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Biomedical subjects

M MacNeil

Publications and source records attributed to M MacNeil.

7 recordsLinked to original sources
PubMed1992

Quality control in nerve conduction studies with coupled knowledge-based system approach.

Contemporary equipment used for nerve conduction studies is usually capable of computerized measurement of latency, amplitude, duration, and area of nerve and muscle action potentials and resulting conduction velocities. Abnormalities can be due to technical error or disease. Identification of technical error is a major element of quality control in electromyography, and artificial intelligence could be useful for this purpose. We have developed a coupled knowledge-based prototype system (QUALICON) to assess the correctness of recording and stimulating characteristics in routine conduction studies. QUALICON extracts numeric features from CMAPs or SNAPs, which are translated into symbolic form to drive a Bayesian network. The network uses high-level knowledge to infer the quality of stimulating and recording electrode placement as well as polarity and stimulus strength making recommendations as to the likely technical error when abnormal potentials are detected. A preliminary assessment shows that QUALICON performs as well as manual assessment performed by professionals.

Action Potentials↗
PubMed1979

Evidence for a noncholinergic site for nicotine's action in brain: psychopharmacological, electrophysiological and receptor binding studies.

In an effort to investigate the possibility of noncholinergic nicotine sites within the brain, psychopharmacological, biochemical and eletrophysiological studies were undertaken with nicotine and various newly synthesized derivatives of nicotine and piperidine. When 1-10 micrograms of (-)-nicotine was injected into the region of the lateral ventricle of rats through implanted cannulae, there resulted a characteristic prostration immobilization syndrome, which was accompanied by seizures and tremors at the higher dose range. The (+)-isomer possessed 1/100 the activity of the natural (-)-isomer. The syndrome could be prevented by pre-treatment, intraventricularly, with the N-benzyl and N-p-nitrophenylazido derivates of either nicotine or piperide. A variety of neurotransmitters and psychotropic agents, including acetylcholine and anticholinergic drugs, were without antagonistic action. After nicotine, recordings of spontaneous electrical activity from electrodes chronically implanted into the region of the dorsal hippocampus showed a marked decrease in the amplitude and number of 6-8 sec discharges, and the change was correlated with the behavioral syndrome. Receptor binding studies were performed with rat brain slices and various neural preparations using 3H-nicotine, 125I-alpha-bungarotoxin and 14C-d-tubocurarine as ligands; and only with 3H-nicotine was it possible to demostrate any competitive effect with the various nicotine and piperidine antagonists. It was possible to demonstrate stereospecific or specific nicotine binding to only glass fiber filters and, to a lesser extent, brain slices, but not to cell-free preparations. It was concluded that there existed specific noncholinergic sites for nicotine's action which have not been hitherto described.

Animals↗
PubMed1978

Phospholipid changes in synaptic membranes by lipolytic enzymes and subsequent restoration of opiate binding with phosphatidylserine.

A study has been made of the role of phosphatidylserine in stereospecific opiate binding to neural membranes, utilizing specific lipolytic enzymes to attack the lipid. At very low concentrations phospholipase A2 from bee venom will preferentially hydrolyze C22:6-fatty acid; and even after a few percent of the total phosphatidylserine is hydrolyzed, opiate binding is greatly inhibited. The addition of brain phosphatidylserine will restore opiate binding; however, when the inhibition approaches 50% restoration is only partial. Exposure of membranes to phosphatidylserine decarboxylase will partially inhibit opiate binding; and the binding returns to the control level after the addition of phosphatidylserine. The partial inhibition of opiate binding by low concentrations of Triton X-100, which presumably remove lipids, can be partially reversed by phosphatidylserine. The binding of 3H-naloxone, an opiate antagonist, is similar to agonists in its behavior towards phospholipases and phosphatidylserine; however, binding of naltrexone, also an antagonist, is far less responsive. It is concluded that the phosphatidylserine associated with the opiate receptor is the C18:0, 22:6-diacyl form, which is closely associated with protein.

Animals↗
PubMed1977

Enhancement of opiate binding by various molecular forms of phosphatidylserine and inhibition by other unsaturated lipids.

A study was undertaken on the possible involvement of phospholipids on stereospecific opiate binding to a rat brain membrane fraction comprised mainly of synaptic membranes. The addition of acidic phospholipids such as phosphatidylserine, phosphoinositides, and phosphatidic acid significantly enhanced opiate binding. With the exception of phosphatidylserine, when the acidic phospholipids contained a polyunsaturated acyl group, they were actually inhibitory, along with neutral phospholipids derived from brain. Both the C18:0, C18:1 form (derived from myelin) and the C18:0, C22:6 form of phosphatidylserine (derived from synaptic membranes) produced as much as a 45% enhancement in opiate binding. Unsaturated fatty acids were highly inhibitory, the degree of inhibition being related to the degree of unsaturation. Both phospholipase A and C were inhibitory; and the inhibitory effect of A could not be prevented by albumin or overcome with the addition of phosphatidylserine. With the use of the cross-linking agent, dinitrodifluorobenzene, it could be demonstrated that the phosphatidylserine of synaptic membranes appeared to be preferentially associated with membrane protein. The enhancement of opiate binding by phosphatidylserine diminished with increasing degree of cross-linking.

Animals↗
PubMed1976

Stereospecific opiate binding in human erythrocyte membranes and changes in heroin addicts.

Stereospecific opiate binding has been demonstrated in human erythrocyte membranes, having a Kd of 9-10(-9) M. In most respects the binding characteristics resemble those of synaptic membranes. These included the correlation of binding affinity and pharmacological potency of opiates; competition by naloxone; inhibition by Ca2+ and Na+; and sensitivity to phospholipases and trypsin. A comparison of stereospecific opiate binding in control human subjects and heroin addicts revealed a 43% increase in the addict group.

Adult↗