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Anorexia is a debilitating disorder which affects significant numbers of young women. Brumberg has suggested a causal relationship in young women between feminism and anorexia. In this study, traditional-aged female college students completed the Attitudes Toward Women Scale and the Eating Attitudes Test. The hypothesized relationship between feminism and anorexia was not found.
Occupational therapy is a predominantly female profession; 93% to 95% of occupational therapists are women. The implications and ramifications of this reality have seldom been directly addressed. In this article, beliefs about balance, activity, environment, and autonomy are explored from the perspectives of occupational therapy, feminism, holistic health, and medicine. The assertion that occupational therapy has more in common philosophically with feminism and holistic health than it does with medicine is supported. This awareness provides a new framework for examining current issues of concern to the profession, such as support for purposeful activity, existence outside the mainstream of power holders, and problems and powers inherent in being seen as a women's profession. Recommendations are made that occupational therapists commit more money and energy to encourage, facilitate, and support female leadership; develop innovative strategies for keeping members who take time out to raise families informed; support more holistic and feminist reorganization of work settings; instill awareness of these issues in our students; and address our strengths as a women's profession. All occupational therapists must also confront their own anti-women prejudice.
Radioreceptor assay and thermostability test for the androgen receptor in two cases with complete testicular feminization syndrome were performed in regard to the fibroblasts cultured from genital skin on the basis of dispersed whole cell binding assay (Eil et al., 1980). No [3H]dihydrotestosterone binding to the androgen receptor was observed in case 1 (receptor negative), while maximum binding capacity and dissociation constant of androgen receptor for [3H]dihydrotestosterone in case 2 were 21000 sites per cell and 1.67 x 10(-10) M (receptor positive). The specific binding of [3H]dihydrotestosterone to the androgen receptor in case 2 decreased remarkably to 6.6% after high temperature (42 degrees C) incubation in comparison with that at 22 degrees C incubation. The specific binding of [3H]dihydrotestosterone to the androgen receptor in normal controls decreased down to 81.6% at high temperature incubation. Thermostability test was useful to demonstrate qualitative abnormality of androgen receptor in receptor positive testicular feminization syndrome.
PURPOSE: We document the postpubertal outcome of feminizing genitoplasty. MATERIALS AND METHODS: A total of 14 girls, mean age 13.1 years, with congenital adrenal hyperplasia were assessed under anesthesia by a pediatric urologist, plastic/reconstructive surgeon and gynecologist. Of these patients 13 had previously undergone feminizing genitoplasty in early childhood at 4 different specialist centers in the United Kingdom. RESULTS: The outcome of clitoral surgery was unsatisfactory (clitoral atrophy or prominent glans) in 6 girls, including 3 whose genitoplasty had been performed by 3 different specialist pediatric urologists. Additional vaginal surgery was necessary for normal comfortable intercourse in 13 patients. Fibrosis and scarring were most evident in those who had undergone aggressive attempts at vaginal reconstruction in infancy. CONCLUSIONS: These disappointing results, even in the hands of specialists, highlight the importance of late followup and challenge the prevailing assumption that total correction can be achieved with a single stage operation in infancy. Although simple exteriorization of a low vagina can reasonably be combined with cosmetic correction of virilized external genitalia in infancy, we now believe that in some cases it may be best to defer definitive reconstruction of the intermediate or high vagina until after puberty. The psychological issues surrounding sexuality in these patients are inadequately researched and poorly understood.
This paper reports on a 56-year-old patient with a history of "testicular feminization syndrome" who was admitted to hospital because of a rapid gain in her abdominal girth (106 cm). A benign cyst was removed laparotomically which, histologically, was equivalent to a cystadenofibroma. Based on this case report, the clinical significance of testicular feminization syndrome and the necessity for gonadectomy due to the risk of growth of a possibly malignant tumor are discussed.
In the nematode Caenorhabditis elegans, the zinc finger transcriptional regulator TRA-1A directs XX somatic cells to adopt female fates. The membrane protein TRA-2A indirectly activates TRA-1A by binding and inhibiting a masculinizing protein, FEM-3. Here we report that a part of the intracellular domain of TRA-2A, distinct from the FEM-3 binding region, directly binds TRA-1A. Overproduction of this TRA-1A-binding region has tra-1-dependent feminizing activity in somatic tissues, indicating that the interaction enhances TRA-1A activity. Consistent with this hypothesis, we show that tra-2(mx) mutations, which weakly masculinize somatic tissues, disrupt the TRA-2/TRA-1A interaction. Paradoxically, tra-2(mx) mutations feminize the XX germ line, as do tra-1 mutations mapping to the TRA-2 binding domain. We propose that these mutations render tra-2 insensitive to a negative regulator in the XX germ line, and we speculate that this regulator targets the TRA-2/TRA-1 complex. The intracellular domain of TRA-2A is likely to be produced as a soluble protein in vivo through proteolytic cleavage of TRA-2A or through translation of an XX germ line-specific mRNA. We further show that tagged derivatives of the intracellular domain of TRA-2 localize to the nucleus, supporting the hypothesis that this domain is capable of modulating TRA-1A activity in a manner reminiscent of Notch and Su(H).
We report the case of a 14-year-old girl with a testicular feminization syndrome. The inguinal cryptorchid testis contained plurifocal hamartomas ranging from 0.5 to 1 cm. They were composed of tubules lined by cylindrical Sertoli cells immunoreactive for alpha-inhibin and p30/32(MIC2). The stroma contained few Leydig cells. Ultrastructural study showed tubules with immature Sertoli cells. The testicular feminization syndrome is caused by mutations of the androgen receptor gene. Patients with male genotype 46, XY have a female morphotype with external sexual organs without ambiguity. They have neither uterus nor ovary but two cryptorchid testis in which sex-cord stromal tumors can develop. Their malignant transformation is rare but requires preventive bilateral orchidectomy.
A case of a 31-year-old patient showing the typical features of testicular feminization is presented.--Laparotomy was performed, and a large cystic tumour at the place of the right gonad was removed. Microscopically dysgenetic testicular tissue was found. The cyst was lined with cuboid epithelium. Its wall contained smooth muscle fibers.--Probably this cyst was a derivative of the Muellerian ducts.--Today, androgen resistance of the target organs is considered to be the cause of testicular feminization, while the production of hormones of the fetal gonads is normal.--In cases with rudiments of the Muellerian ducts there may be an insufficiency of the oviduct repressor.
Feminizing ovarian tumors and polycystic ovarian disease may cause endometrial cancer by abnormal, unopposed endogenous estrogenic stimulation. We reviewed the clinical course of 72 endometrial cancer patients with a concomitant feminizing ovarian tumor or polycystic ovarian disease and compared tumor characteristics and treatment results with those exhibited by 523 patients treated for endometrial cancer alone. With functioning ovarian tumor and with polycystic ovaries, the cancer tended to be more often low-grade, low-stage, and superficial than did endometrial cancer alone. The high 5-year and 10-year survival rates observed in our functioning ovarian tumor-polycystic ovary patients support the conclusion that endometrial carcinoma with a coexistent endogenous estrogenic stimulus has a more favorable prognosis (P less than 0.01) than endometrial carcinoma alone.
A light microscopical study of an excised testis from a 14 1/2-year-old girl with incomplete type of testicular feminization syndrome revealed a carcinoma-in-situ pattern in a part of the gonad. An identical histological pattern has repeatedly been demonstrated in infertile men who developed gross testicular germ cell tumours. It is suggested that germ cell carcinomas in patients with testicular feminization syndrome may be preceded by this characteristic intratubular germ cell abnormality.
Although it has long been known that the lack of androgen dependent differentiation in patients with testicular feminization is secondary to end organ insensitivity, the molecular basis of this genetic disorder has not been elucidated. In the present report a rodent model for testicular feminization is described. The Stanley-Gumbreck pseudohermaphroditic rat has an inherited disorder characterized by a female phenotype, a male genotype and tissue insensitivity to androgens. Even though male differentiation does not occur when these animals are treated with physiologic doses of testosterone, some androgen dependent growth is evident when 100-fold larger doses of testosterone are given. Studies of androgen metabolism in the psuedohermaphroditic animals indicate that testosterone transport and metabolism to dihydrotestosterone are normal. However, intranuclear retention of dihydrotestosterone is defective. These findings suggest that the androgen insensitivity of the pseudohermaphroditic rat is due to an inherited abnormality of a regulatory protein which renders the nucleus of the cell incapable of concentrating androgens at their proposed intracellular site of action. The pseudohermaphroditic rats also have a defect of testicular and adrenal steroid synthesis in addition to the androgen insensitivity. The relation of these two abnormalities in rat and in man are discussed.
Thermolability of androgen binding was compared in fibroblasts cloned from normal female skin, skin from a subject with testicular feminization whose mutation is known to be associated with a thermolabile androgen receptor, and from the mother of the subject with testicular feminization. Seven of 28 clones studied from the mother exhibited thermolability of binding, indicating that the mutant gene that causes thermolability of binding, like the gene responsible for the normal androgen receptor, is X-linked.
Is the H-Y antigen released by the Rat embryo testis responsible for the feminization of the Chick embryo testis, when culturing both organs side by side in vitro? The results of the present study point rather to testosterone as the feminizing agent.
This is a case of a young woman who had testicular feminization syndrome and developed a seminoma in an undescended intrapelvic testis. Androgen insensitivity (testicular feminization) syndrome is a rare inherited form of male pseudohermaphroditism that occurs in phenotypically normal women with adequate breast development, normal external genitalia, a vagina of variable depth, absent uterus, and sparse or absent pubic and axillary hair. The gonad (undescended testes) may be intraabdominal, inguinal, or labial. These patients characteristically have male karyotype (XY) and negative sex chromatin and are at increased risk of undergoing malignant transformation of the undescended gonad. We review the literature emphasizing the biochemical and endocrinologic abnormalities leading to the syndrome, as well as the morphologic abnormalities (light microscopic) of the undescended testes, diagnosis, and therapeutic management.
The construction of social definitions is important, as these definitions are ultimately translated into public policies. This article explores the emergence of the concepts of the advantaged elder and the feminization of poverty. It is a paradox that society has simultaneously embraced these two concepts when the elderly population, especially the subpopulation of those who are very old, is overwhelmingly women. The theoretical shortcomings of both concepts are examined, and a broader model of economic well-being that emphasizes the interactive nature of gender, race, and class is proposed. The implications of societal perceptions of the advantaged elder and the feminization of poverty for older women are addressed.
A case of complete testicular feminization (Morris syndrome) in a male pseudohermaphrodite is described. The results of the hormone analyses and the histological features of the resected gonad are presented. The literature is reviewed with special reference to whether gonadectomy should be performed in the pre or post-pubertal period. We advocate early castration because of the high incidence of germ cell neoplasia and the possibility of virilization in case of incomplete androgenic resistance. Our approach is based on the satisfactory feminization achieved by exogenous estrogen therapy.
A 31-year-old patient with incomplete testicular feminization syndrome characterized by a 46, XY karyotype in a phenotypic female with absent müllerian structures, marked clitoromegaly, testes and wolffian duct structures, partial labioscrotal fold fusion, and male levels of circulating androgens is described. She was challenged with estradiol benzoate (EB) to simulate the preovulatory surge of estradiol seen in cycling women. This EB challenge resulted in a negative feedback response for FSH but an LH surge similar to that induced with EB in cycling women. This suggests that in the incomplete testicular feminization syndrome there is hypothalamic or pituitary resistance to the blocking effects of androgens on LH surge production.
The steroid response of testes to exogenous gonadotropin administration was studied before castration in a patient with the complete form of the testicular feminization syndrome. Urinary steroid determination were made along with measurements of plasma testosterone during adrenal suppression with dexamethasone and after stimulation with human menopausal gonadotropin (HMG) and HMG plus human chorionic gonadotropin (HCG). Our data provide evidence that the gonads in the testicular feminization syndrome synthesize steroids normally. Estrogens and testosterone are secreted by the testes, and the Leydig cells of the testes are capable of responding to exogenous HMG and HCG stimulation. These findins are consistent with the hypothesis that there is no abnormal testicular steroidogenesis in these genotypic males. Additional evidence is provided that these gonads secrete testosterone in amounts comparable to those of normally functioning testes. Failure of virilization in the presence of androgen secretion as indicated by previous authors is probably the result of a deficiency of androgenic action at the end organs. The presence of sparse pubic and axillary hair in the mother and the finding of the same type of karyotype (46,XY) in a sibling suggest that hereditary factors play a role in this disorder.