masculinization - Synonyms for masculinization

Examples of "masculinization"
Fetal masculinization of female external genitalia is usually due to enzyme abnormalities involved in adrenal steroid biosynthesis, resulting in congenital adrenal hyperplasia (CAH); fetal masculinization of female external genitalia is much less frequently due to maternal use of androgenic steroids.
As of 2000, there had been published reports of fetal masculinization of female external genitalia in:
Defeminization and masculinization are the processes that a fetus goes through to become a male.
The incidence of fetal masculinization of female external genitalia varies with the drug and dosage.
As of 2000, there had been published reports of fetal masculinization of female external genitalia in:
The first drugs reported to cause fetal masculinization were the androgens methandriol and methyltestosterone in the mid 1950s.
Normal LHCGR functioning is critical for male fetal development, as the fetal Leydig cells produce testosterone to induce masculinization.
Neural masculinization is a developmental process where different sex hormones assist in the expression of male behavior.
The brain is also affected by this sexual differentiation; the enzyme aromatase converts testosterone into estradiol that is responsible for masculinization of the brain in male mice. In humans, masculinization of the fetal brain appears, by observation of gender preference in patients with congenital diseases of androgen formation or androgen receptor function, to be associated with functional androgen receptors.
Due to excess testosterone secreted by the tumour, one-third of female patients present with a recent history of progressive masculinization. Masculinization is preceded by anovulation, oligomenorrhoea, amenorrhoea and "defeminization". Additional signs include acne and hirsutism, voice deepening, clitoromegaly, temporal hair recession, and an increase in musculature. Serum testosterone level is high.
Defeminization involves the suppression of the development of female typical morphology (development of the Müllerian ducts into the fallopian tubes, uterus and vagina) and behavioural predispositions. Masculinization involves the production of male typical morphology (development of the Wolffian ducts into male reproductive structures) and behavioural predispositions. Both defeminization and masculinization are required for a mammalian zygote to become a fully reproductively functional male.
Voice masculinization is the opposite of voice feminization, being the change of a voice from feminine to masculine. Voice masculinization is not generally required for transgender men as the masculinising effects of testosterone on the larynx are usually sufficient to produce a masculine voice. However, Alexandros N. Constansis has stated that "apart from being unfair to transmen, [this assumption] is also overtly simplistic" and cites Davies and Goldberg in saying that "testosterone doesn’t always drop pitch low enough for FTMs to be perceived as male". Many transgender men also choose not to take testosterone, and use voice masculinization as an alternative way to deepen their voices.
Due to its androgenic activity, ethisterone has been associated with the masculinization of female fetuses in women who have taken it during pregnancy.
The terminal half-life of testosterone in blood is about 70 minutes, so it is necessary to have a continuous supply of the hormone for masculinization.
His book "Huevos y la Mujer Latina: The De-Masculinization of the Macho" was critiqued in the "New York Daily News" in 2007 by Dolores Prida.
The management of 17-beta-hydroxysteroid dehydrogenase III deficiency can consist, according to one source, of the elimination of gonads prior to puberty, in turn halting masculinization.
In a March 1960 "JAMA" article, pediatric endocrinologist Lawson Wilkins at Johns Hopkins reported on 34 cases of fetal masculinization of external genitalia of female infants born from 1950 to 1959 to mothers treated with high-dose (20–250 mg/day) ethisterone to prevent miscarriage, and 35 cases of fetal masculinization of external genitalia of female infants born from 1957 to 1959 to mothers treated with high-dose (10–40 mg/day) norethisterone to prevent miscarriage.
The majority of Leydig cell tumors are found in males, usually at 5–10 years of age or in middle adulthood (30–60 years). Children typically present with precocious puberty. Due to excess testosterone secreted by the tumour, one-third of female patients present with a recent history of progressive masculinization. Masculinization is preceded by anovulation, oligomenorrhea, amenorrhea and "defeminization". Additional signs include acne and hirsutism, voice deepening, clitoromegaly, temporal hair recession, and an increase in musculature. Serum testosterone level is high.
5α-Reductase inhibitors like finasteride and dutasteride can be used to slow or prevent androgenic alopecia (pattern hair loss) and various other adverse androgenic symptoms (e.g., acne) in transgender men taking testosterone. However, they may also slow or reduce a few aspects of masculinization, such as facial and body hair growth and clitoral enlargement. A potential solution is to start taking a 5α-reductase inhibitor after these desired aspects of masculinization have been established.
The first six grades of the scale, grades 1 through 6, are differentiated by the degree of genital masculinization. Quigley describes the scale as one depicting "severity" or "defective masculinization". Grade 1 is indicated when the external genitalia is fully masculinized, and corresponds to mild androgen insensitivity syndrome. Grades 6 and 7 are indicated when the external genitalia is fully feminized, corresponding to complete androgen insensitivity syndrome.