Vascular opacification and leakage in X-linked (juvenile) retinoschisis.

A 22-year-old man had X-linked retinoschisis with extensive vascular sheathing in the posterior pole and dendritic opacified retinal vessels in the periphery. Detailed fluorescein angiographic studies were performed. In the far periphery areas of capillary nonperfusion were seen. Sluggish circulation was present in the majority of dendritic opacified vessels in the areas of schisis. Late staining of the disc and posterior arteries and veins was noted. Scattered intraretinal fluorescein leakage was present even in clinically nonschitic retina, which suggests that the vascular changes may precede the retinoschisis. The patient's half-brother also had X-linked retinoschisis, but the schisis and the vascular changes were much less prominent. Although the retinal vascular changes with X-linked retinoschisis are similar to those seen with the Favre-Goldmann syndrome, a differentiation of the two diseases can be made by family studies, the presence or absence of nyctalopia, examination of the macular areas, measurement of dark adaptation, and electroretinogram determinations.     

Plasma levels, half-life values, and correlation with physiologic assays for growth and immunity

To assess the gonadal effects of chlorambucil given to prepubertal and pubertal boys, testicular function of 21 adolescents or young men, treated with chlorambucil for nephrotic syndrome before or during puberty, have been evaluated. Evaluations have been based on penis and testicular size, serum FSH, LH and testosterone values, and sperm count. Nine patients have testicular hypotrophy, 13 have significantly elevated FSH, 17 have azoospermia, two have severe oligospermia, and repetitive sperm counts show no improvement. A quiescent state of the epithelium of the seminiferous tubules does not protect against chlorambucil toxicity, which seems to be related to the cumulative dose. Chlorambucil should be used with caution, even in children.     

Effects of hydrocortisone and immobilization on tryptophan metabolism in brain and liver of rats of different ages

Hydrocortisone sodium succinate (5 mg/kg i.p.) led to a larger absolute increase in hepatic tryptophan pyrrolase activity in younger (26, 46 and 66 days) than older (107 and 225 days) rats. Activity in control animals was lower in the older rats and there was no obvious correlation between percentage change and age. Responses of male and females were comparable. Consistent with previous findings brain 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) decreased 6 hr after hydrocortisone only at ages when a large absolute increase of pyrrolase activity occurred (26, 46 and 66 days). Brain 5-HT and 5-HIAA levels both before and after hydrocortisone were comparable in males and females. Immobilization led to pyrrolase induction and brain 5-HT changes in 66-day but not in 225-day old rats. Studies with different hydrocortisone preparations showed that the soluble succinate salt caused a more rapid increase of pyrrolase activity than the insoluble acetate salt or free base and a more marked brain 5-HT decrease. Results are discussed in relation to the suggested association between liver tryptophan pyrrolase activity and the subsequent changes in brain 5-HT and 5-HIAA.     

Neuromuscular blocking and antimuscarinic activity of a series of bis-atropinium and N-n-alkyl atropinium compounds

Measurements of neuromuscular blocking and antimuscarinic activity have been made in a series of bis-atropinium (BA) and N-n-alkyl atropinium (N-AA) compounds. That the second atropinium group contributed to the neuromuscular blocking activity of BA compounds was shown by the relative lack of such activity in the N-AA series of compounds. Peak neuromuscular blocking activity occurred when two atropinium groups were separated by a chain of either 10 or 11 methylene groups. Members of both series of compounds displayed antimuscarinic properties but estimates of activity differed according to whether they were obtained by determination of affinity constants on guinea-pig isolated ileum or production of mydriasis in mice. From measurements of affinity constant on the guinea-pig ileum it is concluded that BA compounds interact with only one muscarinic receptor. However, the high activity of the deca- and undecamethylene BA compounds in producing mydriasis suggest that these compounds possibly interact with two receptors at once.     

The Accuracy of Methods of Diagnosis in Patients with Suspected Recurrent Ulcer after Vagotomy

This paper reports a critical analysis of the results of the investigations used to establish a diagnosis in, 37 patients submitted to a second operation for presumed recurrent or unhealed ulcer. The results of investigations have been correlated with the operative and histopathological findings.     

Studies on the post-ictal rise in seizure threshold

Seizure thresholds were determined by timed infusion of a convulsant drug. Following an electroconvulsive shock (ECS) rats exhibited a raised seizure threshold to infusion of the GABA antagonist drugs, pentylenetetrazol, bicuculline and isopropyl-bicyclophosphate, but not to the glycine antagonist strychnine or the 5-HT agonist, quipazine. The increase in threshold was seen following a bicuculline-induced seizure and 30 min following the last of a course of ECS given once daily for 10 days. The rise in seizure threshold still occurred when animals were pretreated with alpha-methyl-p-tyrosine (200 mg . kg-1), p-chlorophenylalanine (200 mg . kg-2), naloxone (1 mg . kg-1) or indomethacin (20 mg . kg-1). Diazepam (2 mg . kg-1), flurazepam (10 mg . kg-1) and sodium valproate (400 mg . kg-1) elevated basal seizure threshold and a further rise followed the ECS. Phenytoin (40 mg . kg-1) and carbamazepine (40 mg . kg-1) had no effect on basal seizure threshold or the ECS-induce rise. (?Propranolol (20 mg . kg-1) did not affect basal seizure threshold but prevented the ECS-induced increase. The rise in seizure threshold following a convulsion may be an important adaptive mechanism which could be related to the reported increase in specific benzodiazepine binding following a seizure.