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Biomedical subjects

M Nielsen

Publications and source records attributed to M Nielsen.

At least 325 records · Page 18Linked to original sources

Granular cell myoblastoma in the parotid gland.

Granular cell myoblastomas develop most commonly in the head and neck region, but their occurrence in the salivary glands has been reported in only one case, in the submaxillary gland. The authors report a case of granular cell myoblastoma in a previously undescribed localization, the parotid gland.

Female↗

The influence of ionic strength and incubation time on the sensitivity of methods using papainized red cells.

The sensitivity of a combination of various papain methods with normal and low ionic strength (lis) of the serum-cell mixture for the detection of red cell antibodies was tested after varying periods of incubation of the mixture. The mixture was centrifuged before reading when the period of incubation was short. The maximum sensitivity without centrifugation was always reached after a period of 60 min. With a longer incubation the sensitivity decreased. A sensitivity that equalled the maximum sensitivity without centrifugation could be obtained after only 10 min of incubation, if it was followed by a centrifugation before reading. Lis consistently increased the sensitivity of the papain methods, especially after 45--60 min of incubation.

Antibodies↗

The influence of ionic strength, albumin and incubation time on the sensitivity of the indirect Coombs' test.

The sensitivity of the indirect Coombs' test was investigated using saline, albumin, or low ionic strength (LIS) in the incubation phase and an incubation time varying from 5 to 120 min. Titration of 41 antibodies showed that LIS always resulted in a higher or almost the same mean scores as the other solutions after the same incubation time. The maximum mean score was always higher with LIS than with saline and was reached after a shorter period of incubation, only 20--40 min even with the weakest antibodies. With LIS, a longer incubation time than 40 min resulted in a sudden decrease in mean score. The maximum mean score using saline or albumin was reached after 40--60 min incubation. The same mean score was obtained after only 15--20 min, when LIS was used. Albumin gave only slightly higher mean scores than saline.

Antibodies↗

Carcinoma of the parotid gland following sialography with thorotrast. Report of two cases.

Two cases are presented of malignant tumour of the parotid gland following sialography with Thorotrast, 28 and 45 years previously. Both cases were histologically established as squamous cell carcinoma and the presence of Thorotrast in the tumours was confirmed by autohistoradiography. It is suggested that the tumours may have developed from metaplastic ductal epithelium after many years of exposure to the alpha radiation from Thorotrast deposits in the gland.

Autoradiography↗

Benzodiazepine receptor in brain.

The evidence that the brain possesses specific receptors for benzodiazepines is summarized. Further we present a series of brain lesion experiments in rats showing that specific neuronal destructions by 6-hydroxydopamine, kainic acid in the striatum, X-ray irradiation of the hippocampus, intraperitoneal 3-acetyl-pyridine or hemisection at the thalamic level do not reduce the level of benzodiazepine receptors in striatum, hippocampus, cortex or cerebellum. These results show that the benzodiazepines are not positioned on dopamine or noradrenaline terminals, cholergic or GABA-ergic neurons in the striatum, granular cells in the hippocampus or climbing fibers in the cerebellum.

Animals↗

Partial purification of human renin substrate.

A two-step purification method is described for the preparation of renin substrate from human plasma. Pooled plasma from women on oral contraceptives is used for the purification. The overall yield of renin substrate is 57%, with a twenty-fold purification. The specific renin substrate content of the preparation, as determined by enzymatic degradation with an excess of human renin, is 2 mug angiotensin I per mg protein. The product has a very low endogenous renin activity and is free from angiotensinase activity. An additional purification step involving affinity chromatography is described. In pilot studies a renin substrate yield of 37% has been achieved, with a hundred-fold purification. The final product has a specific renin substrate content of 10 mug angiotensin I per mg protein. The preparation contains up to 12 different plasma proteins, nine of which have been identified and quantitated.

Angiotensin II↗

A method for the assay of conjugated 3,4-dihydroxyphenylglycol, a major noradrenaline metabolite in the rat brain.

We present the first published procedure for the measurement of endogenous conjugated 3,4-dihydroxyphenylglycol (DOPEG) in the rat brain. Conjugated DOPEG is estimated from brain extracts after enzymic hydrolysis, isolation of hydrolysed DOPEG on alumina, methylation of DOPEG to 3-methoxy-4-hydroxyphenylglycol (MOPEG) and gas chromatographic quantification of MOPEG. The level of conjugated DOPEG in the CNS of rats (65.7 +/- 0.7 ng/g whole brain tissue corrected for recovery) almost equals the level of conjugated MOPEG. The sensitivity of the method is about 6 ng/g brain tissue. After inhibition of monoamine oxidase with clorgyline (30 mg/kg) conjugated DOPEG and MOPEG both disappeared from the brain with a half-life of about 1 h. Turnover calculations indicate that conjugated DOPEG and MOPEG are the two major noradrenaline end-metabolites in the rat brain. The method of estimating conjugated DOPEG also allows the measurement of noradrenaline, dopamine and total MOPEG in an extract from one half of a rat brain.

Aluminum Oxide↗

Regulation in the central norepinephrine neurotransmission induced in vivo by alpha adrenoceptor active drugs.

The level of the two major norepinephrine metabolites, 3-methoxy-4-hydroxyphenylglycol (MOPEG) and 3,4-dihydroxyphenylglycol (DOPEG), was estimated in the central nervous system of rats to study receptor-mediated regulation of release in vivo as reflected in biochemical changes. The norepinephrine receptor stimulating drug clonidine (0.02-0.5 mg/kg) decreased the level of endogenous total MOPEG. The accumulation of 3H-MOPEG and 3H-DOPEG was decreased by clonidine (0.5 mg/kg) regardless of whether 3H-tyrosine or 3H-dopamine was used as precursor of 3H-norepinephrine. In contrast to clonidine, the two alpha adrenoceptor blocking drugs, phenoxybenzamine (20 mg/kg) and aceperone (20 mg/kg), induced an increase in endogenous total MOPEG and also an increase in 3H-MOPEG and 3H-DOPEG regardless of the precursor used. These results indicate that clonidine decreases the release of norepinephrine in vivo and that phenoxybenzamine and aceperone increase the release of norepinephrine. Clonidine inhibited completely the effect of phenoxy benzamine or aceperone on endogenous MOPEG. On the contrary, it was not possible to block completely the effect of small doses of clonidine by pretreatment with either phenoxybenzamine, yohimbine (2 mg/kg) or a high dose of aceperone. These results indicate that clonidine may act on a different target than the alpha adrenoceptor blocking drugs. In vitro experiments with occipital cortex synaptosomes did not indicate a direct effect of clonidine on tyrosine hydroxylation in noradrenergic nerve terminals.

Animals↗

The effect of amitriptyline, desipramine and imipramine on the vivo brain synthesis of 3H-noradrenaline from 3H-L-dopa in the rat.

3H-L-Dopa was given to rats after a peripheral decarboxylase inhibitor Ro 4-4602 (50 mg/kg) and the effect of 30 min pretreatment with antiptyline (10 mg/kg), desipramine (10 mg/kg) and imipramine (10 mg/kg) on the brain formation of 3H-dopamine, 3H-noradrenaline and their major metabolites was investigated. Desipramine produced a decrease in the level of labelled noradrenaline and its major metabolites free and conjugated 3-methoxy-4-hydroxyphenyleneglycol and 3,4-dihydroxyphenyleneglycol. Imipramine decreased labelled noradrenaline and 3-methoxy-4-hydroxyphenyleneglycol, whereas amitriptyline produced no significant effect on noradrenaline metabolism. The thymoleptic drugs produced no significant effect on endogenous brain noradrenaline and dopamine. These findings provide a strong indication that desipramine and imipramine inhibit the 3H-noradrenaline biosynthesis from 3H-L-Dopamthe effect seems closely related to the well-known membrane inhibitory effect of these drugs, since desipramine produced a more marked effect than imipramine and amitriptyline showed no effect. No conclusive evidence for the precise mechanism of action was obtained but it is possible that the decreased 3H-noradrenaline synthesis is related to interference of desipramine and imipramine with the precursor (s) 3H-L-Dopa or 3H-dopamine at sites of 3H-noradrenaline biosynthesis.

3,4-Dihydroxyphenylacetic Acid↗

Intra- and extraneuronal formation of the two major noradrenaline metabolites in the cns of rats.

The two major noradrenaline metabolites in the rat brain, total 3-methoxy-4-hydroxyphenylglycol (MOPEG) and total 3,4-dihydroxyphenylglycol (DOPEG), were measured by a new analytical procedure after intraventricular (i.v.t.) injection of (3-H) noradrenaline or (3-H) dopamine. I.v.t. injection of (3-H) noradrenaline to rats with a 6-hydroxydopamine-induced destruction of nerve terminals in the central nervous system, resulted in an increased accumulation of 3-H-MOPEG compared to 3-H-DOPEG. On the contrary, reserpine induced a greater increase in 3-H-DOPEG than in 3-H-MOPEG accumulation when these two metabolites were formed from (3-H) noradrenaline synthesized in vivo by i.v.t. injection of (3-H) dopamine. These results indicate that the formation of DOPEG and MOPEG occur with some preference intra- and extraneuronally, respectively. The results, however, also show that these two formations sites should not be considered as specific.

Animals↗