Publications by authors named "Fog R"

Using microautoradiography ex vivo we tested the effect of forced running on a roller drum for 3 h on the nuclear incorporation of [5-(3)H uridine] in mouse brain. Specific neuron types with increased nuclear labelling included primary motor cortex layer 5 nerve cells with nuclei greater than 12 microm (+38%) and large neuron nuclei in putamen (+58%). Mice running for 45 min do not show any change in the labelling of nerve cell nuclei compared with mice moving freely in the cage.

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New diagnostic vistas.

Int Clin Psychopharmacol

January 1995

There are many difficulties in establishing criteria for better drug compliance and improved quality assurance in the treatment of schizophrenic patients. The most serious problem (especially with first episodes) is that of diagnosis. Since no biological markers for schizophrenia have been found the clinician is referred to "symptom collecting"--including collecting social data.

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Neuronal uridine metabolism.

Acta Neurol Scand Suppl

November 1992

Uridine and other nucleic acids form part of RNA, DNA, coenzymes, second messengers, etc. Uridine uptake in nerve cells is an expression of neuronal RNA synthesis. More knowledge of uridine functions in neurones may give a better understanding of mechanisms underlying dementia, and they could be useful in treating brain tumors.

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Sixty, 3-month-old, male Theiler mice were injected with 1 mg 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) each i.p. Six groups of 5 animals each were then injected with 0.

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During the last seven years 65 patients with Gilles de la Tourette's syndrome have been treated. Pimozide was used as the preferred drug because of our experience of treating other hyperkinesias which indicated fewer side-effects than with haloperidol. Of the 65 patients with Gilles de la Tourette's syndrome, 59 were treated with pimozide alone or in combination with tetrabenazine or clonidine.

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In a double blind, cross-over study 10 chronic schizophrenic patients with productive symptoms in spite of neuroleptic treatment received the methionine-enkephalin analogue FK 33-824 2 mg i.m. daily for 7 consecutive days.

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Neuropharmacology of tics.

Rev Neurol (Paris)

April 1987

In pharmacological treatment of Gilles de la Tourette's syndrome neuroleptic (antipsychotic) drugs have been the most effective. This has led to the hypothesis of a relative dopaminergic overactivity in the brain. Animal studies with neuroleptic drugs different in their affinity to different dopamine areas as well as studies with drugs different in their selectivity to different receptors have, however, not shown direct correlations to the clinical response in the treatment of hyperkinetic syndromes.

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Male white mice were exposed to electroshock and then injected intravenously with 5-[3H]uridine immediately after the shock. After 5, 30, or 60 min or 6, 12, or 24 h, the mice were killed, microautoradiographs were prepared, and grains were counted in the cortex, hippocampus, and basal ganglia. The results of the grain counts were compared with grain counts in the cortex, hippocampus, and basal ganglia of mice exposed to anoxia for 25 s and then treated in the same manner as the first groups.

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Two hundred and sixteen psychiatric patients (183 men and 33 women) hospitalized in Sct. Hans Hospital were treated with clozapine between 1971-1983. All had been treated previously with one or more neuroleptic(s) and had either failed to respond adequately, or their response was limited by side effects.

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Dopamine antagonists are effective in suppressing hyperkinetic symptoms in patients with tardive dyskinesia, spontaneous oral dyskinesia, Huntington's chorea, and Gilles de la Tourette's syndrome. These neuroleptics have no curative effect upon the conditions and may even aggravate symptoms in the long term. In many cases a single neuroleptic drug may lose its effect.

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Following intravenous injection of tritiated uridine to a grivet monkey, the uptake in nerve cell nuclei was determined autoradiographically in different brain regions, in the choroid plexus, liver and kidney. It is shown (1) that there are obvious differences in the labelling in different brain areas, and (2) that the labelling, compared with earlier results in mice, is the same in some regions but different in others. The uridine labelling was inversely related to the microspectrophotometrically determined cytoplasmic concentration of ribonucleic acid.

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Following a stab wound in the brain, mice were injected with 3H-thymidine intravenously 15 min before sacrifice. In a first series, the cells in the synthesis phase (S-cells) in the stab canal, in the adjacent areas and in the rest of the section were counted. The animals were sacrificed from 15 min to 3 days after the stab wound.

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In vivo experiments in mice demonstrated that 5% CO(2) content in the air inhaled did not change the labelling in autoradiograms from animals injected with [(3)H]uridine, [(3)H]orotic acid, [(3)H]hypoxanthine, [(3)H]lysine or [(3)H]cytidine. At 20% CO(2) content there was a significant decrease in labelling of brain cells with [(3)H]uridine and [(3)H]cytidine, but not following [(3)H]lysine; there was no labelling of nerve cells with [(3)H]orotic acid or [(3)H]hypoxanthine, but a control group was not included. The labelling of choroid plexus and hepatocytes was independent of the CO(2) concentration.

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The uptake of a nucleic acid precursor as related to age was studied in mice. Newborn, young (3-month-old) and old (18 to 24-months-old) mice were given 3H-uridine orally through a plastic tube and sacrificed 4 and 21 hours later. Uptake was studied autoradiographically in nerve cells of the fifth layer of parietal cortex, the epithelial cells of the choroid plexus, the hepatocytes of the liver and the epithelium of the small intestine.

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