ライフサイエンスコーパス: offspring

1 ing in standard diet but not in WD F1 female offspring.

2 ituitary-adrenal (LHPA) axis activity in the offspring.

3 ation and long-term microglial activation in offspring.

4 new neurons from neural stem cells (NSC), in offspring.

5 subset of nuclei that will be transmitted to offspring.

6 n secretion in male but not female F1 and F2 offspring.

7 crease the risk for psychiatric disorders in offspring.

8 tem relative to both control subjects and BD offspring.

9 e risk of long-term metabolic dysfunction in offspring.

10 nsights into the origins of risk of NAFLD in offspring.

11 energy homeostasis and metabolic function in offspring.

12 competent and were used to produce DDX4 null offspring.

13 nd second-generation (F2) C57BL/6J male mice offspring.

14 urity-related morbidity and mortality in the offspring.

15 has rarely been investigated in young adult offspring.

16 cyte function and correlates with obesity in offspring.

17 nd behavioural abnormalities in MIA-affected offspring.

18 associated with lifetime disease risk in the offspring.

19 depression and promoted hyperactivity in F1 offspring.

20 ated with leptin, adiponectin, or HOMA-IR in offspring.

21 regnancy on risk of severe mental illness in offspring.

22 tiate into oocytes that fertilize to produce offspring.

23 of KCC2 transcription in prenatally exposed offspring.

24 and offspring than between mothers and their offspring.

25 owth, trh-1 mutants have a reduced number of offspring.

26 resulted in a decreased production of winged offspring.

27 ical trigger of egg activation can result in offspring.

28 rectly targeted allele in up to 100% of live offspring.

29 isioning of an egg meal to the newly hatched offspring.

30 sting as metabolic dysfunction in adult male offspring.

31 MI) were not associated with NAFLD in female offspring.

32 n germ cells and phenotypic effects in their offspring.

33 on alleles in 8.5-100% of the resulting live offspring.

34 EPA and DHA, affected adipose development in offspring.

35 when on an obesogenic diet compared with HFD offspring.

36 ongenital anomalies and childhood cancers in offspring.

37 attention-deficit/hyperactivity disorder in offspring.

38 ndent of sex) and insulin resistance in male offspring.

39 ntal cortex of immune-challenged and control offspring.

40 leads to numerous adverse health outcomes in offspring.

41 y be associated with harm for the developing offspring.

42 ternal stress during pregnancy and TL in the offspring.

43 ght gain, were associated with NAFLD in male offspring.

44 increased in male, but not in female, F1 WD offspring.

45 t her life in danger in order to protect her offspring.

46 he current generation, and the latter create offspring.

47 genotype shape microbiota populations in the offspring.

48 ficantly higher in LG-IH male but not female offspring.

49 both for their health and for that of their offspring.

50 D(+) levels and citrate synthase activity in offspring.

51 ential for long-term prevention of asthma in offspring.

52 4Y and subsequent sexual orientation in male offspring.

53 ergen-specific regulatory T (T reg) cells in offspring.

54 g scans were collected from 127 nonpsychotic offspring 8 to 18 years of age (average age = 13.5 years

55 either MAC or PAC are associated with LTL in offspring across the age range, or when considering only

56 to test the effects of low n-6/n-3 ratios on offspring adipogenesis and adipogenic potential.

57 maternal dietary fatty acid profile programs offspring adipose development.

58 uring pregnancy and severe mental illness in offspring, adjusting for measured covariates and unmeasu

59 By buffering offspring against environmental perturbation without jeo

60 haracteristics and NAFLD in 1,170 adolescent offspring aged 17 years participating in the Western Aus

61 4 years in 1987 through 1988 and their adult offspring aged 21 to 84 years in 2005 through 2008.

62 sociations of parental clinical outcome with offspring allergic disease were estimated with multinomi

63 germination and defence phenotypes in their offspring, along with the roles of phytohormone signalli

64 tcomes suggest conflicts between parents and offspring and among siblings over optimal mating strateg

65 lation patterns in both adult mice and their offspring and engendered behavioral alterations.

66 al stress in both Japanese quail mothers and offspring and examined the consequences for several stre

67 to the same overall strategy, producing more offspring and exhibiting greater V k* in the second sex.

68 4 having survived to age 50 (n = 661,031) to offspring and fathers (n = 691,124).

69 We also observed fewer viable offspring and increased developmental deformities in the

70 t medication use during pregnancy with ID in offspring and investigate the importance of parental men

71 subsequent effects of prenatal conditions on offspring and parental performance in the burying beetle

72 Cannibals must ensure avoiding their own offspring and targeting only unrelated young.

73 METHODS AND Participants from the Framingham Offspring and Third Generation Cohorts (n=3318; aged 48.

74 aive and free of cancer at baseline from the offspring and third-generation cohorts of the community-

75 as detected in 29.2% of parents and 10.3% of offspring, and anti-Toxocara spp.

76 expenditure and locomotor activities in male offspring, and increased number of pro-inflammatory macr

77 e of testicular atrophy was noted in exposed offspring, and limited changes in other reproductive par

78 ther studies with relevant data on maternal, offspring, and paternal genotype are required to obtain

79 This study compared maternal and offspring anthropometry for moderately malnourished preg

80 4 in clinical practice, its effects on adult offspring are not well known nor have sex-specific diffe

81 easonal environments, where prolonged parent-offspring associations are likely to be less costly.

82 of group living, including prolonged parent-offspring associations.

83 Offspring asthma with hayfever was more strongly associa

84 scores on tests of cognitive function in the offspring at age 4 and 6-12 y.

85 YLR1 mutant females produced mixed paternity offspring at high frequency, indicating acceptance of mu

86 a small causal effect on DNA methylation in offspring at three CpG sites, which was replicated for o

87 white adipose browning and thermogenesis in offspring at weaning accompanied by persistent beneficia

88 ting that reduced buoyancy evolves only when offspring bear symbionts.

89 n early stage and recover as the rejuvenated offsprings become the majority.

90 Whole-cell recordings were conducted in male offspring between 4 and 10 weeks old.We found that PE le

91 ith a 0.25 SD (95% CI 0.21-0.29) increase in offspring BMI at age 7, with similar results at later ag

92 ing pregnancy was positively associated with offspring BMIZ (adjusted beta per serving increase per d

93 Offspring body mass index z scores (BMIZs) were calculat

94 : parents born 1945-1972 (n = 171) and their offspring born 1969-2003 (n = 264).

95 fic IgEs from 1991 to 1993, and data on 9100 offspring born 1972-2012.

96 ng time with the risk of hyperglycemia among offspring born to GDM mothers in Tianjin, China.

97 The unadjusted RR of ID was increased in offspring born to mothers treated with antidepressants d

98 n the development of clinical TSE disease in offspring born to muntjac dams infected with chronic was

99 d-derived mesenchymal stem cells (uMSC) from offspring born to normal-weight and obese mothers, we te

100 ess exposures have in changing the course of offspring brain development.

101 low birth-weight and changes in young adult offspring brain, mimicking those in human neuropsychiatr

102 Maternal obesity impairs offspring brown adipocyte function and correlates with o

103 l prenatal stress and TL was observed in the offspring but not in mothers may be attributable to a hi

104 the adverse effects of prenatal lead on the offspring, but epigenome-wide methylation data for low l

105 sly been associated with adverse outcomes in offspring, but to our knowledge, the association with in

106 nd cat sensitization (5.65[1.92-16.6]) among offspring, but was not associated with allergic outcomes

107 g exposure induces a protective phenotype in offspring by enhancing metabolic tolerance to xenobiotic

108 g can prevent the onset of food allergies in offspring by instructing T reg formation via neonatal Fc

109 inocephalosaurus determined the sex of their offspring by sex chromosomes rather than by environmenta

110 guineous unions are more likely to result in offspring carrying homozygous loss-of-function mutations

111 of transgenerational effects that influence offspring characteristics and performance later in life.

112 A total of 2,639 participants from the Offspring Cohort of Framingham Heart Study were enrolled

113 alcoholic fatty liver disease (NAFLD) in the offspring cohort of the Framingham Heart Study (FHS) par

114 9 participants of the Framingham Heart Study Offspring cohort, an observational study of the offsprin

115 5,124 individuals were recruited to form the Offspring Cohort.

116 e translation to humans, we developed baboon offspring cohorts from mothers fed ad libitum (control)

117 etween prenatal stressful events and risk of offspring conduct disorder and hyperactivity.

118 7), we identified pregnancies complicated by offspring congenital heart defects or early preterm pree

119 increased risk for nonaffective psychosis in offspring, consistent with historical studies on materna

120 We assessed multivariate-adjusted mother-offspring correlations in selected nutrients and food gr

121 role of maternal smoking during pregnancy in offspring depression, rather observed associations may r

122 circadian disruption would negatively impact offspring development and adult function.

123 h changes in response to PREMS varied across offspring developmental periods as predicted.

124 Mother-adult offspring dietary resemblance in this Australian cohort

125 ng of intrauterine conditions that influence offspring disease susceptibility is warranted to inform

126 perturbation growth, necking and budding of offspring droplets from a bulk body are observed.

127 ring period increases the risk of obesity in offspring during childhood, but high prepregnancy BMI ha

128 y after 10 days, recombinants produced fewer offspring early on, leading to an increased female-biase

129 ates, group growth rates, offspring mass and offspring eclosion success, relative to high larval-dens

130 this rule are budding bacteria, in which new offspring emerges de novo from a morphologically invaria

131 ed number of apoptotic cells, and adult male offspring exhibited higher fitness.

132 events may be an independent risk factor for offspring externalizing symptoms, regardless of maternal

133 mother's (F0) smoking during pregnancy, the offspring (F2) would be at increased risk of autism.

134 ciations between maternal protein intake and offspring fasting insulin and homeostasis model assessme

135 al fecundity while slow development benefits offspring fecundity.

136 Analysis of F2 offspring found no differences in wheel running or adipo

137 (IFA-LNS), 3) IFA (as above) and MNP for the offspring from 6 to 24 mo (IFA-MNP), and 4) IFA (as abov

138 d the first 6 mo postpartum and LNSs for the offspring from 6 to 24 mo (LNS-LNS), 2) iron and folic a

139 s comparatively map virulence loci using the offspring from a P. yoelii YM and N67 genetic cross, and

140 Analyses in the AA adolescent/young adult (offspring from COGA families) subsample indicated associ

141 t year of life, an effect not present in the offspring from high fat-fed dams that had trained.

142 AED exposure was available in the subset of offspring from July 1, 2005, to December 31, 2011.

143 We report the first GWAS of offspring from preeclamptic pregnancies and discovery of

144 rly during pregnancy and lactation, protects offspring from WD-induced developmental programming of h

145 joint (QMJ), increases with size among guppy offspring, from 11.7 degrees in the smallest neonates to

146 -0.87) and 2.50 (95% CI -4.12, -0.59) lower offspring GCI and IQ scores, respectively.

147 eased risk of allergic manifestations in the offspring generation, but not among parents.

148 ces for several stress-related traits in the offspring generation.

149 environments can have substantial effects in offspring generations.

150 In this sense, PREMS effects on offspring growth allow mother and offspring to make the

151 reproduction and at the same time accelerate offspring growth and possibly maturation and reproductiv

152 parental energy and nutrient restriction on offspring growth in rural Gambia.

153 intake during pregnancy in association with offspring growth through age 7 y among high-risk childre

154 At weaning, HFD offspring had lower thermogenesis in brown and white adi

155 rations in the cortex and hippocampus of MIA offspring have been described, less evidence exists on t

156 moking and autism spectrum disorder (ASD) in offspring have produced conflicting findings, and prior

157 In contrast, paternal birth season predicted offspring HAZ at 24 mo (crude: -0.21, P = 0.005; adjuste

158 rdiac magnetic resonance imaging to evaluate offspring heart function in early adulthood.

159 that intrauterine growth restriction (IUGR) offspring hearts would show impaired function and a prem

160 ncreased risk of congenital heart defects in offspring; however, the results are inconsistent.

161 stress on several phenotypic traits in their offspring in a functionally relevant context using a ful

162 foraging areas laid nests that produced more offspring in all but one year of the study.

163 ng pregnancy increases asthma sensitivity in offspring in an HDM-specific manner, suggesting that ver

164 pregnant women on neurodevelopment of their offspring in areas where schoolchildren were iodine suff

165 ds are typically unwinged but produce winged offspring in response to high population densities and d

166 t Th1 immunity can be imparted to Th2-biased offspring; in some instances, it can be greater than tha

167 Of the 1 680 219 offspring included in the analysis, 816 775 (48.61%) wer

168 an increased risk of neurologic disorders in offspring, including attention deficit/hyperactivity dis

169 ines and chemokines in the cerebellum of MIA offspring, including increase in the neuroinflammatory c

170 S at birth was associated with NAFLD in male offspring independent of adolescent obesity.

171 ve correlations between maternal factors and offspring insulin resistance.

172 ms, regardless of maternal mental health and offspring internalizing.

173 Deciding when to terminate care of offspring is a key consideration for parents.

174 se to improve the metabolic health of female offspring is important, as this intervention could comba

175 Concomitantly, the pace of offspring life history is recalibrated to partly compens

176 st study to test for parental age effects on offspring LTL in a wild mammal population, and the resul

177 ssociated with a 3% increase in incidence of offspring lymphoid neoplasms (hazard ratio = 1.03, 95% c

178 arly reproductive rates, group growth rates, offspring mass and offspring eclosion success, relative

179 A third mode of transmission, from mother to offspring, may be underappreciated.

180 The primary outcome was new-onset offspring MDD, and the secondary outcome was the total D

181 Overall, 8,112 offspring met the inclusion criteria; 13.6% had a parent

182 ociation of protein intake in pregnancy with offspring metabolic health at age 9-16 y in a longitudin

183 sity leads to the most pronounced effects on offspring metabolism.

184 Our findings suggest that maternal BMI-offspring metabolome associations are likely to be large

185 24 weeks, blood samples were collected from offspring mice for lipid profiles and insulin resistance

186 de of the impact of parental environments on offspring molecular phenotypes is poorly understood.

187 th immune components were related to ADHD in offspring: multiple sclerosis (adjusted odds ratio [OR]

188 and cognitive characterization of the adult offspring (n = 12 per group), unbiased capture array bis

189 3.5 years) of a parent diagnosed with SZ (SZ offspring; n = 28) or BD (BD offspring; N = 60) and comm

190 sed with SZ (SZ offspring; n = 28) or BD (BD offspring; N = 60) and community control subjects (n = 3

191 iation of prenatal exposure to fluoride with offspring neurocognitive development.

192 tion of intergenerational parental stress in offspring neurodevelopment and disease risk, and the cur

193 ess exposures are implicated in the risk for offspring neurodevelopmental and neuropsychiatric disord

194 Surgical BAT ablation in 3-month-old LP offspring normalizes body temperature and causes postpra

195 iated with a >2-fold increase in the risk of offspring obesity at ages 6-11 y (adjusted RR: 2.39; 95%

196 why the combination of maternal obesity and offspring obesity leads to the most pronounced effects o

197 e is known about possible adverse effects in offspring of A(H1N1)-vaccinated mothers beyond the perin

198 Moreover, finding no RC deficits in offspring of BD patients suggest a differential effect o

199 ith impaired glucose tolerance compared with offspring of chow-fed dams throughout their first year o

200 Here we show that adult drug-naive male offspring of cocaine-exposed sires have memory formation

201 tibodies to a novel antigen were elevated in offspring of dams exposed to dLAN.

202 ories: delaying reproduction to care for the offspring of dominant breeders or dispersing early to br

203 Offspring of elevated pCO2-treatment adults were signifi

204 t changes were determined in F1 and F2 adult offspring of F0 mothers exposed to two relevant human ex

205 Offspring of HDM-exposed B-cell-deficient mothers also d

206 Male, but not female, offspring of LPD mothers consistently displayed anxiety-

207 s that may underlie cognitive impairments in offspring of mothers that abuse marijuana during pregnan

208 Previous reports suggest that offspring of mothers who smoke during pregnancy have gre

209 GDM-exposed offspring of mothers with a protein intake in the lowest

210 most metabolically challenged (HFD-consuming offspring of obese mothers).

211 ared treadmill exercise and NMN injection in offspring of obese mothers.

212 They were first-generation offspring of parents with neovascular AMD.

213 Using offspring of PBS- or HDM-exposed mothers, the magnitude

214 including microcephaly, in the foetuses and offspring of pregnant women and (b) GBS in any populatio

215 PM increased the detection rate of MMc among offspring of primigravidae and secundigravidae, and both

216 Adult offspring of RES-treated mothers showed increased energy

217 omical RC connectivity in nonpsychotic young offspring of SZ patients.

218 spring cohort, an observational study of the offspring of the original Framingham Heart Study and the

219 the presence and level of cord blood MMc in offspring of women with and without PM.

220 0.93% in 2565 pregnancies) compared with the offspring of women without epilepsy (2.51% in 2154 pregn

221 of nsv823469, has a tendency to transmit to offspring or siblings (P = 0.010) and is associated with

222 upport causal effects of maternal obesity on offspring outcomes, which are mediated at least partly t

223 egnancy was related to a 10% reduced risk of offspring overweight or obesity at 7 y of age (aRR: 0.90

224 community-dwelling twin, sib-sib, or parent-offspring pairs (n = 138), comprising 69 individuals ran

225 uture generations, but it is unclear whether offspring phenotypes represent specific responses to par

226 t of the onset of metabolic dysregulation in offspring predisposed to altered beta-cell function and

227 ed with all outcomes compared with unexposed offspring (preterm birth odds ratio [OR], 1.47 [95% CI,

228 ly, this locus underlies a trade-off between offspring production and dispersal.

229 ssful hitchhiking, but at expense of reduced offspring production.

230 direct benefits, enabling males to maximize offspring production.

231 can lessen the impact of maternal smoking on offspring pulmonary function and decrease the incidence

232 s apparently "hedge their bets" with current offspring rather than gamble on future offspring which h

233 The degree to which offspring remain near their parents or disperse widely i

234 Agreement between parental hip fracture from offspring reports and diagnoses in administrative data w

235 The sensitivity of offspring reports was 0.70 (95% confidence interval: 0.6

236 t rats causes reproductive disorders in male offspring, resulting from suppression of intratesticular

237 subtly influence the neurodevelopment of the offspring, resulting in increased risk for neurodevelopm

238 hat prions can be transferred from mother to offspring, resulting in the development of clinical TSE

239 renatal exposure to PCBs and OCPs influences offspring risk of ASD and intellectual disability withou

240 ions between maternal vitamin B12 status and offspring's cognition.

241 Leopard mothers appear sensitive to their offspring's demands, and adjust levels of care according

242 ervations suggest altered development of the offspring's immune system, which in turn results in dysr

243 ncies, while few studies have focused on the offspring's risk of adult cancer.

244 dence for effects of maternal obesity on her offspring's risks of obesity, coronary heart disease, st

245 nd varied by nutrients, food groups, and the offspring's sex and living arrangements.

246 that parents had lower childhood SES, their offspring showed worse asthma outcomes across multiple i

247 all, correlations appeared to be stronger in offspring still living with their parents than with thei

248 et al. described the sampling design of the Offspring Study and presented selected baseline characte

249 tal and mammary gland cell types to optimize offspring success.

250 They are likely to raise their offspring successfully, but experience a relatively shor

251 nd wives have slightly lower fertility; (ii) offspring suffer from inbreeding depression; (iii) paren

252 wheel running or adiposity in male or female offspring, suggesting that changes in the F1 generation

253 vels were similar between all four groups of offspring, suggesting that in both cases post-transcript

254 d cardiovascular risk in mothers having male offspring suggests a maternal disease specific mechanism

255 ther maternal allergen sensitization affects offspring susceptibility to food allergy, we epicutaneou

256 wth condition, which is referred to as large offspring syndrome (LOS).

257 s between maternal body mass index (BMI) and offspring systemic cardio-metabolic profile are causal,

258 tly between siblings and between fathers and offspring than between mothers and their offspring.

259 inth exposure in Norway was less frequent in offspring than parents; however, Toxocara spp. seroposit

260 ges in voluntary physical activity in female offspring that are differentially influenced by VTA lept

261 ired less effort were more likely to produce offspring that failed.

262 ody weight and adiposity index in adult male offspring that is paralleled by epigenomic alterations a

263 er weaning is not "catch-up growth," because offspring that were small for age grew slower.

264 g/mL, reduced asthma/recurrent wheeze in the offspring through age 3 years, suggesting that higher vi

265 ental effects on the long-term health of the offspring through non-genetic mechanisms.

266 dietary refined carbohydrates may predispose offspring to an obese phenotype, indicating a potential

267 is may serve mothers to better prepare their offspring to cope with later environments where the same

268 effects on offspring growth allow mother and offspring to make the best of a bad start.

269 lent pregnancy complications that predispose offspring to neurodevelopmental disorders, including aut

270 l viral e antigen to educate immunity of the offspring to support its persistence after vertical tran

271 f 2,871 CHD probands, including 2,645 parent-offspring trios, implicated rare inherited mutations in

272 est identified by exome sequencing of parent-offspring trios.

273 tal n-6/n-3 PUFA ratio exposure in wild-type offspring under standard maternal dietary fat amounts to

274 sts should pass mutualist symbionts to their offspring (vertical transmission) [3-8].

275 nd effects on the physiology and behavior of offspring via epigenetic modifications.

276 apomixis results in the production of clonal offspring via seed and can provide reproductive assuranc

277 Western diet age-specifically alters female offspring voluntary physical activity and dopamine- and

278 (approach 2), 1.04 (1.01-1.07) if the first offspring was a boy, and 1.06 (1.01-1.10) if the first t

279 sruption in anatomical RC connectivity in SZ offspring was associated with increased modularity of th

280 ncreased wheel running in juvenile female WD offspring was associated with up-regulated dopamine rece

281 ons between maternal PFAS concentrations and offspring weight and adiposity at birth, and secondarily

282 ations between maternal diseases and ADHD in offspring were analyzed using logistic regression models

283 e recruited during early pregnancy and whose offspring were born after 34 weeks' gestation.

284 a boy, and 1.06 (1.01-1.10) if the first two offspring were boys (approach 3).

285 After delivery, the offspring were followed for 7 months.

286 SZ offspring were found to show connectivity deficits of th

287 Furthermore, the offspring were invited to complete a questionnaire (74%

288 eetle Nicrophorus vespilloides We found that offspring were smaller at hatching when females laid egg

289 ht gain were associated with NAFLD in female offspring, whereas lower family SES at birth was associa

290 ppies were more likely to produce successful offspring, whereas mothers whose nursing style required

291 rrent offspring rather than gamble on future offspring which have a small probability of surviving.

292 and white adipose tissues compared with CON offspring, which was recovered by maternal RES supplemen

293 trol promotes beige adipocyte development in offspring white adipose tissue.

294 DD before the study or at baseline (n = 27), offspring with an episode of MDD that had remitted by fo

295 High fat-fed sedentary dams produced female offspring with impaired glucose tolerance compared with

296 ) parents alter selection pressures on their offspring with important consequences for their phenotyp

297 Offspring with MDD before the study or at baseline (n =

298 tinal TH17 cells were more likely to produce offspring with MIA-associated abnormalities.

299 that had remitted by follow-up (n = 4), and offspring with missing baseline MDD data (n = 2) were ex

300 us sensitization and oral challenge of their offspring with OVA.