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Query: UMLS:C0848255 (female puberty)
 121 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

By using the odd-numbered Murdock-White SCCS societies, Brown's three hypotheses on female puberty rites were tested. Only matrilocal/ambilocal residence was significantly associated with female puberty rites. But after an adjustment for data quality control, even this relationship became insignificant. Female physiology as symbolized by menstruation is suggested as a better predictor for female puberty rites.
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PMID:Female puberty rites: reconsideration and speculation. 666 21

Ovaries of 23- and 35-day-old rats were transplanted under the kidney capsules of 31- and 23-day-old females, respectively. The recipient rats were ovariectomized on the fourth day after transplantation, and the onset of puberty was recorded. Neither the age and body weight at vaginal opening and first ovulation nor the length of the first ovarian cycle differed significantly between the experimental rats and sham-transplanted or untreated controls. Estimation of the serum FSH an LH concentrations before and after ovariectomy provided no evidence that different gonadotropic responses had masked puberty-delaying or puberty-advancing effects of the implanted immature and prepuberal ovaries, respectively. The results suggest that the developmental stage of the ovaries is not a decisive factor in the control of the onset of female puberty.
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PMID:Failure to demonstrate a significant influence of ovarian maturity on the onset of puberty in female rats. 679 8

Caryovolumetric investigation of hippocampal neurons performed in intact female rats at 21, 26, 32 and 36 days of age, and on the day of the first vaginal estrus revealed distinct prepubertal changes of nuclear volumes of pyramidal neurons located in the ventral hippocampus close by the subiculum. The caryovolumetrically demonstrable activity of these neurons increased significantly between days 21 and 26 and showed a subsequent decrease up to day 36. It was again significantly enhanced at the time of the first vaginal estrus. In contrast to the ventral hippocampus, neuronal activity of the dorsal hippocampus was at a constant level throughout the prepubertal development. Neonatal ovariectomy reduced significantly the nuclear volumes in both hippocampal regions and, simultaneously, prevented completely the prepubertal fluctuation of neuronal activity recorded in the ventral hippocampus of intact rats. The results suggest that the prepubertal activity of hippocampal neurons depends on the integrity of the cerebro-hypophyseo-gonadal axis. They furthermore support the conclusion derived from experimental studies that the hippocampus may be involved in the neurohormonal control of female puberty.
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PMID:[Caryovolumetrically demonstrable relationship between activity of the hippocampus and sexual maturation in female rats (author's transl)]. 719 54

Studies in female rats have shown that transforming growth factor alpha (TGF alpha) stimulates release of luteinizing hormone-releasing hormone (LHRH), the neuropeptide controlling sexual maturation, and that expression of the TGF alpha gene in the hypothalamus increases during both the initiation of normal puberty and after hypothalamic lesions that induce sexual precocity. Since blockade of epidermal growth factor receptors (EGFR), which mediate TGF alpha actions, delayed the normal timing of puberty, it was postulated that TGF alpha/EGFR contributes to the neuroendocrine process that underlies the initiation of normal female puberty. The present study was undertaken to examine the hypothesis that hypothalamic expression of the TGF alpha gene and its receptor changes in relation to the stage of sexual development in nonhuman primates, and to determine whether these changes are accompanied by corresponding alterations in LHRH gene expression. DNA fragments complementary to the coding regions of the rhesus monkey TGF alpha, EGFR and LHRH genes were cloned by reverse transcription-polymerase chain reaction (RT-PCR), sequenced and used to prepare monkey-specific antisense RNA probes. A quantitative RT-PCR was developed in which the cloned sequences were utilized to prepare RNA standards for the quantitation of tissue mRNA levels. Both TGF alpha and EGFR mRNA levels in the medial basal hypothalamus and preoptic area of female monkeys were elevated during neonatal life (1 week to 6 months of age), when FSH secretion is also high, decreased during juvenile development (8-18 months of age), when secretion of both FSH and LH is low, and markedly increased during the expected time of puberty (30-36 months of age). No such changes were observed in either the cerebellum or the cerebral cortex, two brain regions irrelevant to neuroendocrine reproductive control. In contrast to the pronounced alterations in hypothalamic TGF alpha/EGFR gene expression observed during sexual development, LHRH mRNA levels did not vary significantly during this time. Hybridization histochemistry revealed the presence of both TGF alpha and EGFR mRNAs in cells scattered throughout the hypothalamus, but more predominantly in the median eminence, suprachiasmatic nuclei, optic chiasm and cells along the wall of the third ventricle. These results demonstrate that increases in TGF alpha and EGFR gene expression, specific to the neuroendocrine brain, occur during developmental phases in which gonadotropin output is also elevated--most noticeably at the time of puberty.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Developmental expression of the genes encoding transforming growth factor alpha and its receptor in the hypothalamus of female rhesus macaques. 754 71

Although bone mineral status in children has been measured with various techniques, information about development of the actual bone mass density during childhood and adolescent growth is scarce. Our modified radiographic absorptiometry (RA) determines bone mass density (BMaD) three dimensionally at the diaphyseal and metaphyseal site of the middle phalanx of the left second digit, representing predominantly cortical (50% site) and trabecular bone compartments (25% site), respectively. The objectives of this study were to establish reference curves with 95% prediction intervals of BMaD in relation to bone age (BA) during childhood and adolescence (N = 303) determined by RA. The specific effects of female puberty on BMaD were studied comparing the values of 110 untreated girls with Turner syndrome (TS) with those of the female reference group. For either sex, a piecewise linear model with one inflection point (IP) was postulated for the relationship of both the 25% and 50% site with BA. The IPs appeared at exactly the same BA (11.5 "years") for both the 25% and 50% site in boys and for the 25% site in girls. However, in girls the 50% site IP appeared 0.25 "years" later. All BMaD values to the left of the IPs showed little increase with age. In contrast, the slopes to the right of the IPs showed in both genders regression coefficients of approximately 0.05 for the 25% site. For the 50% site, the regression coefficient in girls was markedly higher (0.075) than in boys (0.058), resulting only in girls in a significant difference between the 25% and the 50% site to the right of the IP (p = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Radiographic absorptiometry of the phalanges in healthy children and in girls with Turner syndrome. 757 61

Recent findings have led to the concept that transforming growth factor alpha (TGF alpha) contributes to the neuroendocrine regulation of female puberty by stimulating the release of luteinizing hormone-releasing hormone (LHRH), the neurohormone controlling sexual development. It was postulated that this effect is mediated by epidermal growth factor receptors (EGFR) and that EGFR may not be located on LHRH neurons, so that TGF alpha-induced LHRH release would require an intermediate cell-to-cell interaction, presumably of glial-neuronal nature. The present study was undertaken to characterize the presence of EGFR in rat hypothalamus and to determine if changes in EGFR gene expression and EGFR protein occur at the time of puberty. RNA blot hybridization demonstrated that the hypothalamus expresses all mRNA species known to encode EGFR. RNase protection assays revealed that alternative splicing of the EGFR primary mRNA transcript occurs in the hypothalamus and produces a predominant transcript encoding the full-length EGFR and a much less abundant, shorter mRNA encoding a truncated, and presumably secreted form of EGFR. EGFR-like immunoreactive material was found in several hypothalamic regions including the organum vasculosum of the lamina terminalis, supraoptic, suprachiasmatic, and paraventricular nuclei, ependymal cells lining the third ventricle, some astrocytes associated with blood vessels, astrocytes of the pial surface, and tanycytes and glial cells of the median eminence (ME). Low levels of EGFR mRNA were detected by hybridization histochemistry in cells of the same areas containing EGFR-like immunoreactivity. Double-immunohistochemistry revealed that even though LHRH neurons are in close proximity to EGFR-positive cells, they do not contain EGFR. In the ME, EGFR-immunonegative LHRH nerve terminals tightly coexist with EGFR-positive cells, presumably tanycytes and glial astrocytes. EGFR mRNA levels measured by quantitative reverse transcription-polymerase chain reaction assay (RT-PCR) in the ME-arcuate nucleus region at the time of puberty decreased in the morning of the first proestrus, i.e., preceding the first preovulatory surge of gonadotropins, and rebounded at the time of the surge. Functional EGFR protein levels, detected by the ability of the receptor to autophosphorylate in response to ligand or divalent antibody-induced activation, changed in a similar manner at the time of puberty. No such changes were observed in the cerebellum, a brain region irrelevant to neuroendocrine reproductive control. These results demonstrate the existence of EGF receptors in the prepubertal female rat hypothalamus and suggest that changes in EGFR gene expression and biologically active EGFR protein contributes to the neuroendocrine process underlying the first preovulatory surge of gonadotropins.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Expression of epidermal growth factor receptor changes in the hypothalamus during the onset of female puberty. 808 23

In several species, including humans, circulating insulin-like growth factor I (IGF-I) levels increase during the onset of puberty, suggesting that this peptide contributes to attaining sexual maturity. Because IGF-I elicits LHRH release from the median eminence (ME) of immature female rats in vitro, we hypothesized that it may represent one of the peripheral signals suspected to link somatic development to the LHRH-releasing system at puberty. We now present evidence in support of this concept. Quantitation of IGF-I messenger RNA (mRNA) levels by ribonuclease protection assay revealed that expression of the IGF-I gene did not change in the medial basal hypothalamus or preoptic area of female rats during peripubertal development. In contrast, the contents of both IGF-Ia and IGF-Ib mRNA, the two alternatively spliced forms of the IGF-I gene, increased significantly in the liver during the early proestrous phase of puberty. This change was followed by an elevation in serum IGF-I levels during the late proestrous phase of puberty along with a concomitant increase is serum gonadotropin levels. The proestrous change in serum IGF-I levels was accompanied by a selective increase in IGF-I receptor (IGF-IR) mRNA in the ME. Small doses of IGF-I (2-200 ng), administered intraventricularly, effectively induced LH release in both juvenile and peripubertal female rats, an increase prevented by prior immunoneutralization of LHRH actions. Importantly, intraventricular injections of IGF-I (20 ng), administered twice daily in the afternoon to immature animals, significantly advanced puberty. Thus, these results suggest that IGF-I of peripheral origin contributes to the initiation of female puberty by stimulating LHRH release from the hypothalamus, an effect that appears to be amplified by the increased synthesis of IGF-I receptors in the ME during first proestrus.
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PMID:Insulin-like growth factor I of peripheral origin acts centrally to accelerate the initiation of female puberty. 875 38

Immature female rats (21 days of age) were chronically intraperitoneally treated with guanethidine or muscarinic agents. The effects on the timing of puberty and ovarian wet weight, protein and total RNA and DNA contents were studied. While guanethidine (20.0 mg/kg/day) was ineffective, trihexyphenidyl and especially propantheline (15.0 mg/kg/day) delayed vaginal opening (by 23%) and the first vaginal oestrus (by 28%), and lowered ovarian weight (by 37%) and other ovarian growth parameters. Carbachol (0.2 mg/kg/day) reversed the effects of propantheline. Thus, in contrast to the adrenergic system, the cholinergic system appears to substantially contribute to the accurate onset of female puberty and ovarian growth in the rat.
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PMID:Involvement of muscarinic receptors in the control of female puberty in the rat. 885 Nov 72

The sense of shame seems to vanish for more than a decade now, manifested e.g. by an increasing tolerance toward the naked female body. However, it is supposed that shame has still its significance especially during female puberty. Psychological considerations referring to shame and to the puberty of girls are reported and the significance of feeling ashamed in this salient segment of female development is delineated. Finally a concept is proposed within which the feeling of shame is understood as a possibility to create accordance between the positive aspects of being ashamed and the tendency of going beyond the borders of shame usually guaranteed by social rules.
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PMID:[Disappearance of shame and puberty in girls]. 915 94

Concentrations of LH and FSH are known to increase during normal pubertal development, but changes in the isoforms of the gonadotropins at this time have not been investigated in depth. We examined the median charge of serum LH and FSH using agarose suspension electrophoresis in 81 normal children at pubertal stages I-V. In pubertal girls there were no significant (P > 0.05) differences in the median charge of LH, but there was a small (P = 0.05) shift to more acidic FSH isoforms between pubertal stages I and IV. In boys there was a significant (P < 0.01) shift to more acidic isoforms for both LH and FSH by pubertal stage II. Further changes were not found later in puberty. Except for LH at pubertal stage I, where the median charge was similar (P > 0.05) for both sexes, the median charge was more basic (P < 0.001) for both LH and FSH in girls compared with boys at all five pubertal stages. The degree of charge heterogeneity of FSH, estimated as the peak width at half the peak height, was significantly (P < 0.01) larger at pubertal stage I than at pubertal stages III-V in both boys and girls. The charge heterogeneity of LH was similar for all pubertal stages in both sexes. In conclusion, there were few qualitative changes in the gonadotropins during normal female puberty, whereas in the male there was a dramatic shift to more acidic isoforms of LH and FSH early in puberty. This information may assist our understanding of normal and pathological processes during puberty and may be of clinical relevance in detecting the initiation of puberty in boys.
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PMID:Changes in the isoforms of luteinizing hormone and follicle-stimulating hormone during puberty in normal children. 928 52


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