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Biomedical subjects

H Oepen

Publications and source records attributed to H Oepen.

16 recordsLinked to original sources
PubMed1981

[Monoamine oxidase activity in brain regions and organs of patients with Parkinson's disease and Huntington's disease and serum MAO activity of patients with Huntington's disease as compared with neurologically healthy individuals (author's transl)].

The MAO activity (tyramine substrate) was measured in 17 different brain regions, the spinal cord, and 13 different organs of four patients with Huntington's disease and three patients with Parkinson's disease. The values were compared with those measured in corresponding tissues from neurologically healthy patients. The serum MAO activities of 12 patients with Huntington's disease were compared with those of 137 normal persons (benzylamine substrate). A comparison of the MAO activities in the brain regions of patients with Huntington's disease, Parkinson's disease, and normal controls showed only minor differences in the cerebral gray matter, corpus callosum, striatum, caudate nucleus, pons, putamen, nucleus niger, dentatus, cerebellar gray matter, and cerebellar white matter. Larger differences in MAO activity were observed in the Ammon's horn, the striatal fundus, and the olfactory region. Slightly increased MAO activities were found in the pallidum of patients with Huntington's disease and Parkinson's disease. In patients with Huntington's disease the MAO activity is considerably increased in the medulla oblongata (25%) and the spinal cord (nearly 50%) as compared to patients with Parkinson's disease and normal controls. The brain MAO activity in the rat remained unchanged after movement anomalies had been induced by application of 2,3-diaminobutyric acid; the neurolathyrogenic substance iminodipropionitrile (IDPN), which causes chloreiform movements in the rat that last for life did not considerably change the MAO activity of the brain. The enzyme values were essentially the same in pancreas, spleen, kidney, adrenal, jejunum, ileum, colon, rectum, and testis of patients and control individuals. The MAO activities in the thyroid glands of patients with Parkinson's disease and Huntington's disease were slightly reduced in comparison with the control group. MAO activity in the liver of patients with Huntington's disease was reduced to approximately 50%. In the heart it was increased by approximately 30%, and that in the lungs was five times higher. A comparison of serum MAO activities in Huntington's disease patients and normal subjects did not reveal any essential differences. The increased MAO values in the sera of female patients with Huntington's disease may be related to hormonal influences.

Adult↗
PubMed1981

[Symptomatic therapy in a possible animal model for Huntington's chorea].

This is a report on first symptomatic therapy trials of a possible animal model with beta,beta-iminodipropiontrile (IDPN) for Huntington's disease. 1. Experiments to quantitatively measure the choreiform head movements of the rat after IDPN-application were not successful. 2. Of all substances tested, thyroxine was the only one that prevented the choreiform movement disturbances in the rat induced by IDPN. 3. Glucosamine, isonicotinic acid, -hydrazide (isoniazid) and bromocriptine caused a slight retardation of the occurrence of the IDPN-symptoms in the rat for about 1-2 days. 4. Thyroxine does not improve the IDPN-symptoms in the rat. 5. All the other substances tested (mephenytoin, glucosamine, isonicotinic acid-hydrazide, bromocriptine and isonicotinic acid-hydrazide in combination with glucosamine) do temporarily improve the choreiform movement disturbances induced by IDPN. Furthermore during the treatment, these rats were calmer and their landing showed better results. 6. After these first results, the IDPN-model would appear to be a suitable animal model for Huntington's disease in man. With this animal model, new drugs for the symptomatic treatment of this disease can be tested.

Animals↗
PubMed1980

A pharmacological and behavioural study on beta, beta'-iminodipropionitrile (IDPN)-treated brine shrimp Artemia salina L.

The neurotoxic substance beta, beta-iminodipropionitrile (IDPN), which induces hyperkinesia in some mammals, was found to be neurotoxic to the brine shrimp Artemia salina L. (Crustacea, Anostraca) inducing discoordination of limb-movement and sedation of motility. Up to 9 metabolities of IDPN were detected in Artemia, including beta-alanine, cyanoacetic acid, and beta-aminopropionitrile (BAPN). Brine shrimp, especially nauplius (1 day), may be a useful test animal for the biological assay of IDPN.

Aging↗
PubMed1980

[On age-dependent effects of IDPN in the rat (author's transl)].

We report on age-dependent IDPN-effects in the rat. IDPN induces in rats irreversible movement disorders, which rise qualitatively and quantitatively with increasing age. IDPN-application causes a weight loss in rats, which correlates with the animals' ages. An equal IDPN-dose/kg body weight, in young rats (2 weeks old) causes only a temporary stagnation of the weight increase. Rats older than 2 weeks old suffer from a weight loss which rises with increasing age. In 7 months old rats, the weight loss amounts to as much as 50% of the weight at the start of the experiment. IDPN has an age-dependent strongly, deleterious effect on the rat eye (bleeding in the inner eye, buphthalmos with or without cataract) which finally leads to the loss of the eyes. If young animals (about 35 days old) receive the same IDPN-dose, these eye damages are essentially absent.

Aging↗
PubMed1976

[Fatty acid patterns and glucose tolerance in Huntington's chorea (author's transl)].

Fatty acid patterns of plasma lipids and glucose-tolerance in Huntington's chorea. 25 patients with Huntington's chorea of various manifestation (9 predisposed symptomefree, 5 with light and 11 with severe manifestation) had studies of carbohydrate and lipid metabolism. These studies measured glucose-tolerance tests, insulin-, HGH-secretion, serum lipids and plasma fatty acid conposition of the cholesterylesters, triglycerides and phospholipids. The reactive insulin- but not HGH-levels were significantly raised, 32 % of the patients with Huntington's chorea had abnormal glucose-tolerance tests, compared with 3.2 % in a control group. Duration of symptoms correlated with higher cholesterol levels. Minor deviations were found in the fatty acid patterns in various lipid clases.

Cholesterol↗