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Relevant bibliographies by topics / Precocious puberty

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Academic literature on the topic 'Precocious puberty'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 March 2023

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Journal articles on the topic "Precocious puberty"

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Begum, Poly, Dipti Rani Saha, and Md Kamrul Hassan. "Precocious Puberty A Case Report." Bangladesh Journal of Obstetrics & Gynaecology 30, no. 2 (December 30, 2016): 109–12. http://dx.doi.org/10.3329/bjog.v30i2.30906.

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The parents of a 04-year-old girl bring her to a Gynaecologist because of breast development, appearance of pubic hair and periodic per vaginal bleeding. Her medical history is unremarkable. The parents are of average height, and the mother reports first menstruating when she was 11 years old. At physical examination, the girl is 100 cm tall , weighs 17 kg, and has a bodymass index of 17. Her pubertal development is classified as Tanner stage 3 breast development and Tanner stage 2 pubic hair development. She was diagnosed as a case of precocious puberity. Appearance of secondary sexual development before the age of 9 in a male child and before the age of 8 in a female child is called precocious puberty. When the cause of precocious puberty is premature activation of the hypothalamic-pituitary axis, it is called central or complete precocious puberty and she was a case of central precocious puberty. After proper consult she was treated by GnRHa suppressor of pituitary till 11 years of age.Bangladesh J Obstet Gynaecol, 2015; Vol. 30(2) : 109-112

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Sultana, Nusrat, Faria Afsana, Nazma Akhtar, Yasmin Aktar, Mohammad Feroz Amin, Sharmin Chowdhury, Shah Md Emran, et al. "Precocious puberty: diagnosis and management." BIRDEM Medical Journal 12, no. 1 (December 30, 2021): 62–69. http://dx.doi.org/10.3329/birdem.v12i1.57228.

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Precocious puberty is commonly defined as puberty that starts before age 8 years in girls and 9 years in boys. The causes of it may range from a variant of normal development to various pathologic conditions. The etiology of precocious puberty is classified by the underlying pathogenesis into gonadotropin dependent central precocious puberty and peripheral precocious puberty which is independent of gonadotropin but due to different other causes. Variants of precocious puberty include premature thelarche, premature puberche and isolated premature menarche which imply onset of isolated changes without any other signs of sexual development. Precocious puberty might have an impact on final stature owing to premature epiphyseal fusion and also it has got influence on psychosocial wellbeing. Evaluation includes a detailed history, physical examination, biochemical testing and imaging directed towards suspected etiology. Gonadotropin releasing hormone (GnRH) analogues are effective for treatment of central precocious puberty. Treatment of peripheral precocious puberty should be based on the specific cause. Pubertal variants are usually non-progressive and need no treatment but should be monitored carefully. BIRDEM Med J 2022; 12(1): 62-69

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P., Pallavee, and Rupal Samal. "Precocious puberty: a clinical review." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 7, no. 3 (February 27, 2018): 771. http://dx.doi.org/10.18203/2320-1770.ijrcog20180853.

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Precocious puberty is defined as pubertal development occurring more than 2.5 standard deviations earlier than the average age. It may comprise of central or gonadotropin-dependent precocious puberty and peripheral or gonadotropin-independent precocious puberty. Variants of precocious puberty include premature thelarche, premature pubarche and isolated premature menarche which principally implies onset of menstruation without any other signs of sexual development. Precocious puberty may have long-term consequences including short stature later on in adulthood owing to premature epiphyseal fusion as also psychosocial problems. Evaluation includes a detailed history, physical examination, biochemical tests and imaging directed towards detecting the cause. Gonadotropin Releasing Hormone (GnRH) analogues are effective for treatment of central precocious puberty. Treatment of peripheral precocious puberty should be based on the cause. Isolated variants are usually normal but should be closely monitored. Multi-speciality consultation with involvement of pediatricians and enocrinologists may improve treatment outcomes in these children, who otherwise pose significant challenges to the gynaecologist.

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Muir, Andrew. "Precocious Puberty." Pediatrics in Review 27, no. 10 (September 29, 2006): 373–81. http://dx.doi.org/10.1542/pir.27-10-373.

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Long, D. "Precocious Puberty." Pediatrics in Review 36, no. 7 (July 1, 2015): 319–21. http://dx.doi.org/10.1542/pir.36-7-319.

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Pescovitz, O. H. "Precocious Puberty." Pediatrics in Review 11, no. 8 (February 1, 1990): 229–37. http://dx.doi.org/10.1542/pir.11-8-229.

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Root, A. W. "Precocious Puberty." Pediatrics in Review 21, no. 1 (January 1, 2000): 10–19. http://dx.doi.org/10.1542/pir.21-1-10.

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Finlay, Fiona, and Rosemary Jones. "Precocious Puberty." Pediatrics 106, no. 1 (July 1, 2000): 162.3–163. http://dx.doi.org/10.1542/peds.106.1.162-b.

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Root, Allen W. "Precocious Puberty." Pediatrics In Review 21, no. 1 (January 1, 2000): 10–19. http://dx.doi.org/10.1542/pir.21.1.10.

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Pescovitz, Ora Hirsch. "Precocious Puberty." Pediatrics In Review 11, no. 8 (February 1, 1990): 229–37. http://dx.doi.org/10.1542/pir.11.8.229.

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The child with premature sexual development requires a thorough history, physical, and appropriate laboratory evaluation. The physician and other medical staff should remain sensitive to the family's concerns and the child's emotional adaptation. Counseling and open discussion of the psychosocial and sexual issues may greatly assist both the child and family. Making the correct diagnosis is critical to the selection of the appropriate form of therapy. Fortunately, in most cases in which therapy is warranted, it is extremely effective. In the remaining conditions, promising new forms of therapy are being investigated.

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Dissertations / Theses on the topic "Precocious puberty"

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Maquivar, Martin G. "Nutritional Regulation of Precocious Puberty in Heifers." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1322586535.

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Gasser, Chad Lamar. "Ovarian and endocrine dynamics associated with sexual maturation in beef heifers and the influence of diet, weaning age, and other factors during early reproductive development." Connect to this title online, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1122295880.

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Thesis (Ph. D.)--Ohio State University, 2005.
Title from first page of PDF file. Document formatted into pages; contains xvii, 181 p. : ill. Includes bibliographical references (p. 159-181). Available online via OhioLINK's ETD Center

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Gasser, Chad L. "Ovarian and endocrine dynamics associated with sexual maturation in beef heifers and the influence of diet, weaning age, and other factors during early reproductive development." The Ohio State University, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=osu1122295880.

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Hai, Lan. "EFFECT OF CONSTITUTIVELY ACTIVATED LUTEINIZING HORMONE RECEPTOR ON THE MOUSE REPRODUCTIVE SYSTEM." OpenSIUC, 2016. https://opensiuc.lib.siu.edu/dissertations/1208.

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AN ABSTRACT OF THE DISSERTATION OF LAN HAI, for the Doctor of Philosophy degree in Molecular Cellular and Systemic Physiology, presented on 11th December, 2015 at Southern Illinois University Carbondale. TITLE: EFFECT OF CONSTITUTIVELY ACTIVATED LUTEINIZING HORMONE RECEPTOR ON THE MOUSE REPRODUCTIVE SYSTEM MAJOR PROFESSOR: Dr. Prema Narayan The luteinizing hormone/chorionic gonadotropin receptor (LHCGR) is crucial for fertility, and genetic mutations in LHCGR cause adverse effects in reproductive development. Among the activating mutations identified in LHCGR, replacement of aspartic acid 578 by glycine (D578G) is the most common inherited mutation. Boys with this mutation undergo puberty by 2-4 years, caused by elevated testosterone in the context of prepubertal luteinizing hormone levels and present with Leydig cell hyperplasia. Clinically, these symptoms are associated with familial male-limited precocious puberty (FMPP). Our lab has published a mouse model for FMPP (KiLHRD582G) with D582G mutation equivalent to D578G in human LHCGR. We have previously demonstrated that KiLHRD582G male mice exhibited precocious puberty, Leydig cell hyperplasia and elevated testosterone and was a good model for FMPP. However, unlike women with the D578G mutation who show no abnormal phenotype, our studies revealed that female KiLHRD582G mice were infertile. KiLHRD582G female mice exhibit precocious puberty and irregular estrous cyclicity. A temporal study from 2-24 weeks of age indicated elevated steroid levels and upregulation of steroidogenic acute regulatory protein as well as several steroidogenic enzyme genes. Ovaries of KiLHRD582G mice exhibited significant pathology with the development of large hemorrhagic cysts as early as 3 weeks of age, extensive stromal cell hyperplasia with luteinization, numerous atretic follicles and granulosa cell tumors. Anovulation could not be rescued by exogenous gonadotropins. The body weights of the KiLHRD582G mice was higher that wild type counterparts, but there were no differences in the body fat composition. Hyperandrogenism and polycystic ovary phenotype was not accompanied by impaired glucose tolerance. Blocking the androgen action and estrogen synthesis indicated that reproductive phenotype was primarily due to excess estradiol. These studies demonstrate that activating LHCGR mutations do not produce the same phenotype in humans and mice and clearly illustrates species differences in the expression and regulation of LHCGR in the ovary. As we use male KiLHRD582G mice as breeders, we observed that the KiLHRD582G mice became progressive infertile, and only 8% of KiLHRD582G were fertile at 6 months of age despite normal sperm production. The infertile KiLHRD582G males were not able to form copulatory plugs in WT females, and mating studies suggested that the KiLHRD582G males were not capable of mating and/or ejaculating. Sexual behavioral testing revealed that the infertile KiLHRD582G males were capable of mounting the receptive WT females but were unable to achieve ejaculation indicating a problem with erectile and/or ejaculatory function. To address the reason for the ejaculatory dysfunction, we performed histopathological analysis of the accessory glands and penis. Hematoxylin and eosin staining showed that the normal columnar epithelium was replaced by pseudostratified columnar epithelium in the ampulla and several aggregates of chondrocyte metaplasia were apparent in the penile body of KiLHRD582G male mice. A temporal study indicated the histopathological changes in ampulla and penile body initiated at 7-8 and 12 weeks of age, respectively. Immunohistochemistry indicated that the chondrocytes stained positive for collagen type II, SOX9 and androgen receptor in the nucleus and for LHCGR in the cytoplasm. Penile fibrosis is a major cause of erectile dysfunction and is characterized by an increased collagen/smooth muscle ratio. However, our Image J analysis, hydroxyproline assay and western blot showed that KiLHRD582G penile body exhibited reduced levels of smooth muscle actin but similar total collagen content compared to WT mice. Thus, penile fibrosis was not responsible for the progressive infertility of adult KiLHRD582G mice. We also observed Leydig cell adenoma and disruption of spermatogenesis at 1 year of age. Our results suggest FMPP patients may be susceptible to infertility and testicular tumors later in their life and a follow-up study of FMPP patients is recommended.

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Cavalcante, Celso Junior Wanderley. "Puberdade precoce central em crianÃas atendidas em serviÃo especializado de Fortaleza: caracterÃsticas epidemiolÃgicas e perspectivas em saÃde pÃblica." Universidade Federal do CearÃ, 2012. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=7911.

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IntroduÃÃo: A Puberdade Precoce (PP) Ã problema cada vez mais freqÃente em todo o mundo. CrianÃas em PP estÃo em risco de iniciaÃÃo sexual mais cedo, abuso sexual, baixa estatura na vida adulta, risco aumentado de obesidade, hiperinsulinemia e hipertensÃo arterial. O estudo trata da freqÃÃncia e condiÃÃes associadas Ã PP, visando propor medidas de SaÃde PÃblica para reduÃÃo deste problema e de suas possÃveis seqÃelas. MÃtodos: O estudo transversal, desenvolve abordagem analÃtica das crianÃas acometidas de PP, atendidas no ambulatÃrio de endocrinologia do Hospital UniversitÃrio Walter CantÃdio (HUWC) no perÃodo 1994 a 2010, contando com uma amostra de 342 crianÃas de 1 a 11 anos. As variÃveis analisadas incluÃram as caracterÃsticas biolÃgicas, sÃcioeconÃmicas, familiares e nutricionais. A anÃlise dos dados foi realizada atravÃs do programa SPSS,utilizando-se o teste do qui-quadrado para medir associaÃÃes, com o valor alfa de 5%. Resultados: Encontrou-se uma razÃo feminino: masculino de 37:1. As caracterÃsticas mais freqÃentes das crianÃas com PP foram: cor da pele parda, 64,1%; adotadas, 7,3%; sobrepeso e obesidade, 27,1 e 25,1%, respectivamente; inÃcio da puberdade abaixo dos 5 anos, 27,1%; altura dos pais abaixo da mÃdia populacional, 80%. CrianÃas com PP atendidas tardiamente pelo serviÃo especializado tenderam a apresentar mais cedo sinais da puberdade (p<0,001) e a pertencerem a famÃlias de menor renda (p<0,002). ConclusÃes: Encontraram-se elevadas proporÃÃes de crianÃas com PP que haviam sido adotadas e que apresentavam sobrepeso/obesidade, dois fatores de risco importantes na gÃnese do problema. O retardo na atenÃÃo especializada esteve associado ao aparecimento muito precoce dos sinais da puberdade e Ã baixa renda familiar, sugerindo a necessidade de aÃÃes de saÃde pÃblica que promovam a detecÃÃo e a atenÃÃo ao problema nas camadas mais pobres da populaÃÃo
Introduction: Precocious puberty (PP) is an increasingly common problem worldwide. PP children are at risk of early sexual initiation, sexual abuse, short stature in adult life, increased risk of obesity, hyperinsulinemia and hypertension. The study addresses the frequency and conditions associated with PP in order to propose measures to reduce this public health problem and its possible sequels. Methods: A cross-sectional study develops analytical approach to children affected by PP, who were given assistance at the clinic of Endocrinology, in the University Hospital Walter CantÃdio (HUWC) in the period from 1994 to 2010, with a sample of 342 children aged 1 to 11 years. The variables looked over included the biological, socio-economic, family and nutrition features. Data analysis was performed by using the SPSS program by means of the chi-square test to evaluate any association with the alpha value of 5%. Results: A ratio female-male of 37:1 was found. The most frequent features of children with PP were: dark skin, 64.1%; adopted, 7.3%; overweight and obesity, 27.1 and 25.1%, respectively; onset of puberty under 5 years, 27.1%; parental height below the average population, 80%. Children with late PP assistance by specialized service tended to show early signs of puberty (p <0.001) and belong to households with lower income (p <0.002). Conclusions: It was found a high proportion of children with PP which had been adopted and that had overweight/obesity, two important risk factors in the genesis of the problem. The delay in specialized care was associated with signs of very early onset of puberty and low household income, which suggests that public health actions are required to encourage detection and attention to the problem among the poorest strata of the population.

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Matsuzaki, Cezar Noboru. "Análise dos genes CYP1A1,CYP1B1 e CYP17 em meninas com puberdade precoce central." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5139/tde-18122013-153911/.

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INTRODUÇÃO: Os fatores genéticos que influenciam o início da puberdade precoce ainda não são totalmente conhecidos. Assim, investigar os mecanismos gênicos que estariam envolvidos na sua gênese é muito importante, pois, além de possibilitar o diagnóstico em fases iniciais, pode contribuir para o desenvolvimento de novas terapias, com melhora do prognóstico. Para alguns investigadores, o estradiol também seria um fator contribuinte no determinismo da puberdade. OBJETIVOS: Estudar três genes que codificam enzimas relacionadas à esteroidogênese (CYP1A1, CYP1B1 e CYP17) em meninas com puberdade precoce central. Avaliar a associação entre variações na sequência desses genes e a puberdade precoce central. MÉTODOS: Foram incluídas 177 pacientes, divididas em dois grupos: Grupo Controle - formado por 104 meninas sem puberdade precoce, acompanhadas no Setor de Ginecologia da Infância e da Adolescência da Divisão de Clínica Ginecológica do HC-FMUSP por outros diagnósticos; Grupo Caso - composto por 73 meninas com diagnóstico de puberdade precoce central, acompanhadas no mesmo setor. Foi avaliada a presença de mutação em genes envolvidos no metabolismo do estrogênio (CYP1A1, CYP1B1 e CYP17) pela técnica de RFLP (Restriction Fragment Length Polymorphism), utilizando DNA obtido a partir de sangue periférico. RESULTADOS: A distribuição dos genótipos de CYP1A1 MspI (p=0,86) e CYP17 (p=0,12) não apresentou diferença significante entre os grupos. Para o CYP1B1 Eco571, o genótipo mutado C/C foi mais frequente no Grupo Controle que no Grupo Caso (p=0,03). CONCLUSÃO: Nossos dados sugerem que a variação do gene CYP1B1 Eco571 poderia estar associada ao determinismo da puberdade
INTRODUCTION: The genetic factors influencing onset of precocious puberty are not as yet fully known. Therefore, it is very important to investigate the genetic mechanisms involved in its genesis, for the resulting knowledge would not only enable diagnosis in the early stages but also contribute to the development of new therapies for improvement in prognosis. According to some researchers, estradiol would also be a contributory factor in puberty timing. OBJECTIVES: To investigate three genes which codify enzymes associated with steroidogenesis (CYP1A1, CYP1B1, and CYP17) in girls with central precocious puberty by focusing on the association between the sequence variation of these genes and central precocious puberty. METHODS: A total of 177 patients was included and divided into two groups: Control Group with 104 girls without precocious puberty who were being treated for other diagnoses at the Sector of Gynecology of Childhood and Adolescence, Division of Gynecology Clinic, HC-FMUSP; Case Group with 73 girls diagnosed with central precocious puberty. Mutations in genes involved in estrogen metabolism (CYP1A1, CYP1B1, and CYP17) were assessed by the RFLP (restriction fragment length polymorphism) technique using DNA obtained from peripheral blood. RESULTS: No significant difference in the distribution of the CYP1A1 MspI (p=0.86) and CYP17 (p=0.12) genotypes was detected between the two study groups. As for CYP1B1 Eco571, the mutated C/C genotype was found to be more frequent in the Control Group than in the Case Group (p=0.03). CONCLUSION: Our data suggest the CYP1B1 Eco571 gene variation is associated with puberty timing

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Junqueira, Flávia Raquel Rosa. "Uso do análogo do GnRH para diagnóstico de puberdade precoce." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/17/17145/tde-21062008-112920/.

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Introdução - A puberdade precoce verdadeira ou dependente de GnRH apresenta importante morbidade: a baixa estatura, conseqüência da rápida progressão da idade óssea, além das seqüelas psico-emocionais do desenvolvimento sexual secundário precoce. Daí a importância da realização de um diagnóstico precoce e preciso, a fim de que a terapêutica adequada seja instituída o quanto antes. O uso do análogo do GnRH (aGnRH) em teste diagnóstico vem sendo utilizado com este objetivo. Neste estudo avaliou-se os valores de corte para o diagnóstico de puberdade precoce verdadeira, usando-se o teste do aGnRH. Material e métodos - Estudo prospectivo, com 44 meninas, com desenvolvimento dos caracteres sexuais secundários antes dos 8 anos de idade, atendidas no Ambulatório de Ginecologia Infanto-Puberal do Hospital das Clínicas da Faculdade de Medicina de Ribeirão Preto da Universidade de São Paulo. Realizou-se, em todos os casos, o teste do aGnRH, que consistiu na coleta de amostra sanguínea basal para dosagem de FSH e LH, seguida da aplicação subcutânea de 500µg de acetato de leuprolida (Lupron®). Novas amostras sanguíneas foram realizadas após 3 horas, para dosagem de FSH e LH, e após 24 horas da aplicação, para dosagem de estradiol Compararam-se os níveis de LH e FSH basais, de 3 horas e a relação LH/FSH obtida, além do estradiol de 24h, com a evolução clínica das pacientes. Este foi o padrão ouro utilizado para análise do teste, sendo que, após 6 meses, as pacientes foram divididas em 2 grupos: puberdade progressiva (puberdade precoce verdadeira) e não-progressiva. Para análise estatística, utilizou-se curvas ROC, estabelecendo-se sensibilidade, especificidade e melhor nível de corte para o diagnóstico de puberdade precoce verdadeira, para os diferentes critérios analisados. Além disso, avaliou-se a concordância entre os diversos tipos de análise do teste, através do coeficiente kappa. Resultados - O LH de 3 horas apresentou valor de corte > 4,5 mUI/mL, sensibilidade 59,1% e especificidade 86,4%, com área sobre a curva de 0,723. O valor de kappa foi de 0,45, com concordância de 0,73. O estradiol de 24 horas apresentou valor de corte > 40,6 pg/mL, sensibilidade 70% e especificidade 73,7%, com área sobre a curva de 0,703. O valor de kappa foi de 0,436, com concordância de 0,718. Dentre todos os critérios analisados, o melhor deles foi a relação LH/FSH de 3 horas, com valor de corte > 0,14, sensibilidade 72,7% e especificidade 77,3%, com área sobre a curva de 0,771. O valor de kappa foi de 0,5, com concordância de 0,75. Conclusões - Em nossa avaliação, a relação LH/FSH de 3 horas foi superior ao valor de LH de 3 horas ou estradiol de 24 horas, que haviam sidos os melhores critérios diagnósticos no trabalho pioneiro na utilização deste teste.
Introduction - True or GnRH-dependent precocious puberty involves important morbidity such as short stature due to the rapid progression of bone age, as well as psycho-emotional sequels of precocious secondary sexual development. Thus, it is important to make an early and precise diagnosis so that appropriate treatment can be instituted as early as possible. The GnRH analogue (aGnRH) in the diagnostic test has been used for this purpose. In the present study, the sensitivity and specificity of different laboratory criteria for the diagnosis of true precocious puberty were compared using the aGnRH test. Material and methods - This was a prospective study conducted on 44 girls with the development of secondary sexual traits before 8 years of age attended at the Childhood-Pubertal Gynecology Outpatient Clinic of the University Hospital, Faculty of Medicine of Ribeirão Preto, University of São Paulo. The aGnRH test was performed in all cases, consisting of collection of a basal blood sample for the determination of FSH and LH, followed by subcutaneous application of 500 µg leuprolide acetate (Lupron®). New blood samples were obtained after 3 hours, for the determination of FSH and LH, and after 24hours of application, for determination of estradiol. Basal LH and FSH levels and levels after 3 hours, the LH/FSH ratio obtained 3 hours after the administration of 500 µg Lupron®, and 24 hour estradiol levels were compared with the clinical course of the patients. This was the gold standard used for the analysis of the test and after 6 months the patients were divided into 2 groups: progressive puberty (true precocious puberty) and non-progressive puberty. ROC curves were used for statistical analysis, with the determination of the sensitivity, specificity and best cut-off value for the diagnosis of true precocious puberty of the different criteria analyzed. In addition, the agreement of the various types of test analysis was evaluated using the kappa coefficient. Results - Three hour LH presented a cut-off value of > 4.5 mIU/mL, 59.1% sensitivity and 86.4% specificity, with an area under the curve of 0.723. The kappa value was 0.45, with 0.73 agreement. Twenty-four hour estradiol presented a cut-off value of > 40.6 pg/mL, 70% sensitivity and 73.7% specificity, with an area under the curve of 0.703. The kappa value was 0.436, with 0.718 agreement. The best of all criteria used was the 3 hour LH/FSH ratio, with a cut-off value of > 0.14, 72.7% sensitivity and 77.3% specificity, with an area under the curve of 0.771. The kappa value was 0.5, with 0.75 agreement. Conclusions - In the present evaluation, the 3 hour LH/FSH ratio was superior to the 3 hour LH value and the 24 hour estradiol value, which had been the best diagnostic criteria in the pioneering study using this test.

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Paula, Junior Delcides Ferreira de. "Alterações dentofaciais em meninas com puberdade precoce." Universidade Federal de Goiás, 2016. http://repositorio.bc.ufg.br/tede/handle/tede/6822.

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The objective of this study was to evaluate the prevalence of malocclusion, the need for orthodontic treatment and dentofacial changes in girls with Precocious Puberty (PP). This work gave rise to two distinct studies and data analyzes including descriptive statistics, Pearson's correlation analysis, paired t-test and t-test for one sample: 1- the cross-sectional study included 39 girls (6 to 11 years old) with confirmed PP diagnosis. The Dental Aesthetic Index (DAI) and the Index of Orthodontic Treatment Need (IOTN) were used for malocclusion evaluation and need for orthodontic treatment. Cephalometric analyzes were performed for the diagnosis of facial growth abnormalities. There was a high prevalence (64.1%) of severe and very severe malocclusion (DAI grades 3 and 4) and 82.1% of cases requiring moderate to high treatment (IOTN grades 3 and 4). 2- the control case study included 39 girls (6 to 11 years old) with confirmed PP diagnosis (case group). In this group, dental panoramic and hand and wrist radiographs were made. The control group consisted in 78 panoramic radiographs of girls without PP, randomly selected. Each panoramic radiograph of the 39 from case group was compared with two radiographs from control group, that is, a ratio of 1: 2. The chronological chart of dental mineralization of Nicodemus was used to identify the dental age. A significant difference (p <0.001) was found between chronology and bone age. Dental age (mean = 117) was lower than bone age (mean = 123) in girls with PP, but higher than dental age (mean = 111.5) in the control group. There was a significant correlation between chronological age and dental age. It was concluded that PP can have an impact on the development of dentition and craniofacial growth, a relevant factor for the diagnosis and the choice of the best moment for orthopedic / orthodontic intervention in malocclusion.
O objetivo deste estudo foi avaliar a prevalência de maloclusão, necessidade de tratamento ortodôntico e alterações dentofaciais em meninas com Puberdade Precoce (PP). Este trabalho deu origem a dois estudos distintos e as análises dos dados incluíram estatística descritiva, análise de correlação de Pearson, teste t pareado e teste t para uma amostra: 1- o estudo transversal incluiu 39 meninas (6 a 11 anos) com diagnóstico confirmado de PP. O Dental Aesthetic Index (DAI) e o Index of Orthodontic Treatment Need (IOTN) foram utilizados para a avaliação da maloclusão e necessidade de tratamento ortodôntico. Análises cefalométricas foram realizadas para o diagnóstico de anormalidades do crescimento facial. Foi observada alta prevalência (64,1%) de maloclusão grave e muito grave (DAI graus 3 e 4) e 82,1% dos casos com necessidade de tratamento moderada a alta (IOTN graus 3 e 4). 2- o estudo caso controle incluiu 39 meninas (6 a 11 anos) com diagnóstico confirmado de PP (grupo caso). Foram feitas, nesse grupo, radiografias panorâmicas e de mão e punho. O grupo controle foi composto por 78 radiografias panorâmicas de meninas sem PP, selecionadas aleatoriamente. Cada radiografia panorâmica das 39 do grupo caso foi comparada com duas radiografias do grupo controle, ou seja, uma razão de 1:2. A tabela cronologica de mineralização dental de Nicodemo foi utilizada para identificação da idade dentária. Foi encontrada uma diferença significativa (p<0,001) entre a idade cronologia e óssea. A idade dentária (média=117) foi menor que a idade óssea (média=123) nas meninas com PP, mas foi maior que a idade dentária (média= 111,5) do grupo controle. Houve correlação significativa entre a idade cronológica e a idade dentária. Concluiu-se que a PP pode ter impacto sobre o desenvolvimento da dentição e crescimento craniofacial, fator relevante para o diagnóstico e escolha do melhor momento para a intervenção ortopédica/ortodôntica da maloclusão

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Barnes, Robert 1967. "Gonadotrophin-releasing hormone analogue treatment of idiopathic central precocious puberty presenting in girls after age five years : a multi-centre follow-up to final adult height." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=32753.

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Idiopathic central precocious puberty may compromise adult height. Gonadotrophin-releasing hormone analogues (GnRHa) suppress puberty and increase final height prediction, but their influence on final height is unclear, especially in girls with pubertal onset just below eight years of age, the traditional limit of normal.
At seven children's hospitals, we identified 53 treated and 24 untreated patients (24 and 7 to final height, respectively) whose pubertal onset was between ages 5--8 years. At baseline, bone age advancement and predicted adult height were similar in the two groups. In both groups, the predicted adult height slightly overestimated the final height. What role, if any, GnRHa therapy played in preventing a shorter adult height is uncertain in these borderline cases. The substantial intra- and inter-observer variability in bone age readings compromised the utility of the height prediction method.
The methodological challenges inherent to this study are identified and discussed.

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Pazolini, Marina Cunha Silva. "Avanços no diagnóstico genético da puberdade precoce central." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-23102018-094359/.

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Avanços recentes na etiologia da puberdade precoce foram obtidos a partir da análise do genoma por sequenciamento global. Mutações inativadoras do gene MKRN3 representam uma causa importante de puberdade precoce central (PPC) familial (33-46% dos casos). O objetivo do estudo foi a análise do DNA genômico de pacientes com PPC de origem familial ou esporádica sem mutações deletérias no gene MKRN3. Foram selecionados 68 indivíduos com PPC (37 com a forma familial e 31, aparentemente, esporádicos). O DNA genômico foi extraído do sangue periférico ou da saliva dos pacientes com PPC. A técnica de sequenciamento genômico em larga escala (ILLUMNA -Clonal Single Molecule Array Technology - CSMA) foi usada na busca de novos genes implicados com o desenvolvimento puberal prematuro em seis indivíduos, sendo três afetados e três não afetados, pertencentes a uma grande família brasileira com PPC (Família 1). Mutações em um gene candidato foram pesquisadas em 64 pacientes por sequenciamento automático direto (método de Sanger). Em um subgrupo de pacientes, foi realizada a técnica de MLPA com sondas customizadas na busca de deleções. Por sequenciamento genômico global, foi identificado um novo complexo rearranjo no gene DLK1, caracterizado por uma deleção de, aproximadamente, 14.000 pb na região 5\' não traduzida (5\'UTR), englobando o início do exon 1, associada a uma duplicação de uma região do intron 3 de 269 pb. O gene DLK1 está localizado no braço longo do cromossomo 14 (14q32.2) e sofre imprinting materno. Este lócus está associado à síndrome de Temple, uma doença complexa com múltiplas manifestações, incluindo puberdade precoce central em até 90% dos casos. Para investigar o efeito dessa deleção genômica, as concentrações séricas da proteína DLK1 pelo método ELISA foram medidas nas pacientes afetadas da Família 1. Valores indetectáveis de DLK1 foram encontrados nestas pacientes. O fenótipo das pacientes afetadas da Família 1 caracterizou-se por uma PPC típica, sem sinais sindrômicos (excluída a síndrome de Temple). Posteriormente, por meio do sequenciamento direto, duas novas mutações inativadoras no gene DLK1 foram identificadas (p.Val272Cysfs*14 e p.Pro160Leufs*50) em duas famílias (Famílias 2 e 3) com PPC ou história de menarca precoce. O estudo de segregação nas Famílias 1 e 2 confirmou o padrão de herança autossômico dominante com penetrância completa e transmissão exclusiva pelo alelo paterno. A média de idade de início da puberdade nas pacientes afetadas do sexo feminino foi de 5,4 anos. A técnica de MLPA com sondas customizadas para o gene DLK1 não encontrou outras deleções no subgrupo estudado. Em conclusão, foram identificadas três mutações inativadoras no gene DLK1 associadas à PPC familial de origem paterna. O DLK1 é o segundo gene imprintado associado a distúrbios puberais em humanos. Este achado sugere um papel dos genes imprintados no controle da puberdade. O mecanismo pelo qual esse gene afeta a puberdade ainda é desconhecido
Recent advances in the etiology of precocious puberty were obtained from the whole-genome sequencing analysis. Inactivating mutations of the MKRN3 gene represent a major cause of familial central precocious puberty (CPP) (33%- 46% of the cases). The objective of the study was to analyze the genomic DNA of patients with familial or sporadic CPP without deleterious mutations in the MKRN3 gene. Sixty-eight individuals with CPP (37 with familial form and 31 apparently sporadic cases) were selected. The genomic DNA was extracted from the peripheral blood or saliva of patients with CPP. We used the whole-genomic sequencing technique (ILLUMNA - Clonal Single Molecule Array Technology - CSMA) searching for a new candidate genes implicated in premature pubertal development in 6 individuals, 3 affected and 3 non-affected, belonging to a large Brazilian family with CPP (Family 1). Mutations in one candidate gene were investigated in 64 patients through automatic sequencing (Sanger\'s method). In a subgroup of patients, MLPA using synthetic MLPA probes was performed to search for deletions. A new complex rearrangement in the DLK1 gene characterized by a deletion of approximately 14.000pb in the 5\' untranslated (5\'UTR), encompassing the start of exon 1, associated with a duplication of a region of intron 3 of 269 bp was identified by whole-genomic sequencing. The DLK1 gene is located on the long arm of chromosome 14 (14q32.2) and it is maternally imprinted gene. This locus is associated with Temple syndrome, a complex disorder with multiple alterations, including central precocious puberty in up to 90% of cases. To investigate the effect of this genomic deletion, a serum measurement of DKL1 protein using ELISA method was performed in the affected patients from Family 1. Undetectable serum DLK1 levels were found in these patients. The phenotype of affected patients from Family 1 was characterized by a typical CPP, without syndromic signs (excluding Temple syndrome). Posteriorly, two new inactivating mutations in the gene DLK1 were identified (p.Val272Cysfs*14 and p.Pro160Leufs*50) through direct sequencing in two families (Families 2 and 3) with CPP or precocious menarche history. The segregation studies in Families 1 and 2 confirmed the pattern of dominant autosomal inheritance with complete penetrance and exclusive transmission by the paternal allele. The average age of puberty onset in the affected female patients was 5.4 years. The MLPA technique with synthetic MLPA probes for the DLK1 gene did not find other deletions in the studied subgroup. In conclusion, we identified 3 paternally inherited inactivating mutations in the DLK1 gene associated with familial CPP. The DLK1 is the second imprinted gene associated with pubertal disorders in humans. This finding suggests a role of the imprinted genes in puberty control. The mechanism through which this gene affects puberty is still unknown

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Books on the topic "Precocious puberty"

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Pescovitz, Ora H., and Emily C. Walvoord, eds. When Puberty is Precocious. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-499-5.

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National Institutes of Health (U.S.), ed. Facts about precocious puberty. [Bethesda, Md.?]: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, 1986.

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1941-, Grave Gilman D., and Cutler Gordon B, eds. Sexual precocity: Etiology, diagnosis, and management. New York: Raven Press, 1993.

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Steingraber, Sandra. The falling age of puberty in U.S. girls: What we know, what we need to know. [San Francisco, Calif.]: Breast Cancer Fund, 2007.

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Steingraber, Sandra. The falling age of puberty in U.S. girls: What we know, what we need to know. [San Francisco, Calif.]: Breast Cancer Fund, 2007.

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Steingraber, Sandra. The falling age of puberty in U.S. girls: What we know, what we need to know. [San Francisco, Calif.]: Breast Cancer Fund, 2007.

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Er tong xing zao shu 150 wen. Beijing: Jun shi yi xue ke xue chu ban she, 2010.

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Andrews, V. C. Scattered leaves. New York, NY: Pocket Books, 2007.

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Andrews, V. C. Scattered Leaves. London: Simon & Schuster, 2008.

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Guy, Arthyr A. Precocious Puberty in Provincetown. Authorhouse, 2001.

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Book chapters on the topic "Precocious puberty"

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Léger, Juliane, and Jean-Claude Carel. "Precocious Puberty." In Puberty, 137–54. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32122-6_10.

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Fudge, Elizabeth. "Precocious Puberty." In Endocrinology and Diabetes, 219–33. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8684-8_18.

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Zhu, Jia. "Precocious Puberty." In Endocrine Conditions in Pediatrics, 253–58. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-52215-5_43.

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Misra, Madhusmita, and Sally Radovick. "Precocious Puberty." In Pediatric Endocrinology, 589–615. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-73782-9_26.

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Bhansali, Anil, Anuradha Aggarwal, Girish Parthan, and Yashpal Gogate. "Precocious Puberty." In Clinical Rounds in Endocrinology, 171–210. New Delhi: Springer India, 2016. http://dx.doi.org/10.1007/978-81-322-2815-8_6.

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Kaplowitz, Paul B. "Precocious Puberty." In Practical Pediatric and Adolescent Gynecology, 87–90. Oxford, UK: Blackwell Publishing Ltd., 2013. http://dx.doi.org/10.1002/9781118538555.ch15.

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Lee, Peter A., and Christopher P. Houk. "Precocious Puberty." In Pediatric, Adolescent, & Young Adult Gynecology, 159–70. Oxford, UK: Wiley-Blackwell, 2009. http://dx.doi.org/10.1002/9781444311662.ch18.

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Al-Salem, Ahmed H. "Precocious Puberty." In Pediatric Gynecology, 23–42. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-49984-6_3.

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Klein, Jason, and Patricia M. Vuguin. "Precocious Puberty." In Abnormal Female Puberty, 23–45. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-27225-2_2.

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Baker, Marsha B., and Mitchell E. Geffner. "Precocious Puberty." In Management of Common Problems in Obstetrics and Gynecology, 384–88. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444323030.ch88.

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Conference papers on the topic "Precocious puberty"

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Tuteja, Geetanjali, S. Unmesh, S. Shree, and S. Rudra. "Juvenile granulosa cell tumor." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685332.

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The differential diagnosis for precocious puberty in a young female includes peripheral causes. This case report documents a rare cause of isosexual precocious puberty, a juvenile granulosa cell tumour of the ovary–and a brief literature review. A one year-old baby girl presented with mass abdomen, vaginal discharge and rapid onset of pubertal development. She underwent an exploratory laparotomy for tumour resection. Pathology reported a juvenile granulosa cell tumour of the ovary. Early stage granulosa cell tumor surgically treated has good prognosis. Adjuvant chemotherapy is not indicated in this setting.

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Tuteja, Geetanjali, S. Unmesh, S. Shree, and S. Rudra. "Juvenile granulosa cell tumor." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685322.

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The differential diagnosis for precocious puberty in a young female includes peripheral causes. This case report documents a rare cause of isosexual precocious puberty, a juvenile granulosa cell tumour of the ovary–and a brief literature review. A one year-old baby girl presented with mass abdomen, vaginal discharge and rapid onset of pubertal development. She underwent an exploratory laparotomy for tumour resection. Pathology reported a juvenile granulosa cell tumour of the ovary. Early stage granulosa cell tumor surgically treated has good prognosis. Adjuvant chemotherapy is not indicated in this setting.

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Routledge, LM, S. Morris, and B. Sakamudi. "G577(P) Precocious puberty in a five-year-old girl." In Royal College of Paediatrics and Child Health, Abstracts of the RCPCH Conference and exhibition, 13–15 May 2019, ICC, Birmingham, Paediatrics: pathways to a brighter future. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-rcpch.558.

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Ferreira Simões, Marina, Isabela Tambelli Pires Cardoso, Daniela Gomes Chicre Oliveira, Carlos Eduardo Garcez Teixeira, Simone Appenzeller, Gil Guerra Junior, and Lilian TL Costallat. "Precocious central puberty and systemic lupus erythematosus. Similar risk factors." In SBR 2021 Congresso Brasileiro de Reumatologia. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2021.1983.

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Minjie Zhang and Yong Xu. "Association of gene mutation with central precocious puberty: A meta-analysis." In 2011 International Conference on Remote Sensing, Environment and Transportation Engineering (RSETE). IEEE, 2011. http://dx.doi.org/10.1109/rsete.2011.5964030.

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Braovac, Duje, Filip Jadrijević-Cvrlje, Vesna Kušec, Hrvoje Jednačak, and Miroslav Dumić. "221 Precocious puberty caused by germ cell tumor of the central nervous system – case report." In 10th Europaediatrics Congress, Zagreb, Croatia, 7–9 October 2021. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2021. http://dx.doi.org/10.1136/archdischild-2021-europaediatrics.221.

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Lee, Ji Eun, Hye Young Ahn, and Hye Seon Choi. "A Study of Body Image, Self-esteem and Depression in Girls with Precocious Puberty and Normal Girls." In Healthcare and Nursing 2015. Science & Engineering Research Support soCiety, 2015. http://dx.doi.org/10.14257/astl.2015.116.05.

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VALADARES, Luciana Pinto, Renata Santarem de OLIVEIRA, Cibelle Bueno do Nascimento AVELAR, Anna Beatriz Gomes da SILVA, juliana forte MAZZEU, and Adriana Lofrano Alves PORTO. "Investigation of genomic copy number variations in patients with central precocious puberty and additional dysmorphisms or congenital malformations." In Anais do I Congresso Internacional de Farmacologia Molecular Aplicada. Recife, Brasil: Even3, 2019. http://dx.doi.org/10.29327/16216.1-2.

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Liang, Zhe-Hao, and Wei Lu. "Prediction of the basic gonadotrophic hormone levels in girls with precocious puberty using ultrasonic union artificial neural network." In 2011 Seventh International Conference on Natural Computation (ICNC). IEEE, 2011. http://dx.doi.org/10.1109/icnc.2011.6022283.

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Šepec, Marija Požgaj, Lavinia La Grasta Sabolić, Magdalena Avbelj Stefanija, Jernej Kovač, and Gordana Stipančić. "202 Central precocious puberty in dizygotic twin sisters caused by mutation in the makorin RING finger protein 3 gene." In 10th Europaediatrics Congress, Zagreb, Croatia, 7–9 October 2021. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2021. http://dx.doi.org/10.1136/archdischild-2021-europaediatrics.202.

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Reports on the topic "Precocious puberty"

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Xu, Dan, Xueying Zhou, Junfei Wang, Xi Cao, and Tao Liu. The Value of Urinary Gonadotropins in the Diagnosis of Central Precocious Puberty: A Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2021. http://dx.doi.org/10.37766/inplasy2021.12.0076.

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Review question / Objective: Precocious puberty is defined as the onset of secondary sexual characteristics before the age of 8 years in girls and 9 years in boys. It can be differentiated into central precocious puberty (CPP) and peripheral precocious puberty, and it is more common in girls than in boys. CPP may result in a decreased final adult height, an early age at menarche, and psychological and health problems in adulthood. Gonadotropin-releasing hormone (GnRH) GnRH stimulation test has been indispensable in the diagnosis of CPP. GnRH stimulation test is not only invasive, time-consuming and expensive, but also sometimes difficult to have patients cooperate. Nocturnal urinary LH and FSH can represent gonadotropin excretion in children with normal and early puberty. And urinary sample collection and evaluation are more convenient, more acceptable, cheaper, and noninvasive. This meta-analysis aims to assess the value of first-voided urinary luteinizing hormone (LH) and the ratio of urinary luteinizing hormone and follicle-stimulating hormone (FSH) in the diagnosis of female CPP and to compare the accuracy between urinary gonadotropins and serum GnRH-stimulated gonadotropins.

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Zhao, Xue, Zi Wei Hou, MingYue Wang, huishan Shi, and Xiaoxia Zhang. Efficacy of integrated traditional Chinese medicine and Western medicine in the treatment of female precocious puberty A protocol for systematic review and meta-analysis of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2022. http://dx.doi.org/10.37766/inplasy2022.10.0060.

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Yaron, Zvi, Martin P. Schreibman, Abigail Elizur, and Yonathan Zohar. Advancing Puberty in the Black Carp (Mylopharyngodon Piceus) and the Striped Bass (Morone Saxatilis). United States Department of Agriculture, August 1993. http://dx.doi.org/10.32747/1993.7568102.bard.

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The black carp (bc)GtH IIb cDNA was amplified and isolated, cloned and sequenced. Comparison of the bcGtH IIb deduced a.a. sequence with that of GtH IIb from other teleosts revealed high homology to cyprinid species and a lower homology to salmonid or perciform fish. The gene coding for the GtH IIb was isolated and sequenced. Three bc recombinant phages which hybridized to the goldfish GtH Ib cDNA probe were isolated and are currently being characterized. The region coding for the mature GtH IIb was expressed in a bacterial expression vector resulting in the production of a recombinant protein. In vitro folding resulted in a protein only 1.3% of which displaced the native common carp GtH II in a RIA. Therefore, the common carp GtH RIA was utilized for the physiological studies at the current phase of the project. Two non-functional sites were identified along the brain-pituitary gonadal axis in the immature black carp. The pituitary is refractory to GnRH stimulation due to a block proximal to the activation of PKA and PKC probably at the level of GnRH receptors. The gonads, although capable of producing steroids, are refractory to gonadotropic stimulation but do respond to cAMP antagonists, indicating a block at the GtH receptor level. Attempts to advance puberty in 2 and 3 y old black carp showed that testosterone (T) stimulates GtH synthesis in the pituitary and increases its sensitivity to GnRh. A 2 month treatment combining T+GnRH increased the circulating GFtH level in 3 y old fish. Addition of domperidone to such a treatment facilitated both the accumulation of GtH in the pituitary and its response to GnRH. The cDNA of striped bass GtH a, Ib and IIb subunits were amplified, isolated, cloned and sequenced, and their deduced a.a. sequences were compared with those of other teleosts. A ribonuclease protection assay was developed for a sensitive and simultaneous determination of all GtH subunits, and of b-actin mRNAs of the striped bass. GnRH stimulated dramatically the expression of the a and GtH IIb subunits but the level of GtH Ib mRNA increased only moderately. These findings suggest that GtH-II, considered in salmonids to be involved only in final stages of gametogenesis, can be induced by GnRH to a higher extent than GtH-I in juvenile striped bass. The native GtH II of the striped bass was isolated and purified, and an ELISA for its determination was developed. The production of all recombinant striped bass GtH subunits is in progress using the insect cell (Sf9) culture and the BAC-TO-BAC baculovirus expression system. A recombinant GtH IIb subunit has been produced already, and its similarity to the native subunit was confirmed. The yield of the recombinant glycoprotein can reach 3.5 mg/ml after 3 days culture. All male striped bass reach puberty after 3 y. However, precocious puberty was discovered in 1 and 2 y old males. Females become vitellogenic during their 4th year. In immature 2 y old females, T treatment elevates the pituitary GtH II content while GnRH only potentiates the effect. However, in males GnRH and not T affects GtH accumulation in the pituitary. Neither GnRH, nor T treatment resulted in gonadal growth in 2 y old striped bass, indicating that either the accumulated GtH II was not released, or if released, the gonads were refractory to GtH stimulation, similar to the situation in the immature black carp. In 3 y old female striped bass, 150 day GnRHa treatment resulted in an increase in GSI, while T treatment, with or without GnRHa, resulted in a decrease in oocyte diameter, similar to the effect seen in the black carp. Further attempts to advance puberty in both fish species should take into account the positive effect of T on pituitary GtH and its negative effect of ovarian growth.

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Yaron, Zvi, Abigail Elizur, Martin Schreibman, and Yonathan Zohar. Advancing Puberty in the Black Carp (Mylopharyngodon piceus) and the Striped Bass (Morone saxatilis). United States Department of Agriculture, January 2000. http://dx.doi.org/10.32747/2000.7695841.bard.

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Abstract:

Both the genes and cDNA sequences encoding the b-subunits of black carp LH and FSH were isolated, cloned and sequenced. Sequence analysis of the bcFSHb and LHb5'flanking regions revealed that the promoter region of both genes contains canonical TATA sequences, 30 bp and 17 bp upstream of the transcription start site of FSHb and LHb genes, respectively. In addition, they include several sequences of cis-acting motifs, required for inducible and tissue-specific transcriptional regulation: the gonadotropin-specific element (GSE), GnRH responsive element (GRE), half sites of estrogen and androgen response elements, cAMP response element, and AP1. Several methods have been employed by the Israeli team to purify the recombinant b subunits (EtOH precipitation, gel filtration and lentil lectin). While the final objective to produce pure recombinantGtH subunits has not yet been achieved, we have covered much ground towards this goal. The black carp ovary showed a gradual increase in both mass and oocyte diameter. First postvitellogenic oocytes were found in 5 yr old fish. At this age, the testes already contained spermatozoa. The circulating LH levels increased from 0.5 ng/ml in 4 yr old fish to >5ng/ml in 5 yr old fish. In vivo challenge experiments in black carp showed the initial LH response of the pituitary to GnRH in 4 yr old fish. The response was further augmented in 5 yr old fish. The increase in estradiol level in response to gonadotropic stimulation was first noted in 4 yr old fish but this response was much stronger in the following year. In vivo experiments on the FSHb and LHb mRNA levels in response to GnRH were carried out on common carp as a model for synchronom spawning cyprinids. These experiments showed the prevalence of FSHP in maturing fish while LHP mRNA was prevalent in mature fish, especially in females. The gonadal fat-pad was found to originate from the retroperitoneal mesoderm and not from the genital ridge, thus differing from that reported in certain amphibians This tissue possibly serves as the major source of sex steroids in the immature black carp. However, such a function is taken over by the developing gonads in 4 yr old fish. In the striped bass, we described the ontogeny of the neuro-endocrine parameters along the brain-pituitary-gonadal axis during the first four years of life, throughout gonadal development and the onset of puberty. We also described the responsiveness of the reproductive axis to long-term hormonal manipulations at various stages of gonadal development. Most males reached complete sexual maturity during the first year of life. Puberty was initiated during the third year of life in most females, but this first reproductive cycle did not lead to the acquisition of full sexual maturity. This finding indicates that more than one reproductive cycle may be required before adulthood is reached. Out of the three native GnRHs present in striped bass, only sbGnRH and cGnRH II increased concomitantly with the progress of gonadal development and the onset of puberty. This finding, together with data on GtH synthesis and release, suggests that while sbGnRH and cGnRH II may be involved in the regulation of puberty in striped bass, these neuropeptides are not limiting factors to the onset of puberty. Plasma LH levels remained low in all fish, suggesting that LH plays only a minor role in early gonadal development. This hypothesis was further supported by the finding that experimentally elevated plasma LH levels did not result in the induction of complete ovarian and testicular development. The acquisition of complete puberty in 4 yr old females was associated with a rise in the mRNA levels of all GtH subunit genes, including a 218-fold increase in the mRNA levels of bFSH. mRNA levels of the a and PLH subunits increased only 11- and 8-fold, respectively. Although data on plasma FSH levels are unavailable, the dramatic increase in bFSH mRNA suggests a pivotal role for this hormone in regulating the onset and completion of puberty in striped bass. The hormonal regulation of the onset of puberty and of GtH synthesis and release was studied by chronic administration of testosterone (T) and/or an analog of gonadotropin-releasing hormone (G). Sustained administration of T+G increased the mRNA levels of the PLH subunit to the values characteristic of sexually mature fish, and also increased the plasma levels of LH. However, these changes did not result in the acceleration of sexual maturation. The mRNA levels of the bFSH subunit were slightly stimulated, but remained about 1/10 of the values characteristic of sexually mature fish. It is concluded that the stimulation of FSH gene expression and release does not lead to the acceleration of sexual maturity, and that the failure to sufficiently stimulate the bFSH subunit gene expression may underlie the inability of the treatments to advance sexual maturity. Consequently, FSH is suggested to be the key hormone to the initiation and completion of puberty in striped bass. Future efforts to induce precocious puberty in striped bass should focus on understanding the regulation of FSH synthesis and release and on developing technologies to induce these processes. Definite formulation of hormonal manipulation to advance puberty in the striped bass and the black carp seems to be premature at this stage. However, the project has already yielded a great number of experimental tools of DNA technology, slow-release systems and endocrine information on the process of puberty. These systems and certain protocols have been already utilized successfully to advance maturation in other fish (e.g. grey mullet) and will form a base for further study on fish puberty.

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