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Biomedical subjects

K Akasofu

Publications and source records attributed to K Akasofu.

31 records · Page 2Linked to original sources
PubMed1992

Effect of testosterone on the development of bladder tumors and calculi in female rats.

In order to study the effect of testosterone on bladder calculi and tumor formation in female rats, Wistar rats were administered testosterone for 12, 18 or 24 weeks. Testosterone was found to increase the incidence of both bladder calculi and tumors in intact, but not in oophorectomized rats. It is suggested that testosterone in combination with estrogen may contribute to hyperplasia formation, in turn leading to an increased incidence of bladder calculi and tumors.

Animals↗
PubMed1992

A lactating adenoma of the breast.

A lactating adenoma of the breast was first examined at the 24th week of gestation, and had doubled in size by the 37th week. After delivery, administration of bromocriptine (5 mg/day) reduced its size, and it was surgically removed on the 10th day. Histologically, the glandular epithelial cells of the adenoma showed the physiological changes normally seen during lactation, and retained much of their lactating activity (especially protein secretion). The myoepithelial cells contained an increased number of lysosomes and also some autophagosomes, implying that the tumor had partly undergone involution similarly to the normal breast tissue.

Adenoma↗
PubMed1992

Uterine leiomyoma associated with ascites and hydrothorax.

Uterine leiomyoma associated with ascites and hydrothorax was apparently cured by total hysterectomy. This is believed to be the 15th recorded case of this type of Pseudo-Meigs' syndrome and the first in a patient with severe curvature of the spine and dorsolumbar scoliosis. The association with ascites and hydrothorax was investigated using 99mTc-labeled macroaggregated albumin.

Ascites↗
PubMed1992

Cerebral arteriovenous malformations in a pregnancy with twins: case report.

The natural course of cerebral arteriovenous malformations during pregnancy is not well known. An inoperable cerebral arteriovenous malformation was diagnosed by angiography, computed tomography, and magnetic resonance imaging before pregnancy and followed by magnetic resonance imaging during pregnancy. No significant changes were detected in the size of the cerebral arteriovenous malformation during pregnancy, and healthy twins were born by cesarean section.

Cerebral Angiography↗
PubMed1991

Treatment of an antenatally diagnosed fetal ovarian cyst by needle aspiration during the neonatal period.

An ultrasound scan revealed an ovarian cyst in the fetal lower abdomen at 29 weeks of gestation. Repeated examinations demonstrated that the cyst increased in size to 6.5 cm x 6.1 cm x 5.0 cm at 33 weeks of gestation, and the cyst showed no complications between 29 weeks of gestation and early infancy. The female infant was vaginally delivered at 41 weeks of gestation without any complications. Transabdominal needle aspiration of the cyst fluid was performed on the 14th day after birth. The concentrations of estrone, estradiol, estriol, and progesterone in the cyst fluid were almost the same as those in the infant's serum, while the concentration of pregnenolone was six times that in the infant's serum. Cytology of the cyst fluid was negative. The cyst thus seems to have been a non-functioning simple cyst of ovarian origin. Follow-up until the baby was one year old showed no recurrence of the cyst.

Adult↗
PubMed1991

Changes in 40 serum proteins of post-menopausal women.

Sera were sampled from 83 people (pre- and post-menopausal women and men). Climacteric symptoms of 23 women were treated with conjugated estrogen. Sera were sampled serially until the 21st day of estrogen administration. Serum concentrations of 40 protein components were measured by micro single radial immunodiffusion. The serum proteins were classified into 5 types according to changes after menopause and estrogen therapy, respectively. Type 1 (decreased after menopause and increased by estrogen; alpha 1-antitrypsin, alpha 2-HS - glycoprotein, beta 2-glycoprotein III, Gc-globulin, alpha 1-lipoprotein and alpha 2-AP-glycoprotein), type 2 (unchanged and increased; ceruloplasmin), type 3 (increased and decreased; alpha 1-acid glycoprotein, haptoglobin, serum amyloid P-component, Zn-alpha 2-glycoprotein, beta-lipoprotein and C1-components), type 4 (unchanged and decreased; hemopexin, antithrombin III, beta 2-glycoprotein I, prealbumin and retinol-binding-protein), type 5 (unchanged by estrogen; immunoglobulin M (IgM), IgG and others). Estrogen replacement therapy restored pre-menopausal levels of serum proteins, types 1 and 3. However, estrogen therapy was associated with significantly abnormal levels of proteins, types 2 and 4 in post-menopausal women. Serum levels of type 1 proteins and some type 5 proteins (IgM, alpha 1B-glycoprotein, C9-component and alpha 2-macroglobulin) were higher in pre-menopausal women than in men, whereas type 3 proteins were the opposite.

Adult↗
PubMed1991

A new cause of female pseudohermaphroditism: placental aromatase deficiency.

A description is presented of the first documented case of placental aromatase deficiency. The deficiency caused maternal virilization during pregnancy and pseudohermaphroditism of the female fetus. A 24-yr-old primigravida showed progressive virilization during the third trimester. Urinary excretion of estrogen was less than 14 mumol/day between 35-38 weeks of pregnancy, although nonstress tests showed reactive patterns and serum levels of human placental lactogen were above 460 nmol/L. Maternal serum levels of estrogens were low, and those of androgens were high in the third trimester. A dehydroepiandrosterone sulfate loading test induced a marked increase in maternal serum levels of androgens, whereas no such increase was observed in estrogens. The woman delivered vaginally a live full-term infant who exhibited female pseudohermaphroditism. Cord serum levels of estrogens were extremely low, while those of androgens were high. The aromatase activity of the placenta, determined by the conversion of [7-3H]androstenedione to 17 beta-[7-3H]estradiol and [7-3H]estrone, were less than 0.03 fmol/microgram protein.min (control, 9.6 +/- 2.2 fmol/microgram protein.min). The sulfatase activity of the placenta was 0.63 pmol/microgram protein.min compared to 0.46 +/- 0.16 pmol/microgram protein.min in controls. The rate of aromatization by normal control placentas was the same as that obtained during coincubation of samples of normal placentas and that of the patient. Thus, the presence of aromatase inhibitor in the patient's placenta was excluded.

Adult↗
PubMed1981

Changes of serum concentrations of dehydroepiandrosterone, its sulfate, 11-deoxy-17-ketosteroids, cortisol, estradiol, testosterone, prolactin and gonadotropins in normal prepubertal and pubertal females.

The concentrations of serum dehydroepiandrosterone (DHA), DHA sulfate (DHA-S), 11-deoxy-17-ketosteroids (11-deoxy-17-KS), cortisol (F), estradiol (E2), testosterone (T), prolactin (PRL), follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were measured by means of radioimmunoassays in 157 prepubertal and pubertal girls whose age ranged from 5 to 16. Among the hormones studied, DHA exhibited a first significant increment at age 8, ahead of all other hormones. The significant increases of 11-deoxy-17-KS and DHA-S occurred at age 9 and 10, respectively. After the occurrence of the significant increment, the concentrations of these androgens increased progressively with age. DHA/DHA-S ratio showed a decreasing trend with the advance of age. F did not show any significant variation with age. E2 increased significantly at age 11 and T at age 10. PRL increased significantly at age 12 but its concentration did not seem to vary very much with age after 9. FSH and LH started to increase after age 9, with their significant increases occurring at age 10 and 9, respectively. These results confirm that during the course of pubertal development in girls, adrenal androgens increase first, which is followed by pituitary gonadotropins and then gonadal estrogen.

17-Ketosteroids↗