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66. Cellular algorithms for binary matrix operations.

Author

Goos, G., Hartmanis, J., Brauer, W., Hansen, P. Brinch, Gries, D., Moler, C., Seegmüller, G., Stoer, J., Wirth, N., Händler, Wolfgang, and Katona, E.

Abstract

Binary matrixes (matrixes having only 0 and 1 elements) occur in many theoretical and practical areas (e.g. in the theory of graphs and relations, grammars, coding, etc.) therefore the binary matrix operations have high importance in these topics. It is an obvious idea to use cellular processor consisting of micro-cells for the execution of these operations. The present paper gives a powerful cellular algorithm for the multiplication of two binary matrixes, taking into account the cellprocessor architecture developed by T. Legendi. Moreover, on the basis of this solution cellular algorithms are given for coding and for the computation of the m-th power of a binary matrix. [ABSTRACT FROM AUTHOR]

Published
1981
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68. Effects of Simvastatin on Serum Paraoxonase Activity.

Author

Balogh, Z., Fülöp, P., Seres, I., Harangi, M., Katona, E., Kovacs, P., Kosztáczky, B., and Paragh, G.

Subjects
HIGH density lipoproteins, LOW density lipoproteins, HYPERLIPOPROTEINEMIA, PHYSIOLOGY
Abstract

Background: High density lipoprotein (HDL)-associated paraoxonase activity may play an important role in the inhibition of low density lipoprotein (LDL) oxidation. Previous studies have demonstrated that serum paraoxonase activity is decreased in patients with hyperlipoproteinaemia and coronary heart disease, and a few investigators have suggested that the lipid-lowering statins may increase paraoxonase levels. Objective: To examine the effect of short-term treatment with simvastatin on lipids and paraoxonase activity in patients with hyperlipoproteinaemia. Design: Prospective nonblind single-group sequential study. Patients: 112 (52 male and 60 female) hyperlipoproteinaemic patients with Fredrickson type IIa and IIb hyperlipoproteinaemia (mean age 52.15 ± 7.99 years, mean body mass index 27.53 ± 4.30 kg/m). Methods: Serum cholesterol, lipoproteins, triglycerides, apolipoproteins and liver function were measured, and serum paraoxonase activity was determined spectrophotometrically using paraoxon as substrate. Simvastatin 20 mg/day was administered for 1 month, and measurements were repeated. Results: Simvastatin significantly decreased serum cholesterol [from 10.25 ± 2.73 (SD) to 8.85 ± 2.02 mmol/L], triglyceride (from 3.95 ± 2.51 to 3.15 ± 1.47 mmol/L), LDL (from 6.36 ± 1.70 to 4.94 ± 1.48 mmol/L) and apolipoprotein B100 (from 1.93 ± 0.41 to 1.56 ± 0.35 g/L) levels, whereas HDL and apo A1 levels did not change significantly (from 1.19 ± 0.34 to 1.22 ± 0.39 mmol/L, and from 1.56 ± 1.99 to 1.64 ± 0.24 g/L, respectively). HDL-associated paraoxonase activity did not change significantly (from 182.25 ± 37.21 to 166.49 ± 35.01 U/L) after simvastatin therapy. Conclusion: Short-term administration of simvastatin did not increase the activity of the HDL-associated antioxidant enzyme paraoxonase. [ABSTRACT FROM AUTHOR]

Published
2001
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69. The Golgi complex.

Author

Sturgess, J., Katona, E., and Moscarello, M.

Abstract

The ultrastructural arrangement of membranes of the Golgi complex has been characterized in Golgi fractions isolated from rat liver. Procedures for isolation of these fractions have been modified to provide a good yield of Golgi membranes (60 to 70%) with greater than 50-fold purification of sialyl transferase, an enzyme specific for the Golgi complex. The isolated membranes appear well preserved and both the dimensions and appearance of the Golgi complex observed by negative staining and in sections of the isolated membranes correlate well with that in liver sections. The Golgi complex consists of a series of platelike structures, each consisting of a central sac or cisterna from which a network of fine tubules arises. The tubules increase in diameter towards the periphery of the plate and are associated with the formation of vacuoles or secretory vesicles. The structure of the Golgi complex has been related to its role in glycoprotein biosynthesis. [ABSTRACT FROM AUTHOR]

Published
1973
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74. Val34Leu polymorphism of plasma factor XIII: biochemistry and epidemiology in familial thrombophilia

Author

Balogh, Istva´n, Szo^ke, Gabriella, Ka´rpa´ti, Levente, Wartiovaara, Ulla, Katona, E´va, Koma´romi, Istva´n, Haramura, Gizella, Pfliegler, Gyo¨rgy, Mikkola, Hanna, and Muszbek, La´szlo´

Abstract

Val34Leu polymorphism of the A subunit of coagulation factor XIII (FXIII-A) is located in the activation peptide (AP) just 3 amino acids away from the thrombin cleavage site. This mutation has been associated with a protective effect against occlusive arterial diseases and venous thrombosis; however, its biochemical consequences have not been explored. In the current study it was demonstrated that the intracellular stability and the plasma concentration of FXIII of different Val34Leu genotypes are identical, which suggests that there is no difference in the rate of synthesis and externalization of wild-type and mutant FXIII-A. In contrast, the release of AP by thrombin from the Leu34 allele proceeded significantly faster than from its wild-type Val34 counterpart. By molecular modeling larger interaction energy was calculated between the Leu34 variant and the respective domains of thrombin than between the Val34 variant and thrombin. In agreement with these findings, the activation of mutant plasma FXIII by thrombin was faster and required less thrombin than that of the wild-type variant. Full thrombin activation of purified plasma FXIII of different genotypes, however, resulted in identical specific transglutaminase activities. Similarly, the mean specific FXIII activity in the plasma was the same in the groups with wild-type, heterozygous, and homozygous variants. Faster activation of the Leu34 allele hardly could be associated with its presumed protective effect against venous thrombosis. No such protective effect was observed in a large group of patients with familial thrombophilia.

Published
2000
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77. A lattice model for cellular (systolic) algorithms

Author

Katona, E.

Abstract

In this paper a lattice model (here ‘lattice’ means a net of points) is introduced for homogeneous cellular algorithms. On the basis of this model a transformation methodology is developed, which makes it possible to produce many different versions of a given cellular algorithm. These versions may have quite different structural properties, but they perform the same computation as the original algorithm. In this way a great variety of cellular algorithms can be offered to choose the best version in practice and, on the other hand, cellular algorithms can be classified according to their inherent structures.

Published
1986
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96. Endocannabinoid-mediated CB1 receptor activation attenuates the vasoconstrictor effect of angiotensin II and other Ca2+-mobilizing GPCR agonists in skeletal muscle resistance vasculature.

Author

Szekeres, M., Nádasy, G. L., Turu, G., Soltész-Katona, E., Szabó, E., Tóth, Z. E., Takáts, Z., and Hunyady, L.

Subjects
G protein coupled receptors, ANGIOTENSINS, VASOCONSTRICTION
Abstract

Calcium-mobilizing G protein-coupled receptor (GPCR) agonists, such as angiotensin II (AngII), endothelin and vasopressin induce vasoconstriction. Activation of AT1 angiotensin- and other Gq/11 protein-coupled receptors leads to diacylglycerol (DAG) formation, which can be converted to 2-arachidonoylglycerol (2-AG), an important endocannabinoid by the effect of DAG lipase (1,2). Cannabinoids via CB1 cannabinoid receptors (CB1R) have peripheral hypotensive and vasodilator actions. We tested the hypothesis that 2-AG release can modulate the vasoconstrictor action of AngII and other calcium-mobilizing hormones in rodent vascular tissue. Male Wistar rats (300-350g), C57BL6 and CB1R knockout mice (21-25g, 3) were anaesthetised with pentobarbital (50mg kg-1 ip.). Rat skeletal muscle (gracilis) arterioles and mouse saphenous arteries were isolated, pressurized and subjected to microangiometry. Also, rats (200-250g) were anaesthetised and aorta was removed for vascular smooth muscle cell (VSMC) isolation. Vascular expression of CB1R was demonstrated with immunohistochemistry. In accordance with the functional relevance of these receptors WIN55212, a CB1R agonist caused vasodilation, which was absent in CB1R knockout mice. In gracilis arterioles dose-dependent vasoconstrictions for AngII, norepinephrine (NE), endothelin, vasopressin and prostaglandin (PG)F2α were obtained. Inhibition of CB1Rs with neutral antagonist O2050 in gracilis arterioles augmented the vasoconstriction induced by AngII, NE, endothelin and vasopressin (from 29.1±5.8% to 47.5±3.2% and from 38.8±7.6% to 76.3±4.8%, effects of 10nM AngII and 1µM NE, respectively, p<0.05) but did not influence the contractile effect of PGF2α (45.6±9.9% and 36.9±9.8% at 1µM, n.s.). Inhibition of CB1Rs enhanced AngII-induced vasoconstrictor action in saphenous arteries of wild type, but not of CB1R knockout mice. Inhibition of DAG lipase by tetrahydrolipstatin (THL) also augmented the vasoconstrictor effect of AngII, suggesting the role of 2- AG in CB1R activation. In VSMCs AngII-stimulated 2-AG formation was inhibited by THL but potentiated by JZL184, an inhibitor of monoacylglycerol lipase, an enzyme catalyzing degradation of 2-AG. Inhibition of CB1R also increased the sustained phase of AngII-induced calcium signal and this effect was found to be independent of nitric oxide synthase activity and of endothelial function. These data demonstrate that vasoconstrictor effects of calcium mobilizing GPCR agonists are physiologically attenuated by agonist-induced endocannabinoid release and consequent CB1R activation. It is proposed that this effect may serve as a beneficial control mechanism by moderating the microvascular tone in high contractile states. [ABSTRACT FROM AUTHOR]

Published
2013

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