876 resultados para Sexual hormones
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A disfunção sexual corresponde a alterações em uma ou mais fases da resposta sexual humana e apresenta maior prevalência na população feminina. Ademais, a participação de alguns fatores como obesidade e níveis dos hormônios esteroidais na disfunção sexual feminina (DSF) permanece incerta. O presente estudo deteve-se na análise da ocorrência de DSF numa população de mulheres portadoras de obesidade, cadastradas no Ambulatório de Cirurgia Bariátrica do Hospital Universitário Onofre Lopes, da Universidade Federal do Rio Grande do Norte, no município de Natal, RN. O estudo foi realizado em uma amostra composta por trinta e uma mulheres, com idade entre 20 e 50 anos, com índice de massa corpórea (IMC) > 30 Kg/m2. A todas as pacientes foi aplicado um questionário composto por uma seção com dados socio-econômicos, e outra abordando a saúde sexual feminina, sendo esta última correspondente ao Female Sexual Function Index (FSFI), para diagnóstico de DSF. A partir dessa caracterização, as pacientes foram reunidas nos grupos CD (pacientes com disfunção, n= 9) e SD (sem disfunção, n= 22). Para a análise do efeito da obesidade na DSF, as pacientes foram reunidas nos grupos 1 (6 pacientes com IMC grau I e II: entre 30 e 40 Kg/m2) e 2 (25 com IMC grau III: acima de 40). Para o estudo da participação dos hormônios esteroidais foram determinadas as concentrações séricas de cortisol, estradiol e dehidroepiandrosterona (DHEA) pelo método de quimiluminescência. A análise estatística dos dados foi realizada usando os testes ANOVA, MANOVA (Pillai), além de análise de Cluster. Para identificar as diferenças entre os domínios do FSFI, foi usado o teste T de Student. A significância considerada para todos os testes foi para p< 0,01. Das pacientes estudadas, 25,8% apresentaram DSF de acordo com o escore total do FSFI. A análise estatística posterior evidenciou que as diferenças ocorreram para os domínios desejo, excitação e orgasmo. Não foi encontrada relação da presença de DSF com os diferentes graus de obesidade ou com os níveis hormonais dos esteróides cortisol, estradiol ou DHEA. Contudo, foi encontrado aumento significativo nos níveis séricos de estradiol para o grupo 1, que corresponde ao de menor índice de IMC. Estes resultados mostram que a prevalência de DSF não diferiu entre os graus I,II e III de obesidade das pacientes deste estudo mas, quando presente, a disfunção ocorre nos domínios desejo, excitação e orgasmo. A maior concentração de estradiol encontrada nas pacientes de menor índice de IMC sugere uma possível relação entre as duas variáveis que precisa ser investigada em estudos futuros.
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The so-called endocrine disruptors have been described as compounds which interfere with the estrogen action in their receptors and may exert a crucial role in the development of the reproductive tract and in the brain sexual differentiation. Thus, conducts and/or exposure to these drugs in the perinatal period that apparently do not endanger the neonate may cause side effects. During embrionary development, the gonads, through discharge of a small quantity of reproductive hormones, will guarantee the phenotype of male or female at birth, as well as actuate in specific areas sexual differentiation of the central nervous system. Several experimental models have shown an interference of drugs acting as endocrine disruptors in hypothalamic sexual differentiation. Thus, reproductive function is impaired by exposure to estrogen in the perinatal life of rats and the mechanisms involved in this effect are distinct for males and females. Perinatal exposure to drugs which may be considered endocrine disrupters may induce an incomplete masculinization and defeminization of the central nervous system. Alterations in these processes, if present, generally are perceived only at puberty or adult reproductive life. These later alterations may include anomalies in the process of fertility or in sexual behavior.
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Pós-graduação em Ciências Biológicas (Biologia Celular e Molecular) - IBRC
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In Brazil, the increase in the reported cases of degenerative diseases of articular cartilage is 20% per year, meaning that 200,000 Brazilians develop degenerative joint diseases every year, which have a negative impact on bone mass. This study shows evidence that hormone production of sexual steroids (estrogens, progestogens, and androgens) have an influence on cartilage quality, as well as on bone mass. Therefore, this review aimed to analyze literature data on the molecular and genic action of sexual steroids on hyaline cartilage and bone physiology, as well as osteoarthritis interference on the quality of these structures.
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Introduction. Physical exercise including pelvic floor muscle (PFM) training seems to improve the sexual function of women with urinary incontinence. This effect in postmenopausal women who are continent has not yet been determined. Aim. The aim of this study was to assess the effect of a 3-month physical exercise protocol (PEP) on the sexual function and mood of postmenopausal women. Methods. Thirty-two sedentary, continent, sexually active women who had undergone menopause no more than 5 years earlier and who had follicle stimulating hormone levels of at least 40 mIU/mL were enrolled into this longitudinal study. All women had the ability to contract their PFMs, as assessed by vaginal bimanual palpation. Muscle strength was graded according to the Oxford Modified Grading Scale (OMGS). A PEP was performed under the guidance of a physiotherapist (M. M. F.) twice weekly for 3 months and at home three times per week. All women completed the Sexual Quotient-Female Version (SQ-F) and the Hospital Anxiety and Depression Scale (HADS) before and after the PEP. Main Outcome Measures. SQ-F to assess sexual function, HASDS to assess mood, and OMGS to grade pelvic floor muscle strength. Results. Thirty-two women (24 married women, eight women in consensual unions) completed the PEP. Following the PEP, there was a significant increase in OMGS score (2.59 +/- 1.24 vs. 3.40 +/- 1.32, P < 0.0001) and a significant decrease in the number of women suffering from anxiety (P < 0.01), but there was no effect on sexual function. Conclusion. Implementation of our PEP seemed to reduce anxiety and improve pelvic floor muscular strength in sedentary and continent postmenopausal women. However, our PEP did not improve sexual function. Uncontrolled variables, such as participation in a long-term relationship and menopause status, may have affected our results. We suggest that a randomized controlled trial be performed to confirm our results. Lara LAS, Montenegro ML, Franco MM, Abreu DCC, Rosa e Silva ACJS, Ferreira CHJ. Is the sexual satisfaction of postmenopausal women enhanced by physical exercise and pelvic floor muscle training? J Sex Med 2012; 9: 218-223.
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Human sexual determination is initiated by a cascade of genes that lead to the development of the fetal gonad. Whereas development of the female external genitalia does not require fetal ovarian hormones, male genital development requires the action of testicular testosterone and its more potent derivative dihydrotestosterone (DHT). The "classic" biosynthetic pathway from cholesterol to testosterone in the testis and the subsequent conversion of testosterone to DHT in genital skin is well established. Recently, an alternative pathway leading to DHT has been described in marsupials, but its potential importance to human development is unclear. AKR1C2 is an enzyme that participates in the alternative but not the classic pathway. Using a candidate gene approach, we identified AKR1C2 mutations with sex-limited recessive inheritance in four 46,XY individuals with disordered sexual development (DSD). Analysis of the inheritance of microsatellite markers excluded other candidate loci. Affected individuals had moderate to severe undervirilization at birth; when recreated by site-directed mutagenesis and expressed in bacteria, the mutant AKR1C2 had diminished but not absent catalytic activities. The 46,XY DSD individuals also carry a mutation causing aberrant splicing in AKR1C4, which encodes an enzyme with similar activity. This suggests a mode of inheritance where the severity of the developmental defect depends on the number of mutations in the two genes. An unrelated 46,XY DSD patient carried AKR1C2 mutations on both alleles, confirming the essential role of AKR1C2 and corroborating the hypothesis that both the classic and alternative pathways of testicular androgen biosynthesis are needed for normal human male sexual differentiation.
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Every year around 100 million male piglets are castrated in the EU, usually without anaesthesia or post-operative analgesia. This surgical intervention is painful and stressful. Several main players within the pig industry have voluntarily agreed to end the practice of surgical pig castration in the EU by 2018. One alternative to castration is entire male pig production. However, entire males behave differently than castrates, for example, by performing more mounting behaviour, which is suggested to be a welfare problem. The aim of our study was to develop a comprehensive ethogram of different types of mounting and to investigate properties, causes and consequences of mounting behaviour in finishing pigs. The study included 80 entire male and 80 female pigs from two farrowing batches born six weeks apart. Mixed sex and single-sex housing of pigs are both common in pig farming, so to ensure our study was representative, the 160 pigs were assigned to social groups of 20 in three treatments: entire male pigs only (MM, 2 groups, n = 40), entire females only (FF, 2 groups, n = 40) and entire males and females mixed together (MF, 4 groups, n = 80). Measurements took place during the final six weeks before slaughter (between 63.5 and 105.5 kg). Observations of mounting behaviour on 12 days per batch suggested that: (i) males mounted more than females, (ii) within sex, there was no effect of treatment on the amount of mounting (although the statistical power of the study to detect these effects was low), and (iii) there were individual differences in mounting that were stable over time (within sex). Classification of mounting into different categories revealed that sexual mounting was most common overall and in males but only rare in females. Compared to other types of mounting (e.g. caused by crowding or during a fight), sexual mounts lasted longer and provoked more screaming by the recipient. There were no relationships between mounting behaviour on the one hand and dominance rank in food competition tests, the circulating levels of sex hormones (oestradiol, testosterone and progesterone) at the end of the study, the health scores (lameness and scratches) or weight gain on the other hand. The stable individual differences of mounting over time suggest that mounting behaviour is a trait of the individual rather than the appearance of random outbreaks. However, these differences in mounting cannot be explained by dominance behaviour or by differences in sex hormone concentrations that could indicate the onset of puberty. Mounting behaviour and in particular sexual mounting provoked high pitched screaming of the recipients indicating that mounting is a welfare problem. For the welfare assessment of entire male pig production the performance of mounting behaviour should be considered. (C) 2013 Elsevier B.V. All rights reserved.
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Obesity has a complex, multi-factorial etiology. Infectious agents have recently emerged as a possible contributor to the current obesity epidemic. Seven viruses have demonstrated an association with obesity in animals; however, Adenovirus-36 (Ad-36) is the only known virus associated with obesity in humans. The primary aim of this research was to determine the association between Ad-36 infection and the expression of obesity related hormones in children. Additionally, this study proposed to compare the mean three year change in the level of obesity related hormones between Ad-36 positive and negative children. This study utilized pilot data collected from 98 children at baseline and year three of the Project Heartbeat! cohort. Fasting serum samples were analyzed for the concentration of adiponectin, insulin and leptin. The crude analysis uncovered Ad-36 positive children had significantly lower mean concentrations of insulin (p=0.039) and leptin (p=0.038) at baseline compared to Ad-36 negative children. The results of the adjusted analysis indicated the leptin association with Ad-36 infection at baseline was statistically significant even after controlling for age, sex, ethnicity, and BMI percentile. The longitudinal evaluation revealed individuals with a history of Ad-36 infection experienced a larger mean decrease in adiponectin, a larger mean increase in leptin, and a smaller mean increase in insulin levels over a three year period compared to individuals without a history of infection. These results suggest Ad-36 infection may produce changes in hormone expression. The only statistically significant findings in the crude and adjusted longitudinal analysis occurred at baseline when the children were younger, suggesting physical changes that occur during sexual maturation may mask or enhance Ad-36 induced changes in hormone expression. Furthermore, the longitudinal analysis revealed the duration and course of Ad-36 infection may influence changes in the expression of obesity-related hormones. Taken together, the results of this pilot study are suggestive of an association between Ad-36 infection and the expression of obesity-related hormones.^
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With assays of hormone-sensitive behaviors, it is possible to demonstrate both direct and indirect actions of genes on mammalian social behaviors. Direct effects of estrogen receptor gene expression and progesterone receptor gene expression figure prominently in well analyzed neuroendocrine mechanisms for sex behavior, operating through a neural circuit that has been delineated. Indirect effects, notably the consequences of sexual differentiation, display complex dependencies. In a human condition, Kallmann syndrome, the data show a clear, indirect genetic influence on an important human social behavior, in which damage at chromosome Xp-22.3 works through at least six discrete steps to affect libido. Altogether, simplistic extrapolations from lower animals, especially during brief summaries for nonscientists, do not appear justified as we discover and conceptualize genetic influences on mammalian brain and behavior.
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Whereas adult sex differences in brain morphology and behavior result from developmental exposure to steroid hormones, the mechanism by which steroids differentiate the brain is unknown. Studies to date have described subtle sex differences in levels of proteins and neurotransmitters during brain development, but these have lacked explanatory power for the profound sex differences induced by steroids. We report here a major divergence in the response to injection of the γ-aminobutyric acid type A (GABAA) agonist, muscimol, in newborn male and female rats. In females, muscimol treatment primarily decreased the phosphorylation of cAMP response element binding protein (CREB) within the hypothalamus and the CA1 region of the hippocampus. In contrast, muscimol increased the phosphorylation of CREB in males within these same brain regions. Within the arcuate nucleus, muscimol treatment increased the phosphorylation of CREB in both females and males. Thus, the response to GABA can be excitatory or inhibitory on signal-transduction pathways that alter CREB phosphorylation depending on the sex and the region in developing brain. This divergence in response to GABA allows for a previously unknown form of steroid-mediated neuronal plasticity and may be an initial step in establishing sexually dimorphic signal-transduction pathways in developing brain.
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Mode of access: Internet.
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Thesis (Ph.D.)--University of Washington, 2016-06
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Sex differences occur in most non-communicable diseases, including metabolic diseases, hypertension, cardiovascular disease, psychiatric and neurological disorders and cancer. In many cases, the susceptibility to these diseases begins early in development. The observed differences between the sexes may result from genetic and hormonal differences and from differences in responses to and interactions with environmental factors, including infection, diet, drugs and stress. The placenta plays a key role in fetal growth and development and, as such, affects the fetal programming underlying subsequent adult health and accounts, in part for the developmental origin of health and disease (DOHaD). There is accumulating evidence to demonstrate the sex-specific relationships between diverse environmental influences on placental functions and the risk of disease later in life. As one of the few tissues easily collectable in humans, this organ may therefore be seen as an ideal system for studying how male and female placenta sense nutritional and other stresses, such as endocrine disruptors. Sex-specific regulatory pathways controlling sexually dimorphic characteristics in the various organs and the consequences of lifelong differences in sex hormone expression largely account for such responses. However, sex-specific changes in epigenetic marks are generated early after fertilization, thus before adrenal and gonad differentiation in the absence of sex hormones and in response to environmental conditions. Given the abundance of X-linked genes involved in placentogenesis, and the early unequal gene expression by the sex chromosomes between males and females, the role of X- and Y-chromosome-linked genes, and especially those involved in the peculiar placenta-specific epigenetics processes, giving rise to the unusual placenta epigenetic landscapes deserve particular attention. However, even with recent developments in this field, we still know little about the mechanisms underlying the early sex-specific epigenetic marks resulting in sex-biased gene expression of pathways and networks. As a critical messenger between the maternal environment and the fetus, the placenta may play a key role not only in buffering environmental effects transmitted by the mother but also in expressing and modulating effects due to preconceptional exposure of both the mother and the father to stressful conditions.
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Advances in digital photography and distribution technologies enable many people to produce and distribute images of their sex acts. When teenagers do this, the photos and videos they create can be legally classified as child pornography since the law makes no exception for youth who create sexually explicit images of themselves. The dominant discussions about teenage girls producing sexually explicit media (including sexting) are profoundly unproductive: (1) they blame teenage girls for creating private images that another person later maliciously distributed and (2) they fail to respect—or even discuss—teenagers’ rights to freedom of expression. Cell phones and the internet make producing and distributing images extremely easy, which provide widely accessible venues for both consensual sexual expression between partners and for sexual harassment. Dominant understandings view sexting as a troubling teenage trend created through the combination of camera phones and adolescent hormones and impulsivity, but this view often conflates consensual sexting between partners with the malicious distribution of a person’s private image as essentially equivalent behaviors. In this project, I ask: What is the role of assumptions about teen girls’ sexual agency in these problematic understandings of sexting that blame victims and deny teenagers’ rights? In contrast to the popular media panic about online predators and the familiar accusation that youth are wasting their leisure time by using digital media, some people champion the internet as a democratic space that offers young people the opportunity to explore identities and develop social and communication skills. Yet, when teen girls’ sexuality enters this conversation, all this debate and discussion narrows to a problematic consensus. The optimists about adolescents and technology fall silent, and the argument that media production is inherently empowering for girls does not seem to apply to a girl who produces a sexually explicit image of herself. Instead, feminist, popular, and legal commentaries assert that she is necessarily a victim: of a “sexualized” mass media, pressure from her male peers, digital technology, her brain structures or hormones, or her own low self-esteem and misplaced desire for attention. Why and how are teenage girls’ sexual choices produced as evidence of their failure or success in achieving Western liberal ideals of self-esteem, resistance, and agency? Since mass media and policy reactions to sexting have so far been overwhelmingly sexist and counter-productive, it is crucial to interrogate the concepts and assumptions that characterize mainstream understandings of sexting. I argue that the common sense that is co-produced by law and mass media underlies the problematic legal and policy responses to sexting. Analyzing a range of nonfiction texts including newspaper articles, talk shows, press releases, public service announcements, websites, legislative debates, and legal documents, I investigate gendered, racialized, age-based, and technologically determinist common sense assumptions about teenage girls’ sexual agency. I examine the consensus and continuities that exist between news, nonfiction mass media, policy, institutions, and law, and describe the limits of their debates. I find that this early 21st century post-feminist girl-power moment not only demands that girls live up to gendered sexual ideals but also insists that actively choosing to follow these norms is the only way to exercise sexual agency. This is the first study to date examining the relationship of conventional wisdom about digital media and teenage girls’ sexuality to both policy and mass media.