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Biomedical subjects

W H Habig

Publications and source records attributed to W H Habig.

57 records · Page 4Linked to original sources

Preparation and purification of glucanase and chitinase from bean leaves.

Glucanase (endo-beta-1, 3-glucan 3-glucanohydrolase, EC 3.2.1.6, laminarinase, callase) and chitinase (poly-beta-1, 4-[2-acetamido-2-deoxy] -d-glucoside glycanohydrolase, EC 3.2.1.14) were extracted from ethylene-treated bean (Phaseolus vulgaris L. cv. Red Kidney) leaves and purified on hydroxyapatite and carboxymethyl Sephadex columns. The glucanase prepared was homogeneous as judged by analytical centrifugation data, electrophoresis, and antibody-antigen reactions. On the basis of gel filtration, antibody-antigen reactions, and amino acid analysis, the molecular weight was estimated to be between 11,500 and 12,500. However, ultracentrifugation gave a higher estimate of 34,000. The glucanase had an isoelectric point near pH 11 and was specific for beta-1, 3-linkages. The chitinase was only partially purified as judged by electrophoretic behavior.

Journal Article↗

Differential toxicity of chronic exposure to phenytoin, phenobarbital, or carbamazepine in cerebral cortical cell cultures.

The effects of phenytoin (30 micrograms/ml), phenobarbital (64 micrograms/ml), and carbamazepine (24 micrograms/ml) were assessed in cerebral cortical cell cultures. After antiepileptic drug exposure for eleven days, cultures were assayed for total protein, number of neurons, tetanus toxin fixation, high-affinity uptake of gamma-aminobutyric acid and beta-alanine, activity of choline acetyltransferase, and benzodiazepine binding. Carbamazepine-exposed cultures demonstrated minimal effects, whereas highly significant deficits related to generalized toxicity were observed in cultures exposed to phenytoin or phenobarbital.

Animals↗

Differential neurochemical effects of chronic exposure of cerebral cortical cell culture to valproic acid, diazepam, or ethosuximide.

We have assessed the relative neurochemical effects of valproic acid, ethosuximide, and diazepam on dissociated cultures of mouse cerebral cortex. Cultures were exposed chronically (11 days) to each antiepileptic drug and assayed for number of neurons, total protein, tetanus toxin fixation, high-affinity uptake of gamma-aminobutyric acid and beta-alanine, choline acetyltransferase activity, and specific and clonazepam-displaceable benzodiazepine binding. Ethosuximide-exposed cultures did not evidence neuronal toxicity; exposure to valproic acid and diazepam resulted in modest neuronal toxicity. However, exposure to each of these drugs resulted in a marked reduction in benzodiazepine binding. This effect may relate to a common mechanism of action of drugs used to treat absence seizures.

Animals↗