ライフサイエンスコーパス: adolescence

1 rm and prevent disordered eating problems in adolescence.

2 hs at risk for initiating alcohol use during adolescence.

3 rted having self-harmed at least once during adolescence.

4 ynapses on PV interneurons are pruned during adolescence.

5 underlies the maturation of cognition during adolescence.

6 ing continues to improve from childhood into adolescence.

7 al outcomes associated with self-harm during adolescence.

8 tion to inhalant allergens from childhood to adolescence.

9 disrupting typical synaptic pruning in late adolescence.

10 nt throughout the 8000 days of childhood and adolescence.

11 atric disorders, many of which emerge during adolescence.

12 ume (GMV) and cortical thickness (CT) during adolescence.

13 mately 10-year period spanning childhood and adolescence.

14 xcitatory synapses on PV interneurons during adolescence.

15 affected by ongoing brain development across adolescence.

16 ated variation from middle childhood to late adolescence.

17 ll as early environment during childhood and adolescence.

18 lopment of dental caries from childhood into adolescence.

19 dhood, or broken limb bones in childhood and adolescence.

20 that their mental health problems started in adolescence.

21 lood pressure between midchildhood and early adolescence.

22 from increased pruning of excess synapses in adolescence.

23 ry monitoring from late childhood into early adolescence.

24 ly associated with persistent asthma through adolescence.

25 s were observed during interactions in early adolescence.

26 These risks are particularly salient during adolescence.

27 diagnosed with diabetes during childhood and adolescence.

28 tization with the persistence of asthma into adolescence.

29 n magnitude for traits assessed during later adolescence.

30 transcription of which is initiated in early adolescence.

31 sitizations decrease from early childhood to adolescence.

32 ezing had additive effects on asthma risk at adolescence.

33 n adult rats, mimicking the imbalance during adolescence.

34 e brain imaging through school age and early adolescence.

35 o nicotine (and other drugs of abuse) during adolescence.

36 dwide, and use is typically initiated during adolescence.

37 6.44)], and ADHD [OR = 3.14 (1.07, 9.19)] in adolescence.

38 od and--on average--little change during mid-adolescence.

39 ns, a fundamental adult skill refined during adolescence.

40 orking memory improvement typical of primate adolescence.

41 ing that may be particularly relevant during adolescence.

42 n-making in adults who abused alcohol during adolescence.

43 lower rs-FC and poorer amygdala recovery in adolescence.

44 experience-dependent change in childhood and adolescence.

45 fashion, with greatest patience during late adolescence.

46 jected to weaker GABAergic inhibition during adolescence.

47 Preclinical CVD may start during adolescence.

48 bout the effects of stress on the LAT during adolescence.

49 ll-Being Assessment at 15.5 years of age) in adolescence.

50 4betadelta GABARs are anti-convulsant during adolescence.

51 r to be associated with changes in AA during adolescence.

52 ter development in late school age and early adolescence.

53 neurodevelopmental outcomes in childhood and adolescence.

54 and motor disorders in offspring up to early adolescence.

55 intelligence between preadolescence and late adolescence.

56 se symptoms are most likely to continue into adolescence.

57 ty for patients with ccTGA, especially after adolescence.

58 showed evidence of sex stratification during adolescence.

59 shrinkage and myelination over the course of adolescence.

60 to grow from the striatum to the PFC during adolescence.

61 cademic functioning was assessed during late adolescence.

62 iety-related behaviors both during and after adolescence.

63 t (with implications for functioning) during adolescence.

64 velopment and approaches adult values during adolescence.

65 ation of this circuitry across childhood and adolescence.

66 ork, CEN), which are still developing during adolescence.

67 t have been shown to evolve in childhood and adolescence.

68 largest after 5 y of age and persisted into adolescence.

69 ges of specific social brain regions in late adolescence.

70 red trajectories started to diverge in early adolescence.

71 it is unclear whether the effects persist to adolescence.

72 academic performance in childhood and early adolescence.

73 es predicted functional outcomes during late adolescence.

74 ted or alcohol-related and violent injury in adolescence.

75 ng childhood may influence adiposity through adolescence.

76 ated variation from middle childhood to late adolescence.

77 er estimate = 0.007; 95% CI, 0.001-0.021) in adolescence.

78 evening preference (i.e., chronotype) during adolescence.

79 er volumes and school grade average in early adolescence.

80 of brain anatomy develop differently across adolescence.

81 in the emergence of psychiatric disorders in adolescence.

82 n difficulties during childhood versus later adolescence.

83 How does human brain structure mature during adolescence?

84 tly through early childhood (3-10 years) and adolescence (11-20 years; mean difference, 1.1; 95% CI,

85 was determined in childhood (6 to 12 years), adolescence (12 to 18 years), and young adulthood (18 to

86 dependently associated with self-harm during adolescence (2.27, 1.09-4.69).

87 tionally active compared to adulthood or pre-adolescence [2, 5, 9, 10].

88 ean age 15.9 years (SD 0.5; waves 3-6 during adolescence, 6 months apart) and ending at mean age 35.1

89 osomy 7 (37%, all ages) reaching its peak in adolescence (72% of adolescents with monosomy 7).

90 f adaptations within these substrates making adolescence a particularly susceptible developmental sta

91 pressive disorder (MDD) often emerges during adolescence, a critical period of brain development.

92 Anxiety disorders peak in incidence during adolescence, a developmental window that is marked by dy

93 fest as anxiety and negative symptoms during adolescence, a greater focus on these phenotypes rather

94 pment of the prefrontal cortex occurs during adolescence, a period of increased independence marked b

95 This is of particular concern during adolescence, a period often associated with increased co

96 be related to the development of obesity in adolescence, a relatively novel observation with potenti

97 ermine whether a stressful experience during adolescence affects adult behavior, we exposed adolescen

98 behavioral, and dermoscopic factors in early adolescence (age, 14 years) that are associated with a m

99 sociated with a mole-prone phenotype in late adolescence (age, 17 years).

100 ional study of a school-based cohort in late adolescence (aged 18-19 years: The Tromso Study Fit Futu

101 uggest that the extended human childhood and adolescence allows a balance between exploration and exp

102 pment of body mass index (BMI) from birth to adolescence among 2,818 children with and without asthma

103 hese disorders frequently begin in childhood/adolescence, an understanding of fear-extinction learnin

104 gh levels of depressive symptoms during both adolescence and adulthood (odds ratio = 1.96, 95% confid

105 mimicking n-3 PUFA dietary deficiency during adolescence and adulthood, we found strong increases in

106 of this ability from early childhood through adolescence and adulthood.

107 memory, but not in face perception, both in adolescence and adulthood.

108 ptual reasoning, and verbal comprehension in adolescence and adulthood.

109 Most late-onset cases displayed onset in adolescence and an adolescence-limited presentation.

110 iation between body-mass index (BMI) in late adolescence and death from cardiovascular causes in adul

111 We aimed to examine these risks during late adolescence and early adulthood among people admitted to

112 uld predict favorable oral health beliefs in adolescence and early adulthood, which in turn would pre

113 t until plateauing around the period of late adolescence and early adulthood, which temporally coinci

114 ood and to greater educational attainment in adolescence and early adulthood.

115 recipients has been found to increase during adolescence and early adulthood.

116 al autoimmune encephalomyelitis (EAE) during adolescence and early young adulthood, while an increase

117 findings help specify social learning across adolescence and generate hypotheses about social dysfunc

118 igher in nutrients that are of importance in adolescence and lower in energy density.

119 d a number of dietary factors present during adolescence and midlife to be associated with pancreatic

120 k was higher for high fat intake during both adolescence and midlife.

121 al volume growth across school age and early adolescence and suggest an early childhood sensitive per

122 hythms changes on addiction vulnerability in adolescence and suggest areas that warrant additional re

123 the hippocampus in reinforcement learning in adolescence and suggest that reward sensitivity in adole

124 etween high levels of depressive symptoms in adolescence and T2DM in adulthood in the National Longit

125 ed the associations between self-harm during adolescence and the outcome measures at 35 years (wave 1

126 Glycemic control often deteriorates during adolescence and the transition to young adulthood for pa

127 ion, school start times are often earlier in adolescence and the use of electronic devices at night i

128 n human blood: children at birth, childhood, adolescence and their mothers during pregnancy and middl

129 rn of caries development from childhood into adolescence and to explore the role of potential risk fa

130 mmunodeficiency virus (HIV) are surviving to adolescence and transitioning to adult care, yet there a

131 These effects persisted into adolescence and were not moderated by maternal identity.

132 Late adolescence and young adulthood coincide with greater mo

133 ognitive deficits that affect development in adolescence and young adulthood, and influence education

134 or tanning and sunburns, particularly during adolescence and young adulthood, increase the risk of de

135 ociated with reduced myopia, particularly in adolescence and young adulthood.

136 eir Fontan in early childhood, but also into adolescence and young adulthood.

137 to substance use increases substantially in adolescence and young adulthood.

138 activity and academic performance throughout adolescence and young adulthood.

139 ioid use disorder (OUD) frequently begins in adolescence and young adulthood.

140 ssue sarcoma that is often discovered during adolescence and young adulthood.

141 for suicidal behavior that often develops in adolescence and young adulthood.

142 ocial, psychological, and health outcomes in adolescence and young adulthood; role transitions, and l

143 prefrontal cortex (PFC) increases throughout adolescence and, by establishing precisely localized syn

144 zation and cognitive functions in childhood, adolescence, and adulthood among 2,232 members of the U.

145 ildhood and a host of outcomes in childhood, adolescence, and adulthood.

146 ween BMI and disordered eating in childhood, adolescence, and adulthood.MR analyses were conducted wi

147 nditions that mostly begin during childhood, adolescence, and early adulthood.

148 een vitamin D status measured in prepuberty, adolescence, and early adulthood.

149 marijuana (Cannabis sativa) often begins in adolescence, and heavy adolescent marijuana use is often

150 These alterations emerge during adolescence, and mature animals in which VIP interneuron

151 lude extracolonic tumors, onset of polyps in adolescence, and rapid progression of some polyps to adv

152 dala undergoes maturational processes during adolescence, and therefore may be more vulnerable to har

153 HD symptom trajectories across childhood and adolescence, and to examine whether higher genetic liabi

154 nal adjustment for common mental disorder in adolescence; and (4) final additional adjustment for ado

155 tcomes of regular substance use initiated in adolescence; and the offspring of young people who use s

156 ces in heart rate and blood pressure in late adolescence are associated with lifetime major psychiatr

157 d body mass index (BMI) during childhood and adolescence are sentinels for the future population card

158 Conduct problems in childhood and adolescence are significant precursors of crime and viol

159 the environment on food preferences in late adolescence are unknown.

160 mental model for bipolar disorder (BD), with adolescence as a critical period in its development.

161 nisotropic in the brain during childhood and adolescence, as fibre bundles develop and myelinate.

162 f cardiovascular risk factors from childhood/adolescence associate with worse midlife cognitive perfo

163 gonist 7,8-dihydroxyflavone (7,8-DHF) during adolescence at doses that stimulated ERK42/44 corrected

164 y, but experimenter administration of WIN in adolescence, at doses previously reported in the literat

165 In adolescence basal insulin secretion was significantly hi

166 ticipants were assessed for self-harm during adolescence (between waves 3 and 6).

167 During adolescence, both rodent and human studies have revealed

168 cellular mechanisms that are altered during adolescence but are only manifested in adulthood.

169 he amygdala of males subjected to CUS during adolescence, but not in males that experienced CUS durin

170 Perturbations during adolescence can alter the developmental trajectory of th

171 vestigate the associations between childhood/adolescence cardiovascular risk factors and midlife cogn

172 Emerging evidence suggests that during adolescence, changes in eCB signaling contribute to the

173 k of developing obesity during childhood and adolescence compared with children without asthma at bas

174 condition such as sickle cell disease during adolescence constitutes a significant challenge for the

175 ior cingulate cortex (ACC) maturation during adolescence contributes to or underlies the development

176 e methyl donor supplementation (e.g., during adolescence) could ameliorate executive function deficit

177 itional deficits in dietary n-3 PUFAs during adolescence decreased n-3 PUFAs in both medial prefronta

178 Adverse experiences in childhood and adolescence, defined as subjectively perceived threats t

179 Having a friend who experienced SV in adolescence did however increase the respondent's odds o

180 Thus, SA of a rewarding cannabinoid in adolescence does not produce long-term cognitive dysfunc

181 s occurring before birth, in childhood or in adolescence ('early-life risk factors') could influence

182 h cohort studies is similar in childhood and adolescence/early adulthood.

183 riences (ACEs; occurring during childhood or adolescence; eg, child maltreatment or exposure to domes

184 a history of subchronic cocaine exposure in adolescence engaged habit-based response strategies at t

185 (10 mg/kg) or vehicle for 10 days during mid-adolescence-equivalent period.

186 rats reared in social isolation (SI) during adolescence exhibit augmented ethanol intake and anxiety

187 nsistent with a sensitive period ending with adolescence for the amygdala-mPFC circuit.

188 ng scans at 3 times (early, middle, and late adolescence) from ages 11 to 20 years.

189 ation was the opposite; men diagnosed during adolescence had lower HRs than survivors of childhood ca

190 Consumption of alcohol during adolescence has been associated with increased impulsivi

191 peated binge-like exposure to alcohol during adolescence has been reported to perturb prefrontal cort

192 with the lowest, carbohydrate intake during adolescence (hazard ratio (HR) = 0.87, 95% confidence in

193 of substance use disorders is highest during adolescence; however, many adolescents experience a natu

194 irst live birth among women diagnosed during adolescence (HR, 0.89), but the HR was lower among women

195 1.18, 1.95) and those who lost a sibling in adolescence (i.e., between the ages of 12 and 18 years)

196 However, CKD progressed much faster during adolescence in ADCK4 than in WT1 and NPHS2 nephropathy,

197 tter increases are typically observed during adolescence in anterior cortices.

198 port neurodevelopmental abnormalities during adolescence in BDI in anterior cortices, including alter

199 nd track the growth of dopamine axons across adolescence in mice.

200 s into height variation during childhood and adolescence in populations representing different ethnic

201 ditions explained 20% of deaths in childhood/adolescence in the VLBW group, with deaths from neoplasm

202 erences had a moderate genetic basis in late adolescence, in keeping with findings in children.

203 dults who had undergone the operation during adolescence, in the Follow-up of Adolescent Bariatric Su

204 Cocaine use during adolescence increases vulnerability to drug dependence a

205 ry-based risk factors and lipids measured in adolescence independently predicted preclinical atherosc

206 se model of n-3 PUFA deficiency lasting from adolescence into adulthood.

207 y fat varied with both age and height during adolescence, invalidating the standard weight-to-height

208 Adolescence is a critical period for emotional maturatio

209 during adolescence supporting the idea that adolescence is a critical period of the development that

210 Late adolescence is a crucial, but underexplored, development

211 Adolescence is a developmental period marked by heighten

212 Adolescence is a highly susceptible period for mammary c

213 Adolescence is a period of development in neural circuit

214 Adolescence is a period of life characterised by changes

215 Here we show that adolescence is a sensitive period for the emergence of p

216 days beginning at PND70 to determine whether adolescence is a sensitive time period when stress can h

217 Adolescence is a time of significant cortical changes in

218 Adolescence is a time of significant neural and behavior

219 Adolescence is a time of tumultuous behavior that may re

220 Adolescence is a time period in development when the bra

221 al learning processes.SIGNIFICANCE STATEMENT Adolescence is a unique developmental period of heighten

222 Specifically, we find that lower SES during adolescence is associated with an increase in methylatio

223 Cannabis abuse in adolescence is associated with increased risk of psychot

224 Severe obesity in adolescence is associated with reduced life expectancy a

225 To assess whether concussion in childhood or adolescence is associated with subsequent multiple scler

226 continued neurobiological maturation through adolescence is increasingly invoked in discussions of yo

227 factors for the persistence of asthma out to adolescence is not established.

228 The regular use of cannabis during adolescence is of particular concern because use by this

229 cence and suggest that reward sensitivity in adolescence is related to adaptive differences in how ad

230 Adolescence is the peak time for initiation of substance

231 but whether the negative effects remain into adolescence is unknown.

232 cases displayed onset in adolescence and an adolescence-limited presentation.

233 Type 2 diabetes in adolescence manifests as a severe progressive form of di

234 n the evolution of cerebral perfusion during adolescence may be a critical element of the affective n

235 men, suggesting that this particular week in adolescence may be a specific period of maturation and f

236 Obesity in childhood and adolescence may continue into adulthood and lead to adve

237 progress faster during early childhood than adolescence (mean difference, 10.0; 95% CI, -2.2 to 22.2

238 Clinically, SPG5 manifested in childhood or adolescence (median 13 years).

239 ADCK4 nephropathy presented during adolescence (median age, 14.1 years) with nephrotic-rang

240 ncer survivors diagnosed during childhood or adolescence; men were particularly vulnerable.

241 as been suggested that reward sensitivity in adolescence might be adaptive, but evidence of an adapti

242 During subsequent adolescence, mPFC-BLA circuits are further modified by e

243 emic performance or cognitive performance in adolescence on a population level.

244 limited access to alcohol in gelatin during adolescence only.

245 uals from four families with a childhood- or adolescence-onset neurodegenerative disorder characteriz

246 reater risk of substance-related problems in adolescence or adulthood.

247 than 30 years in France, those currently in adolescence or early adulthood have the highest risk of

248 s comparing the risk of graft failure during adolescence or early adulthood to other periods were est

249 oking impairing pulmonary development during adolescence or early adulthood, thereby preventing catch

250 Psychosis commonly develops in adolescence or early adulthood.

251 % of patients dying suddenly in childhood or adolescence or undergoing cardiac transplantation are af

252 At adolescence (P28), an increase in burst frequency (>50 H

253 INTERPRETATION: Head trauma in adolescence, particularly if repeated, is associated wit

254 Exposing rats to alcohol during early-mid adolescence (PD28-42) increased the density of long/thin

255 ring about fear emotion during the important adolescence period.

256 to late (mean [SD] age, 19.08 [0.460] years) adolescence, predominantly in the temporal lobes (tempor

257 tical dopamine axon density increases across adolescence remains unknown.

258 Therefore, late adolescence represents a potentially underrecognized win

259 It has long been appreciated that adolescence represents a uniquely vulnerable period when

260 esting that working memory maturation during adolescence requires pruning of excitatory inputs to PV

261 ivity during childhood and the transition to adolescence shaped future resting-state connectivity, co

262 Finally, inhalation of hydrogen gas in adolescence significantly increased the resilience to ac

263 susceptible to the effects of toluene during adolescence supporting the idea that adolescence is a cr

264 re dramatic alterations in self-views during adolescence than other phases of the lifespan.

265 round cell sarcoma with a peak incidence in adolescence that is driven by a chimeric oncogene create

266 study imply that induction of BDNF following adolescence THC exposure may serve as a homeostatic resp

267 During adolescence, the human cortex undergoes substantial remo

268 diagnosed with diabetes during childhood or adolescence, the prevalence of complications and comorbi

269 s on diet quality during the transition from adolescence to adulthood are understudied.This study exa

270 atric disorder typically diagnosed from late adolescence to adulthood.

271 arrhythmias in patients with ARVC spans from adolescence to advanced age, reaching its peak between a

272 6, 0.99), as was a change from low intake in adolescence to high intake in midlife (HR = 0.71, 95% CI

273 ic and environmental factors may interact in adolescence to influence the development and function of

274 es of the GABAergic system in the PFC during adolescence to provide an insight into the increased sus

275 with depressive symptoms that persisted from adolescence to young adulthood [OR = 2.05 (1.04, 4.03)].

276 ge in emotional and behavioral problems from adolescence to young adulthood among individuals with an

277 ution increased with age and was greatest in adolescence (up to 0.83 in boys and 0.76 in girls).

278 y, smoking, and alcohol consumption) in late adolescence using a cross-cohort comparison and to explo

279 o bullying to mental health in childhood and adolescence using a twin differences design to strengthe

280 e examined the prevalence of food allergy in adolescence using objective measures such as oral food c

281 ased solely on nonlaboratory risk factors in adolescence versus a lipid model based on nonlaboratory

282 Concussion in adolescence was associated with a raised risk of MS, pro

283 es, within the accepted normal range, during adolescence was associated with increased cardiovascular

284 ysician-diagnosed asthma during childhood or adolescence was reported by 2694 children (21%).

285 found anatomical change in the cortex during adolescence was thinning, with the largest decreases obs

286 ributor to cortical volume reductions during adolescence was thinning.

287 or borderline high and high triglycerides in adolescence were associated with high cIMT in adulthood.

288 ear response may be most advantageous during adolescence when animals are prone to explore novel, pot

289 activity disorder (ADHD) often persists into adolescence, when motor vehicle crash risk peaks.

290 This occurs during adolescence, when the maturation of PFC lags behind that

291 d drugs in the United States, and use during adolescence--when the brain is still developing--has bee

292 etween problematic eating attitudes in early adolescence, which can lead to disordered eating behavio

293 ty at the entry into middle childhood and in adolescence, which differ across domains.

294 undergo coordinated cortical thinning during adolescence, which is in part governed by evolutionary n

295 f working memory processing stabilize during adolescence, while those affecting sensorimotor processe

296 a rare disorder presenting in childhood and adolescence with central visual disturbance and sparse s

297 ge dynamic neurodevelopmental changes during adolescence with the potential to extinguish pathologica

298 whether any of these GPCs are associated, in adolescence, with classical risk factors of CVD, namely

299 Thus, increased pruning throughout adolescence would likely result in a deficit of large sp

300 ed through schools and one focusing on later adolescence, would provide phase-specific support across