

38 hat protected, until risk increases again in adolescence.

39 opt anti-school roles, particularly in later adolescence.

40 me course, which is completed only by end of adolescence.

41 the risk of asthma and allergic disease into adolescence.

42 ntially methylated in relation to smoking in adolescence.

43 eural processing of sounds in late childhood/adolescence.

44 al impact of cigarette smoking behaviours in adolescence.

45 sample, 14 107 (25%) first gave birth during adolescence.

46 utive function, and behavioral function into adolescence.

47 itude ratio that progresses from juvenile-to-adolescence.

48 e predicted higher externalizing problems in adolescence.

49 unctional reorganization of the brain during adolescence.

50 an overactive but desynchronized PFC before adolescence.

51 underlying mechanisms are already mature by adolescence.

52 r puberty with self-report sleep duration in adolescence.

53 ormance on the memory task was better during adolescence.

54 pus functional connectivity before and after adolescence.

55 risk factors and asthma-related outcomes in adolescence.

56 th severe asthma outgrow their asthma during adolescence.

57 Latino; 54% female) were followed into early adolescence.

58 between ages 13 and 24, peaking during late adolescence.

59 icted axial eye elongation and myopia during adolescence.

60 biological locus of memory improvements into adolescence.

61 ficant developmental changes from birth into adolescence.

62 arkers of sex-specific asthma acquisition in adolescence.

63 The majority of children with NPC die in adolescence.

64 asthma-related outcomes and lung function in adolescence.

65 s can be debilitating for self-management in adolescence.

66 then in mid-childhood (7-9 years) and early adolescence (10-12 years) using Wechsler Intelligence Sc

67 dies in healthy developmental samples (i.e., adolescence [10-18 years of age] and emerging adulthood

68 In adolescence (15 y; n = 115), error monitoring event-rela

69 he basis of age at first birth: 10-19 years (adolescence), 20-24 years (young adulthood), and 25 year

70 ong those with asymptomatic sensitization in adolescence, 53%-78% developed allergic rhinitis in adul

71 ce suggests this is particularly true during adolescence, a developmental period involving substantia

72 PFC undergoes significant maturation during adolescence, a period when cannabis use in humans has be

73 outh during the transition from childhood to adolescence, a period when self-regulatory capacities ra

74 has focused mainly on early life rather than adolescence, a potentially important developmental life

75 striatum dopamine (DA) system through human adolescence, a time of increased sensation seeking and v

76 These processes continue to develop during adolescence, a time of significant social change, and ar

77 -related disorders peak in prevalence during adolescence, a window of rapid behavioral development an

78 ut some experience the first symptoms during adolescence/adulthood.

79 By adolescence (age 16), subjects in FE trajectory were sig

80 escents from whom data were collected during adolescence (ages 11-18 years) and adulthood (ages 24-32

81 d that ADHD symptoms may emerge later during adolescence and adult life in some individuals although

82 tigated the impact of stress exposure during adolescence and adulthood on the activity of putative py

83 ter animals complete their maturation during adolescence and are absent if the NMDAR is deleted durin

84 ognized predictor of early heart failure, in adolescence and being diagnosed with cardiomyopathy in a

85 ression of threat response regulation during adolescence and beyond.

86 whether miR-218 regulates Dcc expression in adolescence and could serve as an early predictor of lif

87 This study highlights the transition between adolescence and early adulthood as a critical period and

88 We examined trajectories across adolescence and early adulthood for 2 major dietary patt

89 during the critical developmental period of adolescence and early adulthood is a major challenge.

90 ory airflow in these individuals during late adolescence and early adulthood with that of control ind

91 During adolescence and early adulthood, learning when to avoid

92 ere less likely to be overweight or obese in adolescence and early adulthood.

93 in proximal femur shape can be discerned in adolescence and early adulthood.

94 s among survivors of cancer diagnosed during adolescence and early young adulthood have not been char

95 Adolescence and emerging adulthood are periods of height

96 tly downregulate PV levels in the PFC during adolescence and examined its impact on prefrontal GABAer

97 An association between body weight in adolescence and future cardiomyopathy among men was rece

98 al activity initiation increasing throughout adolescence and higher immunogenicity for younger vaccin

99 the development of flexible cognition during adolescence and how these neural systems are affected in

100 ng axons toward the prefrontal cortex during adolescence and in the maturational organization and adu

101 population and that often has its genesis in adolescence and in vulnerable individuals associated wit

102 s and sexual minorities are present early in adolescence and increase throughout the school years, pe

103 forcement-learning mechanisms that change in adolescence and into adulthood.

104 y of basal ganglia iron concentration during adolescence and its association with cognition are less

105 e development of brain iron concentration in adolescence and its relationship to cognition are less w

106 gain of GABAergic function in the PFC during adolescence and its susceptibility to the impact of tran

107 layer V apical dendrites that emerges during adolescence and persists into adulthood.

108 oncentration across the basal ganglia during adolescence and provide evidence that diminished iron co

109 nlinear patterns of threat responding during adolescence and the continued development of the underly

110 and academic outcomes typically accompanying adolescence and the middle school transition.

111 t modes of PSI of somatosensory afferents in adolescence and throughout adulthood.

112 why schizophrenia typically manifests after adolescence and which neurobiological mechanisms are und

113 suicidal ideation and hazardous drinking in adolescence and young adulthood as well as opioid use in

114 nd DMN function may be tightly linked during adolescence and young adulthood, and reduced DMN connect

115 y mild to moderate, tended to decline during adolescence and young adulthood.

116 verweight or obesity of grandchildren during adolescence and young adulthood.

117 carriage of Neisseria meningitidis peaks in adolescence and young adulthood.

118 erate fluorosis severity was observed across adolescence and young adulthood.

119 ity of exhibiting any behavior of despair in adolescence and young adulthood.

120 ) lower risk of overweight or obesity during adolescence and young adulthood.

121 with greater iron concentration through late adolescence and young-adulthood.

122 substantial development across childhood and adolescence, and aberrations in these trajectories are r

123 n do not appear to be the same in childhood, adolescence, and adult life.

124 hat were weak at 14 y became stronger during adolescence, and connections that were strong at 14 y be

125 ny mental health disorders first manifest in adolescence, and early treatment may affect the course o

126 ed morphologic and functional changes during adolescence, and it is believed that these changes serve

127 tation accumulation rates are established in adolescence, and later menarche in women is associated w

128 and hippocampal volume across school age and adolescence, and measures of emotion regulation and depr

129 ldren from preschool (ages 3 to 5 y) to late adolescence, and which includes prospective assessments

130 never-institutionalized children widened by adolescence; and (iii) early difficulties in visual-spat

131 In particular, PSs during adolescence appear to be a nonspecific precursor of diff

132 The causes of obesity in childhood and adolescence are complex and multifaceted, presenting res

133 odevelopmental adaptations that occur during adolescence are hypothesized to underlie age-related imp

134 cational experiences that span childhood and adolescence are independently related to level of cognit

135 Poor dietary patterns established in adolescence are likely to track into early adulthood, pa

136 mpal development during middle childhood and adolescence are not sensitive enough.

137 maturation linked to pubertal development in adolescence are thought to affect multiple aspects of br

138 s in asthma status changes from pre- to post-adolescence are unclear.

139 es-mediated input mapping in mice to uncover adolescence as a developmental stage when frontal top-do

140 Our findings point to early adolescence as a phase of rapid change in cooperative be

141 sts in late adolescence or for SFSS in early adolescence as a robust correlate of well-being or predi

142 In addition, we emphasise adolescence as a sensitive period for the confluence of

143 cidence of psychotic experiences during late adolescence as well as an unmet need for care in young p

144 Notably, circulating miR-218 levels in adolescence associate with vulnerability to social defea

145 in DNAm (males vs females) from pre- to post-adolescence at asthma-associated CpGs.

146 ooperative behaviour remains constant across adolescence, but adjustment requiring cooperative behavi

147 ethylation is also observed in childhood and adolescence, but not adulthood. Birthweight-related CpGs

148 top-down neuron activity selectively during adolescence, but not later periods, produces long-lastin

149 asthma often improves between childhood and adolescence, but refractory cases have been noted.

150 human brain organization is disrupted during adolescence by remodeling of FC between association cort

151 Exposure to nicotine during adolescence can harm the developing brain, which may aff

152 Stress in adolescence can regulate vulnerability to traumatic stre

153 Whether exposure to EE during adolescence can restore normal hippocampal function and

154 amygdala undergoes extensive growth through adolescence, coinciding with the acquisition of complex

155 es of secondhand smoke exposure in childhood/adolescence consisted of parental self-reports of smokin

156 aturation of the somatosensory system during adolescence contributes to the improved motor control.

157 How adolescence contributes to the maturation of top-down ne

158 By contrast, protein restriction during adolescence decreased nucleus accumbens dopamine release

159 the behavioral level, MK-801 exposure during adolescence did not disrupt the acquisition of trace fea

160 requiring liver transplantation (LT) during adolescence, disparity on the waiting list and post-LT o

161 ry effects during early life periods such as adolescence due to its late maturation.

162 c affliction manifested behaviorally at late adolescence/early adulthood.

163 a standardised, classroom-based life skills Adolescence Education Program (AEP), compared to AEP alo

164 ults indicate NMDA receptor signaling during adolescence enables the gain of prefrontal GABAergic fun

165 uggests that psychoactive cannabinoid use in adolescence enhances the behavioral effects of cocaine.

166 standing the health effects of childhood and adolescence exposure to multiple industrial carcinogens

167 of prefrontal GABAergic transmission during adolescence for maintaining proper levels of excitatory-

168 ampus and highlight the utility of EE during adolescence for restoring normal hippocampal function.

169 identifying morphological sex differences in adolescence from those of the National Consortium on Alc

170 ividuals in the lower quartiles of intake at adolescence generally continuing to have low intake in y

171 ors for surgery included CD diagnosis during adolescence, growth impairment, NOD2/CARD15 polymorphism

172 eased mostly from puppyhood (0.5-1 years) to adolescence (> 1-2 years), then continued to decrease in

173 ally disadvantaged area during childhood and adolescence has a long-lasting negative association with

174 Frequent cannabis use during adolescence has been associated with alterations in brai

175 rtunity for nutritional interventions during adolescence has been postulated.

176 nterneurons interacts with maturation during adolescence has not been clarified yet.

177 onal brain growth from the newborn period to adolescence has not been described.

178 lood of infants and children with AD through adolescence have not been explored.

179 slowly, reaching maturity only at the end of adolescence; however, the mechanisms controlling the tim

180 institutionalized children persisted through adolescence; (ii) the gap in spatial working memory betw

181 t to study if and how THC consumption during adolescence impacts adult behavior.

182 y during pregnancy and diet quality in early adolescence in a contemporary cohort.

183 during a critical period equivalent to early adolescence in humans to optimize the ability of organis

184 d control offspring-an age comparable to mid adolescence in humans.

185 in a reversal-learning task improves during adolescence in male and female Long-Evans rats and demon

186 e assessed whether exposure to MK-801 during adolescence in male rats triggers a state of excitatory-

187 osure with neurodevelopment in childhood and adolescence in the Center for the Health Assessment of M

188 lood pressures increased more quickly during adolescence in the EP group than in the control group.Co

189 ich gray and white matter develop throughout adolescence in typically developing youth as well as in

190 occurs alongside behaviors that characterize adolescence, including deepening cognitive sophisticatio

191 and hypersensitivity to social rejection in adolescence increase the likelihood of both risky and pr

192 on dopamine release but the same diet during adolescence induced a frequency-dependent increase in st

193 ulants, and sedatives or tranquilisers) from adolescence into adulthood, assess the extent to which d

194 Adolescence is a critical developmental stage.

195 Adolescence is a formative phase of the life course with

196 Adolescence is a peak time for the onset of psychiatric

197 Adolescence is a period of dramatic developmental transi

198 Adolescence is a period of increased vulnerability to ps

199 Adolescence is a period of major brain reorganization sh

200 EE during adolescence is a promising method of enhancing impaired

201 Adolescence is a time of significant neurobiological dev

202 Adolescence is a vulnerable period of development when l

203 Adolescence is a vulnerable time for personality develop

204 Research has demonstrated that adolescence is an important time for self- and other-ori

205 er exposure to parental smoking in childhood/adolescence is associated with midlife cognitive functio

206 Adolescence is characterised by a substantial increase i

207 Adolescence is characterized by significant changes in s

208 of prefrontal cortex (PFC) maturation during adolescence is crucial to reveal which neural processes

209 man studies suggest that cannabis use during adolescence is linked to long-term negative psychologica

210 e PV upregulation observed in the PFC during adolescence is necessary for refinement of prefrontal GA

211 we hypothesized that PV upregulation during adolescence is necessary to sustain the increase in GABA

212 ses a nuclear envelopathy whose prognosis in adolescence is relatively good in comparison to that of

213 of the developing brain during childhood and adolescence is shaped by complex brain-environment inter

214 Youth (including both childhood and adolescence) is a period when the brain undergoes dramat

215 cannabis legalization and consumption during adolescence, it is essential to expand knowledge on the

216 lls are immature (DCX+PSA-NCAM+), and during adolescence many transition into mature (TBR1+VGLUT2+) n

217 Our findings indicate that stress during adolescence may accelerate the development of BLA-PFC pl

218 , obesity, and the combination of the two in adolescence may be related to risk for disability in adu

219 Psychological stress during adolescence may cause enduring cognitive deficits and an

220 onic occupancy of CB1Rs by Delta9-THC during adolescence may competitively decrease the functional ex

221 Rationale: Growth and development during adolescence may modify the respiratory and vascular diff

222 miR-218 expression in adolescence may serve both as a marker of risk and as a

223 Five children died in childhood or adolescence (mean age of death: 9 years), mainly as a re

224 erience of chronic peer victimization during adolescence might induce psychopathology-relevant deviat

225 Heightened error monitoring in adolescence moderated higher levels of adult internalizi

226 onsortium on Alcohol and Neurodevelopment in Adolescence (NCANDA), and determining the bone age from

227 term (EP) individuals in childhood and early adolescence.Objectives: To assess the trajectory of resp

228 tudinal changes in adiposity indices through adolescence on arterial stiffness.

229 ed, consanguineous families with a childhood/adolescence onset of a myopathy associated with homozygo

230 icant associations in mid-childhood and from adolescence onwards.

231 impact of protein restriction either during adolescence or adulthood on the function of the mesolimb

232 n can also be mild with onset of symptoms in adolescence or adulthood.

233 n severe cases, kidney failure occurs during adolescence or early adulthood, so most research has foc

234 o suggest that these features emerge in late adolescence or early adulthood.

235 matory biomarkers or cognitive tests in late adolescence or for SFSS in early adolescence as a robust

236 no studies have extended these findings into adolescence or identified periods of heightened suscepti

237 High CVH in late adolescence or young adulthood was associated with very

238 When measured in adolescence or young adulthood, cardiovascular health (C

239 ether parents being overweight in childhood, adolescence, or adulthood is associated with asthma in t

240 Using data from infancy to adolescence, our analysis of longitudinal wheeze phenoty

241 This altered plasticity during adolescence overlapped with a reduction in calcium-perme

242 n trajectories through juvenility (PD28) and adolescence (PD38;PD48).

243 By late adolescence, perceptions of subjective family social sta

244 lear whether dietary patterns established in adolescence persist into adulthood.

245 hanged by stress, and if such changes during adolescence persist or recover in young adulthood.

246 n escalating doses (2.5-10 mg/kg/ip) through adolescence (postnatal day 29-43).

247 tion of footshock/restraint stress in either adolescence (postnatal day 31-40) or adulthood (postnata

248 slices revealed that MK-801 exposure during adolescence preferentially reduces the presynaptic funct

249 triatal white matter microstructure early in adolescence, prior to alcohol use.

250 ial direct current stimulation (tDCS) during adolescence, prior to schizophrenia-relevant behavioral

251 KC normally has its onset in adolescence, progressively worsening through the third t

252 ed, downregulation of miR-218 in the mPFC in adolescence promotes resilience to stress in adulthood.

253 articipants who restored normal total FMI in adolescence (PWV 5.8 m/s [5.7-5.9] for metabolically hea

254 eport that reversal-learning trajectories in adolescence reliably predicted reversal performance in a

255 Adolescence represents a vulnerable time for individuals

256 and that 15 days of access to THC-gelatin in adolescence resulted in the down-regulation of cannabino

257 We conclude that avoiding childhood/adolescence secondhand smoke exposure promotes adulthood

258 ice that had received Delta9-THC only during adolescence showed a significant (1) decrease in the ext

259 ed with poorer cognitive ability during late adolescence.SIGNIFICANCE STATEMENT Brain tissue iron is

260 ties during the transition from childhood to adolescence.SIGNIFICANCE STATEMENT Few imaging studies o

261 erizing the ways in which they change across adolescence.SIGNIFICANCE STATEMENT Working memory is a f

262 onsortium on Alcohol and NeuroDevelopment in Adolescence) study.

263 ontinue to develop across childhood and into adolescence, studying episodic memory maturation can pro

264 y continues to develop through childhood and adolescence, suggesting that the neural mechanisms that

265 olonged development, often lasting well into adolescence, suggests that children, teens, and adults m

266 l, and social changes across the duration of adolescence that are known or thought to be related to a

267 nt knowledge regarding the unique aspects of adolescence that may serve as risk factors for schizophr

268 identify circuit-specific treatments during adolescence that prevent the onset of the adult deficits

269 ps to support memory in middle childhood and adolescence, the extent to which ongoing maturation with

270 of postnatal brain development occurs during adolescence, the period between childhood and adulthood.

271 In adolescence, the status of allergic sensitization was as

272 we show behaviorally that over the course of adolescence there is a within-person increase in model-b

273 expression in the mPFC increases from early adolescence to adulthood and correlates negatively with

274 le changes in GFR during the transition from adolescence to adulthood and overestimation of GFR in yo

275 These results highlight the transition from adolescence to adulthood as a period of dynamic maturati

276 I sensitization increased significantly from adolescence to adulthood mostly due to increased sensiti

277 ture and function changed significantly from adolescence to early adulthood in participants with yout

278 ry cortical response strength decreases from adolescence to early adulthood Somatosensory cortical re

279 was characterized by a slower increase from adolescence to middle adulthood, and by a lack of substa

280 ng samples (N = 2423), spanning childhood or adolescence to middle age, with prospective or family-ba

281 deaths, 84% would occur in males, mostly in adolescence to middle age.

282 atory fitness and healthy body weight during adolescence to prevent later chronic disease.

283 n interact with postnatal development during adolescence, triggering pathophysiological mechanisms re

284 of blunted threat extinction learning during adolescence, underpinned by brain structures such as the

285 .02 (95% CI 1.46, 14.59) points higher IQ in adolescence versus the declining trajectory group.

286 Self-harm in adolescence was assessed through interviews at age 18.

287 advantaged neighborhood during childhood and adolescence was associated with a higher level of depres

288 ed that asthma acquisition from pre- to post-adolescence was associated with changes in DNAm during t

289 r pattern: recent depression severity during adolescence was associated with more focal hyporeactivit

290 arly poverty and self-reported depression in adolescence was explained by serial mediation through te

291 NAm changes and sex on asthma acquisition in adolescence were found at 13 of the 535 CpGs in IOWBC (P

292 these 10 CpGs, opposite DNAm changes across adolescence were observed between sexes in both cohorts.

293 s, and may explain why symptoms appear after adolescence when the expression of many sex-specific gen

294 inal study design spanning from childhood to adolescence, where participants underwent polysomnograph

295 1:D2 density ratio increased in females from adolescence, whereas it was stable in males.

296 Many with asymptomatic sensitization in adolescence will develop allergic rhinitis in adult life

297 ls without T2D) in individuals followed from adolescence with youth-onset T2D.

298 Adolescence, with its increased focus on transitioning t

299 We hypothesized that stress in adolescence would increase adult trauma vulnerability by

300 ntinues to substantially increase throughout adolescence, yet the significance of this increase remai