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G Cohen

Publications and source records attributed to G Cohen.

At least 361 records · Page 20Linked to original sources

Transcutaneous nerve stimulation: its significance and applications in podiatry.

In summation, the neuranatomy and neurophysiology of pain have been presented. Three of the classical theories of pain transmission were also discussed, these being the specificity, pattern, and gate control theories. The gate control theory postulates that stimulation of large diameter sensory nerve fibers blocks pain sensation at the level of the substantia gelatinosa in the dorsal horn of the spinal cord. This theory is used as the basic explanation for the function of the TNS, a device that can control pain by stimulation of the skin through surface electrodes. TNS stimulation appears to be most efficacious when the electrodes are placed either directly over or just proximal to the painful region. Podiatric application appears to lend itself quite naturally to TNS therapy. Several surgical and nonsurgical cases were presented where TNS therapy was employed and in this preliminary study approximately a 63% improvement in pain state was shown. We believe this modality is useful for patients who should limit their intake of analgesic medications, whether they are medically compromised, allergic to various pain medication, or simply are highly intolerant to pain. TNS is also useful in patients who do not respond well to the more traditional and conventional podiatric treatments. Our study illustrates TNS to be efficacious in pain states of a surgical, chronic or acute nature and even pain secondary to systemic disease. It should be noted that TNS is not curative, per se, but is a useful adjunct in the therapeutic regime. This form of therapy, although not without hazard, is relatively safe and easy to use, and although it is not the answer to all pain states, it is highly recommended when applicable.

Achilles Tendon↗

Potassium-induced release of [3H]catecholamine from brain: effects of pre-exposure to catecholamine uptake inhibitors.

Cocaine, nomifensine, mazindol, dita and desmethylimipramine markedly decreased the potassium-stimulated release of [3H]-dopamine from rat striatum, an area of brain enriched with dopamine. In contrast, only desmethylimipramine had a similar effect on the release of (3H]norepinephrine from the occipital cortex, a brain area comprised mainly of norepinephrine nerve terminals. These results were obtained under the following experimental conditions: the brain tissue was labeled with the appropriate [3H]catecholamine, incubated with a drug, rinsed twice with drug-free medium and subsequently stimulated with 20 mM potassium ions to induce release of the [3H]catecholamine. The radioactivity present in the medium before, during and after stimulation was primarily the unmetabolized [3H]catecholamine. The diminished response to potassium-stimulation in the striatum after exposure to drug was not related to the ability or potency of the drug to act as an inhibitor of neuronal uptake of catecholamines. The data indicate a relatively selective interaction of the drugs with dopamine nerve terminals rather than norepinephrine nerve terminals.

Acetophenones↗

Role of hydroxyl radicals in the iron-ethylenediaminetetraacetic acid mediated stimulation of microsomal oxidation of ethanol.

The microsomal oxidation of ethanol or 1-butanol was increased by ferrous ammonium sulfate-ethylenediaminetetraacetic acid (1:2) (Fe-EDTA) (3.4-50 microM). The increase was blocked by hydroxyl radical scavenging agents such as dimethyl sulfoxide or mannitol. The activities of aminopyrine demethylase or aniline hydroxylase were not affected by Fe-EDTA. The accumulation of H2O2 was decreased in the presence of Fe-EDTA, consistent with an increased utilization of H2O2. Other investigators have shown that Fe-EDTA increases the formation of hydroxyl radicals in systems where superoxide radicals are generated. The stimulation by Fe-EDTA appears to represent a pathway involving hydroxyl radicals rather than catalase because (1) stimulation occurred in the presence of azide, which inhibits catalase, (2) stimulation occurred in the presence of 1-butanol, which is not an effective substrate for catalase, and (3) stimulation was blocked by hydroxyl radical scavenging agents, which do not affect catalase-mediated oxidation of ethanol. A possible role for contaminating iron in the H2O or buffers could be ruled out since similar results were obtained with or without chelex-100 treatment of these solutions. The stimulatory effect by Fe-EDTA required microsomal electron transfer with NADPH, and H2O2 could not replace the NADPH-generating system. In the absence of microsomes or catalase, Fe-EDTA also stimulated the coupled oxidation of ethanol during the oxidation of xanthine by xanthine oxidase. These results suggest that during microsomal electrom transfer, conditions may be appropriate for a Fenton type or a modified Haber-Weiss type of reaction to occur, leading to the production of hydroxyl radicals.

Animals↗

Role of hydroxyl radicals in microsomal oxidation of alcohols.

A series of hydroxyl radical (.OH) scavenging agents competitively inhibited microsomal oxidation of ethanol and 1-butanol. The inhibition by the scavengers was specific since these agents had no effect on catalase-dependent oxidation of ethanol, microsomal drug metabolism or microsomal electron transfer. Chemical evidence for production of .OH during microsomal electron transfer was provided by the generation of appropriate products from .OH scavenging agents. H2O2 was shown to play a role as a precursor of .OH. Fe-EDTA increased microsomal oxidation of ethanol without affecting drug metabolism. A role for cytochrome P-450 in catalyzing . OH generation remains to be evaluated. These results suggest that the molecular mechanism underlying the oxidation of ethanol by liver microsomes reflects the ability of ethanol to interact with .OH generated from microsomal electron transfer.

Alcohols↗

Isodense acute subdural hematoma.

An unusual isodense acute subdural hematoma is reported. Its causes may have included dilution with cerebrospinal fluid and a local or disseminated coagulopathy. Detection of such lesions requires a high incidence of suspicion based on subtle abnormalities found on computed tomography and the use of enhancement, particularly with the aid of advanced scanners. When a significant shift of the midline is seen, other alternatives would be angiography or placement of an exploratory burr hole on the "swollen" side.

Absorptiometry, Photon↗

Regional distribution of glutathione peroxidase in the adult rat brain.

Glutathione peroxidase activity was measured in 10 areas of perfused adult rat brain with the use of a fluorometric assay coupled to NADPH oxidation. The caudate-putamen and the substantia nigra had the highest activities. Cortical areas and several nuclear areas had somewhat lower activity. Activity was lowest in a white matter structure (corpus callosum). High activity of glutathione peroxidase may be related to the need to reduce hydrogen peroxide arising in the course of monoamine metabolism.

Animals↗

Ethanol oxidation by rat brain in vivo.

Can brain metabolize ethanol? We present data demonstrating that brain catalase in conjunction with endogenous H2O2 will oxidize ethanol in vivo. The method is based on an H2O2-dependent inhibition of brain catalase in vivo by 3-amino-1,2,4-triazole and its prevention by ethanol. The irreversible inhibition of catalase by aminotriazole is known to proceed via the reaction of (catalase-H2O2) compound I with aminotriazole. Inhibition can be prevented by compounds that are oxidized by compound I. Ethanol is one such compound. Prevention of the inhibition of brain catalase in vivo by prior administration of ethanol constitutes indirect evidence for the oxidation of ethanol to acetaldehyde in rat brain. The catalase content of the tissues represented catalase in the brain parenchyma, from which erythrocytes and capillaries had been excluded. Ethanol did not alter the levels of aminotriazole in brain. These results constitute the first demonstration of ethanol oxidation by living brain.

Amitrole↗