ライフサイエンスコーパス: offspring

1 13 (n = 4,255,196 unique pairs and 8,343,951 offspring).

2 ht gain predict future obesity status of the offspring.

3 r activity and anxiety-like behaviour in the offspring.

4 ate species that exhibits biparental care of offspring.

5 ed with adverse outcomes in both mothers and offspring.

6 of a core full-sibship we term the pedigree offspring.

7 P5 intron 7, site 6 methylation in Holocaust offspring.

8 biparental inheritance of mtDNA in 0.06% of offspring.

9 implying transgenerational effects on their offspring.

10 ategy is often to disperse a set fraction of offspring.

11 rease the cost of reproduction per surviving offspring.

12 and protect against HFD-induced adiposity in offspring.

13 to reverse the sociability phenotypes in MIA offspring.

14 ited to the gonads and can be transmitted to offspring.

15 onse to ozone was examined in Long-Evans rat offspring.

16 -specific adipogenic programming in the IUGR offspring.

17 sponse times of germ cells to protect future offspring.

18 on the sex-related behavior of their female offspring.

19 lacental efficiency and glucose tolerance in offspring.

20 l (n = 5-8/group) and juvenile (n = 8/group) offspring.

21 other to enable her to feed and care for her offspring.

22 differences in maternal transfer of MeHg to offspring.

23 ure to trauma prior to conception can affect offspring.

24 ion-deficit/hyperactivity disorder (ADHD) in offspring.

25 ternal F0 Pb exposure produced runting in F3 offspring.

26 ns, such as schizophrenia and autism, in the offspring.

27 ncreased risk of congenital heart defects in offspring.

28 by schizophrenia-like behavior in the adult offspring.

29 nd insulin, and increased adiponectin in HFD offspring.

30 revented the above-mentioned deficits in the offspring.

31 ic-induced head-twitch behavior in adult MIA offspring.

32 ke phenotypes early and persistently in male offspring.

33 are associated with epigenetic aging in the offspring.

34 into fewer, better provisioned (i.e. larger) offspring.

35 -specific adipogenic programming in the IUGR offspring.

36 ed liver adenomas at 45 weeks of age in male offspring.

37 ect the immune response of their undisturbed offspring.

38 cumulative incidence for SCZ and BIP in the offspring.

39 uture fitness as well as more investment per offspring.

40 n the maternal serum and the brains of fetal offspring.

41 romosomes critical for production of healthy offspring.

42 les produced greater clutch sizes and larger offspring.

43 ompartments and causes behavioral changes in offspring.

44 ng with the transmission of parental cues to offspring.

45 ogenous stores or exogenous food intake into offspring.

46 loidy in gametes and compromise viability in offspring.

47 verse psychiatric and behavioral outcomes in offspring.

48 asting glucose, compared with mothers of AGA offspring.

49 and maintain health and genetic fidelity in offspring.

50 icts a preference for palatable foods in the offspring.

51 , thereby ensuring proper development of the offspring.

52 creased cortical neural activity in MIA male offspring.

53 ities in brain function and behaviour of the offspring(4).

54 Adult male and female offspring (8 weeks old) were assessed across a battery o

55 A) receptor (5-HT(2A)R) density in the adult offspring, a phenotype previously observed in postmortem

56 association between gestational glycemia and offspring AA measured by MRI in the neonatal period and

57 th uncertainty is to spread the emergence of offspring across multiple years via dormancy.

58 cy was strongly associated with psychosis in offspring (adjusted odds ratio=1.8, 95% CI=1.2-2.7) and

59 c phenotype, especially pronounced in female offspring after developmental exposure to environmentall

60 ization with the trivalent vaccine protected offspring against nHSV-disseminated disease and mortalit

61 lationship between maternal HMO profiles and offspring allergic diseases up to age 18 years.

62 reproductive success), the random number of offspring an individual produces over its lifetime.

63 nalyses, performed in a larger sample of 147 offspring and 40 control subjects that included the 31 p

64 as been shown to improve metabolic health in offspring and confers protection against the development

65 le of GBS-specific IgG production in exposed offspring and juvenile mice at age 12 and 14 days, respe

66 HLA matches, as would be expected between an offspring and parent.

67 ac or smooth muscle cells resulted in viable offspring and remodeled vasculature and did not recapitu

68 an elevated risk for psychotic disorders in offspring and that the association varies by infection s

69 different transcriptional profiles in their offspring, and sons and daughters strongly differed in t

70 ffects of maternally transmitted hormones on offspring, and their role in adapting to changing enviro

71 alth consequences, the effects of MIA on the offspring appear to be variable.

72 omen with small or large for gestational age offspring are at increased risk of cardiovascular diseas

73 atory, females increased relative effort per offspring as the reproductive season progressed; smaller

74 ory diet, was associated with higher risk of offspring asthma (OR: 1.35; 95% CI: 1.10, 1.65; per 1-SD

75 ring pregnancy was associated with increased offspring asthma severity in a dose-dependent manner.

76 cy with emotional and behavioral symptoms of offspring at 7 to 10 years of age.

77 n females, while number, size and quality of offspring at birth remained unaffected.

78 and tight junction protein expression in the offspring at pre-weaned age.

79 , and the brown progenitor cells sorted from offspring BAT demonstrated attenuated brown adipogenic c

80 quences of maternal e-cigarette use on adult offspring behavior and neuroimmune outcomes.

81 tered by Pb, PS, or combined Pb and PS in F1 offspring: behavioral performance [fixed-interval (FI) s

82 utrition offered to pregnant women and their offspring below the age of 6 years was associated with a

83 plements offered to pregnant women and their offspring below the age of 6 years were not associated w

84 mining the effects of ME during pregnancy on offspring body composition and development of NAFLD whil

85 stfledging survival cost for each individual offspring, but parents benefitted through a 14.0% increa

86 ysiological adaptations to enable caring for offspring, but the underlying CNS changes are poorly und

87 at reflect the amount of energy allocated to offspring by mothers, such as infant body mass, are pred

88 9-mediated Arrayed Mutagenesis of Individual Offspring (CAMIO) to achieve comprehensive analysis of a

89 modulate maternal diet and improve long-term offspring cardiometabolic health.

90 effect of birthweight associated variants on offspring cardiometabolic risk factors after adjusting f

91 pring cardiovascular well-being, programming offspring cardiovascular function through both sperm and

92 impact of sub-optimal paternal nutrition on offspring cardiovascular well-being, programming offspri

93 ess disorder, age at Holocaust exposure) and offspring characteristics (i.e., childhood trauma exposu

94 imiquimod (5.0 mg/kg) induces a phenotype in offspring characterized by reduced anxiety-like behavior

95 We used data from the Framingham Heart Study Offspring Cohort exams 5 through 9.

96 rticipants from the Framingham Heart Study's Offspring Cohort who had 3 ceramides measured (n = 1561,

97 chasticity, derived communities give rise to offspring communities that faithfully re-establish paren

98 reduce infestation by parasites and increase offspring condition [1,2].

99 ollectively, our results suggest that parent-offspring conflict and associated parental benefits expl

100 The association between GI and GL and offspring congenital heart defects was estimated by logi

101 beverages and a moderately increased risk of offspring congenital heart defects was observed.

102 sugar-sweetened drinks increased the risk of offspring congenital heart defects.

103 on criteria were linked to the data of their offspring contained within the National Korea Health Scr

104 reduced brain age compared to those without offspring, corroborating our cognitive function results.

105 The lack of this defence mechanism in offspring could have dramatic negative consequences (e.g

106 when exposed to kairomones and AgNPs, their offspring could not develop such adaptive defensive trai

107 with vasectomized male mating, we generated offspring derived from either NPD or LPD sperm (devoid o

108 the negative effects of maternal obesity on offspring development and adult health.

109 oad on placental function directly affecting offspring development and/or leading to chronic disease

110 ts on maternal physiological functioning and offspring development, resulting in increased risk for l

111 al nutrients consumed contemporaneously with offspring development.

112 maternal DHCR7 heterozygosity, combined with offspring DHCR7 heterozygosity might represent a vulnera

113 al germ cell epigenetics in association with offspring disease risk, a framework must first be built

114 the resulting maternal mutant Dot1l(mat-/+) offspring displayed normal development and fertility, su

115 6-OH-BDE-47 and a MAPK inhibitor resulted in offspring displaying similarly increased frequency of mu

116 The dispersion parameter of the offspring distribution in the inferred transmission chai

117 A stratified analysis of sex of offspring donors to female recipients demonstrated that

118 n hepatic metabolism are already seen in the offspring early life.

119 al investment in response to a deteriorating offspring environment: allocating greater resources to l

120 g previous correlations between parental and offspring environments, and interfering with the transmi

121 rental environments are highly predictive of offspring environments.

122 nic blow fly (females produce female or male offspring, exclusively) by separately sequencing and ass

123 ermore, IL-17A-condition male but not female offspring exhibited reduced anxiety-like behavior.

124 and characterize subgroups of isogenic mouse offspring exposed to identical MIA, which was induced in

125 ablish that the social behaviour deficits in offspring exposed to MIA can be temporarily rescued by t

126 Moreover, male and female offspring exposed to PG/VG with and without nicotine had

127 , and experiments were then conducted in the offspring exposed to these drugs via lactation.

128 For a given number of offspring, females that weaned more sons than daughters

129 re predicted to have long-lasting effects on offspring fitness.

130 e influence of infection on reproduction and offspring fitness.

131 xpression, and neuroendocrine measures) with offspring FKBP5 methylation.

132 and neuroimmunological consequences to adult offspring following maternal e-cigarette exposure during

133 rsed XY mice were able to give birth to live offspring following mating to stud-males.

134 , psychological, and psychiatric features of offspring from extended pedigrees selected for high-dens

135 Significantly, this approach protected offspring from long-term behavioral morbidity.

136 attenuated activity of DA midbrain neurons, offspring from mothers exposed to HFD feeding exhibited

137 dala of postnatal days 22-28 male and female offspring from normal bedding or LB mothers.

138 Enhanced performance of offspring from parents exposed to high conditions was ma

139 Offspring from the rural site were heavier at fledging t

140 offspring to carefully constructed synthetic offspring from the same parents to determine statistical

141 Both LC-like and DC offspring from this progenitor carried the BRAF mutation

142 ion of ITGA6(+)ITGB4(+) mitotic cells, whose offspring further segregated into a TNFRSF12A(hi) subfra

143 aplotype algorithm to obtain the conditional offspring genotype distribution under the null hypothesi

144 ed the interactions between maternal SDB and offspring growth and adiposity measurements after contro

145 vailability is the key factor limiting urban offspring growth and survival, at least in this well-stu

146 Significant changes in F2 neonatal offspring growth and tissue angiotensin-converting enzym

147 In contrast, offspring GRS is strongly related to many cardiometaboli

148 iometabolic risk factors after adjusting for offspring GRS.

149 Women with small for gestational age (SGA) offspring had 1-2 mmHg higher systolic and diastolic blo

150 , women with large for gestational age (LGA) offspring had higher measures of adiposity, ~0.1 mmol/l

151 at in both sexes, subjects with two or three offspring had significantly reduced brain age compared t

152 oups that originate through the retention of offspring have a clear reproductive divide with distinct

153 etween prenatal Tdap vaccination and ADHD in offspring (hazard ratio = 1.00, 95% confidence interval:

154 ations between paternal life experiences and offspring health and disease outcomes.

155 lthough the impact of maternal diet on adult offspring health is well characterized, the role that a

156 atal life has substantial influence on adult offspring health.

157 d the transcriptome profiles of genes in the offspring hippocampus.

158 is related to adverse health outcomes in the offspring; however, its effect on the daughters' breast

159 erinatal cytokines and abnormal behaviors in offspring, human epidemiological studies in this area re

160 ered thyroid hormone levels in both dams and offspring in a dose-dependent manner, but did not change

161 mothers' concentrations, and examined their offspring in adulthood.

162 X/Y heterogametic amphogeny (male and female offspring in similar ratios) sex determination systems e

163 dative stress) causes various disruptions in offspring, including ones in white matter/glia, glucocor

164 que fathers transmit more mutations to their offspring, increasing the per generation mutation rate b

165 g development on the cardiac function of the offspring, independent of additional effects on the moth

166 an inflammatory microglial phenotype in the offspring induced by maternal immune activation (MIA).

167 mune challenge had smaller effects on mother-offspring interactions.

168 The amount of care parents provide to the offspring is complicated by an evolutionary conflict of

169 Genetic diversity in offspring is induced by meiotic recombination, which is

170 The percentage of FMPD in AMD offspring is nearly twice that reported for the general

171 possible long-term risks for users and their offspring is needed.

172 f the mother's energy needs and those of her offspring is presumably fundamental to maximizing lifeti

173 investigate maternal age effects on several offspring life-history traits: condition, reproductive s

174 udy, we focus on how maternal age influences offspring life-history trajectories and performance in a

175 he age of parents at reproduction can affect offspring lifespan and other fitness-related traits is i

176 llocating greater resources to late-produced offspring likely enhances maternal fitness.

177 ternal survival and adequate provisioning of offspring, likely presenting strains on their metabolism

178 from social interactions between parents and offspring may underlie signal evolution.

179 sus LGA offspring, where giving birth to SGA offspring might primarily reflect adverse maternal vascu

180 adverse maternal vascular health whereas LGA offspring might reflect the mother's metabolic health.

181 ), and the maternal cumulative prevalence of offspring mortality (mOM) bring theoretical and practica

182 On PND 40, F1 offspring (n = 10/group/sex) were exposed to air or 0.8

183 preconception exposure to these drugs alters offspring neurodevelopment.

184 e-carrying fish in several traits related to offspring number and fitness.

185 rauterine growth restriction (IUGR) leads to offspring obesity.

186 igher among offspring of affected women than offspring of affected men.

187 observed that epilepsy risk is higher among offspring of affected women than offspring of affected m

188 Adult offspring of both sexes exposed to + Nic exhibited eleva

189 ing test revealed no differences between the offspring of CORT-treated breeders compared to controls.

190 retained, with modest attenuations, for the offspring of heterotypic pairs.

191 esolved the balance of risks and benefits to offspring of medication use during pregnancy.

192 The predominance of this effect in offspring of mothers exposed during childhood implicates

193 Offspring of mothers from the Danish National Birth Coho

194 istent with improved neonatal tolerance, the offspring of mothers with T1D had reduced cord blood CD4

195 eratures had a greater effect on survival of offspring of native O. hecate compared to introduced O.

196 of smokers are more likely to smoke than the offspring of nonsmokers, this sets the stage for more se

197 sing brief-access taste testing, with female offspring of obese dams showing an enhanced response to

198 ficits and reversed leptin resistance in the offspring of obese dams.

199 rotect foveal MPOD architecture in Caucasian offspring of parent(s) with AMD.

200 Offspring of parents exposed to high pCO(2) had greater

201 Offspring of pedigrees with a high density of AUD or DA

202 ally, small, infected females produced fewer offspring of poorer condition, while in contrast, large,

203 bortions and congenital malformations in the offspring of ruminants.

204 Since the offspring of smokers are more likely to smoke than the o

205 We reared F1 offspring of unexposed and predator-exposed F0 males und

206 (i.e., overall and disproportionate) in the offspring of women attending a high-risk pregnancy clini

207 ee relatives (3776 siblings, 4258 parents or offspring) of 2122 unrelated vitiligo probands.

208 living donor liver allograft from either an offspring or a nonoffspring, with exactly 3 HLA matches,

209 hether deleterious effects are direct on the offspring or secondary to alterations in uteroplacental

210 Offspring ornamentation typically occurs in taxa with pa

211 GDM) thresholds, are associated with adverse offspring outcomes, with DNA methylation proposed as a m

212 vascular anatomy, and donor, recipient, and offspring outcomes.

213 A) was reduced in FMPD offspring vs. control offspring (P = 0.04).

214 We studied 212 mother-offspring pairs from the HOME Study.

215 In 940 mother-offspring pairs, we performed gas chromatography-mass sp

216 re estimated by quantile regression for 6227 offspring-parent pairs.

217 Quantile-specific offspring-parent regression slopes (beta(OP)) were estim

218 ility is that sex-of both the parent and the offspring-plays an important role in driving the evoluti

219 In BAT of DEX offspring, Ppargc1a expression was suppressed, together

220 16ac provides an instructive function to the offspring, priming future gene activation.

221 ttle evidence to support the hypothesis that offspring prioritize their same-sex parent's experience.

222 p and subordinate group members help to rear offspring produced by breeders.

223 Crabs were assessed for offspring production and quality, as well as measures of

224 sterile males also showed enhanced late-life offspring production when allowed to reproduce, indicati

225 high elevation pursue strategies that favour offspring quality over offspring quantity.

226 effect of position in the laying sequence on offspring quality.

227 trategies that favour offspring quality over offspring quantity.

228 t that lifestyle factors accompanying having offspring, rather than the physical process of pregnancy

229 protein diet modified F1 neonatal and adult offspring renin-angiotensin system activity and cardiova

230 cell frequency in blood and its BRAF-mutated offspring reported response to chemotherapy.

231 high GI and GL in midpregnancy and increased offspring risk of congenital heart defects.

232 d overweight status (potential mediator) and offspring's asthma with or without nasal allergies (outc

233 ulted in robust sex-based differences in the offspring's behavioural responses during adulthood.

234 tion by maternal food choices could limit an offspring's brain function for life.

235 age 8 years, puberty, and age 30 years with offspring's childhood overweight status (potential media

236 where to lay your eggs, are critical for the offspring's fitness and survival in any species.

237 ed, the role that a father's diet has on his offspring's health remains poorly defined.

238 ternal probiotic supplementation can improve offspring's neurodevelopmental outcomes.

239 ect or indirect effects mediated through the offspring's own overweight status.

240 Regarding the F1 offspring, screening for anxiety-related behaviours usin

241 over the subsequent 40 years, stratified by offspring sex and presence of reported parental mental i

242 association varies by infection severity and offspring sex.

243 2.7) and varied by severity of infection and offspring sex.

244 Cep55-knockout offspring show microcephaly and primary neural progenito

245 Study of Atherosclerosis, and the Framingham Offspring Study, known cohorts with available measures o

246 en analyzed in a separate cohort (Framingham Offspring Study; n=2045, age 55+/-10 years, 51% women),

247 energy compensation are less likely to rear offspring successfully.

248 on dominant female fecundity, body mass, and offspring survival and growth using an additive modellin

249 rstand the effects of maternal allocation on offspring survival and growth, we estimated the effects

250 nes (THs) exert context-dependent effects on offspring survival and physiology by manipulating both e

251 n 2 and 7 y experienced faster senescence in offspring survival in old age.

252 urthermore, maternal and paternal effects on offspring survival were non-additive: offspring with a p

253 resilience may exert a salubrious effect on offspring telomere biology and highlight the importance

254 probabilities and produced fewer recruiting offspring than noninbred individuals.

255 lloparental care, where individuals care for offspring that are not their own, but usually the behavi

256 l offspring, we identified a subgroup of MIA offspring that displayed elevated peripheral production

257 g pregnancy results in chronic conditions in offspring that manifest in adulthood.

258 ht the existence of subgroups of MIA-exposed offspring that show dissociable behavioral, transcriptio

259 No offspring that was heterozygous for both Cre and the con

260 osures to oil alone did not affect survival, offspring that were subsequently exposed to full spectru

261 In their offspring, those chicks whose parents were exposed to CH

262 n of the effects of parental exposure to the offspring through epigenetic changes in the germline.

263 e to nutritionally program gilthead seabream offspring through fish oil (FO) replacement by vegetable

264 posed digital twin test compares an observed offspring to carefully constructed synthetic offspring f

265 se in the likelihood of raising at least one offspring to independence.

266 n the brain of maternally exposed Dhcr7(+/-) offspring to levels approaching those seen in a mouse mo

267 A total of 279 offspring to parent and 241 nonoffspring donor liver tra

268 m greater energetic investment in many small offspring towards investing less total energy into fewer

269 earch exome-sequence data from 31,058 parent-offspring trios of individuals with developmental disord

270 rformed whole-exome sequencing of 250 parent-offspring trios, and observed enrichment of damaging de

271 ful between-population dispersers) and their offspring using 29 years of monitoring from North Americ

272 r seminal fluid at conception impaired adult offspring vascular function in response to both vasocons

273 a sup-optimal paternal low protein diet for offspring vascular homeostasis and define the sperm and

274 ates yield additive genetic benefits through offspring viability, thereby maximizing chooser fitness.

275 cosahexaenoic acid (DHA) was reduced in FMPD offspring vs. control offspring (P = 0.04).

276 pendent cohort containing 50 MIA and control offspring, we identified a subgroup of MIA offspring tha

277 ade-offs between the quantity and quality of offspring, we sought to examine the potential for dimini

278 These offspring were about 4 years younger than those without

279 The lifelong metabolic improvements in the offspring were accompanied by reductions in proinflammat

280 F3 offspring were generated from each of these lineages and

281 mon environment for one generation, and then offspring were grown in ambient or elevated [CO(2) ] gro

282 Male and female offspring were tested using a comprehensive sequence of

283 Male offspring were weaned at postnatal Day 21 and then fed a

284 hanges in the gut microbiome and immunity of offspring when exposed to direct or prenatal maternal st

285 levels of cardiovascular risk factors among offspring when they were young adults.

286 lower risk of cardiovascular disease in the offspring when they were young adults.

287 r risk profiles in mothers of SGA versus LGA offspring, where giving birth to SGA offspring might pri

288 ansmit somatic mutations and epimutations to offspring, which in turn can affect fitness.

289 ing antepartum depressive symptoms delivered offspring who exhibited lower fecal sIgA concentrations

290 easures of adiposity, compared to women with offspring who were appropriate for gestational age (AGA)

291 By parent-offspring whole genome sequencing, we estimate a mutatio

292 insulin at 9 months of age, as compared with offspring with a father or sibling with T1D.

293 cts on offspring survival were non-additive: offspring with a predator-exposed father, but not two pr

294 treated epididymal epithelial cells produced offspring with altered neurodevelopment and adult stress

295 The primary outcome was offspring with asthma or recurrent wheeze by age 3 years

296 Offspring with dual-affected, single-affected, and unaff

297 on in the maternal provisioning of lipids to offspring, with a positive correlation between lipid con

298 Ai9 offsprings, with and without Cre, were reared under a no

299 ortant question: as past research shows that offspring would benefit-improve postfledging survival-by

300 sk of schizophrenia and related psychoses in offspring, yet there has been limited research focused o