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Biomedical subjects

M Nielsen

Publications and source records attributed to M Nielsen.

At least 289 records · Page 16Linked to original sources
PubMed1983

Morphological changes in the aorta of rabbits with chronic renal failure.

The morphological changes in the thoracic aorta induced by chronic renal failure (CRF) were studied in female albino rabbits after seven weeks of CRF. The effect of three and eight months duration of CRF was studied in the proximal part of the abdominal aorta. Renal impairment was induced by electrocoagulation of part of the renal parenchyma of one kidney and subsequent contralateral nephrectomy two weeks later. In the media wavy elastic membranes were the first histological change observed. After long-term CRF necrosis and calcifications with thickening of the vessel wall became frequent and in some rabbits the aorta was changed grossly into a stiff calcified tube. In the intima focal thickenings were found with increasing frequency and severity with increasing duration of the renal insufficiency.

Animals↗
PubMed1983

Penicillamine-induced dermatomyositis. A case history.

A 69-year-old woman with classical rheumatoid arthritis developed a severe dermato-myopathy during treatment with penicillamine. Remission occurred on withdrawal of the drug. Penicillamine (dimethylcysteine) is a pharmacological agent used for its chelating properties in the treatment of Wilson's disease and heavy metal poisoning, and in cysteinuria because of soluble disulphide formation. Within the last 17 years penicillamine has been increasingly applied in the treatment of rheumatoid arthritis, the mechanism of action still being unknown. A great number of side effects have been reported, including less common auto-immune disorders such as drug-induced systemic lupus erythematosus, myasthenia gravis and polymyositis. These and other possible side effects have been well reviewed by others (1, 2). To our knowledge only a few earlier cases of dermatomyositis as a complication to penicillamine treatment of rheumatoid arthritis have been reported (3, 4, 5). We describe here another case.

Aged↗
PubMed1982

Anxiety.

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Animals↗
PubMed1982

Does the reversal of the anticonflict effect of phenobarbital by beta-CCE and FG 7142 indicate benzodiazepine receptor-mediated anxiogenic properties?

In mice and rats, the high affinity ligand for brain benzodiazepine (BZ) receptors beta-CCE, and the more stable congener FG 7142, failed to exert anticonflict activity in conflict situations but instead reversed the anticonflict effect of lorazepam. In contrast to Ro 15-1788, beta-CCE and FG 7142 also antagonized the anticonflict effect of phenobarbital in rats. This effect suggests that beta-CCE and FG 7142 may produce anxiety by either inducing a conformational change in the BZ receptors which is directly opposite to that induced by the benzodiazepines, or binding to a particular subclass of BZ receptors.

Animals↗
PubMed1982

Interaction of convulsive ligands with benzodiazepine receptors.

The gamma-aminobutyric acid (GABA)-benzodiazepine receptor complex, which is composed of distinct proteins embedded in the neuronal plasma membrane, is important for several effects of benzodiazepines, including protection afforded against convulsions. During structural modification of ethyl beta-carboline-3-carboxylate an agent was discovered which has high affinity for brain benzodiazepine receptors but which is a potent convulsant. Also in contrast to benzodiazepines, this type of benzodiazepine receptor ligand favors benzodiazepine receptors in the non-GABA-stimulated conformation, which may explain the convulsive properties.

Allosteric Regulation↗
PubMed1982

The benzodiazepine/GABA receptor complex during severe ethanol intoxication and withdrawal in the rat.

The benzodiazepine/GABA (gammaaminobutyric acid) receptor complex was investigated during severe ethanol intoxication and withdrawal in the rat. The intragastric intubation technique was used to establish physical ethanol dependence in the animals. Cerebral cortex from male Wistar rats was studied 1) after 3 1/2 days of severe ethanol intoxication, 2) during the ethanol withdrawal reaction and 3) in a control group. The effect of GABA-ergic activation by muscimol and THIP (4,5,6,7-tetrahydroisoxazole(5,4-c)pyridin-3-01) on 3H-diazepam binding was unchanged during ethanol intoxication and withdrawal, as was the affinity constant (KD) and the maximal number of binding sites (Bmax) for 3H-flunitrazepam. In conclusion, the benzodiazepine/GABA receptor complex is unlikely to play any causal part in physical ethanol dependence.

Alcoholic Intoxication↗
PubMed1982

Peripheral metabolism of beta-carboline-carboxylic acid esters.

Esters of beta-carboline-3-carboxylic acid have recently been identified as potent inhibitors of brain benzodiazepine receptors in vitro. Ethyl beta-carboline-3-carboxylate (beta-CCE), however, is a rather weak inhibitor in vivo of benzodiazepine receptors in mice. The ED50-value was 91 mg/kg intraperitoneally 35 min after administration (ED50 is that dose which inhibits by 50% the specific binding of 3H-flunitrazepam intravenously). ED50 for beta-CCE was 2-20 fold lower in mice pretreated with organophosphorus esterase inhibitors, concomitantly with the observation of strong inhibition of liver and kidney hydrolyzing activity, using 3H-propyl beta-carboline-3-carboxylate as substrate. The rat brain contains only approximately 0.1% of the hydrolyzing activity as compared to the liver. It is concluded that some esters of beta-carboline-3-carboxylate exhibit only weak effects on benzodiazepine receptors in living animals due to hydrolysis outside the brain.

Animals↗
PubMed1982

Osteosclerosis of the femoral head in long-term uraemic rabbits.

The morphology of the femoral head of rabbits was studied by histomorphometric analysis of undecalcified sections after four and eight months' duration of surgically induced chronic renal failure. A significant increase in trabecular bone mas and osteoid tissue was found in the uraemic rabbits. Signs of osteonecrosis or increase bone resorption were not seen. 99mTechnetium-methylenediphosphonate osteoscintigrams showed increased uptake in the axial skeleton and all periarticular regions in uraemic rabbits. The serum concentrations of calcium and phosphate in the uraemic rabbits were increased.

Animals↗
PubMed1982

Cutaneous lymphocytomas: clinical and histological aspects.

25 cases of cutaneous lymphocytoma were reviewed, of which 13 were benign lymphocytoma of the skin and 15 lymphocytic infiltration of the skin (Jessner). The clinical diagnosis benign lymphocytoma of the skin was in agreement with the histology, except in 2 patients where lymphocytic infiltration of the skin (Jessner) was the most likely clinical diagnosis. Of the 15 patients treated, 8 went into complete remission and 5 into partial remission. Eight patients suffered a relapse after partial and complete remission. The duration of the follow-up period varied between 2 months and 22 years. The histological diagnosis lymphocytic infiltration of the skin (Jessner) tallied in 9 patients with the clinical diagnosis, whereas in 6 patients the clinical diagnosis was benign lymphocytoma or pseudolymphoma. None of the patients developed systemic malignancy within the lymphoreticular system. A suspicious-looking skin lesion should always require further examination in order to exclude cutaneous manifestations of a systemic malignant lymphoreticular disease. The present histologic review demonstrates some uncertainty in diagnosing cutaneous lymhocytomas.l

Humans↗
PubMed1981

[3H]Propyl beta-carboline-3-carboxylate as a selective radioligand for the BZ1 benzodiazepine receptor subclass.

Ethyl beta-carboline-3-carboxylate (beta-CCE) is a mixed-type inhibitor of [3H]flunitrazepam ([3H]FNM) binding to benzodiazepine receptors in noncerebellar regions of rat brain. These findings may represent the presence of either receptor multiplicity or negative cooperativity among benzodiazepine receptors. [3H]Propyl beta-carboline-3-carboxylate ([3H]PrCC) has previously been shown to bind specifically to benzodiazepine receptors of rat cerebellum. In the present study we found no indication of the presence of true negative cooperativity among benzodiazepine receptors when [3H]PrCC was used as radioligand. However, we observed that [3H]PrCC labelled only 57% of [3H]FNM binding sites in rat hippocampus (Bmax values) and 71% in rat cerebral cortex, whereas the number of receptors labelled by both ligands was equal in the cerebellum. Hofstee analyses of the shallow inhibition curves seen in hippocampus and cerebral cortex when [3H]FNM binding was inhibited by beta-CCE indicate that beta-CCE and some other beta-carboline-3-carboxylate derivatives interact preferentially with a subclass of receptors, and that the percentage of this subclass is equivalent to the number of receptors labelled by [3H]PrCC. We conclude that [3H]PrCC at low concentration (0.3-0.4 X 10(-9) M) labels a subclass of benzodiazepine receptors, BZ1, while another class, BZ2 receptors, are not labelled by [3H]PrCC when filtration assays are used. By parallel determinations of the proportion between [3H]FNM and [3H]PrCC binding we calculated the percentage of BZ1 receptors in several regions of rat, guinea pig and calf brain and in mouse forebrain. The values ranged from approximately 50% in hippocampus to 90% in the guinea pig pons.

Animals↗
PubMed1981

[3H]propyl beta-carboline-3-carboxylate binds specifically to brain benzodiazepine receptors.

Ethyl beta-carboline-3-carboxylate has recently been isolated from human urine and it was proposed that derivatives of this compound might be related to an endogenous ligand for benzodiazepine receptors. In the present study we investigated high-affinity binding of [3H]propyl beta-carboline-3-carboxylate ([3H]PrCC) to rat brain membranes. [3H]PrCC binds specifically and with high affinity (half-maximal binding at ca. 1nM) to rat brain membranes. The regional and subcellular distributions of specific [3H]PrCC binding are similar, but not identical, to the distributions of [3H]flunitrazepam or [3H]-diazepam binding. The total numbers of binding sites labelled by [3H]PrCC and [3H]flunitrazepam in rat cerebellum are closely similar, and both ligands bind to cerebellar membranes in a mutually exclusive way. The pharmacological selectivity of [3H]PrCC and [3H]diazepam binding is almost identical. Binding of [3H]PrCC like binding of [3H]diazepam, can be increased in vitro by muscimol, GABA and SQ 20.009. Although subtle differences in binding characteristics were observed, these results indicate that [3H]PrCC and benzodiazepines bind to a common recognition site on benzodiazepine receptors.

Animals↗