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Biomedical subjects

J Nauman

Publications and source records attributed to J Nauman.

At least 55 records · Page 3Linked to original sources

Thyrotrophin binding glycoprotein isolated from bovine thyroid.

A butanol-water extraction of bovine thyroid plasma membranes was used to solubilize a thyrotrophin receptor. This method was found to solubilize approximately 12% of membrane proteins and 40% of the binding capacity of thyroid membranes for [125I]TSH. Thyrotrophin binding proteins were further purified 10 times over the butanol-water extract and 70 times over the plasma membranes by means of chromatography on DEAE-cellulose and AcA-54 Ultrogel columns. Purified fractions were found to be glycoproteins containing galactose, mannose, galactosamine, glucosamine and sialic acid. A minute amount (6.0 micrograms per sample) of two glycoprotein fractions obtained after chromatography on AcA-54 Ultrogel caused about 50% inhibition of [125I]TSH binding to thyroid plasma membranes. This inhibition was due to specific interaction between thyrotrophin and isolated glycoproteins.

Animals↗

Presence of gangliosides in the structure of membrane receptor for thyrotrophin.

Thyroid gangliosides were isolated from bovine thyroid tissue. Neutral lipids and glycolipids were removed by chromatography on a DEAE-cellulose column and residual acidic phospholipids by alkaline degradation. Thyroid gangliosides were separated by chromatography on a silica acid column into 9 different fractions. Thyroid gangliosides were found to be active in the inhibition of [125I]TSH binding to thyroid plasma membranes and this results from a direct action between thyrotrophin and gangliosides. The most active fraction contained gangliosides with two sialic acids per molecule. Pre-incubation of thyroid plasma membranes for 4 hours at 37 degrees C with gangliosides and removal of the unbound gangliosides increased the [125I]TSH binding to pre-treated membranes by 10-20%. Anti-ganglioside antibodies obtained by immunisation of rabbits inhibited [125I]TSH binding to thyroid plasma membranes by 60 to 80%. The thyroxine (T4) level in blood serum of immunized animals was significantly decreased after the first immunization and T4 become almost undetectable after the booster injection implying that antibodies against thyroid gangliosides produce severe impairment of thyroid cell function.

Animals↗

Effects of beta-blocking agent Metipranolol on metabolic variables in patients with ischemic heart disease, hyperkinetic syndrome, hyperthyreosis and in healthy subjects.

Metabolic effects of Metipranolol, a new beta adrenergic blocking agent, have been studied in patients with ischemic heart disease, hyperkinetic syndrome, hyperthyreosis and in healthy subjects. Administration of the drug (30 mg per day for one week) resulted in the decrease of noradrenaline excretion, blood free fatty acid level, and in lowering of blood pressure and heart rate, particularly in patients with ischemic heart disease and hyperkinetic syndrome. These alterations were accompanied by alleviation of clinical symptoms. It is suggested that Metipranolol by suppressing the activity of sympathetic nervous system and thereby diminishing lypolysis, exerts favourable clinical effects, most probably related to diminution of myocardial oxygen consumption.

Adrenergic beta-Antagonists↗

Evidence for the detrimental effect of adrenaline infused to healthy dogs in doses imitating spontaneous secretion after coronary occlusion.

We have previously shown that acute coronary occlusion in the dog is often accompanied by increased adrenaline release into the blood. In the present study the consequences of this humoral reaction were studied in anaesthetised healthy mongrel dogs subjected to adrenaline infusion administered at a rate relevant to spontaneous release of this amine in coronary occlusion. Adrenaline was infused in a dose of 1.2 microgram.kg-1.min-1 for 4 h. Dogs receiving saline served as the control. Adrenaline administration led to the decrease in insulin/glucose ratio, to a significant fall in serum triiodothyronine and in blood pH. Free fatty acid levels doubled. Histochemically, a diminution in succinic dehydrogenase and ATPase activity in adrenaline-treated hearts was found. A significant fall in the activity of mitochondrial hexokinase in these hearts was detected spectrophotometrically. Electron microscopic study revealed alterations in the mitochondrial structure. These findings indicate that an excess of adrenaline in ammounts similar to that seen in experimental infarction leads to profound metabolic and hormonal disturbances and exerts a detrimental effect upon myocardium.

Animals↗