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Feminism and nursing.

Feminism provides a personal, philosophic and political means for analyzing the realities of women's lives as lived in patriarchal systems. It is not a single line of thought; multiple approaches have been developed that provide diverse avenues for confronting systematic injustices while learning to value ourselves as women. Jo Ann Ashley, recognizing that new realities must emerge from within nursing rather than from other groups, states: "For many years we have heard that nursing is at the crossroads. Nursing never seems to get over being at a crossroads. Indeed, nursing has been at a crossroads many times, but instead of taking a new road, leaders in the profession always choose to continue bearing the burden of continuing to live out the subservient role under the patriarchal system, rather than taking a new road that can lead beyond patriarchy. Nursing is no longer at a crossroads. It is at a turning point. It needs to turn away from being the "token torturer" of itself and other women. It needs to turn toward the health awaiting women in a woman-defined, woman-created world that lies beyond patriarchal ideas and institutions." Movement in this direction requires becoming familiar with feminist literature and the insights that women scholars have provided. In nursing, a feminist perspective requires an uncompromising questioning of the forces that divide us from one another, the ethics of our actions, and our co-optation into the unhealthy environment of the current health care system.

Female↗

Ultrastructure of the gonad in the testicular feminization syndrome.

The ultrastructural findings on the gonad from a patient with testicular feminization syndrome (TFS) are reported. One gonad was the site of dysgerminoma. The other was a dysgenetic testis composed of seminiferoud and Sertoli cell tubules and ovarian cortical stroma-like tissue. Ultrastructurally the tubules were lined by immature Sertoli cells and cells indistinguishable from dark ovarian stromal cells. Similar and/or identical cells were found in the ovarian-like stroma and in the interstitial tissue between the tubules. There were mature and immature Leydig cells in the intertubular areas. The ovarian cortical-like tissue contained dark and light cells like the normal ovary. Some of the dark cells contained fat droplets like thecoma cells. All these findings point to the dysgenetic nature of the gonad in the TFS as well as the functional activity and or inactivity of certain cells found in it.

Androgen-Insensitivity Syndrome↗

Effect of estrogens on luteinizing hormone release in testicular feminization syndrome before and after gonadectomy.

The effect of exogenous estrogens on luteinizing hormone release was studied in three siblings with complete testicular feminization syndrome. Two subjects, 21 and 20 years old, were postpubertal. The third, 15 years old, was in the early pubertal stage. An estrogen provocation test was performed in which 20 mg of conjugated estrogens were administered intravenously and serum follicle-stimulating hormone and luteinizing hormone levels were assessed every 12 hours for 96 hours under basal conditions, on day 5 of an eight-day treatment with 0.2 mg/day ethinyl estradiol orally, and on day 5 of a subsequent eight-day treatment with 0.2 mg/day ethinyl estradiol and 120 mg/day cyproterone acetate orally. The first two tests were repeated one month after gonadectomy. During pregonadectomy treatments there was an overall luteinizing hormone fall. After gonadectomy, the two postpubertal subjects exhibited luteinizing hormone surges during ethinyl estradiol treatment -in one as a single peak and in the other as multiple peaks. A positive feedback effect was not induced in the youngest patient either before or after gonadectomy as in normal prepubertal and early pubertal females. The data suggest that testosterone or some other testicular factor inhibits estrogen induced positive feedback for luteinizing hormone. This inhibition mechanism acts independently of the testosterone cytosol receptor.

Adolescent↗

Steroid metabolism in the gonads of a patient with testicular feminization. I. Metabolism of cholesterol, pregnenolone, progesterone and dehydroepiandrosterone in vitro.

The metabolism of cholesterol-4-14C, pregnenolone-4-14C, progesterone-4-14C and dehydroepiandrosterone-4-14C in a right abdominal and a left inguinal testis of a patient with testicular feminization was studied by a double isotope method in vitro. One of the main metabolites found in all incubations was testosterone. In incubations with cholesterol the delta4-pathway seems to be preferred. The rate of conversion of cholesterol to testosterone in the right testis was 1,27% and in the left testis 4,90%. Pregnenolone was converted to testosterone in the right testis at a rate of 6,61% and in the left testis at a rate of 3,23%. The conversion for testosterone using progesterone as precursor was 13,19% and 3,88% respectively and 11,97% of dehydroepiandrosterone was converted to testosterone in the right testis and 12,32% in the left testis. These findings are compared with data from the literature and conclusions are drawn.

Adolescent↗

Classical seminoma in a case of testicular feminization syndrome.

The appearance of a seminoma in a 16-year-old patient with testicular feminization syndrome is reported. There is a high incidence of malignant degeneration of the gonads associated with this syndrome. The consensus is that exploration and gonadectomy are indicated immediately after puberty.

Adolescent↗

Psychological characterization of testicular feminization syndrome.

Ten cases with testicular feminization syndrome (TFS) diagnosed at the National Institute of Endocrinology and Metabolism, were studied. The patients were interviewed and subjected to the following psychological tests: Raven's Progressive Matrices, the MMPI, the 16PF, and the TAT. Laboratory determinations included: nuclear chromatin, karyotype, FHS, LH, estradiol, testosterone and nitrogen retention test. Intellectual achievement was found normal, and as far as psychological stability is concerned (MMPI) there was no common profile typical of the group. Psychosexual attitudes showed alterations related to acceptance of body image, fears to be unable to maintain the stability of the couple, and lack of a strong maternal drive. Personality profile manifested two outstanding traits in the group: Dominance (E+) and Shrewdness (N+), the former being remarkably high for a female population. A hypothesis is advanced in regard to the psychological alterations of the possible role of partial androgenization of the central nervous system in these patients.

Adolescent↗

Danazol suppression of gonadal estradiol-17 beta secretion--report of two sibling cases with a complete form of testicular feminization on gonadal ultrastructure and endocrine status.

It has been established that the pathogenesis of a complete form of testicular feminization syndrome (TFM) is due to end-organ unresponsiveness to androgens. In the present study, two sibling cases with TFM have been reported with special reference to the effect of danazol (a derivative of 17 alpha-ethynyltestosterone) on gonadal estradiol-17 beta (E2) secretion in vivo and in vitro. Both patients showed hypergonadotropic-hypergonadism with good response to LH-RH. In one case, peripheral blood E2 levels seemed to fall independently of gonadotropins during danazol administration in vivo. Administrations of danazol to the culture media also inhibited E2 secretion from the cultured monolayered cells of the testes. These results suggest a direct inhibitory effect of danazol on gonadal E2 secretion. However, the feedback mechanisms of hypothalamic-pituitary units to E2 were preserved in both cases. Spermatogeneses were almost undetectable as in immature embryonal testes when using either light or electron microscopies, though spermatogonia were differentiated from Sertoli cells by these techniques. Finally, plasma T and E2 levels in both patients were considerably lower after gonadectomy.

Adult↗

[Ultrastructural findings in testicular feminization].

On the basis of light and electron microscopic findings problems of the morphology of gonads in testicular feminization syndrome (TF) are discussed. Within the tubules 3 cell types (light, dark, intermediate) can be distinguished which are regarded as different functional forms of Sertoli cells. Germ cells were not observed definitely. There are, however, remarkable difficulties in morphological distinction between undifferentiated Sertoli and germ cells. It is underlined that fine structure of gonads and cellular composition of tubules as well as the amount of interstitial cells depend on the age of the individuum and on the form of TF (complete and incomplete).

Adult↗

Ultrastructure of the gonads in the testicular feminization syndrome.

The testicular feminization syndrome is a form of familial male pseudohermaphroditism transmitted by an X-linked gene. The karyotype is 46XY. Affected patients resemble normal females phenotypically. To date, only eight cases of this syndrome have been studied by electron microscope. This study reports the ultrastructural appearance of the gonads in two additional patients. The presence of mature interstitial cells with a rich endoplasmic reticulum suggests that the pathologic defect is not due to a lack of androgenic hormone production by the testes but is caused by peripheral end-organ resistance.

Adolescent↗

Testicular feminization in the Finnish racoon dog (Nyctereutes procyonoides).

The clinical features of testicular feminization in the racoon dog (Nyctereutes procyonoides) are reported. The condition is characterized by a normal male karyotype, but a mixed phenotype consisting of vulva, enlarged clitoris and scrotal testes. Partial spermatogenesis with a relative arrest at the first meiotic division was observed. The likely underlying genetic defect and mode of inheritance are discussed, together with implications for breeding programmes.

Androgen-Insensitivity Syndrome↗

Structural and functional factors related to testicular neoplasia in feminized rats.

Testicular tumors in King-Holtzman hybrid rats with testicular feminization (tfm) were seen as firm, rounded masses of tissue consisting of Leydig cells, myoid cells, and fibroblast-like cells. The cytoplasm of Leydig cells contained well-developed smooth endoplasmic reticulum, pleomorphic mitochondria with numerous cristae, and many lipid droplets. Mitochondria were numerous and varied in size and shape. Their cristae were in the form of tubules, and lipid-like inclusions were frequently seen in the mitochondrial matrix. Lysosomes, rough endoplasmic reticulum, and Golgi bodies were also scattered in the cytoplasm. An in vitro study showed that more testosterone was produced in the tumor than in the testes of rats with tfm; however, the amount in both was less than normal. Testicular tumor-bearing rats with tfm exhibited slightly higher levels of plasma testosterone than did non-tumor-bearing animals with tfm. Levels in both were significantly higher than normal. Testicular tumor cells growing in culture medium supplemented with luteinizing hormone (LH) contained more protein and synthesized more androgen and DNA than did those growing in culture medium without LH. Observed under the scanning and transmission electron microscopes, the LH-stimulated cells had well-developed cytoplasmic organelles and inclusions and surface specializations such as numerous microvilli, large blebs, and other microextensions. They adhered well to the glass surface. These results indicated that Leydig cells in testicular tumors of rats with tfm had morphologic characteristics of steroid-producing cells. In addition these cells were capable of producing steroids, and this capability was enhanced by the presence of LH.

Androgen-Insensitivity Syndrome↗

Testicular feminization syndrome.

The testicular feminization syndrome is an uncommon condition with a familial background. The clinical features of a typical case are presented, as well as its management. It is emphasized that these patients and their parents must be treated with the greatest sensitivity when the condition is explained to them.

Adult↗

The androgen receptor in the testicular feminized (Tfm) mouse may be a product of internal translation initiation.

Androgen insensitivity in the testicular feminized (Tfm) mouse is caused by frame-shift mutation in the androgen receptor (AR) mRNA, which results in a stop codon in the amino terminus. Despite this mutation, a smaller sized protein corresponding to the DNA- and steroid-binding domain of the AR can be synthesized from the cloned Tfm AR cDNA by in vitro translation. The Tfm AR construct was demonstrated to express a protein capable of binding androgen with an affinity similar to the cloned wild-type AR. Although the Tfm AR product failed to transactivate mouse mammary tumor virus-long terminal repeat (MMTV-LTR) promoter when low concentrations (100 ng) of Tfm AR vector were cotransfected, higher concentrations (5000 ng) resulted in a residual amount of transactivation, suggesting lower level transactivating capabilities. By cotransfecting the Tfm AR expression vector with the wild-type receptor, it was demonstrated that the product of the Tfm AR gene is capable of inhibiting the transactivation activity of the wild-type receptor. These data suggest that although the Tfm AR mRNA fails to produce a full-length AR because of the frame-shift mutation, a smaller protein capable of binding both steroid and DNA can be produced by translation from an internal initiation codon. This product could account for the low levels of androgen-binding activity detected previously in the Tfm mouse.

Androgen-Insensitivity Syndrome↗

[Testicular feminization. The androgen insensitivity syndrome. A case report].

Testicular feminization is a syndrome due to androgen insensitivity. It occurs in a complete and incomplete form. The case of a 17 years old girl with complete androgen insensitivity syndrome is reported. Patient came to medical attention because of primary amenorrhea as the only pathology, with normal external, female genitalia. Diagnosis, findings, management and a five months follow up, are described, as well as a review of this subject.

Adolescent↗

Feminizing adrenal adenoma in a boy. Case report and literature review.

Feminizing adrenal tumors in young boys are rare; such patients initially show bilateral gynecomastia, and may have signs of virilization. We present a patient with bilateral gynecomastia, left adrenal adenoma, and elevated estrogen levels but normal levels of 17-ketosteroids.

17-Ketosteroids↗

[The testicular feminization syndrome combined with disseminated hemangiomatosis].

It is described a new born child with many hemangiomas on the liver. It is made a karyogram to exclude. The possibility of chromosome disease. We fixed male karyotype 46 XY--syndrome Morris. We found out that it is a rare combination of testicular feminization with disseminated hemangiomatosis. After the medical treatment with high doses of cortisone the hemangiomas decreased their sizes.

Androgen-Insensitivity Syndrome↗

Bilateral laparoscopic gonadectomy for testicular feminization syndrome.

Defects of androgen receptor gene lead to testicular feminization syndrome, which is one of the most common etiology of male pseudohermaphroditism. A 22-year-old phenotypic female with primary amenorrhea and insomnia is presented. Gross appearance revealed sparse axillary and pubic hair, poor breast development, clitoromegaly and absence of vagina. Ultrasound demonstrated no evidence of the uterus or adnexal structures, but the prostate gland was found. The laboratory data showed elevated follicle-stimulating hormone and a male 46, XY karyotype. Computed tomography localized the position of bilateral undescending testes, which were removed by operative laparoscopy procedures later. The patient was discharged without complication postoperatively.

Adult↗