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Biomedical subjects

Z Argov

Publications and source records attributed to Z Argov.

105 records · Page 6Linked to original sources
PubMed1982

D-Penicillamine-associated myasthenia gravis: immunological and electrophysiological studies.

Immunological and electrophysiological features were investigated in a patient with rheumatoid arthritis who developed myasthenic symptoms after 10 months of treatment with D-penicillamine (D-pen). After an initial rise, acetylcholine receptor (AChR) antibodies gradually fell from 24.4 nmole alpha-bungarotoxin bound/liter to 1.8 nmole/liter following withdrawal of the drug, and this was associated with clinical and electrophysiological improvement. Immunoglobuline synthesis by peripheral blood lymphocytes cultured with pokeweed mitogen and D-pen was significantly increased at D-pen concentrations of 10-100 micrograms/ml in 2 patients with D-pen associated myasthenia gravis and 1 out of 3 normal individuals. Furthermore, lymphocytes from 1 myasthenic patient synthesized detectable AChR antibodies in vitro, and the amount of receptor antibody produced was increased in the presence of the drug. This effect was most marked at a concentration of 10 micrograms/ml which is thought to approximate the concentration in vivo. Our results confirm the in vivo findings of others that D-pen may have different effects on immunoglobulin production in different individuals and may also enhance the snythesis of at least 1 autoantibody, the AChR antibody.

Adult↗
PubMed1980

Congenital myotonic dystrophy: fiber type abnormalities in two cases.

Histometric data on muscle fiber types were studied in two cases of congenital myotonic dystrophy (CMD); one underwent biopsy at the age of 5 months and the other at the age of 10 years. A previously unreported severe deficiency of type IIB fibers were found in both cases. In addition, in the first case, there was type I fiber preponderance and hypotrophy as described in cases of congenital fiber type disproportion (CFTD). It is suggested that an abnormality of motor unit maturation may be common to CMD and to CFTD, and that this results from a disorder of neural trophic influences during muscle development.

Child↗
PubMed1979

The action of chlorpromazine at an isolated cholinergic synapse.

The effects of chlorpromazine (CPZ) on cholinergic transmission were studied at the isolated neuromuscular synapse of the frog. It was found that 5 x 10(-6) M CPZ produces the following effects: (1) a reduction in end-plate potential amplitude, mainly through inhibition of transmitter release at presynaptic nerve terminals; (2) a reduction in amplitude of focally recorded end-plate current without detectable change in nerve terminal potential: (3) a decrease in amplitude of miniature end-plate potentials; and (4) an increase in the frequency of spontaneous liberation of transmitter both in normal and calcium-free Ringer's solution. It is concluded that CPZ inhibits cholinergic transmission by a complex action on presynaptic and postsynaptic elements. The relation of these findings to central cholinergic activities of CPZ is discussed.

Acetylcholine↗
PubMed1979

Drug-induced peripheral neuropathies.

Review of the various drugs in current clinical use showed that over 50 of them may cause a purely sensory or mixed sensorimotor neuropathy. These include antimicrobials, such as isoniazid, ethambutol, ethionamide, nitrofurantoin, and metronidazole; antineoplastic agents, particularly vinca alkaloids; cardiovascular drugs, such as perhexiline and hydrallazine; hypnotics and psychotropics, notable methaqualone; antirheumatics, such as gold, indomethacin, and chloroquine; anticonvulsants, particularly phenytoin; and other drugs, including disulfiram, calcium carbimide, and dapsone. Patients receiving drug treatment who complain of paraesthesie, pain, muscle cramps, or other abnormal sensations and those without symptoms who are receiving drugs that are known or suspected to be neurotoxic should undergo neurological examination and studies of motor and sensory nerve conduction. This will allow the incidence of drug-induced peripheral neuropathy to be determined more precisely.

Anti-Infective Agents↗
PubMed1979

Phenytoin and transmitter release at the neuromuscular junction of the frog.

The effects of phenytoin (diphenylhydantoin, DPH) on transmitter release were studied at the frog neuromuscular junction. It was found that in Ringer's solutions containing a normal concentration of Ca2+ ions, DPH (1-2 X 10(-4) M) depresses neurally evoked transmitter release, whereas in Ca2+-deficient Ringer's solutions it produces an increase in evoked release. Spontaneous transmitter liberation is augmented by DPH under all the above conditions. An abrupt disappearance of the evoked response occasionally occured with stimulation at 0.5 Hz, but a normal response could be elicited by a second stimulus delivered shortly after the first. At 100-200 Hz, DPH regularly induced a partial block in synaptic transmission. In 8 mM MgCl2, this phenomenon appeared at 50 Hz and developed into a total neuromuscular blockade.

Animals↗
PubMed1979

Hyperparathyroidism presenting with unusual neurological features.

A case of hyperparathyroidism, who presented with unusual complex neurological symptomatology is reported. Mental confusion, asterixis and elevated cerebrospinal fluid protein with marked pleocytosis dominated the neurological picture. All these findings subsided upon correction of hypercalcemia, suggesting direct relationship between cerebrospinal fluid abnormalities, asterixis and this metabolic disturbance.

Adenoma↗
PubMed1977

Depression of synaptic transmission by diphenylhydantoin.

Diphenylhydantoin (phenytoin, DPH) depresses synaptic transmission at the frog neuromuscular synapse by presynaptic and postsynaptic mechanisms. In normal Ringer's solution the amplitude of the neurally evoked end-plate potentials and their quantal content are reduced. Somewhat paradoxically, miniature end-plate potential (mepp) frequency is increased by the drug. These effects could result if DPH blocked both calcium transport at the axonal membrane and intracellular calcium sequestration. Mepp amplitude is reduced, and DPH also induces nerve conduction block at high rates of stimulation. The relevance of these effects to the anticonvulsive activity of DPH is discussed.

Animals↗