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Biomedical subjects

J Booth

Publications and source records attributed to J Booth.

At least 91 records · Page 5Linked to original sources

Regression of pituitary microadenoma during and following bromocriptine therapy: persistent defect in prolactin regulation before and throughout pregnancy.

During 5 years of clinical, endocrinologic, and radiologic observations in a woman with a microprolactinoma treated medically with bromocriptine for 29 months, serial hypothalamic-pituitary studies revealed a defect in lactotrope function after prolactin (PRL) concentrations and ovulation were restored to normal. This defect persisted throughout a spontaneously conceived pregnancy in which the PRL, estradiol, and progesterone levels were subnormal, while, the dehydroepiandrosterone sulfate levels were normal and estriol concentrations were elevated. Levels of the beta subunit of human chorionic gonadotropin (hCG) were close to and slightly above the normal ranges. These observations are consistent with a role for PRL, interacting with hCG, in the control of estrogen and progesterone secretion by the fetoplacental unit. Lactation was initiated and maintained post partum. Pituitary function and PrL responses to suckling suggested improved lactotrope function 22 to 25 months after withdrawal of bromocriptine. The impaired lactotrope function, therefore, did not preclude normal implantation, pregnancy maintenance, onset of parturition, fetal development, and lactation.

Adenoma↗

The dexamethasone suppression test in mania.

The results of the overnight 2 mg Dexamethasone Suppression Test administered to 50 manic patients are reported. Twenty-three (46%) cases showed an absence of normal suppression, results which are similar to those seen in endogenous depression and which differ to those of others who have all reported normal suppression in mania. Suppressors and non-suppressors were not shown to differ in the factors of age, weight, polarity or the rated severity of mood.

Adult↗

Enzymic reduction of aromatic hydrocarbon epoxides by the microsomal fraction of rat liver.

1. The oxidation of aromatic hydrocarbons to arene oxides and the reduction of these oxides to the parent hydrocarbons are both catalysed by enzymes in the microsomal fraction of rat liver. A suggested name for the enzyme concerned in the reduction of these epoxides is 'epoxide reductase'. 2. 'Epoxide reductase' is NADPH-dependent and is inhibited by oxygen. 3. Preliminary investigations suggest that the enzyme is specific for both 'K-region' and 'non-K-region' arene oxides.

Animals↗

Glutathione conjugates as metabolites of benz[a]anthracene.

1. [3H]Benz[a]anthracene is converted into water-soluble metabolites by microsomal plus soluble fractions of rat-liver in the presence of NADPH and glutathione. Chromatography on Sephadex G25 gave four radioactive peaks; the first contained hydrocarbon or hydrocarbon derivatives bound to soluble protein while the other three peaks contained glutathione conjugates of hydrocarbon metabolites. 2. Conjugates formed when either of the benz[a]anthracene metabolites, 5,6-dihydro-5,6-dihydroxybenz[a]anthracene or 8,9-dihydro-8,9-dihydroxybenz[a]anthracene, were similarly incubated were probably S-(5,6,8,9-tetrahydro-5,6,9-trihydroxybenz[a]anthracen-8-yl)glutathione and S-(5,6,8,9-tetrahydro-6,8,9-trihydroxybena[a]anthracen-5-yl)glutathione respectively. The corresponding peak obtained in the metabolism of benz[a]anthracene probably contains a mixture of these two isomers. 3. The third peak contained the conjugate, S-(5,6-dihydro-l-hydroxybenz-[a]anthracen-k-yl)glutathione, also formed by the conjugation of the "K-region" epoxide of benz[a]anthracene with glutathione. This was not formed in the metabolism of the dihydrodiols. 4. The fourth peak contained a new type of conjugate that is probably S-(8,9,10,11-tetrahydro-8,9,10-trihydroxybenz[a]anthracen-11-yl)glutathione. This conjugate is chromatographically similar to a product obtained from incubation of the 8,9-dihydrodiol, and is probably formed by microsomal oxidation of the 10,11-bond of the dihydrodiol, followed by conjugation of the resulting diol-epoxide with glutathione.

Animals↗