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

In the following, the authors examine the relationship between hormonal climate and the female voice through discussion of hormonal biochemistry and physiology and informal reporting on a study of 197 women with either premenstrual or menopausal voice syndrome. These facts are placed in a larger historical and cultural context, which is inextricably bound to the understanding of the female voice. The female voice evolves from childhood to menopause, under the varied influences of estrogens, progesterone, and testosterone. These hormones are the dominant factor in determining voice changes throughout life. For example, a woman's voice always develops masculine characteristics after an injection of testosterone. Such a change is irreversible. Conversely, male castrati had feminine voices because they lacked the physiologic changes associated with testosterone. The vocal instrument is comprised of the vibratory body, the respiratory power source and the oropharyngeal resonating chambers. Voice is characterized by its intensity, frequency, and harmonics. The harmonics are hormonally dependent. This is illustrated by the changes that occur during male and female puberty: In the female, the impact of estrogens at puberty, in concert with progesterone, produces the characteristics of the female voice, with a fundamental frequency one third lower than that of a child. In the male, androgens released at puberty are responsible for the male vocal frequency, an octave lower than that of a child. Premenstrual vocal syndrome is characterized by vocal fatigue, decreased range, a loss of power and loss of certain harmonics. The syndrome usually starts some 4-5 days before menstruation in some 33% of women. Vocal professionals are particularly affected. Dynamic vocal exploration by televideoendoscopy shows congestion, microvarices, edema of the posterior third of the vocal folds and a loss of its vibratory amplitude. The authors studied 97 premenstrual women who were prescribed a treatment of multivitamins, venous tone stimulants (phlebotonics), and anti-edematous drugs. We obtained symptomatic improvement in 84 patients. The menopausal vocal syndrome is characterized by lowered vocal intensity, vocal fatigue, a decreased range with loss of the high tones and a loss of vocal quality. In a study of 100 menopausal women, 17 presented with a menopausal vocal syndrome. To rehabilitate their voices, and thus their professional lives, patients were prescribed hormone replacement therapy and multi-vitamins. All 97 women showed signs of vocal muscle atrophy, reduction in the thickness of the mucosa and reduced mobility in the cricoarytenoid joint. Multi-factorial therapy (hormone replacement therapy and multi-vitamins) has to be individually adjusted to each case depending on body type, vocal needs, and other factors.
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PMID:Sex hormones and the female voice. 1049 59

Activation of LH-releasing hormone (LHRH) secretion, essential for the initiation of puberty, is brought about by the interaction of neurotransmitters and astroglia-derived substances. One of these substances, transforming growth factor alpha (TGFalpha), has been implicated as a facilitatory component of the glia-to-neuron signaling process controlling the onset of female puberty in rodents and nonhuman primates. Hypothalamic hamartomas (HH) are tumors frequently associated with precocious puberty in humans. The detection of LHRH-containing neurons in some hamartomas has led to the concept that hamartomas advance puberty because they contain an ectopic LHRH pulse generator. Examination of two HH associated with female sexual precocity revealed that neither tumor had LHRH neurons, but both contained astroglial cells expressing TGFalpha and its receptor. Thus, some HH may induce precocious puberty, not by secreting LHRH, but via the production of trophic factors--such as TGFalpha--able to activate the normal LHRH neuronal network in the patient's hypothalamus.
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PMID:Some hypothalamic hamartomas contain transforming growth factor alpha, a puberty-inducing growth factor, but not luteinizing hormone-releasing hormone neurons. 1059 38

To investigate hormonal changes before the onset of female puberty, we measured LH and FSH in serum samples drawn every 20 min for 24 h and measured testosterone and estradiol hourly for 24 h. Seventeen girls (13 prepubertal and 4 early pubertal) of short stature, from 5.1-11.4 yr of age, participated in this study. LH and FSH were measured using a time-resolved immunofluorometric assay, and testosterone and estradiol were measured using a sensitivity RIA capable of detecting testosterone and estradiol concentrations of 10 and 2 pg/mL, respectively. Diurnal rhythms of LH, FSH, and testosterone were apparent in all subjects, including those aged 5-6 yr. Serum LH and FSH concentrations showed night-day variation in a pulsatile fashion. The serum testosterone concentration was elevated in the early morning in all subjects. The serum estradiol concentration was elevated in the early morning in 4 of 13 prepubertal subjects and all 4 early pubertal subjects. The diurnal pattern of the serum estradiol concentration was similar to that of the serum testosterone concentration. Mean 24-h LH and testosterone concentrations in prepubertal subjects who did not attain puberty for at least 1 yr were 0.07 U/L and 65 pg/mL, respectively, whereas those in prepubertal subjects who attained puberty within 1 yr (0.14 U/L and 106 pg/mL, respectively) were significantly higher. Furthermore, mean 24-h LH, FSH, testosterone, and estradiol concentrations increased with the onset of puberty. In conclusion, the diurnal rhythms of LH, FSH, and testosterone already exist at 5-6 yr of age, and serum LH and testosterone levels increase before the onset of puberty. These results suggest that preparation for the onset of female puberty may begin in 5- to 6-yr-old girls.
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PMID:Diurnal rhythms of luteinizing hormone, follicle-stimulating hormone, testosterone, and estradiol secretion before the onset of female puberty in short children. 1072 42

Transforming growth factor alpha (TGFalpha) is a member of the epidermal growth factor (EGF) family with which it shares the same receptor, the EGF receptor (EGFR or erbB1). Identified since 1985 in the central nervous system (CNS), its functions in this organ have started to be determined during the past decade although numerous questions remain unanswered. TGFalpha is widely distributed in the nervous system, both glial and neuronal cells contributing to its synthesis. Although astrocytes appear as its main targets, mediating in part TGFalpha effects on different neuronal populations, results from different studies have raised the possibility for a direct action of this growth factor on neurons. A large array of experimental data have thus pointed to TGFalpha as a multifunctional factor in the CNS. This review is an attempt to present, in a comprehensive manner, the very diverse works performed in vitro and in vivo which have provided evidences for (i) an intervention of TGFalpha in the control of developmental events such as neural progenitors proliferation/cell fate choice, neuronal survival/differentiation, and neuronal control of female puberty onset, (ii) its role as a potent regulator of astroglial metabolism including astrocytic reactivity, (iii) its neuroprotective potential, and (iv) its participation to neuropathological processes as exemplified by astroglial neoplasia. In addition, informations regarding the complex modes of TGFalpha action at the molecular level are provided, and its place within the large EGF family is precised with regard to the potential interactions and substitutions which may take place between TGFalpha and its kindred.
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PMID:What role(s) for TGFalpha in the central nervous system? 1086 79

Current investigations of bone development mostly focus on bone mass, but bone strength may be functionally more important than mass. Therefore, we compared the developmental changes in cortical bone mass (BMCcort) and parameters of cortical bone strength [polar moment of inertia, section modulus, and strength strain index (SSI)]. Analyses were performed at the 65% site of the proximal radius using peripheral quantitative computed tomography. The study population comprised 469 healthy subjects, 6-40 yr of age (273 females). Both in prepubertal children (pubertal stage 1) and after puberty (pubertal stage 5 and adults) all studied parameters were significantly higher in males. During puberty (pubertal stages 2-4) the gender-specific differences were generally somewhat smaller. All of the measured parameters increased significantly with age and pubertal stage. However, although the percent increase in BMCcort between the youngest children and adults was similar between the genders, the increases in polar moment of inertia, section modulus, and SSI were higher in males. The ratio between section modulus and BMCcort was consistently higher in males after the age of 11 yr and after pubertal stage 2. Similar results were found for ratios between polar moment of inertia or SSI and BMCcort. These results show that for a given bone mass, males have stronger bones than females after pubertal stage 2. This reflects the fact that in puberty males add bone mostly on the periosteal surface, where the effect on bone strength is highest, whereas females add bone on the endocortical surface, which has a small effect on bone stability. The purpose of the mechanically inefficient endocortical apposition in female puberty might be to create a reservoir of calcium for future pregnancy and lactation.
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PMID:The development of bone strength at the proximal radius during childhood and adolescence. 1115 18

Inhibin is a gonadal hormone that inhibits the release of follicle stimulating hormone (FSH) from the anterior pituitary gland. The objective of this study was to determine whether active immunization of male and female rats against inhibin rich, steroid-free bovine follicular fluid would increase inhibin antibody titre, onset of female puberty, pregnancy rate, litter size, testis weights, testosterone concentration and serum FSH. Immunization of rats with steroid free bovine follicular fluid stimulated production of anti-inhibin antibodies that immunoneutralized endogenous inhibins and increased levels of circulating FSH in immunized males. Inhibin immunoneutralization resulted in early vaginal opening in immunized females compared with controls and pregnancy rates were increased when immunized female rats were mated with immunized males. However, serum testosterone, testis weights and potential litter size remained unchanged. We conclude that methods to immunoneutralize inhibin may have merit as therapeutic procedures to enhance reproductive performance in domestic animals.
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PMID:Fertility in rats immunized with steroid-free bovine follicular fluid. 1120 93

Leri-Weill dyschondrosteosis (LWD) (MIM 127300) is a dominantly inherited skeletal dysplasia characterized phenotypically by Madelung wrist deformity, mesomelia, and short stature. LWD can now be defined genetically by haploinsufficiency of the SHOX (short stature homeobox-containing) gene. We have studied 21 LWD families (43 affected LWD subjects, including 32 females and 11 males, ages 3-56 yr) with confirmed SHOX abnormalities. We investigated the relationship between SHOX mutations, height deficit, and Madelung deformity to determine the contribution of SHOX haploinsufficiency to the LWD and Turner syndrome (TS) phenotypes. Also, we examined the effects of age, gender, and female puberty (estrogen) on the LWD phenotype. SHOX deletions were present in affected individuals from 17 families (81%), and point mutations were detected in 4 families (19%). In the LWD subjects, height deficits ranged from -4.6 to +0.6 SD (mean +/- SD = -2.2 +/- 1.0). There were no statistically significant effects of age, gender, pubertal status, or parental origin of SHOX mutations on height z-score. The height deficit in LWD is approximately two thirds that of TS. Madelung deformity was present in 74% of LWD children and adults and was more frequent and severe in females than males. The prevalence of the Madelung deformity was higher in the LWD vs. a TS population. The prevalence of increased carrying angle, high arched palate, and scoliosis was similar in the two populations. In conclusion, SHOX deletions or mutations accounted for all of our LWD cases. SHOX haploinsufficiency accounts for most, but not all, of the TS height deficit. The LWD phenotype shows some gender- and age-related differences.
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PMID:Phenotypes Associated with SHOX Deficiency. 1193 48

Activation of the ErbB-1 receptor is necessary for initiating mammalian female puberty by stimulating the release of LH-releasing hormone. It remains unclear whether ErbB-1 is also required in governing reproduction during adulthood and whether altered ErbB-1 signaling is linked to changes in gonadotropin secretion in aging females. The present study examined these issues. RT-PCR was employed to determine changes in ErbB-1 mRNA levels during proestrus in both young adult (YA) and middle-aged (MA) female rats. Before the LH surge, expression levels in the preoptic area of YA rats increased to a maximal value. No such increase in ErbB-1 mRNA was found in MA rats. This difference was confirmed by the analysis of in situ hybridization histochemistry, where a stronger mRNA signal was observed in the preoptic area of YA rats compared with MA females. ErbB-1 protein levels measured by Western blot reflected this difference. A peak level of ErbB-1 mRNA in the median eminence-arcuate nucleus was detected at 0800 h in YA rats, but it was delayed in MA animals. There were intense ErbB-1 mRNA-positive cells in the arcuate nucleus. Pharmacological blockade of ErbB-1 receptor-mediated signal transduction resulted in the disruption of estrous cyclicity in YA rats. These results indicate that ErbB-1 receptors are necessary for maintaining normal estrous cycles. Consequently, age-related alterations in hypothalamic ErbB-1 gene activity may contribute to a delayed preovulatory LH secretion in aging females. Thus, the ErbB-1 signaling system plays an important role in the control of female reproduction during adulthood.
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PMID:Altered gene activity of epidermal growth factor receptor (ErbB-1) in the hypothalamus of aging female rat is linked to abnormal estrous cycles. 1179 13

Inhibin is a heterodimeric glycoprotein that consists of an alpha-subunit linked to either a betaA subunit (inhibin A) or to a betaB subunit (inhibin B) and it exists in at least six different isoforms. These isoforms can not be measured separately by immunoassays. In boys, serum inhibin B levels change in concert with the increase in gonadotrophins. Associated with the postnatal activation of gonadotrophin secretion, the early inhibin B secretion is sustained until the age of 18-24 months; thereafter serum concentrations subside. In boys, between Tanner stages G1 and G2, serum inhibin B concentration again increases, but then plateaus. Inhibin A levels in human males are below the detection limit, but in girls, during the postnatal activation of gonadotrophin secretion, both serum inhibin A and inhibin B concentrations are measurable. Serum inhibin B levels correlate positively with age several years before the clinical onset of puberty, suggesting increasing follicular activity in late prepuberty. During female puberty, the inhibin B level increases from Tanner stage B1 through stage B3, suggesting high follicular activity before the development of ovulatory menstrual cycles, but serum inhibin A levels become measurable later in puberty, in agreement with the idea that inhibin A is mainly produced by the corpus luteum.
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PMID:Inhibins in childhood and puberty. 1198 97

The mixture of the sexual steroids: estradiol (E2) and dihydrotestosterone (DHT) was injected to the female rats at prepuberty. This hormonal combination has been established to accelerate the different stages of the female rats' puberty--the vaginal opening and first ovulation. The puberty was accompanied with an increase in the estrogen level in the blood and a reduce of the relation between testosterone and E2. The stimulating effect of the hormonal combination on the ovarian folliculogenesis was observed and post-ovulatory corpus luteum were found in the experimental rats. We suggest that DHT blocked overripening the ovarian follicles at estrogenizating, and E2 reduces the negative effect of DHT on the hypophysis. The steroid combination (E2 + DHT) is effective for stimulating female puberty.
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PMID:[Hormonal stimulation of female sexual maturation]. 1212 86


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