Binding site detection via mutual information

Abstract:The frequency of ventricular premature beats (VPBs) has been related to the risk of mortality. However, little is known about the temporal pattern of occurrence of VPBs and its relationship to autonomic activity. Hence, we applied a general correlation measure, mutual information, to quantify how VPBs are generated over time. We also used mutual information to determine the correlation between VPB production and heart rate in order to evaluate effects of autonomic activity on VPB production. We examined twenty subjects with more than 3000 VPBs/day and simulated ran-( dom time series of VPB occurrence. We found that mutual information values could be used to characterize quantitatively the temporal patterns of VPB generation. Our data suggest that VPB production is not random and VPBs generated with a higher value of mutual information may be more greatly affected by autonomic activity.

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Data Screening Methods – Application to Differential Diagnosis in Pancreatic Pathology from Radiological Signs

Methods of Information in Medicine ◽

10.1055/s-0038-1636606 ◽

1978 ◽

Vol 17 (01) ◽

pp. 36-40 ◽

Cited By ~ 4

Author(s):

J.-P. Durbec ◽

Jaqueline Cornée ◽

P. Berthezene

Keyword(s):

Differential Diagnosis ◽

Mutual Information ◽

Data Processing ◽

Screening Methods ◽

Automatic Data ◽

Chronic Calcifying Pancreatitis ◽

Number Of Patients ◽

Calcifying Pancreatitis ◽

Pancreatic Pathology ◽

Data Screening

The practice of systematic examinations in hospitals and the increasing development of automatic data processing permits the storing of a great deal of information about a large number of patients belonging to different diagnosis groups.To predict or to characterize these diagnosis groups some descriptors are particularly useful, others carry no information. Data screening based on the properties of mutual information and on the log cross products ratios in contingency tables is developed. The most useful descriptors are selected. For each one the characterized groups are specified.This approach has been performed on a set of binary (presence—absence) radiological variables. Four diagnoses groups are concerned: cancer of pancreas, chronic calcifying pancreatitis, non-calcifying pancreatitis and probable pancreatitis. Only twenty of the three hundred and forty initial radiological variables are selected. The presence of each corresponding sign is associated with one or more diagnosis groups.

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Antithrombin-mediated Inhibition of Factor Vlla-Tissue Factor Complex by the Synthetic Pentasaccharide Representing the Heparin Binding Site to Antithrombin

Thrombosis and Haemostasis ◽

10.1055/s-0038-1650512 ◽

1996 ◽

Vol 76 (01) ◽

pp. 005-008 ◽

Cited By ~ 22

Author(s):

Jean Claude Lormeau ◽

Jean Pascal Herault ◽

Jean Marc Herbert

Keyword(s):

Binding Site ◽

Tissue Factor ◽

Residual Activity ◽

Coagulation Factors ◽

Heparin Binding ◽

Experimental Conditions ◽

First Order ◽

Heparin Binding Site ◽

Coagulant Activity

SummaryWe examined the effect of the synthetic pentasaccharide representing the minimal binding site of heparin to antithrombin on the antithrombin-mediated inactivation of factor Vila bound to tissue factor. This effect was compared to the effect of unfractionated heparin. Using purified recombinant human coagulation factors and either a clotting or an amidolytic assay for the determination of the residual activity of factor Vila, we showed that the pentasaccharide was an efficient antithrombin-dependent inhibitor of the coagulant activity of tissue factor-factor Vila complex. In our experimental conditions, assuming a mean MW of 14,000 for heparin, the molar pseudo-first order rate constants for ATIII-mediated FVIIa inhibition by ATIII-binding heparin and by the synthetic pentasaccharide were found to be similar with respective values of 104,000 ± 10,500 min-1 and 112,000 ± 12,000 min-1 (mean ± s.e.m., n = 3)

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Localization of a Vitronectin Binding Region of Plasminogen Activator Inhibitor-1

Thrombosis and Haemostasis ◽

10.1055/s-0038-1653876 ◽

1995 ◽

Vol 73 (05) ◽

pp. 829-834 ◽

Cited By ~ 11

Author(s):

Jaya Padmanabhan ◽

David C Sane

Keyword(s):

Binding Site ◽

Plasminogen Activator ◽

Inhibitory Activity ◽

Plasminogen Activator Inhibitor ◽

Structural Homology ◽

Binding Region ◽

Plasminogen Activator Inhibitor 1 ◽

Activator Inhibitor ◽

Pai 1

SummaryThe PAI-1 binding site for VN was studied using two independent methods. PAI-1 was cleaved by Staph V8 protease, producing 8 fragments, only 2 of which bound to [125I]-VN. These fragments were predicted to overlap between residues 91-130. Since PAI-2 has structural homology to PAI-1, but does not bind to vitronectin, chimeras of PAI-1 and PAI-2 were constructed. Four chimeras, containing PAI-1 residues 1-70,1-105,1-114, and 1-167 were constructed and expressed in vitro. PAI-1, PAI-2, and all of the chimeras retained inhibitory activity for t-PA, but only the chimera containing PAI-1 residues 1-167 formed a complex with VN. Together, these results predict that the VN binding site of PAI-1 is between residues 115-130.

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Enhancement of Plasminogen Binding to U937 Cells and Fibrin by Complestatin

Thrombosis and Haemostasis ◽

10.1055/s-0038-1655921 ◽

1997 ◽

Vol 77 (01) ◽

pp. 137-142 ◽

Cited By ~ 20

Author(s):

Kiyoshi Tachikawa ◽

Keiji Hasurni ◽

Akira Endo

Keyword(s):

Binding Site ◽

Binding Affinity ◽

Blood Cells ◽

Aminocaproic Acid ◽

U937 Cells ◽

Biochemical Basis ◽

Equilibrium Binding ◽

Pharmacological Stimulation ◽

Endogenous Fibrinolysis ◽

Stimulation Of

SummaryPlasminogen binds to endothelial and blood cells as well as to fibrin, where the zymogen is efficiently activated and protected from inhibition by α2-antiplasmin. In the present study we have found that complestatin, a peptide-like metabolite of a streptomyces, enhances binding of plasminogen to cells and fibrin. Complestatin, at concentrations ranging from 1 to 5 μM, doubled 125I-plasminogen binding to U937 cells both in the absence and presence of lipoprotein(a), a putative physiological competitor of plasminogen. The binding of 125I-plasminogen in the presence of complestatin was abolished by e-aminocaproic acid, suggesting that the lysine binding site(s) of the plasminogen molecule are involved in the binding. Equilibrium binding analyses indicated that complestatin increased the maximum binding of 125I-plasminogen to U937 cells without affecting the binding affinity. Complestatin was also effective in increasing 125I-plasminogen binding to fibrin, causing 2-fold elevation of the binding at ~1 μM. Along with the potentiation of plasminogen binding, complestatin enhanced plasmin formation, and thereby increased fibrinolysis. These results would provide a biochemical basis for a pharmacological stimulation of endogenous fibrinolysis through a promotion of plasminogen binding to cells and fibrin.

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Regulation of the CD95 gene by the p53 family network- the intronic binding site is essential

Zeitschrift für Gastroenterologie ◽

10.1055/s-2008-1037533 ◽

2008 ◽

Vol 46 (01) ◽

Author(s):

AE Schulze Schleithoff ◽

A Kairat ◽

AF Koch ◽

W Stremmel ◽

PH Krammer ◽

...

Keyword(s):

Binding Site ◽

P53 Family ◽

Family Network

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