Kullback-Leibler and Renormalized Entropy: Applications to EEGs of Epilepsy Patients

Recently, renormalized entropy was proposed as a novel measure of relative entropy (P. Saparin et al., Chaos, Solitons & Fractals 4, 1907 (1994)) and applied to several physiological time sequences, including EEGs of patients with epilepsy. We show here that this measure is just a modified Kullback-Leibler (K-L) relative entropy, and it gives similar numerical results to the standard K-L entropy. The latter better distinguishes frequency contents of e.g. seizure and background EEGs than renormalized entropy. We thus propose that renormalized entropy might not be as useful as claimed by its proponents. In passing we also make some critical remarks about the implementation of these methods.Comment: 15 pages, 4 Postscript figures. Submitted to Phys. Rev. E, 199

The Metalloprotease Meprinβ Processes E-Cadherin and Weakens Intercellular Adhesion

BACKGROUND: Meprin (EC 3.4.24.18), an astacin-like metalloprotease, is expressed in the epithelium of the intestine and kidney tubules and has been related to cancer, but the mechanistic links are unknown. METHODOLOGY/PRINCIPAL FINDINGS: We used MDCK and Caco-2 cells stably transfected with meprin alpha and or meprin beta to establish models of renal and intestinal epithelial cells expressing this protease at physiological levels. In both models E-cadherin was cleaved, producing a cell-associated 97-kDa E-cadherin fragment, which was enhanced upon activation of the meprin zymogen and reduced in the presence of a meprin inhibitor. The cleavage site was localized in the extracellular domain adjacent to the plasma membrane. In vitro assays with purified components showed that the 97-kDa fragment was specifically generated by meprin beta, but not by ADAM-10 or MMP-7. Concomitantly with E-cadherin cleavage and degradation of the E-cadherin cytoplasmic tail, the plaque proteins beta-catenin and plakoglobin were processed by an intracellular protease, whereas alpha-catenin, which does not bind directly to E-cadherin, remained intact. Using confocal microscopy, we observed a partial colocalization of meprin beta and E-cadherin at lateral membranes of incompletely polarized cells at preconfluent or early confluent stages. Meprin beta-expressing cells displayed a reduced strength of cell-cell contacts and a significantly lower tendency to form multicellular aggregates. CONCLUSIONS/SIGNIFICANCE: By identifying E-cadherin as a substrate for meprin beta in a cellular context, this study reveals a novel biological role of this protease in epithelial cells. Our results suggest a crucial role for meprin beta in the control of adhesiveness via cleavage of E-cadherin with potential implications in a wide range of biological processes including epithelial barrier function and cancer progression

St.-Beatenberg und seine Drahtseilbahn : mit zahlreichen Illustrationen

von G. Dumermut

Night sleep electroencephalogram power spectral analysis in excessive daytime sleepiness disorders

A group of 53 patients (40 míales, 13 females) with mean age of 49 years, ranging from 30 to 70 years, was evaluated in the. following excessive daytime sleepiness (EDS) disorders : obstructive sleep apnea syndrome (B4a), periodic movements in sleep (B5a), affective disorder (B2a), functional psychiatric non affective disorder (B2b). We considered all adult patients referred to the Center sequentially with no other distinctions but these three criteria: (a) EDS was the main complaint; (b) right handed ; (c) not using psychotropic drugs for two weeks prior to the all-night polysomnography. EEG (C3/A1, C4/A2) samples from 2 to 10 minutes of each stage of the first REM cycle were chosen. The data was recorded simultaneously in magnetic tape and then fed into a computer for power spectral analysis. The percentage of power (PP) in each band calculated in relation to the total EEG power was determined of subsequent sections of 20.4 s for the following frequency bands: delta, theta, alpha and beta. The PP in all EOS patients sample had a tendency to decrease progressively from the slowest to the fastest frequency bands, in every sleep stage. PP distribution in the delta range increased progressively from stage 1 to stage 4; stage REM levels were close to stage 2 levels. In an EDS patients interhemispheric coherence was high in every band and sleep stage. B4a patients sample PP had a tendency to decrease progressively from the slowest to the fastest frequency bands, in¡ every sleep stage; PP distribution in the delta range increased progressively from stage 1 to stage 4; stage REM levels were between stage 1 and stage 2 levels. B2a patients sample PP had a tendency to decrease progressively from the slowest to the fastest frequency bands, in every sleep stage; PP distribution in the delta range increased progressively from stage 1 to stage 4; stage REM levels were close to stage 2 levels. B2b patients sample PP had a tendency to decrease progressively from the slowest to the fastest frequency bands, in every sleep stage; PP distribution in the delta range increased progressively from stage 1 to stage 3; stage 4 levels were close to stage 3 levels; stage REM levels were close to stage 2. B5a patients sample PP had a tendency to decrease progressively from the slowest to the fastest frequency bands, in every sleep stage; PP distribution in the delta range increased progressively from stage 1 to stage 3; stage REM levels were close to stage 2 levels, Interhemispheric coherences of B4a, B2b, and B5a groups were high in, every band and sleep stage. B4a, B2a, B2b, and B5a power spectral analysis comparison showed higher PP in B2b stage 1 alpha band, as well as, higher PP in B5a stage 2 theta band. The B4a versus. B2a power spectral analysis comparison showed higher PP in B4a stages 1 and REM alpha bands, as well as higher PP in B2a stage REM delta band