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Biomedical subjects

M Burstein

Publications and source records attributed to M Burstein.

At least 37 records · Page 2Linked to original sources
PubMed1985

Biochemical evidence that acetylcholine release from cholinergic nerve terminals is mostly vesicular.

The nature of the intraterminal compartments from which acetylcholine (ACh) is released following presynaptic stimulation was investigated. This was pursued by examining the effects of the anticholinergic drug 2-(4-phenylpiperidino)cyclohexanol (AH5183) on the release of newly synthesized [3H]ACh and of endogenous ACh from purified cholinergic nerve terminals (synaptosomes) which were isolated from the electric organs of Torpedo. Preincubation of the synaptosomes, with AH5183 (1-10 microM), does not affect either the intraterminal synthesis of [3H]ACh or the uptake of its precursors, but results in a marked inhibition (85%) of the release of the newly synthesized [3H]ACh. However, when AH5183 is added following the accumulation of [3H]ACh in the nerve terminals, it does not affect [3H]ACh release. AH5183 also has no effect on the release of preformed endogenous ACh. These findings, together with the previous in vitro demonstrations that AH5183 is a potent inhibitor of ACh uptake into isolated cholinergic vesicles, suggest that most of the synaptosomal ACh is secreted by a vesicular mechanism.

Acetates↗
PubMed1985

Seasonal variations in the muscarinic regulation of acetylcholine release from Torpedo electric organ nerve terminals.

The cholinergic nerve endings of the electric organs of Torpedo ocellata contains presynaptic muscarinic acetylcholine receptors (mAChR) which regulate acetylcholine (ACh) release by negative feedback. The efficiency of this muscarinic regulation varies circannually: maximal inhibition is observed in the winter, much smaller effects in the fall and spring, and no effect is observed during the summer. These variations are accompanied by seasonal changes in the ability of the mAChR to trigger the synthesis of its second messenger (a prostaglandin E-like substance) and in the ability of exogenous prostaglandin E2 to inhibit ACh release. No seasonal changes were found in the number of presynaptic mAChRs. These findings suggest that the observed seasonal variations are due to changes in both the metabolism of prostaglandins in the electric organ and the sensitivity of the ACh-releasing apparatus to the muscarinic second messenger.

Acetylcholine↗
PubMed1984

Metabolism of arachidonic acid and prostaglandins in the Torpedo electric organ: modulation by the presynaptic muscarinic acetylcholine receptor.

We have found that Torpedo electric organ readily synthesizes prostaglandin E2 from both exogenous and endogenous arachidonate and that activation of the presynaptic muscarinic acetylcholine receptor increases the rate of prostaglandin E2 synthesis by inducing the release of tissue arachidonate from its phospholipid pools. The incorporation of radiolabeled arachidonate into tissue phospholipids is slow and Ca2+ independent. However, the electric organ slices readily oxidize the externally added, radiolabeled arachidonate via the cyclo-oxygenase pathway, with prostaglandin E2 being the major product (22 +/- 4% of the initial radioactivity). This process is not affected by either Ca2+ or mepacrine. Torpedo electric organ slices also synthesize prostaglandin E2 from endogenous substrates, and release it into the medium. This process, however, is enhanced by Ca2+ and inhibited by mepacrine. Activation of the Torpedo muscarinic acetylcholine receptor by the agonist oxotremorine results in a dose-dependent atropine-sensitive increase in the synthesis of prostaglandin E2 from endogenous tissue substrates and in the concomitant release of arachidonate into the medium. By contrast, oxotremorine has no effect on either the formation of [14C]prostaglandin E2 from exogenous arachidonate, the incorporation of radiolabeled arachidonate into tissue phospholipids or its liberation from prelabeled slices. These results suggest that activation of the muscarinic acetylcholine receptor induces lipolysis which results in the liberation of endogenous arachidonate and its subsequent conversion to prostaglandin E2.

Animals↗
PubMed1982

[Decreased concentration of low density lipoproteins (LDL) in malignant forms of monoclonal gammopathy].

Low density lipoprotein (LDL + VLDL) concentrations, were measured in 48 patients with multiple myelomatosis, or Waldenström's macroglobulinaemia (malignant monoclonal gammopathies) and in 42 patients with "asymptomatic" benign monoclonal gammopathies (M.G.). In patients with malignant M.G., the level of LDL plus VLDL was significantly lower than in patients with "asymptomatic" M.G. who exhibit a normal level.

Aged↗
PubMed1982

Interaction of heparin with low density lipoproteins. Formation of soluble high molecular weight complexes.

The electrophoretic pattern of low density protein (LDL) in heparinized human serum was analyzed by means of molecular-sieve electrophoresis in polyacrylamide gradient gels. While increasing the electrophoretic mobility of LDL in nonsieving gels (agarose), heparin markedly decreases the electrophoretic mobility of LDL in polyacrylamide gels. This slowing down reflects the formation of large polymers where individual lipoprotein molecules are linked by heparin bridges.

Electrophoresis, Polyacrylamide Gel↗
PubMed1982

Separation and quantitation of subclasses of human plasma high density lipoproteins by a simple precipitation procedure.

Studies in recent years have suggested that measurement of high density lipoprotein (HDL) subclasses may provide significant information beyond that provided by measurement of total HDL. However, conventional methodology for separation of HDL subclasses involves various types of ultracentrifugation that are time-consuming, costly, and not suitable for many clinical or epidemiological studies. We have developed a simple precipitation method for the separation of HDL subclasses in human plasma. After precipitation of apoB-containing lipoproteins with heparin-Mn2+, HDL2 is precipitated by addition of dextran sulfate (mol wt 15,000). HDL2 cholesterol is calculated as the difference between total HDL cholesterol (heparin-Mn2+ supernatant) and HDL3 cholesterol (dextran sulfate supernatant). HDL2 determined by this method correlated well with results obtained by preparative ultracentrifugation (n = 295, r = 0.91) and analytical ultracentrifugation (n = 17, r = 0.92). In the original method final concentration of dextran sulfate was 0.09 g/dl; however further studies indicated that 0.13 g/dl is a more suitable concentration. The chemical compositions of HDL2 and HDL3 isolated by the precipitation method were very similar to those of HDL2 and HDL3 isolated by preparative ultracentrifugation. The concentration of HDL2 cholesterol was 40% higher in normal women than in normal men. In men with coronary heart disease, total HDL was decreased by 28%, HDL2 was decreased by 44%, while HDL3 was 19% lower. A similar pattern of change was found in women with coronary heart disease. In other conditions where total HDL either increased or decreased, the change in HDL2 was always proportionately greater than the change in total HDL. HDL3 showed relatively less change, and in some instances its concentration was unchanged. Thus HDL2 is the more variable component and may be a more meaningful index of altered HDL metabolism.

Chemical Phenomena↗
PubMed1981

[Systematic detection of elevated low density lipoproteins (LDL and VLDL) in a population of 2656 blood donors].

The atherogenic low density lipoproteins were evaluated using two turbidimetric methods: one based on the precipitation of LDL and VLDL by heparin-CaCl2 and the other on the precipitation of the VLDL by sodium dodecyl sulfate. In search of hyperlipoproteinemia, both tests were applied to a population of blood donors aged from 18 to 60 years. when both tests were negative, hyperlipoproteinemia can be excluded without quantitative evaluation of cholesterol and triglycerides levels. If the heparin-CaCl2 test is high and the SDS normal it can be concluded that it is a case of type IIa hyperlipidemia. When both test are high, further investigations are required. In the present study, corresponding to the screening of the sera from 2656 blood donors (including 1280 males and 1376 females), the high level of atherogenic lipoproteins is most frequently observed in the males (10 per cent for men and 2,5 per cent for women). This frequency increases with age.

Adolescent↗
PubMed1978

[Polysulfates, anionic detergents, sodium phosphotungstate and electrophoretic mobility of plasmatic proteins].

Anions with strong electro-negative charges, like sulphuric esters of polysaccharides (heparin, dextran sulphate M.W. 15 00), the sodium salt of polyanethol sulfonic acid (liquoid, Roche), anionic detergents (sodium dodecylsulphate, sodium oleate, sodium deoxycholate), and the sodium salt of phosphotungstic acid were added to human serum or citrated plasma. For each compound several final concentrations were adopted, the highest being 4%. By using microimmunoelectrophoresis and numerous specific antisera against human plasma proteins, it was demonstrated that at pH 8.60 anions increase electrophoretic mobility of the following antigens: lipoproteins alpha and beta; fibrinogen; beta 2-glycoprotein I; beta 2-glycoprotein II ; antithrombin III. All reagents utilized do not react with all these proteins; for instance, only detergents accelerate the migration rate of a lipoproteins. Besides, depending on the protein, this or that reagent may be the most active. Thus, in the polysulphate group, heparin has the highest affinity for antithrombin III, liquoid for fibrinogen and dextran sulphate for beta 2-glycoprotein I.

Blood↗
PubMed1976

[Detergents and precipitation of serum lipoproteins by antisera (author's transl)].

By using gel diffusion methods, it was shown that during immunoelectrophoresis and double diffusion in two dimensions, anionic detergents (sodium oleate, sodium desoxycholate, sodium lauryl-sulfate and sodium decyl-sulfate), added to human serum at the final concentration of 0.5%, do not prevent the formation of an insoluble antigen-antibody complex (precipitation line) when specific antibodies react with serum lipoproteins: LDL, HDL and VLDL. In spite of the presence of anionic detergents, the antigen-antibody interaction in gel occurs even if the amount of lipoproteins in serum was highly reduced. On the contrary, the non ionic detergent tween 80, has a strong inhibitory effect on the specific precipitation of lipoproteins, especially in the case of HDL.

Anions↗
PubMed1976

Purification of rabbit anti-human fibrinogen antibodies cross reactivity of mammalian fibrinogen.

A simple isolation procedure of highly purified and unaltered rabbit antibodies to human fibrinogen is described. The method used is based upon the preferential adsorption of fibrinogen by barium sulfate at acid pH. After redissolution of the specific precipitate and dissociation of the antigen-antibody complexes at pH 2.4, the fibrinogen is removed by adsorption on barium sulfate, while the antibody protein stays in solution. BaSO4 is eliminated by centrifugation and the supernatant is neutralized and concentrated by ammonium sulfate fractionation (40% saturation). A concentrated solution of specific anti-fibrinogen antibodies is thus obtained; the latter can be used to prepare, by selective immunprecipitation, a fibrinogen free plasma, and to analyze precipitin patterns in cross reacting systems.

Animals↗