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Biomedical subjects

E Vogt

Publications and source records attributed to E Vogt.

At least 37 records · Page 2Linked to original sources
PubMed1993

New postnatal growth grids for very low birth weight infants.

OBJECTIVE: To generate contemporary postnatal growth curves for hospitalized very low birth weight infants. DESIGN: Retrospective survey. SETTING: Tertiary intensive care nursery. PATIENTS: All surviving singleton, appropriate-for-gestational age infants with birth weight < or = 1500 g, born January 1, 1987, to May 31, 1991, who did not develop necrotizing enterocolitis (N = 205). MEASUREMENTS AND RESULTS: Macronutrient intakes and body weights were recorded daily, with crown-heel length and occipital-frontal head circumference recorded weekly up to 105 days of age or hospital discharge, whichever occurred first. Growth curves were generated for four birth weight ranges: 501 through 750, 751 through 1000, 1001 through 1250, and 1251 through 1500 g. Compared to previously published growth curves, the current infants regained birth weight more quickly and exhibited larger average daily weight gains. These differences were most apparent in infants of lowest birth weight. CONCLUSIONS: The "premature growth grid" constructed by Dancis et al more than 40 years ago may no longer be a useful standard of early postnatal growth for present-day very low birth weight, appropriate-for-gestational-age infants. The new weight curves are a more accurate reflection of current in-hospital growth trends, especially for infants weighing < or = 1000 g at birth.

Female↗
PubMed1992

Monoclonal antiphospholipid antibody reactivity against human placental trophoblast.

Naturally occurring antibodies against the negatively charged phospholipids cardiolipin (CL) and phosphatidylserine (PS) have been associated with recurrent pregnancy loss. One prevalent hypothesis proposes that antiphospholipid antibody (aPL) mediated pathophysiology is through increased placental thrombosis. In this study we investigated the reactivity of three mouse monoclonal aPLs with term and 26 week human placental preparations. Each monoclonal antibody reacted differently with CL and PS; 3SB9b reacted with PS (CL-/PS+), D11A4 reacted with CL (CL+/PS-) and BA3B5C4 reacted with both CL and PS (CL+/PS+). 3SB9b reacted strongly with the syncytiotrophoblastic layer of both formalin fixed and frozen placental tissue. Sporadic reactivity was observed against the cytotrophoblastic layer. BA3B5C4 reacted strongly and specifically with cytotrophoblastic cells. D11A4 had only weak reactivity in the subtrophoblastic stromal region of the placenta in frozen sections. aPL staining was also observed against extravillous cytotrophoblast. BA3B5C4 stained cytoplasmic structures, whereas 3SB9b stained the plasma membrane region with little cytoplasmic staining. These data suggest that the trophoblastic layer is reactive with aPLs and may potentially be directly damaged through mechanisms unrelated to thrombosis. In addition, the trophoblastic layer directly in contact with the maternal circulation is most reactive with aPLs that are PS+ rather than CL+. The differential reactivity of 3SB9b and BA3B5C4 suggests that the antigenic conformation involving PS on the cytotrophoblast is altered concurrent with fusion into the syncytium.

Antibodies, Monoclonal↗
PubMed1991

Functional reconstitution of the malate carrier of barley mesophyll vacuoles in liposomes.

The malate carrier of barley (Hordeum vulgare L.) mesophyll vacuoles was highly purified by chromatography on hydroxyapatite followed by affinity-chromatography using 5-amino-1,2,3-benzenetricarboxylic acid as ligand. The carrier, reconstituted in asolectin liposomes, had properties similar to those described previously for the carrier in intact vacuoles (Martinoia, E., Flügge, U.I., Kaiser, G., Heber, U. and Heldt, H.W. (1985) Biochim. Biophys. Acta 806, 311-319). The apparent Km for malate uptake was 2-3 mM, and the uptake was inhibited by other carboxylic acids (preferentially tricarboxylic). The sulfhydryl reagent, p-chloromercuribenzenesulfonate, as well as the anion transport inhibitor 4,4'-diisothiocyano-2,2'-stilbenedisulfonic acid, also inhibited malate uptake. The transport was dependent on the membrane potential with an optimum at about 35 mV.

Carrier Proteins↗
PubMed1991

Transport of arginine and aspartic Acid into isolated barley mesophyll vacuoles.

The transport of arginine into isolated barley (Hordeum vulgare L.) mesophyll vacuoles was investigated. In the absence of ATP, arginine uptake was saturable with a K(m) of 0.3 to 0.4 millimolar. Positively charged amino acids inhibited arginine uptake, lysine being most potent with a K(i) of 1.2 millimolar. In the presence of free ATP, but not of its Mg-complex, uptake of arginine was drastically enhanced and a linear function of its concentration up to 16 millimolar. The nonhydrolyzable adenylyl imidodiphosphate, but no other nucleotide tested, could substitute for ATP. Therefore, it is suggested that this process does not require energy and does not involve the tonoplast ATPase. The ATP-dependent arginine uptake was strongly inhibited by p-chloromercuriphenylsulfonic acid. Furthermore, hydrophobic amino acids were inhibitory (I(50) phenylalanine 1 millimolar). Similar characteristics were observed for the uptake of aspartic acid. However, rates of ATP-stimulated aspartic acid transport were 10-fold lower as compared to arginine transport. Uptake of aspartate in the absence of ATP was negligible.

Journal Article↗
PubMed1989

Fish oil affects phosphoinositide turnover and thromboxane A metabolism in cultured vascular muscle cells.

Fish oil has been reported as having beneficial effects on cardiovascular diseases. Elevated serum lipoproteins, prostaglandins and intracellular free calcium concentrations [( Ca2+]i) of the vasculature and thus the phosphoinositide (PI) turnover may be involved in the pathogenesis of these disorders. Therefore, the effect of fish oil on the potency of both low-density lipoprotein (LDL) and angiotensin II (AII) to stimulate the PI turnover in cultured rat vascular smooth muscle cells (VSMC) has been studied. Furthermore, a possible link between PI turnover activity and thromboxane A2 (TXA2) metabolism in these cells has been investigated. In VSMC cultured for up to 7 weeks with either fish oil or n-3 eicosapentaenoic acid (EPA) a decrease to 5-48% of the LDL-induced inositol trisphosphate (IP3) formation (= 100%) was found. A similar range of decreased IP3 synthesis was observed, when AII was used instead of LDL. Both LDL- and AII-stimulated TXA2 synthesis was suppressed concomitantly within the range 34-60%. Blockade of VSMC TXA2 biosynthesis with either indomethacin or TXA2 synthetase blocker (SQ-80338) inhibited LDL-induced formation of IP3 in a dose-dependent manner. Similar results were obtained, when TXA2 receptor coupling antagonists (SQ-27427 or BM-13177) were used. However, blockers of TXA2 synthesis and of TXA2 receptor binding failed to affect AII-induced formation of IP3.

Angiotensin II↗
PubMed1989

Ca2+-channel blockers inhibit the action of recombinant platelet-derived growth factor in vascular smooth muscle cells.

Human platelet-derived growth factor (PDGF) is mainly composed of two polypeptide chains (PDGF-AB). All three possible dimeric forms of PDGF--i.e., PDGF-AA, PDGF-BB and PDGF-AB--exist in nature. We have used two recombinant PDGF homodimers to determine the roles of each isoform in the activation of phosphatidylinositol turnover in vascular smooth muscle cells (VSMC) isolated from rat thoracic aorta, their mitogenic effect on VSMC, and their vasoconstrictor effect on intact strips of aortic vascular tissue. Three Ca2+-channel blockers, nifedipine, verapamil, and diltiazem, were used as antagonists for investigating the PDGF-dependent changes mediated by the homodimers. PDGF-BB had a greater efficacy than PDGF-AA on inositol 1,4,5-trisphosphate release, on the formation of diacylglycerol, and on Ca2+ mobilization, which was also associated with vasoconstrictor activity and effective mitogenicity. PDGF-AA, on the other hand, was more potent than PDGF-BB in stimulating protein kinase C. In all instances, the activation of the phosphatidylinositol turnover by the two homodimers was inhibited by the Ca2+-channel blockers.

Animals↗
PubMed1988

Rapid activation of human platelets by low concentrations of low-density lipoprotein via phosphatidylinositol cycle.

The interaction of low-density lipoprotein (LDL) with the human platelet was investigated with regard to saturable high-affinity binding, shape change, cytosolic free Ca2+ concentration, phosphatidylinositol (PtdIns) turnover, and thromboxane B2 biosynthesis. The experiments show that LDL, at a concentration approximately 100 times lower than in plasma, causes platelet activation concomitantly with stimulation of the PtdIns cycle and thromboxane B2 formation, similarly to other activators of platelets. The effects of LDL were inhibited by high-density lipoprotein. The results suggest that activation of platelets by low concentrations of LDL may play a role in pathophysiological conditions and that platelet can serve as a model for studying the influence of LDL on various target cells.

Binding Sites↗
PubMed1988

Low density lipoprotein causes general cellular activation with increased phosphatidylinositol turnover and lipoprotein catabolism.

Low density lipoprotein (LDL), at concentrations high enough for receptor binding but not high enough to saturate the receptor, induces activation of phosphatidylinositol (PtdIns) turnover in a variety of cell types with various biological functions. Using both biochemical and electron microscopic studies, we have shown that blood platelets take up and degrade LDL in a manner reminiscent of phagocytic cell types. The activation of both PtdIns turnover and LDL metabolism is inhibited by high density lipoprotein. Thus, LDL at hormonal concentrations causes general cellular activation. Since all cell types studied responded to LDL with increased PtdIns turnover and uptake of LDL cholesterol, the PtdIns cycle may also be involved in the cellular regulation of LDL cholesterol metabolism.

Animals↗
PubMed1988

The phosphoinositide turnover of vascular smooth muscle cells is influenced by fish oil.

As the phosphoinositide cycle and high serum levels of low-density lipoprotein cholesterol may be involved in the pathogenesis of both hypertension and atherosclerosis, the effect of fish oil on low-density lipoprotein stimulation of phosphoinositide metabolism was studied in cultured rat vascular smooth muscle cells. Low-density lipoprotein-stimulated synthesis of inositol trisphosphate decreased to 5-48% of control values in vascular smooth muscle cells treated for 4 weeks with either fish oil or n-3 eicosapentaenoic acid (EPA), the active ingredient of fish oil. In addition, low-density lipoprotein-induced biosynthesis of thromboxane A2 was reduced by 50% in vascular smooth muscle cells precultured with either fish oil or EPA. Thus, our results may explain the mechanisms by which fish oil exerts its beneficial effects on both atherosclerosis and hypertension.

Animals↗
PubMed1988

Stimulation of the phosphoinositide signalling system as a possible mechanism for glucocorticoid action in blood pressure control.

Cortisol stimulates the phosphoinositide signalling system in smooth muscle cells of the rat aorta. After stimulation of the cells with cortisol, epinephrine or both compounds, inositol-1,4,5-trisphosphate concentrations were analysed by standardized ion-exchange chromatography procedure. A 15-min stimulation with physiological concentrations of cortisol (0.02-5.0 microgram/ml) led to a dose-dependent increase of the inositol trisphosphate concentrations (up to 500%) and also to a translocation of the calcium- and lipid-dependent protein kinase C activity from the cytosolic to the membranous compartment. Incubation of smooth muscle cells with epinephrine (10(-9) to -5 mol/l) did not lead to an increase in the inositol trisphosphate concentrations. However, after pre-incubation with an average dose of cortisol (0.2 microgram/ml) the inositol trisphosphate response was potentiated by 10(-7) mol/l epinephrine. Our results suggest that stimulation of the phosphoinositide system is a still unknown mechanism of glucocorticoid action in smooth muscle cells, which could influence intracellular free calcium and thus vascular reactivity and blood pressure.

Animals↗
PubMed1988

[The ankle joint fork and tarsus].

Severe soft tissue injury occurring in sprains and dislocations may lead to painful disability after plaster-immobilisation for 6-12 weeks. Therefore, primary operation is indicated for ligamentous repair, osteochondral fracture-fixation and internal K-wire stabilization of dislocations after reduction. After 1 week of immobilisation, the patient should begin active daily muscle exercises; in the 2nd week patients are mobilized with support of a dynamic, partial weight-bearing splint, allowing continued muscle exercises until weight-bearing is possible 6-8 weeks after surgery. In 23 patients undergoing operations for acute dislocations excellent results were obtained in 14 (60%) and fair results in 7 (30%), while two patients (10%) had to have legs amputated because of arterial thrombosis and vascular disease.

Ankle Injuries↗