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PubMedDate not supplied

Genetics and pathology of hereditary adrenal hyperplasia in the rabbit: a model for congenital lipoid adrenal hyperplasia.

One-hundred-twenty-nine cases of adrenal hyperplasia in the rabbit were shown to be associated with a fully penetrant autosomal recessive gene, symbolized ah. The mutant is viable prenatally, may be recognized by gross examination of the adrenal at least as early as 19 days of gestation, but dies soon after birth. There is an external feminizing effect of the gene and the model is similar to the feminizing congenital lipoid adrenal hyperplasia reported in man. This mutant is being maintained in strain IIIVO/ahJ.

Adrenal Glands↗

PubMed2000

Desert hedgehog (Dhh) gene is required in the mouse testis for formation of adult-type Leydig cells and normal development of peritubular cells and seminiferous tubules.

Testes from adult and prepubertal mice lacking the Desert hedgehog (DHH:) gene were examined in order to describe further the role of Dhh in spermatogenesis because, in a previous report, DHH:-null male mice were shown to be sterile. Dhh is a signaling molecule expressed by Sertoli cells. Its receptor, patched (Ptc), has been previously localized to Leydig cells and is herein described as being localized also to peritubular cells. Two phenotypes of the mice were observed: masculinized (7.5% of DHH:-null males) and feminized (92.5%), both of which displayed abnormal peritubular tissue and severely restricted spermatogenesis. Testes from adult feminized animals lacked adult-type Leydig cells and displayed numerous undifferentiated fibroblastic cells in the interstitium that produced abundant collagen. The basal lamina, normally present between the myoid cells and Sertoli cells, was focally absent. We speculate that the abnormal basal lamina contributed to other characteristics, such as extracordal gonocytes, apolar Sertoli cells, and anastomotic seminiferous tubules. The two DHH:-null phenotypes described have common peritubular cell defects that may be indicative of the essential role of peritubular cells in development of tubular morphology, the differentiation of Leydig cells, and the ultimate support of spermatogenesis.

Androgen-Insensitivity Syndrome↗

PubMed2001

Sex, infertility and the molecular biology of the androgen receptor.

Mutations that totally disrupt androgen receptor function cause the well known testicular feminizing syndrome or complete androgen insensitivity syndrome, wherein a 46 XY individual is completely feminized at birth. Recently it has been increasingly obvious that androgen receptor mutations not only result in the complete androgen insensitivity syndrome, but can cause a wide spectrum of milder insensitivity syndromes including ambiguous genitalia in newborn infants, and 'idiopathic' male infertility in otherwise normal males. Characterization of the molecular and structural mechanisms of androgen receptor dysfunction in these cases has led to directed hormonal therapy. Thus the differential response of a Met807Thr mutant androgen receptor to dihydrotestosterone but not testosterone, have been used to restore male genital development in an infant with partial AIS. Of greater significance, because they affect larger numbers of patients, are the mutations and polymorphisms that result in depressed spermatogenesis and male infertility in phenotypic males. Studies involving Singaporean, Australian, North American and Japanese subjects have established that increases in length of a trinucleotide repeat (CAG) tract, encoding a polyglutamine stretch in the transactivation domain of the androgen receptor, are associated with increased risk of defective spermatogenesis and undermasculinization. Independent of the CAG repeats, missense amino-acid substitutions in the ligand-binding domain, involving residues 727, 798 and 886 cause infertility through a novel mechanism. Pathogenicity is transmitted, not through defective ligand binding, but through defective protein-protein interactions between receptor domains and coactivator proteins that are essential for gene transcription. Elucidation of the molecular and structural basis of androgen receptor dysfunction in these cases allows precise genetic counseling and can lead to the design of rational hormonal therapy.

Androgens↗

PubMed1997

Oestradiol and testosterone blood levels in patients with viral cirrhosis and hepatocellular carcinoma.

BACKGROUND: Patients with alcoholic cirrhosis show hypogonadism and feminization associated with sex hormone imbalance due to enhanced aromatization of testosterone and subsequent reduced testosterone and increased oestradiol blood levels. Because oestrogens modulate hepatocyte proliferation and oestrogen receptors are present in liver cirrhosis and hepatocellular carcinoma, it has been proposed that sex hormone imbalance can play a role in liver carcinogenesis. Trials with the oestrogen receptor antagonist tamoxifen have been performed with conflicting results. OBJECTIVES: To investigate oestradiol and testosterone blood levels in men with viral cirrhosis and hepatocellular carcinoma and also to investigate changes in sex hormone circulating levels induced by tamoxifen treatment. PATIENTS AND METHODS: Oestradiol and testosterone blood levels were evaluated in 32 male patients with postviral cirrhosis and hepatocellular carcinoma at the time of diagnosis and during the follow-up, and in 20 healthy controls. In eight patients, hormone levels were also assayed during treatment with tamoxifen (40 mg/day). No patient had a history of high alcohol intake. RESULTS: Oestradiol values observed at the time of diagnosis were 56.1 +/- 54.5 pmol/l, while testosterone values were 13.6 +/- 8.0 pmol/l. There was no relationship between oestrogen values and age, while higher oestradiol values were observed in patients with advanced cirrhosis (Child B and C); conversely, testosterone levels progressively and significantly decreased from cirrhosis Child A (15.1 +/- 9.7) to C (7.7 +/- 7.1) (P < 0.05). Tamoxifen treatment (40mg/day) for 1 month in eight patients increased oestradiol values (62.2 +/- 77.0 vs. 156.4 +/- 83 pmol/l, P < 0.05), while testosterone levels decreased (15.1 +/- 6.8 vs. 8.5 +/- 10.6 pmol/l). However, these changes were not associated with clinical signs or symptoms of feminization. Oestrogen levels decreased after 6 months of tamoxifen treatment. No significant change in hormone levels was observed in patients not treated with tamoxifen. Unlike patients with alcoholic cirrhosis, in male patients with viral cirrhosis and hepatocellular carcinoma there were no significant alterations in blood oestradiol and testosterone levels, although a certain degree of sex hormone imbalance was observed in those with advanced cirrhosis. Treatment with tamoxifen (40 mg/day) did not induce clinical manifestations of sex hormone imbalance.

Age Factors↗

PubMed2005

The association between the fraternal birth order effect in male homosexuality and other markers of human sexual orientation.

Later fraternal birth order (FBO) is a well-established correlate of homosexuality in human males and may implicate a maternal immunization response in the feminization of male sexuality. This has led to the suggestion that FBO may relate to other markers of male sexual orientation which are robustly sexually dimorphic. If so, among homosexual males the number of older brothers should strongly correlate with traits such as spatial ability and psychological gender, indicative of greater behavioural feminization, compared to heterosexual males. The present study failed to find significant associations between number of older brothers and these traits.

Adolescent↗

PubMed1995

Evolution and phylogeny of Wolbachia: reproductive parasites of arthropods.

Wolbachia are cytoplasmically inherited bacteria found in reproductive tissues of many arthropod species. These bacteria are associated with reproductive alterations in their hosts, including parthenogenesis, reproductive incompatibility and feminization. A fine-scale phylogenetic analysis was done using DNA sequences from ftsZ, a rapidly evolving bacterial cell-cycle gene. ftsZ sequences were determined for 38 different Wolbachia strains from 31 different species of insects and one isopod. The following results were found: (i) there are two major division of Wolbachia (A and B) which diverged 58-67 millions years before present based upon synonymous substitution rates; (ii) a general concordance is found between the ftsZ and 16S rDNA phylogenies, indicating that these represent bacterial strain (rather than simply gene) phylogenies; however, a possible example of recombination between A and B division bacteria may have occurred in the feminizing Wolbachia present in an isopod; (iii) extensive horizontal transmission of Wolbachia has occurred between insect taxa, including different insect orders; one strain in particular (designated Adm) shows extensive recent horizontal transmission; (iv) there is an association between the Wolbachia found in a parasitic wasp (Nasonia) and its fly host (Protocalliphora), suggesting exchange of bacteria between these species; (v) parthenogenesis induction has evolved several times among the Wolbachia; and (vi) some insects harbour infections with more than one Wolbachia strain, even within individual insects.

Animals↗

PubMed2003

A bacterial symbiont in the Bacteroidetes induces cytoplasmic incompatibility in the parasitoid wasp Encarsia pergandiella.

Vertically transmitted symbionts of arthropods have been implicated in several reproductive manipulations of their hosts. These include cytoplasmic incompatibility (CI), parthenogenesis induction in haplodiploid species (PI), feminization and male killing. One symbiont lineage in the alpha-Proteobacteria, Wolbachia, is the only bacterium known to cause all of these effects, and has been thought to be unique in causing CI, in which the fecundity of uninfected females is reduced after mating with infected males. Here, we provide evidence that an undescribed symbiont in the Bacteroidetes group causes CI in a sexual population of the parasitic wasp Encarsia pergandiella. Wasps were crossed in all four possible combinations of infected and uninfected individuals. In the cross predicted to be incompatible, infected (I) males x uninfected (U) females, progeny production was severely reduced, with these females producing only 12.6% of the number of progeny in other crosses. The incompatibility observed in this haplodiploid species was the female mortality type; dissections showed that most progeny from the incompatible cross died as eggs. The 16S rDNA sequence of this symbiont is 99% identical to a parthenogenesis-inducing symbiont in other Encarsia, and 96% identical to a feminizing symbiont in haplodiploid Brevipalpus mites. Thus, this recently discovered symbiont lineage is capable of inducing three of the four principal manipulations of host reproduction known to be caused by Wolbachia.

Animals↗

PubMed2004

Neonatal 5HT activity antagonizes the masculinizing effect of testosterone on the luteinizing hormone release response to gonadal steroids and on brain structures in rats.

Hypothalamic 5HT concentrations are transiently lower in male compared to female Wistar rats in the second week post partum (pp) and our previous findings have shown that pharmacologically potentiating 5HT activity over this period feminizes certain aspects of sexually differentiated behaviours in adult males and androgenized females. In order to investigate whether neonatal testosterone and 5HT interact to influence physiological and morphological brain sexual differences, females, androgenized females and males were treated with the 5HT2 agonist (-) [2,5 dimethoxy-4-iodophenyl]-2-amino propane HCl [(-) DOI], over days 8-16 pp. In androgenized females (250 microg testosterone proprionate, day 2 pp) (-) DOI prevented the delay in vaginal opening, but did not prevent the androgen-induced constant oestrus in females treated with 100 microg TP, day 2 pp. (-) DOI overcame the neonatal androgen effect in suppressing the positive feedback of ovarian steroids in a few males and androgenized females. (-) DOI had a feminizing effect on the volume of the anteroventral periventricular nucleus (normally smaller in males), by significantly increasing its volume in male and androgenized females. It also had a significant antagonistic effect on the testosterone-induced increase in the volume of the sexually dimorphic nucleus of the preoptic area in males and androgenized females. These findings support the view that raised 5HT activity in the second week of life antagonizes the masculinizing effect of neonatal testosterone.

Animals↗

PubMed1979

Testicular function in post pubertal male pseudohermaphroditism.

Testicular endocrine function was studied in twelve post pubertal patients with male pseudohermaphroditism and 46 XY chromosomal constitution. Patients were divided into three groups, four subjects who became feminized during puberty, five who became masculinized during puberty and three who were castrated before puberty. Serum dehydroepiandrosterone, progesterone, 17-hydroxyprogesterone, androstendione, testosterone, dihydrotestosterone, LH and FSH were determined by radioimmunoassay. Patients of the first group had the clinical characteristics of testicular feminization secondary to absence of the androgen receptor. One of the five patients of the second group had deficient testosterone secretion but no enzymatic defect could be demonstrated. One of the subjects castrated before puberty had a deficiency in 17,20-desmolase. Therefore, evidence of a failure of the fetal testes could be found in only two of the twelve patients studied.

Adolescent↗

PubMed1989

Increased thymic size and thymocyte interleukin 2 production in androgen-resistant mice.

The functional significance of androgen receptors in thymocytes is unknown. To investigate whether such receptors might mediate androgen-induced effects on thymocyte proliferation or differentiation we examined mice bearing a known defect in the gene coding for the androgen receptor. This mutation, termed testicular feminization (Tfm/Y), renders these mice resistant to the action of androgenic hormones. Testicular feminization mice were found to have large thymuses that were an average of 2.8 times as heavy as those of their unaffected male litter mates, and contained up to 36 times as many thymocytes. Similar findings were observed when Tfm mice were compared with C57Bl/6 control mice. Thymocytes from androgen-resistant mice produced several times more interleukin 2 in culture than did thymocytes from control mice. A small but significant reduction in the population of cells bearing neither CD4 nor CD8 surface markers ('double negatives') was observed in the androgen-resistant mice. These data indicate that androgen resistance is associated in the Tfm/Y mouse with alterations in thymocyte number, phenotype, and function that may be attributable to lack of androgen action during thymic development.

Androgens↗

PubMed1992

Estrogen therapy in Turner's syndrome.

Girls with Turner's syndrome are born short, grow slowly, and usually fail to enter puberty spontaneously and to undergo a pubertal growth spurt. The goal of estrogen therapy is to correct estrogen deficiency in a manner that optimizes height potential, permits attainment of normal bone mass, and provides appropriate feminization with minimal risk of adverse effects. The issues to be resolved include the age at which treatment should be begun, the preparation, route of administration, and dosage to be given, the effect on concurrent growth hormone administration, the rate of dose increase during treatment, the timing and nature of progestin administration, and the total duration of treatment. The available data suggest that treatment should be initiated between the ages of 12 and 14 years. The dose-response relationship between growth rate and estrogen dose is biphasic. Optimal growth stimulation for ethinyl estradiol occurs at approximately 100 ng/kg body weight per day, which is below the dose that produces full feminization. Although suboptimal doses of estrogen and growth hormone appear to have additive effects, estrogen causes only a minor increase in the short-term growth response to an optimal dose of growth hormone. The long-term effects of estrogen combined with growth hormone are unknown. In the absence of data concerning the outcome of different dose schedules, we treated for 2 years at 100 ng/kg/day of ethinyl estradiol, then double the dose annually until menstruation, at which time cyclic monthly progestin therapy is added (medroxyprogesterone acetate 10 mg daily from days 16 to 25). The importance of estrogen in maintaining normal bone mass suggests that treatment should be lifelong. Current research in our clinic is assessing the long-term effect on adult height of ultra-low-dose treatment (25 to 50 ng/kg/day of ethinyl estradiol) during the childhood years (ages 5 to 11), alone or in conjunction with supplemental growth hormone.

Adolescent↗

PubMed1983

Correlations between fibroblast androgen receptor levels and clinical features in abnormal male sexual differentiation and infertility.

Androgen receptor binding of radiolabelled methyltrienolone (3H-R1881) was determined in cultured genital skin fibroblasts from 17 normal male controls and from 65 males with genital abnormalities. Analysis of the results was performed with patients grouped according to the predominant clinical features. Of 16 patients with complete male pseudohermaphroditism, 12 had androgen receptor (AR) deficiency, one had "receptor-positive" Testicular Feminization, and in three, alternative diagnoses were established (17 alpha hydroxylase deficiency; 20,22-desmolase deficiency; mixed gonadal dysgenesis). In contrast, only four of 16 patients investigated for ambiguous genitalia (phallus intermediate between male and female, perineal urethra) showed AR deficiency. Borderline or slightly low AR levels were found in each of four boys in whom the sole abnormality was micropenis. In 26 boys with penile hypospadias, however, only one had low AR. Very low levels of AR (levels comparable to those seen in complete Testicular Feminization) were found in two of three men with infertility associated with abnormally high serum testosterone levels.

Adult↗

PubMed2005

Congenital adrenal hyperplasia and lower urinary tract symptoms.

OBJECTIVES: To assess urinary symptoms in adult women with congenital adrenal hyperplasia (CAH), as feminizing surgery in infancy is current standard practice for CAH and one of the indications for surgery is to reduce urinary symptoms. PATIENTS, SUBJECTS AND METHODS: In a case-control study, 19 women with CAH, of whom 16 had had childhood feminizing genital surgery, and age-matched women with no CAH, were evaluated. Subjects and controls completed the Bristol Female Lower Urinary Tract Symptoms (BFLUTS) questionnaire. RESULTS: Urge incontinence was reported in 13 (68%) patients and three (16%) controls (P = 0.003); stress incontinence was present in 47% and 26%, respectively (P = 0.31). Results from the controls were comparable with those documented in larger studies on normal populations. Nine of the patients felt that their urinary symptoms had an adverse effect on their lives, compared with only one of the controls (P = 0.008). CONCLUSION: Patients with a diagnosis of CAH are more likely to have significant urinary symptoms than normal controls. At present it is not clear whether this is a result of surgery or an effect of CAH. In at least two-thirds of patients surgery did not achieve the objective of reducing urinary symptoms.

Adolescent↗

PubMed1981

Sexual dimorphism and the effects of the X-linked Tfm locus on hexobarbitone metabolism and action in mice.

1 Normal males of the testicular feminized strain of mice (Tfm) had longer hexobarbitone-induced sleeping times than females, and hepatic hexobarbitone hydroxylase activity different in that the Km was higher and the Vmax lower in the male. 2 Castration and androgen replacement studies indicated that testicular androgens were responsible for the sexual differences in drug metabolism found in this mouse strain. 3 Hepatic hexobarbitone metabolism and action were feminized in the intact, androgen-insensitive, genetically male Tfm mouse. Furthermore, hexobarbitone hydroxylase activities were less responsive to large doses of testosterone in Tfm mice than in normal males. 4 The Tfm mouse with a deficiency in androgen receptors responded to the enzyme-inductive effects of phenobarbitone and softwood bedding, indicating that these inducers do not act through the androgen receptors.

Androgen-Insensitivity Syndrome↗

PubMed2003

Professionalization, gender and female-dominated professions: dental hygiene in Ontario.

This paper explores the influence of gender and feminism on the professional projects of female-dominated professions, through a case study of dental hygiene in Ontario. Full professional status has eluded many female-dominated professions, including dental hygiene. Historically, dental hygiene was defined as work for women, to be performed strictly under the control of male dentists. In recent years, dental hygiene has pursued a professional project and struggled for greater independence from dentistry. Ideas about gender and, particularly, feminism have been central to their professional project.

Canada↗

PubMed1994

The sex determination process in maize.

Maize partitions the sexes into different flowers on the plant, a condition called monoecy, which facilitates outcrossing. Sex determination in maize is a complex process involving an interplay between genetic determinants, the environment, and hormones. Unisexuality of flowers is achieved by the process of selective arrest and abortion of the inappropriate organ primordia within a bisexual floral meristem. Floral organ abortion is associated with the degeneration of cells within an immature primordia. Masculinizing genes are required for gynoecial abortion, feminizing genes arrest stamen development, and both types also control secondary sexual traits involving morphological characteristics of floral tissues. Gibberellins, steroid-like plant hormones, appear to play a pivotal role in the stamen abortion process and the feminization of floral tissues.

Genes, Plant↗

PubMed1976

Female phenotype in a male child due to 17-alpha-hydroxylase deficiency.

The discovery of testicles in a 3-year-old girl with XY karyotype led to a diagnosis of testicular feminization. Subsequently, however, hypokalaemia, hypertension, and severe prostration during a mild infection suggested adrenal involvement, and investigations showed a 17-alpha-hydroxylase deficiency. Diagnosis of testicular feminization should not be made without excluding a defect of testosterone synthesis.

Adrenocortical Hyperfunction↗

PubMed1983

Sex steroid induced changes in hepatic enzymes.

Sex differences exist in steroid and xenobiotic metabolism in the liver of a number of species. In the rat, the differences are regulated through the hypothalamo-pituitary axis. The previously postulated "feminizing factor" responsible for a female-type liver metabolism appears to be identical to growth hormone. The different effects of this peptide on hepatic metabolism in male and female rats may be related to the sexual dimorphism of the growth hormone secretory pattern; serum levels of growth hormone do not fluctuate as markedly in female as in male rats and may be simulated by administration of the hormone via osmotic minipumps, a procedure resulting in "feminization" of liver metabolism of male or hypophysectomized rats. This newly discovered system, the hypothalamo-pituitary-liver axis, represents a novel concept in endocrinology.

Androgens↗