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Biomedical subjects

E Yavin

Publications and source records attributed to E Yavin.

123 records · Page 7Linked to original sources

Regulation of phospholipid metabolism in differentiating cells from rat brain cerebral hemipheres in culture. II. Incorporation of [U-14C]ethanolamine into 1-alkenyl,2-acyl-and 1,2 diacyl-ethanolamine phosphoglycerides.

Cultured dissociated cells from rat embryo cerebral hemisphere incorporate [3H]-and [U-14C]ethanolamine into cellular lipids. Nearly all radioactivity in the lipid fractions is incorporated into 1,2-diacylethanolamine phosphoglycerides and 1-alkenyl,2-acylethanolamine phosphoglycerides (plasmalogen). Kinetic data suggest that the rate of labeling of both ethanolamine phospholipids from the phosphorylethanolamine is similar. A relative increase of the plasmalogen labeling is observed when free ethanolamine is continually present in the medium. The rate of incorporation of label from ethanolamine and phosphorylethanolamine into lipids was measured using a double label technique. Based upon these studies, an independent labeling pattern of the ethanolamine moiety of plasmalogens is suggested. A relative delay for the incorporation of label in plasmalogens could be explained by the presence of a variety of cell types which may differ in their capacity for phospholipid biosynthesis. The rate of incorporation of phosphorylethanolamine into the phosphatidylethanolamine was not affected by the presence of high concentrations of either choline or serine.

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Effect of essential fatty acids on proliferation of two neural tumor lines.

A combination of linoleic and linolenic acids has been shown to be able to partly replace serum in maintaining cell division of neural tumor lines. Addition of essential fatty acids to C-6 rat astrocytoma cells grown in serum-deprived medium increased the rate of cell proliferation and restored morphological appearance. Essential fatty acids also restored the rate of 3H-thymidine uptake by N-18 neuroblastoma cells grown in a serum-deprived medium. In the complete absence of serum, neuroblastoma cells were unable to proliferate despite addition of essential fatty acids. These studies indicate the importance of essential fatty acids in controlling the rate of neural tumor proliferation.

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Regulation of eicosanoid synthesis by whole fetal rat brain ex vivo.

Intact cerebral hemispheres from 20-d-old rat fetuses incubated at 37 degrees C in Dulbecco's Modified Eagle Medium (DMEM) synthesize and release a number of arachidonic acid derived metabolites, such as thromboxane B2 (TxB2), 6-keto prostaglandin F1 alpha (6k-PGF1 alpha), and prostaglandin E2 (PGE2) eicosanoids. Synthesis is time-dependent and is stimulated upon addition of the calcium ionophore A23187 (10 microM). Ionophore stimulation is prevented by EDTA/EGTA (5 mM each) ion chelators, dextran-70 (5%), and indomethacin (10 microM), a potent cyclooxygenase inhibitor. Ca2+ (2 mM) enhances ionophore-mediated formation of TxB2, 6K-PGF1 alpha, and PGE2 by 2.5-, 2.9-, and 4.2-fold, respectively; Mg2+ blocks ionophore stimulation. Freezing and thawing enhances release of eicosanoids to a level nearly the same as that obtained in the presence of A23187, indicating a common mode of action.

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Monoclonal antibodies to the thyrotropin receptor: the identification of blocking and stimulating antibodies.

Monoclonal antibodies to the thyrotropin (TSH) receptor have been obtained from fusions of mouse myeloma cells with spleen cells immunized with solubilized thyroid membrane preparations. Two monoclonal antibodies which inhibit 125I-TSH binding and are reactive with the glycoprotein component of the bovine TSH receptor (11E8 and 13D11), are shown to inhibit basal and TSH stimulated adenylate cyclase activity in bovine thyroid membranes and human thyroid cells. Both antibodies also inhibit 125I-TSH binding in vitro, whether binding is measured at pH 6.0 in low salts and at 0-4 C or at pH 7.4 in 50 mM NaCl and at 37 C. The glycoprotein component is thus a portion of the physiologic TSH receptor in vivo and 125I-TSH binding studies apparently measure the high affinity glycoprotein component under nonphysiologic conditions and conditions more representative of the physiologic milieu. A third monoclonal antibody whose interaction with thyroid membranes is prevented by TSH is shown to stimulate adenylate cyclase activity in bovine thyroid membranes and human thyroid cells. This stimulating antibody only weakly inhibits 125I-TSH binding to thyroid membranes or to the glycoprotein component of the TSH receptor. The 22A6 antibody does, however, immunoprecipitate mixed brain gangliosides, in distinct contrast to the monoclonal antibodies to the glycoprotein receptor component, i.e., 11E8 and 13D11. The results support the speculation that autoimmune antibodies which inhibit TSH binding to thyroid membranes are not necessarily identical to antibodies which stimulate function; that antibodies directed at the high affinity initial site of TSH interaction with a cell can behave as blocking rather than stimulating antibodies and that a possible relationship exists between stimulating antibodies and the low affinity TSH binding sites (gangliosides) on thyroid membranes.

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Docosahexaenoic acid accumulation in the prenatal brain: prooxidant and antioxidant features.

Docosahexaenoic acid (DHA; 22:6n-3) is the major polyunsaturated fatty acid (FA) in the adult rat brain and it accumulates significantly more than any other FA prior to birth. Under normal nutritional conditions, fetal-brain DHA accumulation is substantial, with a "DHA accretion spurt" being demonstrated in the last period of gestation. Under stress conditions, this spurt may be harmful owing to an increase in multiple double-bond targets for lipid peroxidation. The "DHA accretion spurt" is supported by the maternal supply of DHA or its precursor. Under maternal dietary n-3 FA deficiency, DHA content in the fetal brain can be restored by direct intraamniotic injection of mM concentrations of ethyl-DHA (Et-DHA). This approach may hold a potential advantage in the event of maternal-fetal insufficiency, a stress that may cause intrauterine growth retardation. It also revealed a potential beneficial effect after in utero ischemic stress; brain slices from Et-DHA-treated fetuses formed less oxidation products, as detected by thiobarbituric acid (TBA), compared to controls. Furthermore, brain-lipid extracts from Et-DHA but not ethyl-oleate treated fetuses, exhibited hydroxyl radical scavenging activity, as demonstrated by electron spin-resonance technique. Part of the beneficial effect of Et-DHA administration on the fetal brain may be attributed to enhanced free-radical scavenging capability, a phenomenon not directly related to vitamin E or lipid-soluble antioxidant levels.

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