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Biomedical subjects

W Hamilton

Publications and source records attributed to W Hamilton.

At least 37 records · Page 2Linked to original sources
PubMed1977

Biochemical determinants in Gender identity.

The purpose of this communication is to report cognate studies which suggest that the nature of the peripheral metabolism of testosterone may impart gender direction to thought construction and motive. In patients with the complete testicular feminizing syndrome [4], the XO/XY syndrome [4], female trans-sexualism [4] and testicular agenesis [5] HCG-tests of 3 days duration were performed, and plasma and urinary testosterone, urinary excretion of 5 alpha-androstane, 3 alpha, 17 beta-diol (5 alpha-diol), 5 beta-androstane, 3 alpha, 17 beta-diol (5 beta-diol) and epiandrosterone before and after stimulation were measured. In addition steroid transformation was examined by incubation studies with human fetal brain tissue. The results of the latter method presented here are in agreement with published work. It seems clear therefore that the peripheral levels of androgens, oestrogens and their metabolites combine with cerebral steroid transformation, metabolism and possible also synthesis in order to establish gender identity. Exploration of the role of peripheral hormones as stimulators of both gender identity and gender function has dictated the need for a new approach to therapy for gender abnormalities in psyche and soma.

Adolescent↗
PubMed1977

Diabetes insipidus, diabetes mellitus, optic atrophy, and deafness. 3 cases of 'DIDMOAD' syndrome.

Three children with diabetes insipidus, diabetes mellitus, optic atrophy, and high-tone deafness were shown to lack vasopressin, indicative of degeneration of the cells of the hypothalamic supraoptic nuclei. The syndrome being due to a single gene defect, inherited as an autosomal recessive, is therefore likely to be the result of an inborn error of metabolism with variable periods of latency in those affected.

Adolescent↗
PubMed1976

Long-term effects of aminoglutethimide on steroid metabolism in congenital adrenal hyperplasia.

Five cases of congenital adrenal hyperplasia due to C21-hydroxylase defect were treated with a combination of aminoglutethimide and prednisolone. In the third year of treatment the urinary levels of 17-oxosteroids increased above normal values while the total 17-hydroxy-corticosteroids were normally low. Specifically, urinary pregnanetriol was normal in 3 cases. To determine the reasons for this disparity the adrenal metabolism of cholesterol, as judged by the urinary steroid metabolites, was studied. Fractionation of urinary steroid metabolites was by thin-layer chromatography (TLC) followed by gas-liquid chromatography (GLC). The results indicate that aminoglutethimide inhibits steroidogenesis less than prednisolone; that a pathway from cholesterol via 17 alpha, 20 alpha-dihydroxycholesterol to dehydroepiandrosterone is likely to operate after long-term aminoglutethimide therapy; that 11 beta-hydroxylase, at least for pregnenes may be inhibited by aminoglutethimide and that the metabolic breakdown of testosterone may be delayed by this drug.

17-Hydroxycorticosteroids↗
PubMed1976

Developing or normocellular bacterial meningitis.

Occult, normocellular bacterial meningitis is described in two cases, and additional records of similar cases reviewed. It is considered necessary to perform bacteriological cultures of all cerebrospinal fluids investigated for possible infective conditions even if of normal cell count, biochemistry, and naked eye appearance.

Anti-Bacterial Agents↗
PubMed1976

Partial trisomy 5 with a carrier parent t(5p-;9p+).

The significance of partial trisomies of the B group is as yet unknown. An infant with multiple congenital anomalies was found to have a partial trisomy 5p+ syndrome. The father of this patient demonstrated a 5/9 translocation carrier state. A discussion of the relationship of the partial 5p+ syndrome to the Cri du chat syndrome is noted. Partial trisomy 5 would not appear, as yet, to represent a clearly definable syndrome.

Adult↗
PubMed1976

Endemic cretinism.

Explore the source record for details and available documents.

Abnormalities, Drug-Induced↗
PubMed1976

Hypoaldosteronism in three sibs due to 18-dehydrogenase deficiency.

Three sibs all presented in the early neonatal period with a salt-losing syndrome. The salt-losing form of congenital adrenal hyperplasia was diagnosed and appropriate treatment with glucocorticosteroids, mineralocorticosteroids, and additional dietary salt started. Although early life was maintained with difficulty, with age all 3 children required decreasing amounts of replacement steroids to maintain normal plasma electrolyte balance. They were reinvestigated at the ages of 15 years and 8 years (twins), when cortisol synthesis and metabolism proved normal, but aldosterone synthesis was blocked by deficiency of 18-dehydrogenase. Rational treatment of these cases of a salt-losing syndrome in which aldosterone synthesis alone is blocked due to lack of the enzyme 18-dehydrogenase requires the administration of a mineralocorticosteroid drug only. Since deoxycorticosterone (acetate or pivalate) requires intramuscular administration, as life-long therapy oral fludrocortisone is preferable. Although fludrocortisone has glucocorticoid activity, the "hydrocortisone equivalent" effect of the small dosage used was unlikely to inhibit either pituitary corticotrophin or growth hormone production.

Adolescent↗
PubMed1976

Changes in tibiotalar area of contact caused by lateral talar shift.

A carbon black transference technique was used to determine the contact area in twenty-three dissected tibiotalar articulations, with the talus in neutral position and displaced one, two, four, and six millimeters laterally. The greatest reduction in contact area occurred during the initial one millimeter of lateral displacement, the average reduction being 42 per cent. With further lateral displacement of the talus the contact area was progressively reduced but the rate of change for each increment of shift was less marked.

Ankle Joint↗
PubMed1975

Raised serum TSH in hypothyroidism.

It is desirable to detect early hypothyroidism of the mildest degree even before conventional tests of thyroid function become abnormal. Serum TSH levels (normal: undetectable to 4 muU/ml) rise in patients with mild hypothyroidism long before serum T4 and T3 levels fall. In the patient described the serum TSH level was 310 muU/ml, while other tests of thyroid function gave normal results. After treatment with thyroxine, serum TSH returned to normal. It should now be accepted that patients with mild hypothyroidism have a raised serum TSH and that thyroid insufficiency can be confidently excluded if the serum TSH concentration is normal. It is thus important to assay serum TSH when suspicion of hypothyroidism is aroused.

Child, Preschool↗