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1 ory peptides are the ultimate gatekeepers of puberty.
2 communities on skin profoundly shift during puberty.
3 have reduced mammary ductal outgrowth during puberty.
4 s the polymorphic variant may resolve around puberty.
5 rt for transgender children below the age of puberty.
6 significantly lower adjusted BMR/RMR during puberty.
7 xin-like, have been linked to alterations in puberty.
8 f the decreased seizure-like activity during puberty.
9 th, with the majority of oocytes lost before puberty.
10 dioxin-like PCBs advance, the timing of male puberty.
11 ing behaviors that are often observed during puberty.
12 involved in epigenetic repression of primate puberty.
13 ber of APP-positive spheroids found prior to puberty.
14 testis of a non-human primate occurs before puberty.
15 ymal epithelium and appear with the onset of puberty.
16 loci but fully restored imprinting prior to puberty.
17 ates Zinc finger (ZNF) genes in timing human puberty.
18 Bs) that form at ductal tips at the onset of puberty.
19 assumed to be minimal before later stages of puberty.
20 al patterns of development to the effects of puberty.
21 duce testosterone do not differentiate until puberty.
22 ced proliferation of epithelial cells during puberty.
23 accurately reflect blood levels during mini-puberty.
24 ation, ductal outgrowth and branching during puberty.
25 ntries, with peak incidence near the time of puberty.
26 orrelations between prepubertal BMI and male puberty.
27 mmary epithelial cell proliferation in early puberty.
28 arious diseases, including rare disorders of puberty.
29 delay or arrest in follicle development and puberty.
30 Little is known about genes regulating male puberty.
31 ed by proportionate increases in dw/dt until puberty.
32 cts, a block to mammary ductal elongation at puberty.
33 required for mammary gland morphogenesis at puberty.
34 reproductive cascades, such as the onset of puberty.
35 mbers of 15 families with central precocious puberty.
36 ately before puberty, and remained low after puberty.
37 hylation of their promoters increased before puberty.
38 d in the absence of nicotine, at least until puberty.
39 ke MFLD values by the species-typical age at puberty.
40 ala, suggesting that expression arises after puberty.
41 y-gonadal axis results in central precocious puberty.
42 ts with CAIS should remain gonadectomy after puberty.
43 erlying the neuroendocrine control of female puberty.
44 the development of the mammary gland during puberty.
45 d the second round commences at the onset of puberty.
46 s adolescent height growth and the timing of puberty.
47 ressing to atrophy and ovarian dysgenesis at puberty.
48 wave inversion decreases significantly after puberty.
49 nclear whether this inequality changes after puberty.
50 ior in NMRs given the opportunity to undergo puberty.
51 ed a size increase of this protrusion during puberty.
52 ding of internal calendar time from birth to puberty.
53 to fast skeletal growth during childhood and puberty.
54 sence of AgRP neuron leptin signaling delays puberty.
55 y dynamic reorganization of the brain during puberty.
56 different trajectories, before the onset of puberty.
57 eclining physical functions before attaining puberty.
58 static cancer, endometriosis, and precocious puberty.
59 ngthened with age and the transition through puberty.
60 tion control-related disorders emerge during puberty.
61 releasing hormone to determine initiation of puberty.
62 valuated for interactions with age, sex, and puberty.
63 heir relative size increased markedly during puberty.
64 ess AIRE (mRNA and protein) than males after puberty.
65 rowth hormone deficiency (12.5%), precocious puberty (12.2%), thyroid-stimulating hormone deficiency
66 of age were subsequently transplanted during puberty (5 weeks) or at maturation (10 weeks) with synge
67 zed across 3 epochs; prepuberty (4-7 years), puberty (8-12 years), and postpuberty (13-20 years).
68 nt, Ptprb expression is downregulated during puberty, a period of extensive ductal outgrowth and bran
71 ovaries and reduced follicle numbers during puberty/adulthood; as similar changes were found for F2
72 kout restores developmental transcription at puberty, alters luminal epithelial homoeostasis, yet rem
74 y have a physiological role for the onset of puberty and a genetic basis for sexual maturation in hum
75 d as a critical permissive signal triggering puberty and a major regulator of the adult female hypoth
79 vated by kisspeptin to regulate the onset of puberty and adult reproductive function, is enriched in
86 to adulthood that begins around the onset of puberty and ends with relative independence from the par
87 endocrine responses, including modulation of puberty and estrous; control of reproduction, aggression
88 prefrontal cortex continues to mature after puberty and into early adulthood, mirroring the time cou
89 ow-up should try to establish the effects of puberty and later dietary or social transitions on these
91 ogenous sex hormones over the lifespan (e.g. puberty and menopause), exogenous sex hormones (e.g. hor
92 s similar between males and females in early puberty and only diverged in midpuberty, with CBF actual
93 ed delays in mammary tissue expansion during puberty and pregnancy, accompanied by increased luminal
94 particularly robust in mammary tissue during puberty and pregnancy, accounting for 34-40% of detected
95 to HDR defects in mammary epithelium during puberty and pregnancy, including in different epithelial
96 ng the miR-193b locus was accelerated during puberty and pregnancy, which coincided with the loss of
101 rganizational effects of ovarian hormones at puberty and provide a potential mechanism by which gonad
102 on the effects that the age of onset of male puberty and rates of spermatogenesis have likely had in
103 hypothalamic-pituitary-gonadal axis controls puberty and reproduction and is tightly regulated by a c
106 ease with an onset commonly immediately post-puberty and stabilization by 40 to 50 years of age.
107 morphogenesis to form branching ducts during puberty and terminate in secretory alveoli during lactat
108 al compartments for ductal elongation during puberty and that loss of RIP140 leads to a catastrophic
109 : The male predominance in prevalence before puberty and the "sex-shift" towards females after pubert
110 time difference between their appearance in puberty and the editing of the lymphocyte repertoire aro
111 t puberty will allow for selection on age at puberty and traits correlated with sow lifetime producti
112 hey show sexual dimorphism, major changes in puberty and typically more pronounced species difference
113 dence, notably in girls, rises sharply after puberty and, by the end of adolescence, the 1 year preva
115 ith age at menarche, a late manifestation of puberty, and body mass, little is known about these vari
117 increased susceptibility to mortality after puberty, and identify peritoneal cells as mediators of p
121 ry, housed under laboratory conditions until puberty, and subsequently used to establish offspring po
122 include maintenance of growth, navigation of puberty, and transition to adult services for long-term
123 lar nature of seminiferous tubules and after puberty androgens may further reinforce this feature.
126 ch into whether the neuroendocrine events of puberty are mechanistically linked to cortical maturatio
128 l environment as children transition through puberty, as well as evaluate the potential for reverse c
129 causes hypogonadotropic hypogonadism (failed puberty associated with low or apulsatile luteinizing ho
130 me, a syndrome of growth failure and delayed puberty associated with massive liver enlargement from g
133 immunoreactivity peaks prior to the onset of puberty before declining markedly to adult levels, where
135 A3, CRF1 binding was greater in males before puberty but decreased during puberty, abolishing the sex
137 (HBsAg), DNA, and RNA levels in mice before puberty, but its effect on HBV after puberty was apparen
139 AD1 or ZNF573 to the rat hypothalamus delays puberty by impairing the transition of a transcriptional
140 erty by hormonal blockade or acceleration of puberty by oestrogen treatment led to increased or decre
141 d children were prospectively followed after puberty by using a newly standardized MeDALL Core Questi
142 omatosensory cortex, suggesting that earlier puberty can advance cortical maturation in a regionally
143 ecause changes in the hormonal milieu during puberty can lead to inadequate suppression of adrenal an
144 the downregulation of CUX2 in male liver at puberty contributes to the developmental changes establi
145 c, CRH overexpression during early-life (pre-puberty, CRHOEdev) in double-mutant mice (Camk2a-rtta2 x
146 ds were retrospectively reviewed and data on puberty, dialysis, and immunosuppressive medication were
147 ion of breeding females and gilts that reach puberty earlier tend to stay in the herd longer and be m
148 7.82) as sites where pads were provided with puberty education (Rural M = 89.74, SD = 9.34; Periurban
150 oped additional brief paroxysmal episodes in puberty, either dystonic/dyskinetic or "shivering" attac
152 structure in children during early stages of puberty, extending our understanding of genotype-phenoty
155 neurogenesis and volume increase, peaking at puberty followed by selective elimination and myelinatio
156 ant, albeit slight, effects included delayed puberty for F1 females, reduced caput epidydimal sperm c
157 ecifically sexual abuse, prior to and during puberty has specific implications for personality develo
159 signals in or near genes involved in delayed puberty, highlighting the first molecular links between
161 steroid hormone titers and delayed onset of puberty; however the pathway by which this occurs remain
162 alamo-pituitary-gonadal axis such as delayed puberty, hypothalamic amenorrhea, and hypogonadotropic h
163 sm through which diet-induced obesity during puberty imposes its long-lasting effects on sleep-wake b
164 ocorticoid exposure influences the timing of puberty in animal models, but the human relevance of tho
165 opment in ChCs, but increases rapidly before puberty in BCs, with an earlier time course in deeper-la
166 iking properties matured before the onset of puberty in both cell types, but following cell type-spec
168 oid hormones, leading to abnormal growth and puberty in children, and affecting general wellbeing and
174 in the uterotrophic assay and did not alter puberty in male and female rats or mammary gland develop
175 vation of GnRH neurons results in precocious puberty in mice and humans, but the mechanisms underlyin
180 ssociations previously identified for age at puberty in the pig and loci for age at menarche in human
183 behavioral response inhibition mature after puberty, in tandem with structural changes in the prefro
185 characterised by failure to progress through puberty, indicating the involvement of this newly descri
186 evidence suggests that calcium intake before puberty influences adolescent height growth and the timi
187 varies between individuals and the timing of puberty initiation is associated with several health out
188 pubertal markers, epidemiological trends of puberty initiation over time, and the mechanisms whereby
189 es the normal GnRH-fuelled run-up to correct puberty initiation, and interfering with this process di
194 cortex in monkeys as they transitioned from puberty into adulthood and compared activity at differen
201 , based in part on animal work, suggest that puberty is associated with neural-level changes that fac
207 lometric growth by the mammary glands around puberty is widely held to be estrogen (E)-dependent.
208 equired for mammary gland development during puberty, it is not clear whether its overexpression alte
209 ifferences and the relation to the timing of puberty jointly explained 67% of the between-subject var
211 The present work shows that obesity during puberty leads to persistently dysregulated patterns of s
215 rgely shaped by transitional periods such as puberty, menopause and pregnancy, while daily fluctuatio
216 ale JDP2 null mice, however, exhibited early puberty, observed as early vaginal opening, larger litte
217 hift towards a sex-balanced prevalence after puberty onset (0.89, 0.74-1.04); sex-puberty interaction
218 idity showed the strongest sex effect before puberty onset (female-male-OR 0.55, 0.46-0.64) and a con
221 rons) plays a critical role in the timing of puberty onset and is involved in fertility regulation th
222 signaling in AgRP neurons is sufficient for puberty onset and normal adult fecundity in both sexes w
225 neurons), but also into neurons critical for puberty onset and the regulation of reproductive functio
227 atal loss, pregnancy rate, gestation length, puberty onset in males, growth, estrous cycles, hormone
230 ty and the "sex-shift" towards females after puberty onset were strongest in multimorbid patients who
231 re-pubertal hormone treatment to model early puberty onset, a phenomenon increasingly observed in gir
232 wider range of deficits, including advanced puberty onset, abnormal negative feedback, and abolished
233 es were morbidly obese and exhibited delayed puberty onset, no evidence of estrous cycles, and minima
234 development, showing dramatic changes after puberty onset, yet few experiments have directly tested
238 ten affected than boys both before and after puberty onset: 0.71, 0.63-0.81 and 0.81, 0.64-1.02, resp
239 girls less often than boys before and after puberty onset: adjusted odds ratio for females vs males
246 rapid increases in albumin excretion during puberty precede the development of microalbuminuria and
248 GATAD1 represses transcription of two key puberty-related genes, KISS1 and TAC3, directly, and red
251 egion in the brain, in relation to change in puberty (self-report and testosterone levels), laborator
252 rodevelopmental trajectories associated with puberty, self-evaluations, and the presumed social reori
254 significantly higher absolute BMR/RMR during puberty (SMD: 1.10-5.93), and all of the studies favored
255 bidity (ie, concurrent asthma and rhinitis), puberty status and allergic sensitization by specific se
257 s and childhood growth in 940 girls from the Puberty Study of the Breast Cancer and Environment Resea
258 nile pheromone produced by young mice before puberty, termed exocrine-gland secreting peptide 22 (ESP
259 vior and undergoes structural changes during puberty that may be driven by gonadal hormone secretion
265 with increased interest in the other sex at puberty, these early emerging biases might help explain
266 -cells can reprogram to produce insulin from puberty through to adulthood, and also in aged individua
267 imals, and no other members exhibit signs of puberty throughout their lives unless they are removed f
271 ate shared aetiologies in both sexes between puberty timing and body mass index, fasting insulin leve
272 ndependent of body mass index (BMI), between puberty timing and risks for breast and endometrial canc
273 the complexity of the genetic regulation of puberty timing and support causal links with cancer susc
274 ancestry, we found that variants that delay puberty timing are associated with a longer parental lif
275 Understanding of the genetic regulation of puberty timing has come largely from studies of rare dis
276 , we report the largest genomic analysis for puberty timing in 55,871 men, based on recalled age at v
277 analyses infer causal influences of earlier puberty timing on earlier first sexual intercourse, earl
279 adjusting the timing of artificially induced puberty to optimise overall outcome with respect to stat
280 se cells change their properties during late puberty to young adulthood, when bone growth and accrual
281 hesis in a large sample of children in early puberty, to compare regional gray matter volumes among i
284 imary spongiosa of long bone in mice at late puberty undergo normal programmed senescence, characteri
285 before puberty, but its effect on HBV after puberty was apparent, with HBV replicating approximately
289 use children have less sebaceous skin before puberty, we compared the fungal communities of primary c
291 ian oocytes are arrested at prophase I until puberty when hormonal signals induce the resumption of m
293 current, reduced activity in 8.5 mM K(+) at puberty, while blockade of alpha5-GABARs had no effect.
294 boy, with a diagnosis of CAH and precocious puberty, who was referred to our department for an ultra
296 ging a developmental pathway linking earlier puberty with reduced pubertal growth (P = 4.6 x 10(-5))
299 genes involved in regulation of the onset of puberty would allow for the improvement of reproductive
300 ition during pregnancy, early childhood, and puberty would avoid not only obesity, but also accelerat
301 ations, we analysed the effects of sex, age, puberty (yes/no) and possible confounders on the prevale
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