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Biomedical subjects

E Heinen

Publications and source records attributed to E Heinen.

At least 127 records · Page 7Linked to original sources
PubMed1976

Comparative ultrastructural study of the effects of serum-free medium and dibutyryl-cyclic AMP on newborn rat astroblasts.

Modifications of cell shape induced in cultured newborn rat astroblasts by serum deprivation or dibutyryladenosine 3'-5' monophosphate (dBcAMP) are described. Serum suppression modifies the adhesitivity of the cells to the substrate, but this modification is not consistent with a true differentiation. The main ultrastructural feature of dBcAMP-treated astroblasts is the presence of an extensive system of 90 A microfilaments, while control cells are relatively devoid of these structures.

Animals↗
PubMed1976

Comparison of the effects of ethidium bromide and of ethidium bromide-deoxyribonucleic acid complex in fibroblasts cultivated in vitro.

Chick embryo fibroblasts cultivated in vitro were treated with ethidium bromide (E.B.) or with DNA-E.B. complex (DNA-E.B.). E.B. (5 mug/ml) provokes morphological alterations and cell death, inhibits DNA synthesis and mitotic activity. DNA-E.B. (E.B. 5 mug/ml) is less toxic to the fibroblasts as far as cell structure, DNA synthesis and mitotic activity are concerned. DNA alone has no apparent effect on the fibroblasts. As shown by fluorescence microscopy, the lower toxicity of DNA-E.B. seems to be related to its mode of penetration into the cells.

Animals↗
PubMed1976

Cytological and cytochemical analysis of the effects of cis-dichlorodiamino platinum (II) on chick fibroblasts cultivated in vitro.

Chick embryo fibroblasts cultivated in vitro and treated with cis-dichlorodiamino platinum (II) have been analysed by cytological and cytochemical methods. Morphological alterations (in the nucleoli, in the chromatin and in the cytoplasm), inhibition of DNA and RNA syntheses and of cell multiplication have been noted. Under some conditions, cells are blocked just before entering into mitosis (G2 block) and can become polyploid. A high degree of cell degeneration has also been observed.

Animals↗
PubMedDate not supplied

Hepatic thyroid hormone levels following chronic alcohol consumption: direct experimental evidence in rats against the existence of a hyperthyroid hepatic state.

To study the effect of chronic alcohol consumption on hepatic levels of thyroid hormones, female Sprague-Dawley rats (n = 24) were pair-fed nutritionally adequate liquid diets containing either ethanol (36% of total calories) or isocaloric carbohydrates for 21 days. Compared to controls, chronic alcohol consumption failed to result in a significant change of hepatic thyroid hormone levels (thyroxine: 14.7 +/- 1.81 ng per gm of liver wet weight vs. 15.0 +/- 1.59; triiodothyronine: 2.60 +/- 0.16 ng per gm of liver wet weight vs. 2.66 +/- 0.18). Similar results were obtained when the hepatic levels of thyroid hormones were expressed per total liver, per gram of liver protein or per 100 gm of body weight. Moreover, prolonged alcohol ingestion led to a significant reduction of serum total thyroxine by 31.6% (p less than 0.001), free thyroxine by 38.9% (p less than 0.02), total triiodothyronine by 40.2% (p less than 0.001) and free triiodothyronine by 56.1% (p less than 0.001) when compared to their pair-fed controls, whereas thyroid-stimulating hormone levels remained virtually unchanged. These data, therefore, clearly show that chronic alcohol consumption is incapable of creating a hyperthyroid hepatic state in rats, and limit the rationale for antithyroid treatment in patients with alcoholic liver disease.

Alcoholism↗
PubMedDate not supplied

Inhibition of peripheral deiodination of 3, 5, 3'-triiodothyronine: an adverse effect of propylthiouracil in the treatment of T3-thyrotoxicosis.

An inhibition of peripheral conversion of T4 to T3 is thought to be of benefit in the treatment of thyrotoxicosis. Therefore, propylthiouracil (PTU) has been considered to be more effective in the therapy of hyperthyroidism than methimazole, since the former has the additional peripheral effect of decreasing the conversion of T4 to T3, From in vitro studies PTU is known, however, to inhibit the deiodination at the 5' as well as at the 5 position of the iodothyronine molecule. To study if PTU blocks degradation in T3 in vivo as well, the effect of PTU on thyroid hormone concentrations in serum and liver tissue during a constant and high administration of T4 or T3 to rats was followed. It was shown that PTU clearly inhibits T4 and reverse T3 degradation. Moreover, simultaneous treatment of the rats with T3 and PTU resulted in a significantly higher increase of T3 concentration in liver tissue (11.5 ng/g liver vs 5.6 ng/g liver) and serum (615 ng/di vs 345 ng/dl) than with T3 alone. This effect may be explained by an inhibition of the T3 degradation by PTU in vivo as well. Provided the results obtained from these animal experiments can be applied to the situation in man, the inhibition of peripheral deiodination could have an adverse effect at least in the treatment of T3-thyrotoxicosis.

Animals↗