Feminizing and non-feminizing Sertoli cell tumors.
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It is a well-known fact that nursing and feminism have enjoyed an uneasy alliance. In recent years, however, nursing has begun to recognize the importance of feminism. Nevertheless, the literature still rarely addresses the relevance of feminism for public health nursing. In this article, I articulate the relevance of feminism for public health nursing knowledge and practice. First, I define and describe feminism and public health nursing and then I discuss the importance of feminism for public health nursing practice. The importance of feminism for the metaparadigm concepts of public health nursing is then reviewed. Finally, I examine several existing challenges relating to feminism and public health nursing research, education, and practice. The thesis of this article is that feminism is vitally important for the development of public health nursing and for public health care.
Feminist criticism of health care and of bioethics has become increasingly rich and sophisticated in the last years of the twentieth century. Nonetheless, this body of work remains quite marginalized. I believe that there are (at least) two reasons for this. First, many people are still confused about feminism. Second, many people are unconvinced that significant sexism still exists and are therefore unreceptive to arguments that it should be remedied if there is no larger benefit. In this essay I argue for a thin, "core" conception of feminism that is easy to understand and difficult to reject. Core feminism would render debate within feminism more fruitful, clear the way for appropriate recognition of differences among women and their circumstances, provide intellectually compelling reasons for current non-feminists to adopt a feminist outlook, and facilitate mutually beneficial cooperation between feminism and other progressive social movements. This conception of feminism also makes it clear that feminism is part of a larger egalitarian moral and political agenda, and adopting it would help bioethics focus on the most urgent moral priorities. In addition, integrating core feminism into bioethics would open a gateway to the more speculative parts of feminist work where a wealth of creative thinking is occurring. Engaging with this feminist work would challenge and strengthen mainstream approaches: it should also motivate mainstream bioethicists to explore other currently marginalized parts of bioethics.
The problem was approached whether the feminizing action of oestrogens or androgens on the chick embryo testes could be antagonized by anti-oestrogens or anti-androgens. 100 micrograms of either tamoxifen, cyproterone acetate or compound RU 23908 were injected into the chick embryo after 4 days of incubation and 100 micrograms of either oestradiol benzoate or diethylstilboestrol or 1 mg of either androsterone, dehydroepiandrosterone, 5 alpha-dihydrotestosterone or 5 alpha-androstanedione were given one day later. The surviving embryos were sacrificed when 14-17 days old and their gonads were examined morphologically and in some cases also histologically. Control embryos were only given oestrogens or androgens. Out of 20 surviving embryos treated with oestradiol only, 10 were genetic females and 10 strongly feminized males. After tamoxifen treatment, out of 20 embryos, 11 were females, 7 normal males and 2 slightly feminized males. Thus, tamoxifen suppressed the feminizing action of oestradiol. It antagonized also the feminizing action of diethylstilboestrol. Neither cyproterone acetate nor compound RU 23908 suppressed the feminizing action of androsterone or diethylstilboestrol. But tamoxifen interfered with the androgens, preventing the feminization of the testes. It is suggested that androgens bind to the oestrogen receptor.
Wolbachia, which forms a group of maternally inherited bacteria in arthropods, often cause reproduction alterations in their hosts, such as cytoplasmic incompatibility, parthenogenesis, male-killing, hybrid breakdown and feminization. To date, Wolbachia-induced feminization has been reported only in isopods. Here we report that a Wolbachia strain feminizes an insect host, Ostrinia furnacalis. Among 79 wild females of O. furnacalis examined, Wolbachia infection was detected in 13 females. Twelve of the 13 infected females produced all-female progenies, and this trait was maternally inherited. Tetracycline treatment of thelygenic matrilines resulted in the production of all-male progenies. The present findings indicate that the Wolbachia infection induces feminization of genetic males in O. furnacalis. Differences in the Wolbachia-induced feminization in O. furnacalis and that in isopods are discussed along with the differences in sex determination mechanisms between insects and isopods. Phylogenetic analysis of the wsp gene sequence of Wolbachia suggests independent evolutionary origins for the Wolbachia-induced feminizations in O. furnacalis and in isopods. Our findings over 5 years suggest that the infection has been maintained at a low prevalence in the O. furnacalis population.
Taenia crassiceps cysticercosis results in an impressive feminization in male mice during chronic infection, characterized by increased serum estradiol levels 100 times their normal values, while those of testosterone and dihydrotestosterone are decreased by 85 and 95% respectively. Concomitantly, the levels of follicle-stimulating hormone and IL-6 are increased 70 and 90 times their normal values in the infected male mice. Since a specific Th1/Th2 shift of the immune response has been previously reported during the chronic infection, and this shift may be associated with the feminization process, we proposed that this shift is induced by immunoendocrine interactions during the disease, and this gives way to a change in the initial resistance to the infection in the male mice, which become as susceptible as female mice. To confirm this hypothesis, we depleted immune system activity in two different ways: total body irradiation and neonatal thymectomy. Our results show that when immune system activity is depleted using either strategy, the male mice do not feminize, and the levels of follicle-stimulating hormone and IL-6 are inhibited. Depletion of IL-6 using IL-6(-/-) knockout mice does not produce the feminization process stated above, while restitution of the IL-6(-/-) knockout, irradiated, and thymectomized mice with murine recombinant IL-6 restores the feminization process. Expression of the IL-6 gene was found only in the testes and spleen of infected animals. Our results illustrate the importance of immunoendocrine interactions during a parasitic disease and show a possible new mechanism of parasite establishment in an initially resistant host.
This research programme commenced in West Africa, where it was found that individuals with kwashiorkor gynaecomastia were feminized. This was also reinforced by the interacting dominant maternal socialization practices (Dawson, 1966). This was confirmed with feminized responses for adult male rats, on the Tolman-Maze (Dawson, 1972), while as well confirmed neonatally, for both feminized male and female rats (Dawson, Cheung and Lau, 1973, 1975). The present experiment tests the interacting effects of various levels of environmental stimulation, high, normal and low (Levitsky and Barnes, 1972), using feminized male rats. Thus castration, oestrogen and castration, and oestrogen feminized males, were contrasted with male and female controls. The results confirmed the physiological growth curves and other anatomical differences. As well, the activity data confirmed the hypothesis, for the combined samples (where high Ns mean more reliability) and also the environmental stimulation (F ratio: d.f. 18 and 57, 11.37, p less than 0.001; low Ns here mean lower reliability). However, for the symmetrical maze, the results for the combined samples, were not as convincing as in Dawson et al. (1973, 1975), although the environmental stimulation produced significant results in many cases, including a significant interaction for the analysis of variance (F ratio: d.f. 18 and 57, 3.12 p less than 0.001).
The relationship between gender-related personality traits, on one hand and drinking, permissiveness towards drinking, and social as well as personal problems associated to drinking on the other, was studied in a general population sample from the City of Morelia, Mexico. Four gender-related traits scales were used for measuring assertive and aggressive masculinity and affective and submissive feminity, in addition to a standardized questionnaire for assessing drinking and other associated behavior. Some of the main results showed that people with high scores in affective feminity were less willing to allow drinking. Men who adopted a submissive feminine role and women with high masculine aggressive scores were more permissive as regards drinking. Among men, assertive masculine and affective feminine traits were more characteristic among those who drank than among abtainers. Drinking among women was related to liberal attitudes towards drinking and to aggressive masculinity. As regards the number of drinks consumed per month, assertive masculinity and liberal attitudes among men and affective feminity and liberal attitudes among women predicted the number of drinks. Affective feminity was negatively related to drinking. Regarding drinking-associated problems, frequency of drunkenness and submissive feminity among males predicted greater personal and social problems. Among women, drunkenness frequency and number of drinks were the most significant predictors. Contrary to what has been found in other countries, gender was a better drinking predictor than gender-related personality traits.
The metabolism of radioactive testosterone simultaneously administered intravenously and either orally or percutaneously has been studied in seven patients with the syndrome of testicular feminization and compared with that of normal males and females. This investigation was carried out in order to determine the relative contribution to urinary 17-oxo and 17beta-hydroxy androstane steroids of labeled testosterone, according to its mode of administration. In normal males the yields of urinary 5alpha-androstane-3alpha,17beta-diol (androstanediol) originating from either an intravenous or a percutaneous dose of testosterone were respectively 3 and 6 times higher than those arising from an oral dose which perfuses the liver directly. These data indicate that in normal males, testosterone might be 5alpha-hydrogenated outside the liver. By contrast in patient with feminizing testes, because the contribution to androstanediol of radioactive testosterone is identical whatever its mode of administration, the extrahepatic 5alpha-reduction of this substrate seems very unlikely. The metabolic abnormalities observed in patients with testicular feminization syndrome may be reproduced in normal males by estrogen treatment. Nevertheless, the sensitivity of the patients to estrogen seems to be 10 times greater than that of normal males. This sensitivity was appreciated from the reduction of radioactive testosterone intravenously injected to urinary 17beta-hydroxy-5alpha-androstan-3-one and androstanediol and also from the level of plasma binding for testosterone. This level was significantly higher (P < 0.05) in patients with feminizing testes than in normal males. The level increased dramatically after administration of a low dose of estrogen whereas this effect was not observed in normal males under the same experimental conditions. In light of these results the defect of extrahepatic 5alpha-reduction of testosterone observed in patients with feminizing testes does not necessarily reflect an enzymatic impairment but might be related to an abnormal synthesis of plasma binding protein(s) under the effect of circulating estrogens so that an abnormally small amount of unbound testosterone may be available in target cells for 5alpha-reduction.
The metabolism of 4-[4-14C]androstene-3,17-dione was studied in the microsomal fraction of rat livers after continuous administration of human GH (hGH) in Alzet osmotic minipumps under varying conditions. hGH caused a complete feminization of hepatic steroid metabolism (i.e. increased the 5 alpha-reductase and decreased the 6 beta- and 16 alpha-hydroxylase activities) in normal male rats when infused at a rate of 5 microgram/h for 7 days. Hypophysectomy and castration or adrenalectomy and thyroidectomy of male rats did not reduce the feminizing capacity of hGH, indicating that the adrenals and the thyroid gland are not involved in the mediation of the feminizing effect of hGH. The same dose (5 microgram/h for 7 days) of hGH was also able to refeminize the liver steroid metabolism in hypophysectomized-ovariectomized female rats. The effect of the homologous hormones, rat PRL and rat GH on hepatic steroid metabolism was also investigated. Either hormone was infused at a rate of 10 microgram/h for 7 days, a dose which was sufficient to increase the serum level of the hormone in hypophysectomized animals. No feminizing effect was seen after the administration of rat PRL, whereas rat GH caused a partial feminization of hepatic steroid metabolism in hypophysectomized male animals. It is concluded that GH or a hormone related to GH is involved in sexual differentiation of liver steroid metabolism.
The purpose of this study was to quantify the various sources of estrone (E1) and 17 beta-estradiol (E2) production in normal men and in women with testicular feminization. The mean production rate of E1 in four young adult men was 58 micrograms/24 h, while that of E2 was 44 micrograms/24 h. In these men, E1 production could be accounted for totally by extraglandular formation through 1) aromatization of plasma androstenedione, 2) conversion of E2 which was formed from the aromatization of plasma testosterone, and 3) conversion of secreted E2. In these men, only 12 micrograms or less of E2 production could not be accounted for by extraglandular formation from plasma C19 precursors, and is presumed to have arisen by testicular secretion. In six women with testicular feminization, the mean production rate of E1 was 99 micrograms/24 h, while that of E2 was 77 micrograms/24 h. THe amount of E2 production that arose by glandular secretion could be computed in four of these women and was considerably greater than that found in the young adult men. In these women with testicular feminization, an average of 44 micrograms/24 h E2 could not be accounted for by extraglandular formation and is presumed to have arisen by testicular secretion. The mean plasma production rate of testosterone in the normal men was 5.7 mg/24 h, while that in the women with testicular feminization was 8.3 mg/24 h. However, the range of plasma production rates of testosterone in the women with testicular feminization was large (1.3--17.0 mg/24 h).
The absence of uterus has been regarded by a number of authors as a condition for the diagnosis of testicular feminization, although cases with a rudimentary uterus have been reported. However, their number within the framework of this syndrome cannot be exactly determined. In the present report on a 22 year-old patient with testicular feminization and uterus bicornis solidus a double uterus malformation identical with that described in the Mayer-Rokitansky-küster syndrome was found. Forms of testicular feminization with rudimentary uterus in genetically-male individuals may be explained by the absence of androgens, or the absence of reactivity on the part of the target organ, and a simultaneous disturbance (lessening) of the function of the so-called X-factor (oviduct repressor) during early embryonal development. Our own observations, as well as reports in the literature, suggest a theory according to which testicular feminization may be regarded as a series of morphological variants, from male-oriented forms with vaginal aplasie, hypertrophy of the clitoris and male distribution of pubic hair, to female-orientated ones with a vagina of normal length and a rudimentary uterus. The absence of a uterus as a condition for the definition of the syndrome can be maintained only so far as no cases have, as yet been observed with a normally-developed uterus in a typical position. The karyogram showed a small Y-chromosome. Functional anomalies may only be surmised, since Y-anomalies are frequent (3% in a random collection). The morphology of the testes mirrored the functional embryonal insufficiency (pre-pubertal, undifferentiated testicular tissue with a varying amount of stroma and Leydig cells); the basal excretion of testosterone, 17-ketosteroid fractions and pregnane in the 24-hour urine was within the normal range for males. Oestrogen production over and above the "adrenal values" was also present. The values for plasma testosterone, which are in accordance with those of males of a similar age, are considered as indicating the importance of "androgen resistance in the periphery" as a factor in the aetiology of testicular feminization.
The hormonal profile of 40 transsexual inmates from a pool of 86 inmates in the California State prison system was studied before and after therapy with feminizing hormones. Clinical and social data were obtained on all 86 inmates; the incidence of human immunodeficiency virus (HIV) seropositivity was examined in 76 of the 86 individuals. Despite similar degrees of feminization in all 40 individuals in whom hormonal studies were performed, variable suppression of serum testosterone concentrations was present. Based on their testosterone concentrations while on feminizing hormone therapy, the transsexual inmates could be divided into three groups. In Group I (the "suppressed" group), the serum testosterone concentrations were markedly depressed (less than 10 ng/dL); in Group II (the "non-suppressed" group), the values of testosterone were normal (446 to 1072 ng/dL); and in Group III (the "intermediate" group), the testosterone values were between those of the suppressed group and the nonsuppressed group. We speculate that feminizing hormone therapy may induce the development of a state of target hormone resistance to testosterone that results in similar degrees of feminization independent of the circulating concentrations of testosterone. The incidence of HIV seropositivity (3/76) was considerably less than anticipated based on previous studies in populations at high risk for developing the acquired immunodeficiency syndrome.
Gonads dissected from 17-day-old normal chick embryos, as well as testes feminized by oestrogen treatment, were labelled in vitro with [35S]methionine and [14C]leucine. The patterns of cytosolic protein synthesis by the gonads were analysed using two-dimensional (2-D) polyacrylamide gel electrophoresis. In the feminized testis, two female-specific proteins appeared, the rate of synthesis of four testis-specific proteins was decreased, and quantitative variations of other synthesized proteins in relation to sex were detected. This altered protein synthesis indicates that the protein synthesis of the testis feminized by oestrogen treatment has in part become similar to that of a normal ovary. The synthesis of female-specific proteins in the feminized testis raises the question of their role in normal ovarian differentiation.
The metabolism of [4-14C]androst-4-ene-3,17-dione, [4-14C]5alpha-androstane-3alpha,17beta-diol and [1,2-3H]5alpha-androstane-3alpha,17beta-diol, 3,17-disulfate in the 105,000 X g supernatant and microsomal fractions of liver was studied in male and female rats after electrothermic lesion of the hypothalamus including the median eminence. Following electrothermic lesion, hepatic steroid metabolism in male rats was generally "feminized" (increased 5alpha-reduction and decreased 6beta- and 16alpha-hydroxylation of 4-androstene-3,17-dione, decreased 2alpha-, 2beta-, 18- and 7beta-hydroxylation of 5alpha-androstane-3alpha, 17beta-diol and induced 15beta-hydroxylation of 5alpha-androstane-3alpha,17beta-diol,3,17-disulfate), whereas hepatic metabolism in female rats remained essentially unchanged. Previous investigations have pointed to the occurrence of a sex-specific secretion of "feminizing factor" from the female pituitary that is responsible for the "feminization" of the basically "masculine" type of metabolism characterizing the rat liver. Taken together with these findings, the present results indicate that the release of the pituitary "feminizing factor" is controlled by means of a release-inhibiting factor from the hypothalamus. This factor is not secreted in female rats; it is suggested that its secretion in male rats is turned on as a result of neonatal imprinting by testicular androgens.