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PubMed1983

Gender reorientation and psychosocial adjustment in male-to-female transsexuals.

This study examined the relationship, in a sample of male-to-female transsexuals, between psychological and social adjustment, on the one hand, and gender reorientation (approximation of the status of the opposite biological sex), on the other. Three gender reorientation variables were studied: exogenous female hormones, vaginoplasty, and social feminization (adoption of the female gender role at home and in the transsexual's social life and the procurement of documents indicating the female sex). These three gender reorientation variables plus age were employed as predictor variables in a series of multiple regression analyses. Five stepwise regression analyses were carried out, one for each of five criterion variables (depression, tension, involvement with a male partner, cohabitation with a male partner, and the MMPI Lie Scale). There was a statistically significant negative correlation between depression and social feminization and between tension and social feminization, and a significant positive correlation between cohabitation with a male partner and vaginoplasty. Neither the MMPI Lie Scale nor the simple fact of having been "involved" with a male partner at some point during the past year correlated significantly with any of the predictor variables. These results indicate that gender reorientation is associated with better psychological and social adjustment in male-to-female transsexuals.

Adult↗
PubMed1976

The age of occurrence of gonadal tumors in intersex patients with a Y chromosome.

A total of 320 intersex patients with a Y chromosome were classified into four groups; (1) gonadal dysgenesis, (2) asymmetrical gonadal differentiation, (3) virilizing male hermaphroditism and (4) feminizing male hermaphroditism (testicular feminization syndrome). Of these 320 cases, 98 were from the files of The Johns Hopkins Hospital and the remainder from the literature. The incidence of tumors in relation to age and clinical classification was analyzed by computer. The results were plotted for each group. It was found that the percentage of tumors rose appreciably soon after the age of puberty in the first three groups, and it was concluded that the gonads were best removed before the age of puberty. In the case of testicular feminization patients, procrastination until the age of 25 could be considered, if one were willing to assume the risk of neoplasia of about 3.6 per cent until then.

Adolescent↗
PubMed1987

Effects of prenatal testosterone propionate treatment on saccharin preference of adult rats exposed to ethanol in utero.

Prenatal exposure to alcohol feminizes saccharin consumption patterns in adult male rats. To study the involvement of testosterone in this effect, testosterone propionate (TP) was administered to pregnant dams in an attempt to reverse that feminized saccharin consumption pattern in the male offspring. Female offspring were also studied to determine the effect of TP on saccharin preference in normal males and females. During the last week of gestation, dams were administered a liquid diet containing 35% ethanol derived calories, an isocaloric liquid diet containing no ethanol, or Purina Lab Chow. Half of the dams in each group received twice daily injections of TP, the other half were injected with the oil vehicle. Saccharin consumption of adult fetal alcohol exposed (FAE) males from dams administered oil or TP was significantly greater than controls, indicating that the feminized pattern of saccharin consumption of FAE males cannot be overcome with TP administration during the prenatal period. In controls, prenatal TP exposure alone was found to increase adult saccharin consumption in both sexes. Prenatal administration of TP was also found to markedly depress body weight of offspring of dams receiving the liquid diets compared to offspring from dams receiving the same diets plus oil injections. Body weights of offspring from TP or oil injected dams receiving the chow fed diets during pregnancy did not differ.

Animals↗
PubMed1987

Effects of ventromedial nucleus lesions on the display of lordosis behavior in the male rat. Interactions with facilitory effects of male urine.

Previous observations showed that exposure to the odor of male urine prior to mating could enhance the display of lordosis behavior in male rats feminized with ovarian hormones. This study was performed to determine in feminized male rats whether the control of lordosis behavior by the olfactory system was mediated by the ventromedial nucleus (VMN) of the hypothalamus. Male rats were orchidectomized (ORCH) as adults and primed with 25 micrograms estradiol benzoate (EB) and 150 micrograms progesterone (P) 40 hr apart. Lordosis behavior was tested 9 +/- 1 hr after P injection. VMN lesions were shown to completely suppress the display of lordosis behavior as compared to sham VMN operated and dorsomedial nucleus (DMN) lesioned animals. Exposure of feminized rats to the odor of male urine by 9 +/- 1 hr before mating significantly increased the proportion of ORCH rats that displayed lordosis behavior in response to male mounts. This effect was abolished by VMN lesions but was maintained in the sham VMN operated and DMN lesioned animals. These results were discussed in the light of the present knowledge on the neuroendocrine and olfactory structures which mediate lordosis behavior in the male rat.

Animals↗
PubMed1988

xol-1: a gene that controls the male modes of both sex determination and X chromosome dosage compensation in C. elegans.

Loss-of-function mutations in the X-linked gene xol-1 cause the feminization and death of XO animals (normally males) by shifting the sex determination and dosage compensation pathways toward their hermaphrodite modes. XO-specific lethality most likely results from the reduction in X chromosome expression caused by xol-1 mutations. Mutations in genes required for the hermaphrodite mode of dosage compensation suppress lethality but not feminization, and restore X chromosome expression to nearly wild-type levels. Mutations in genes that control the hermaphrodite modes of both sex determination and dosage compensation fully suppress both defects. These interactions suggest that xol-1 is the earliest-acting gene in the known hierarchy controlling the male/hermaphrodite decision and is perhaps the gene nearest the primary sex-determining signal. We propose that the wild-type xol-1 gene product promotes male development by ensuring that genes (or gene products) directing hermaphrodite sex determination and dosage compensation are inactive in XO animals. Interestingly, in addition to feminizing XO animals, xol-1 mutations further masculinize XX animals already partially masculinized.

Alleles↗
PubMed1987

Abnormal sexual differentiation and neoplasia.

The prevalence of neoplasia is increased in individuals with certain disorders of sexual differentiation. Etiology and frequency of neoplasia vary with the particular disorder. In uncomplicated cryptorchidism, the testis is at least 10 times more likely to undergo neoplastic transformation than a normal scrotal testis. Neoplasia probably is a function of both testicular location (intraabdominal) and underlying dysgenetic structure. If cryptorchidism is unilateral, and if orchiopexy has not been performed prior to age 6-10 years, orchiectomy should be encouraged. In those forms of gonadal dysgenesis not associated with a Y chromosome (e.g., 45,X; 45,X/46,XX; 46,XX) there is no definite increase in neoplasia, suggesting that elevated gonadotropin levels per se are not carcinogenic. Gonadal tumors are found in at least 30% of individuals with XY gonadal dysgenesis and are particularly frequent (55%) in H-Y antigen-positive patients. These tumors are almost always gonadoblastomas or dysgerminomas. Similar tumors are found in 15%-20% of 45,X/46,XY individuals. In either situation the neoplastic transformation could be a) secondary to the existence of XY gonadal tissue in an inhospitable environment, or b) integrally related to that process--genetic or cytogenetic--producing the dysgenetic gonads. The risk of neoplasia is sufficiently high that most of these patients should be offered early gonadal extirpation. The prevalence of gonadal tumors is not increased in Klinefelter's syndrome, further indicating that gonadotropins are not carcinogenic per se. However, Klinefelter patients are 20 times more likely to develop a carcinoma of the breast than are 46,XY males. Extragonadal germ cell tumors also are more common. In female pseudohermaphrodites there is probably no increased risk of neoplasia, whereas, in true hermaphrodites neoplasia is unusual but does occur. Neoplasia occurs in patients with complete testicular feminization (complete androgen insensitivity) but rarely in those with incomplete testicular feminization/Reifenstein's syndrome, 5 alpha-reductase deficiency, anorchia, agonadia, or testosterone biosynthetic defects. In complete testicular feminization the risk of malignant tumors is small prior to age 25. After age 25, it is about 2%-5%. Orchiectomy is recommended after pubertal feminization.

Disorders of Sex Development↗
PubMed1999

Pretranslational up-regulation of the hepatic microsomal delta4-3-oxosteroid 5alpha-oxidoreductase in male rat liver by all-trans-retinoic acid.

Administration of all-trans-retinoic acid (ATRA; 60 mg/kg daily for 3 days) to male rats increased the rate of 5alpha-dihydrotestosterone (5alpha-DHT) formation from testosterone in microsomal fractions in vitro. The formation of androstane-3alpha,17beta-diol from testosterone was also increased because of the higher concentration of 5alpha-DHT produced in microsomal incubations. Northern analysis confirmed that the increased rate of 5alpha-DHT formation was due to the pretranslational up-regulation in delta4-3-oxosteroid 5alpha-oxidoreductase (EC 1.3.99.5) mRNA expression in ATRA-treated male rat liver. Thus, ATRA elicited in male rat liver a partial feminization of the expression of this enzyme, which normally exhibits a female-selective distribution in the rat. Subsequent experiments evaluated whether the administration of human chorionic gonadotropin or thyroxine to ATRA-treated male rats decreases 5alpha-reductase activity to that observed in untreated male rat liver. Although these treatments did not decrease 5alpha-reductase to untreated male levels, it was found that administration of ATRA to gonadectomized male rats produced complete feminization of the enzyme. Again, up-regulation was confirmed at the mRNA level. The activity of the male-specific cytochrome P450 2C11 (as reflected by microsomal testosterone 16alpha-hydroxylation activity) was correspondingly decreased by treatments that increased steroid 5alpha-reductase activity. Thus, gonadectomy in combination with ATRA administration effected a more pronounced decrease in 16alpha-hydroxylation activity than either treatment alone. These findings suggest that ATRA is a novel positive regulator of the 5alpha-reductase that in combination with the removal of circulating androgen, which normally suppresses 5alpha-reductase levels, feminizes the expression of this enzyme in rat liver.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1989

Total ablation of the penis after circumcision with electrocautery: a method of management and long-term followup.

Four patients who had traumatic loss of the penis were managed after the initial injury with a feminizing genitoplasty. Patient reconstruction ranged from 6 months to 3 years. The technique of feminizing genitoplasty is described. There were no instances of flap necrosis, urinary tract infection or urinary incontinence. Immediate results were considered to be cosmetically satisfactory in all patients. Followup ranged from 8 months to 23 years, with a median of 10.5 years. The long-term results have been particularly gratifying in 2 individuals who have been observed for more than 18 years. Early feminizing genitoplasty offers an excellent method of reconstruction of the external genitalia in the child with traumatic loss of the penis who is assigned a female sex of rearing.

Circumcision, Male↗
PubMed1999

The avian egg as a test system for endocrine disrupters: effects of diethylstilbestrol and ethynylestradiol on sex organ development.

Many environmental contaminants are known or suspected to interfere with hormonal function in animals. In vivo test methods to detect and characterize chemicals that disrupt the endocrine system are therefore urgently needed. In this study, we assessed the usefulness of abnormalities of the reproductive organs as test endpoints for estrogenic activity of xenobiotics in Japanese quail embryos. Two synthetic estrogens, diethylstilbestrol (DES) and ethynylestradiol (EE2), were injected into the yolks of embryonated eggs. At a dose as low as 2 ng EE2/g egg, all male embryos became feminized, containing ovary-like tissue in the left testis. The extent of feminization of the testes was determined by measuring the relative area of the ovary-like component. Persistent Müllerian ducts (oviducts) in male embryos, and malformations of the Müllerian ducts in females occurred at 2 ng EE2/g egg and higher doses. DES was approximately one-third to one-tenth as potent as EE2. The morphological changes studied were dose-dependent, indicating that they are useful as test endpoints for estrogenic activity. Feminization of the left testis in males proved to be the most sensitive endpoint. We propose the quail egg as a simple in vivo test system for estrogenic compounds.

Androgen-Insensitivity Syndrome↗
PubMed2002

Relationships among childhood sex-atypical behavior, spatial ability, handedness, and sexual orientation in men.

Moderate support was obtained in a sample of 101 gay, bisexual, and heterosexual males for the perinatal hormone theory, which hypothesizes that attenuated levels of androgens during critical periods of male fetal development fail to masculinize and defeminize the brain. Affected individuals develop female-typical sexual orientation (assessed here by a pie chart) and cerebral organization, reflected in visual-spatial abilities and gender nonconformity. Handedness, also thought to reflect in utero hormone exposure, was evaluated. Gay and bisexual males reported greater femininity and lesser masculinity than heterosexuals, with bisexuals intermediate in masculinity, suggesting a common biological mediator for homoeroticism and sex atypicality. Among bisexual males, increased masculinity was related to enhanced performance on all spatial tasks. Group mean differences in spatial ability and handedness were not found; however, among bisexuals, poorer visual-spatial performance predicted increased homoeroticism and right-handedness positively correlated with all spatial tasks. If perinatal hormones contribute to a generalized feminization of the brain, the current data indicate that it is most apparent among bisexual males. Sexing of their brains may involve several sexually dimorphic regions that are related in a continuous manner. Inferred cerebral feminization was more circumscribed among gay and heterosexual males, for whom childhood sex atypicality was most highly-distinguishing. Unspecified mechanisms responsible for homoeroticism in them may differ from those that produce same-sex attractions in bisexuals and thus have relatively little impact on other components of cerebral feminization.

Adolescent↗
PubMed1976

On the obligatory role of the hypophysis in sexual differentiation hepatic metabolism in rats.

The hepatic metabolism of 4-[4-14C]androstene-3,17-dione and 5alpha-[4-14C]androstane-3alpha,17beta-diol was studies in castrated and hypophysectomized male rats with a transplanted pituitary under the kidney capsule. The effects of testosterone propionate and estradiol benzoate on liver metabolism were also studied in these experimental animals. It was found that the autonomous pituitary secreted a "feminizing factor" that transformed the male type of steroid metabolism characteristic of hypophysectomized rats into a female type of metabolism Hypophysectomized rats were unresponsive towards androgen action on the liver and did not respond with feminized hepatic metabolism after treatment with estradiol benzoate. It is concluded that estrogenic action on liver enzymes is mediated via modulation of the secretion of a central (probably hypothalamic) "feminizing factor inhibiting factor" and the sex hormonal effects of hepatic metabolism only occur in the presence of a pituitary in situ.

Androstane-3,17-diol↗
PubMed2026

The complete sequence of the silkworm W chromosome uncovers its rapid evolution by large-scale duplications/deletions and translocation of W-linked genes.

The complete sequence of the W chromosome, which carries feminization activity in the silkworm, is crucial for understanding the sex-determination system in Lepidoptera. However, extensive accumulation of transposons due to lack of recombination, the very rare protein-coding genes and almost no information about molecular markers has hindered full W sequencing. We report the first complete silkworm W sequence (T2T_W, 11683305 bp) obtained by combining sequencing-assembly technologies and newly developed error detection methods, evaluated with genetically mapped W-RAPD markers, W-mutants, and W-derived BAC clones. The T2T_W sequence showed that the W is composed of a massive 92% accumulation of transposons and repeat sequences, among which the main constituents are intact LTR/LINE retrotransposons indicating recent expansions. In addition to Fem clusters producing Fem piRNA (Feminizer-derived PIWI-interacting RNA), we found 26 protein-coding genes in the W sequence. These include four gene pairs encoding zinc-finger motifs designated z1:z20 and a gene encoding serine/arginine repetitive matrix protein 1-like (SRRM1-like). To identify candidate genes for female sex-determination and differentiation we also sequenced the shortest W (3.8 Mb) from a translocation mutant with feminizing activity, which harbored four conventional genes: a Fem cluster, a pair of z1:z20 isoforms, z20-S, and a SRRM1-like gene. Phylogenetic analysis revealed that z1:z20 originated from a copy of an autosomal zinc-finger gene pair, z2:z21, translocated onto the W around 2.43 Mya and subsequently amplified to yield 4 W-linked zinc-finger gene pairs. The complete W sequence revealed that large-scale deletions and amplifications played a significant role in W chromosome evolution.

Animals↗
PubMed1989

Genes that implement the hermaphrodite mode of dosage compensation in Caenorhabditis elegans.

We report a genetic characterization of several essential components of the dosage compensation process in Caenorhabditis elegans. Mutations in the genes dpy-26, dpy-27, dpy-28, and the newly identified gene dpy-29 disrupt dosage compensation, resulting in elevated X-linked gene expression in XX animals and an incompletely penetrant maternal-effect XX-specific lethality. These dpy mutations appear to cause XX animals to express each set of X-linked genes at a level appropriate for XO animals. XO dpy animals are essentially wild type. Both the viability and the level of X-linked gene expression in XX animals carrying mutations in two or more dpy genes are the same as in animals carrying only a single mutation, consistent with the view that these genes act together in a single process (dosage compensation). To define a potential time of action for the gene dpd-28 we performed reciprocal temperature-shift experiments with a heat sensitive allele. The temperature-sensitive period for lethality begins 5 hr after fertilization at the 300-cell stage and extends to about 9 hr, a point well beyond the end of cell proliferation. This temperature-sensitive period suggests that dosage compensation is functioning in XX animals by mid-embryogenesis, when many zygotically transcribed genes are active. While mutations in the dpy genes have no effect on the sexual phenotype of otherwise wild-type XX or XO animals, they do have a slight feminizing effect on animals whose sex-determination process is already genetically perturbed. The opposite directions of the feminizing effects on sex determination and the masculinizing effects on dosage compensation caused by the dpy mutations are inconsistent with the wild-type dpy genes acting to coordinately control both processes. Instead, the feminizing effects are most likely an indirect consequence of disruptions in dosage compensation caused by the dpy mutations. Based on the cumulative evidence, the likely mechanism of dosage compensation in C. elegans involves reducing X-linked gene expression in XX animals to equal that in XO animals via the action of the dpy genes.

Animals↗
PubMed1987

A genetic analysis of the sex-determining gene, tra-1, in the nematode Caenorhabditis elegans.

The normal sexes of Caenorhabditis elegans are the self-fertilizing hermaphrodite (XX) and the male (XO). The autosomal gene tra-1 is a major switch gene controlling sexual phenotype. Mutant phenotypes of 43 loss-of-function (lf) tra-1 alleles and 22 gain-of-function (gf) tra-1 alleles are described and discussed. The tra-1(lf) alleles are recessive and, in general, masculinizing. The most severe mutations (such as seven out of eight identified amber alleles) can transform XX animals into fertile males. These mutations have little effect on XO animals (which are male already) but lead to some abnormalities in XO gonadal development, indicating that tra-1 has functions in normal development of both sexes, although its major function is confined to the XX hermaphrodite. Weaker tra-1(lf) alleles lead to incomplete masculinization of XX animals, resulting in a variety of intersexual phenotypes. the tra-1(gf) alleles are dominant and have an opposite, feminizing effect. Six out of 22 can transform XO animals into fertile females or hermaphrodites, whereas the remainder cause partial feminization. All 22 transform XX animals into fertile females. Limited intragenic mapping indicates that the gene is large and that gf alleles map to a location different from lf alleles. The results suggest that the tra-1 gene has several roles in wild-type sexual development. First, tra-1 activity dictates female, as opposed to male, development in all nongonadal tissues of XX animals. Second, tra-1 activity dictates female development in the somatic gonad of XX animals. Third, a high level of tra-1 activity may act to inhibit spermatogenesis in the XX germ line, thereby assisting the switch from spermatogenesis to oogenesis in the hermaphrodite. These three functions are all feminizing and specific to the XX animal; the gene also has minor functions in the XO animal, which are to assist normal male somatic gonad development and to promote abundant spermatogenesis in males. A low level of both spermatogenesis and oogenesis can occur in the absence of tra-1 activity. Both the function and the regulation of this gene must be complex.

Alleles↗
PubMed1994

Florence Nightingale and the women's movement: friend or foe?

The historical analysis of the complex and often contradictory views of Florence Nightingale regarding the rights of women is explored in this paper. Feminism and nursing are often viewed as contradictory and antithetical. The relationship between the two is examined through the link between Florence Nightingale and her contemporary, Barbara Leigh-Smith Bodichon. Leigh-Smith was founder and primary financier of The English Women's Journal that provided a public platform for the major feminist writings of the period. Its offices in Langham Place formed the administrative centre of the Society for Promoting the Employment of Women. Bodichon and her colleagues were often referred to as the 'Langham Place Group'. Unexplored prior to this study was the fact that Leigh-Smith and Nightingale were first cousins. Utilizing techniques of internal and external criticism, primary and secondary sources were surveyed relating to Nightingale and Leigh-Smith. The views of both women on the subjects of the rights of women, women's suffrage, the employment status of women, and the societal place of women are compared and contrasted. The legacy of both Leigh-Smith and Nightingale to twentieth century feminism, the status of women, and the profession of nursing is then elaborated. The exploration of the views of both Nightingale and Leigh-Smith is important to gain a clearer understanding of the existing relationship between nursing and feminism. In keeping with the aims of feminist inquiry, women's experiences, specifically those of Nightingale and Leigh-Smith, are the major 'objects' of investigation. The concluding interpretation provides a synthesis that is emancipatory as well as knowledge generative.

England↗
PubMed1979

Verbal tests and transsexualism.

Gender discriminating vocabulary tests administered to a consecutive series of 53 male transsexuals show different results. The Slater Selective Vocabulary Test, Cohen's factors and the Terman-Miles Attitude Interest Analysis Test (M-F) show male transsexuals to have a higher degree of feminization than normal controls. The Wechsler-Bellevue Vocabulary Test and the Wechsler M-F Test are difficult to interpret, and do not show a clear trend of feminization in transsexual males. The investigation has shown that male transsexuals have a vocabulary which differs from that of normal males in the direction of greater feminization.

Humans↗
PubMed1982

Androgen resistance syndromes.

Hereditary defects that impede androgen action cause resistance to the hormone both during embryogenesis and in later life and hence usually cause developmental defects of the male urogenital tract. In genetic males such defects produce a phenotypic spectrum ranging from infertile but otherwise normal men to individuals with varying degrees of ambiguous genitalia to phenotypic women. These disorders can be classified on the basis of the step in androgen action that is impeded by the individual mutations. 5 alpha-Reductase deficiency is an autosomal recessive enzyme defect that impairs the conversion of testosterone to dihydrotestosterone. The internal male genital tract virilizes normally, but the external genitalia are predominantly female in character. The syndrome is the result of one of several mutations that impair the function of the 5 alpha-reductase enzyme. A variety of disorders influence the androgen receptor that mediates the action of both testosterone and dihydrotestosterone. At least four phenotypic variants can be distinguished: complete testicular feminization, incomplete testicular feminization, the Reifenstein syndrome, and the infertile male syndrome, each of which is inherited as an X-linked trait. Absence of receptor binding is found commonly in complete testicular feminization, but qualitative and/or less severe quantitative defects in receptor function can be associated with all four variants. A third type of disorder, receptor positive resistance, also causes variable defects in male development and is associated with normal 5 alpha-reductase activity and normal androgen receptor. The underlying defect is presumed to lie at the intranuclear site or sites of action of the hormone-receptor complex.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1976

Dihydrotestosterone binding by cultured human fibroblasts. Comparison of cells from control subjects and from patients with hereditary male pseudohermaphroditism due to androgen resistance.

Dihydrotestosterone binding was measured in culture fibroblasts from 14 control subjects and from 12 patients with five different types of hereditary male pseudohermaphroditism. Two assays of binding were used--an intact monolayer assay and density gradient centrifugation of cell extracts. In the intact monolayer assay of normal cells the uptake of [3H]dihydrotestosterone consisted of two components. The first was a high affinity component that exhibited saturation at approximately 1 nM dihydrotestosterone. The second was a low affinity component that was not saturable with concentrations of steroid up to 5 nM. Twice the number of high affinity binding sites were present in fibroblasts grown from genital skin (foreskin, labia majora, and scrotum) as from nongenital sites (37 vs. 14 fmol/mg protein). In the density gradient assay in 5-10% sucrose, the major peak of dihydrotestosterone binding was in the 8S region in low molarity buffer and in the 4S region in 0.5 M KCl. High affinity binding was normal in cells from two patients with familial incomplete male pseudohermaphroditism, type 2, an autosomal recessive defect in which dihydrotestosterone formation is deficient, and in cells from a patient with male pseudohermaphroditism due to 17 beta-hydroxysteroid dehydrogenase deficiency, an autosomal recessive defect of testosterone synthesis. High affinity binding was low by both methods in fibroblasts from five patients with complete testicular feminization. Furthermore, binding by both methods was also low in cells from three subjects with familial incomplete male pseudohermaphroditism, type 1, a presumed X-linked recessive disorder of androgen resistance, and in fibroblasts grown from a subject with the incomplete form of testicular feminization. The finding that dihydrotestosterone binding is abnormal in two forms of hereditary androgen resistance in addition to complete testicular feminization suggests either that these disorders are the result of allelic mutations affecting the function of the androgen-binding protein or that normal dihydrotestosterone binding requires the participation of more than one gene product.

Binding Sites↗