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feminization/atrophy

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The profiles of hepatic drug metabolism were obtained by using young and old male and female rats. The profile obtained from old male rats was completely different from that from young male rats, while it was almost identical to those of females of any ages. This was due to the selective decrease in

[Malignant degeneration in testicular feminization. Apropos of a case].

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The authors describe the main therapeutic features found in a case of testicular feminisation that became malignant. Bilateral gonadal ablation should be carried out after puberty for fear of malignancy. When cancer occurs treatment is best decided on the grounds of extension to the lymph nodes and

Pubertal feminization in a genetic male with testicular atrophy and normal urinary gonadotropin.

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[Endocrinological study of hypogonadism and feminization in patients with bulbar spinal muscular atrophy].

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Classical seminoma in a case of testicular feminization syndrome.

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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.

A Second Look at the Process of Occupational Feminization and Pay Reduction in Occupations.

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Using the IPUMS-USA data for the years 1960-2015, this study examines trends in the effect of occupational feminization on occupational pay in the U.S. labor market and explores some of the mechanisms underlying these trends. The findings show that the (negative) association between occupational

Ciliary neurotrophic factor arrests muscle and motoneuron degeneration in androgen-insensitive rats.

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Steroid hormones and neurotrophic factors exert profound and widespread effects on the developing nervous system, including regulation of the size, connectivity, and survival of neurons. Androgenic control of the survival of motoneurons in the spinal nucleus of the bulbocavernosus (SNB) of rats has

Androgen receptor abnormality in X-linked spinal and bulbar muscular atrophy.

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X-linked spinal and bulbar muscular atrophy (SBMA) is usually associated with feminization and hypogonadism. We were unable to find androgen receptor (AR) in the scrotal skin of three patients with SBMA, and propose that AR abnormality is the cause of the disease.
X-linked spinal and bulbar muscular atrophy (SBMA; Kennedy's disease) is a polyglutamine (polyQ) disease in which the affected males suffer progressive motor neuron degeneration accompanied by signs of androgen insensitivity, such as gynecomastia and reduced fertility. SBMA is caused by CAG repeat

[Inguinal hernia in a young girl; sporadic manifestation of testicular feminization].

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Examination of a woman aged 17 years with primary amenorrhoea revealed normal breasts and external genital organs, hardly any axillary or pubic hair growth, a blind vaginal pouch and no palpable uterus or adnexa. At additional examination, uterus and adnexa proved to be absent, the serum

Effect of androgen insensitivity on diabetogenesis in db/db male mice with testicular feminization (Tfm).

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In C3H mice, a major component of susceptibility to the diabetogenic action of an obesity mutation (diabetes, db) is male gender associated. We tested whether increased male susceptibility was an androgen receptor mediated process. C3H.SW/Lt-derived db/db males were rendered androgen-receptor

[The problem of extirpation of gonads in "testicular feminisation"].

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The 15-year old female patient G. G. was referred to the outpatient department for child gynaecology on account of a primary amenorrhoea. The endocrinal parameters found (testosterone, oestradiol, 17 OHCS, 17 KS), chromosome analysis, vaginoscopy and the result of a laparoscopy led to the clinical

Sexual dimorphism of pancreatic beta-cell degeneration in transgenic mice expressing an insulin-ras hybrid gene.

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The human H-ras oncogene induces cell degeneration and diabetes when expressed in pancreatic beta-cells in transgenic mice. The disease develops predominantly in male mice between 5-8 months of age. Most transgenic female mice do not manifest this phenotype, even at much greater ages. However,

Prenatal flutamide enhances survival in a myogenic mouse model of spinal bulbar muscular atrophy.

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BACKGROUND Spinal bulbar muscular atrophy (SBMA) is caused by a CAG repeat expansion mutation in the androgen receptor (AR) gene, and mutant AR is presumed to act in motoneurons to cause SBMA. However, we found that mice overexpressing wild-type (wt) AR solely in skeletal muscle fibers display the

Complete testicular feminization with normal gonadotropin and high androgen secretion: a case report.

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A patient with a complete form of testicular feminization with normal gonadotropin and high testosterone levels is described here. These findings are in contrast to previous reports that have shown high circulating luteinizing hormone (LH) levels in adults affected by this syndrome. Testicular
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