Biomedical subjects
Publications and source records attributed to S Lal.
Exfoliative dermatitis associated with hepatitis has been reported in leprosy patients taking dapsone in daily dosage of 200 mg daily or more previously. This report concerns a 40 year-old-female who developed exfoliative dermatitis and hepatitis six weeks after starting dapsone in daily dosage of 100 mg for treatment of leprosy. She responded dramatically to administration of corticosteroids.
Concurrent neuroleptic administration is a necessary factor in the therapeutic response to GABAergic agents. In contrast to their effect on the striatum, neither BAC nor NaV influences hypothalamic-pituitary DA function mediating PRL secretion.
A case of secondary sulphone resistant lepromatous leprosy proved by mouse foot-pad tests is reported from Pondicherry, India.
The leucocyte migration inhibition test (LMIT) using Dharmendra's antigen was performed in 21 cases of leprosy classified according to Ridley Jopling Scale (1966). The degree of migration correlated well with the classification as expected thus confirming the immunological validity of Ridley-Jopling classification.
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In this brief report, a 'distributed' computer model of skeletal muscle is described, and its predictions regarding muscle force and EMG are presented. The force and myo-electric signals are produced as the sum of the contributions of independently activated motor units possessing a distribution of properties. The results of the simulation as well as theoretical study show that: (a) asynchronous activity of motor units can be responsible for the fairly regular oscillations observed in muscle tremor; (b) the use, in the case of muscle, of the limit theorem for the superposition of independent point processes leads to erroneous conclusions with respect to the frequency characteristics of the muscle force waveform, and possibly, with regard to those of the EMG.
The few existing neuropathological, neurochemical, and neuropharmacological studies have shed little light on the pathophysiology of spasmodic torticollis (ST). The relevance of experimental ST in animals and drug-induced ST in man to idiopathic ST is unclear. Most pharmacotherapeutic endeavors have focused on drugs affecting basal ganglia function. Unfortunately, problems of sample size, clinical heterogeneity of patient population, research design, objective evaluation of response, documentation of key data, and adequacy of duration of follow-up make interpretation of published results difficult. Because of the heterogeneity of ST, investigations aimed at establishing a neurotransmitter profile for each patient by observing the acute response to a test dose of drugs affecting cholinergic, dopaminergic, serotonergic, and gamma-aminobutyric acid systems may provide a more rational basis to the selection of treatment.
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Naloxone HCl (0.8 mg intravenously; n=9) or levallorphan tartrate (0.25 mg subcutaneously; n=5) had no effect on basal prolactin or growth hormone secretion in normal men. Neither narcotic antagonist inhibited the growth hormone secretory response to apomorphine HCl (0.75 mg subcutaneously). These findings suggest that narcotic antagonists do not block dopamine receptors in the hypothalamic-pituitary axis in man and that if these agents have antischizophrenic properties then these are not mediated by dopamine receptor blockade.
Clozapine had no effect on basal serum growth hormone concentrations in 10 schizophrenic patients but significantly inhibited the apomorphine-induced growth hormone increase that occurred in 7 subjects. Clozapine caused a slight (17%) but significant elevation in basal serum prolactin levels. These data suggest that in man clozapine, like other neuroleptics, blocks dopamine receptors, at least in the hypothalamic-pituitary axis.
The effect of benztropine on haloperidol-induced prolactin secretion was investigated in 10 normal male volunteers. Benztropine had no effect on basal prolactin secretion but significantly enhanced the increased induced by haloperidol. The magnitude of the enhancement, however, was relatively small. These data suggest that in man cholinergic mechanisms have no effect on basal prolactin secretion but exert a weak inhibitory effect under conditions of dopamine receptor blockade. Differences in intrinsic anticholinergic properties may account for some of the variations in potency of different neuroleptics in increasing circulating prolactin concentrations.
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Plasma beta-endorphin was measured in 35 chronic schizophrenic patients (15.47 +/- 15.39 pmol/L) and 3 normal volunteers (19.55 +/- 11.23 pmol/L). There was no significant difference between the levels of the two groups.
Morphine and the opioid peptides leucine-enkephalin (leu-enk), methionine-enkephalin (met-enk) and beta-endorphin had no effect on basal cyclic AMP levels in rat cerebral cortex and hypothalamus, but each inhibited noradrenaline (NA)-stimulated cyclic AMP formation in both brain regions. This inhibition was reversed by naloxone. Naloxone did not reverse phentolamine- or propranolol-induced inhibition of NA-stimulated cyclic AMP formation. The increase in cyclic AMP formation induced by NaF or MnCl2 was unaffected by met-enk or morphine. These data suggest that in rat cerebral cortex and hypothalamus opiates bind to opiate receptors and that the opiate-receptor complex interferes with noradrenergic receptor activity.
Noradrenaline, isoproterenol, adrenaline or clonidine stimulate cyclic AMP formation in human cerebellar cortex 15-20 fold and serotonin or dopamine 3-fold. The increase by noradrenaline or clonidine is dose-dependent. Propranolol completely blocks the increase induced by noradrenaline or isoproterenol but not that by clonidine. Phentolamine was ineffective in blocking cyclic AMP formation induced by noradrenaline, isoproterenol, adrenaline or clonidine. Chlorpromazine completely blocked the increase induced by noradrenaline, isoproterenol, clonidine, serotonin or dopamine.
The effect of lithium on apomorphine-induced growth hormone secretion and haloperidol-induced prolactin secretion was examined in eight male subjects without history of manic-depressive illness. Lithium had no effect on baseline or drug-induced changes in serum growth hormone or prolactin concentrations. These data suggest that lithium does not alter hypothalamic-pituitary dopamine receptor function.