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Biomedical subjects

A J Friedhoff

Publications and source records attributed to A J Friedhoff.

At least 109 records · Page 6Linked to original sources
PubMed1977

Gilles de la Tourette's syndrome. Familial occurrence and precipitation by methylphenidate therapy.

Gilles de la Tourette's syndrome was independently ascertained in two male cousins once removed. Previous studies have shown familial clustering of individuals with tics, but no consistent pattern of inheritance of Tourette's syndrome has been apparent. The onset and later exacerbation of symptoms in our younger patient were associated with the administration of CNS stimulants given for excessive motor activity. The adverse effects of methylphenidate and dextroamphetamine therapy on Tourette's syndrome supports the hypothesis that this condition results from a relative excess of CNS catecholaminergic activity. Physicians prescribing these agents should inquire about the presence of tics in patients and their families.

Adult↗
PubMed1977

In vitro and in vivo studies of extrapineal N-acetyltransferase of rat brain.

In a series of experiments, extrapineal rat brain N-acetyltransferase was further characterized and was demonstrated to have a similar pH optimum and similar activity to that of the low activity daytime pineal N-acetyltransferase. Experiments in vivo indicate that N-acetylation may be a possible alternative metabolic pathway for biogenic amines and that brain N-acetyltransferase activity may be regulated by a beta-adrenergic mechanism.

Acetylation↗
PubMed1977

Reversal of two manifestations of dopamine receptor supersensitivity by administration of L-dopa.

Rats treated chronically with dopamine receptor blockers were found to have an increase in striatal 3H-dopamine binding and adenylate cyclase activity as manifestations of receptor supersensitivity. Both the increase in binding and in adenylate cyclase activity were reversed by chronic 1-dopa treatment, presumably by increasing the supply of specific ligand (dopamine). The use of deliberate receptor sensitivity manipulation may be useful as a treatment for conditions involving disturbances in receptor sensitivity such as tardive dyskinesia and insulin resistant diabetes.

Adenylyl Cyclases↗
PubMed1977

The reaction of 5-hydroxyindoleacetic acid with ortho-phthalaldehyde and cysteine.

The metabolite 5-hydroxyindoleacetic acid, the major metabolic product of serotonin, can be measured by reacting it with orthophthalaldehyde to form a highly fluorescent product. The inclusion of cysteine in this reaction causes an increase in the amount of fluorescence. The rate of fluorescence formation for reaction containing cysteine is much faster than the rate for the reaction without cysteine. The differences observed for both excitation and remission maxima between reaction products formed in the presence and absence of cysteine indicate that these products are different. Furthermore, the significant difference in the regression coefficients of fluorescence of the reaction products versus HC1 concentration adds further evidence that the reaction products formed in the presence and absence of cysteine are different. HC1 appears to influence the reaction of 5-HIAA, OPT and cysteine in several ways: by causing the destruction of 5-HIAA, by affecting the fluorescence of the product formed, and by influencing the amount of reaction product formed.

Aldehydes↗
PubMed1975

5-methyltetrahydrofolic acid is not a methyl donor for biogenic amines: enzymatic formation of formaldehyde.

Contrary to previous reports, 5-methyltetrahydrofolic acid does not mediate the methylation of dopamine to epinine. Instead, this methyl donor is degraded enzymatically to formaldehyde, which condenses with dopamine to form a tetahydoisoquinoline derivative. The latter has chromotographic characteristics very similar to those of epinine, which likely accounts for the original misidentification of the product.

Animals↗