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At least 577 records · Page 32Linked to original sources
PubMed2005

Black skin, 'cowboy' masculinity: a genealogy of homophobia in the African nationalist movement in Zimbabwe to 1983.

This paper examines the intellectual and social origins of racialist homophobia in contemporary Zimbabwean political discourse, exemplified by President Robert Mugabe's anti-homosexual speeches since the mid-1990s. It challenges the notions that such homophobia is either essential to African patriarchy or simple political opportunism. Tracing overt expressions of intolerance towards male-male sexuality back to the colonial period, it focuses on ways in which notions of appropriate, respectable, exclusive heterosexuality within the 'cowboy' culture of White Southern Rhodesia trickled into, or were interpreted in, the African nationalist movement. It concludes that understanding this history could improve efforts to address concerns around sexual health in Zimbabwe and elsewhere in the region, particularly silences around same-sex sexuality in HIV/AIDS education and prevention.

Female↗
PubMed2003

Models of masculinity: sex education, the United States Public Health Service, and the YMCA, 1919-1924.

In 1918, the U.S. Public Health Service (PHS) told American parents that "it is no longer possible for you to choose whether your child will learn about sex or not." According to the PHS, most American boys learned about sex from "improper sources" by the age of nine. The "unfortunate effect of these early impressions" had, PHS warned, not only resulted in a gross misunderstanding of sex, but also been a major factor in the spread of venereal disease (The Parents' Part [the U.S. Public Health Service, 1918], p. 5). To counter and correct this miseducation, PHS joined with the Young Men's Christian Association (YMCA) to create a sex education program aimed at adolescent boys. Officially launched in the spring of 1919, the "Keeping Fit" campaign provides a unique insight into the federal government's attempt to medicalize and regulate American sexuality through the forum of public health.

Adolescent↗
PubMed2007

Prenatal testosterone exposure permanently masculinizes anogenital distance, nipple development, and reproductive tract morphology in female Sprague-Dawley rats.

In mammals, abnormal increases in fetal androgens disrupt normal development of the female phenotype. Due to the recent concern regarding environmental androgen-active chemicals, there is a need to identify sources of fetal androgen variation and sensitive developmental markers for androgenic activity in female rats. Anogenital distances (AGD), nipple retention, reproductive tract, and external genitalia are morphological parameters organized by prenatal androgens and are predictive of altered masculinized/defeminized phenotype in adult female mice and rats. The objectives of this study were to (1) characterize the natural prenatal androgen environment of rats including the magnitude of the intrauterine position (IUP) effect, (2) characterize the permanent effects of prenatal androgen exposure on female rats, and (3) determine the ability of AGD and areolas to predict these permanent androgenic alterations in female rats. Untreated male fetal rats had higher tissue testosterone (T) concentrations than females in the amniotic fluid, reproductive tract, gonad, and fetal body. The intrauterine position (IUP) of male and female fetuses did not affect T concentrations or AGD in male or female rats at gestational day (GD) 22. Female offspring exposed to 0, 1.5, and 2.5 mg/kg/day testosterone propionate (TP) on GDs 14-18 displayed increased AGD at postnatal day (PND) 2 and decreased nipples at PND 13 and as adults. TP-induced changes in neonatal AGD and infant areola number were reliable indicators of permanently altered adult phenotype in female rats. Further, females in the two high-dose groups displayed increased incidences of external genital malformations and the presence of prostatic tissue, not normally found in female rats.

Abnormalities, Drug-Induced↗
PubMed1999

Prenatal testosterone masculinizes synaptic input to gonadotropin-releasing hormone neurons in sheep.

In sheep, the control of tonic and surge GnRH secretion is sexually differentiated by testosterone in utero. However, GnRH neurons are not sexually dimorphic with respect to number, distribution, or gross morphology. Therefore, this study tested the hypothesis that prenatal steroids influence synaptic input to GnRH neurons. We compared the number of synapses on GnRH neurons from male, female, and androgenized female lambs (n = 5 each). Androgenized females were exposed to testosterone during mid-gestation. Yearling lambs were perfused, and GnRH neurons were visualized using the LR-1 antibody. Five to seven GnRH neurons from the rostral preoptic area in each animal were viewed at the ultrastructural level. Afferent synapses and glial ensheathment on each neuron were counted in a single section through the plane of the nucleus. GnRH neurons from females received approximately twice as many contacts (3.6 +/- 0.7 synapses/100 microm plasma membrane) as those from male lambs (1.6 +/- 0.3; p < 0.05), similar to previous reports in rats. In addition, the number of synapses on GnRH neurons from androgenized female lambs (1.5 +/- 0.5) was similar to that from male lambs, suggesting that prenatal steroids give rise to sex differences in synaptic input to GnRH neurons.

Animals↗