1,139 research outputs found
Biometric security based on ECG
Recently the electrocardiogram (ECG) has been proposed as a novel biometric. This paper aims to construct a reliable ECG verification system, in terms of privacy protection. To this end, an improved expression to estimate the capacity in the autocorrelation (AC) of the ECG is derived, which not only gives an upper bound for the number of identifiable subjects using ECG, but also helps to determine the number of independent features needed for verification. This capacity derivation, to our best knowledge, is new and can be easily extended to other biometrics. In addition, we apply the Quantization Index Modulation (QIM) scheme to the verification system for template protection. Based on our database, we found that, the capacity in the AC of ECG is approximately 20 bits information contained in the 23 independent features. We have also shown that compared to unprotected systems, the QIM scheme greatly enhances privacy protection of ECG templates without significant sacrificing of the identification performance
Bench-to-bedside review: genetic influences on meningococcal disease
This review discusses the possible involvement of a variety of genetic
polymorphisms on the course of meningococcal disease. It has been shown
that several common genetic polymorphisms can either influence the
susceptibility to meningococcal disease or can account for a higher
mortality rate in patients. Gene polymorphisms concerning antibody
receptors, lipopolysaccharide (LPS) binding receptors or proteins, innate
complement proteins as well as cytokines and hemostatic proteins are
described. The study of genetic polymorphisms might provide important
insights in the pathogenesis of meningococcal disease and could make it
possible to identify individuals who are at risk of either contracting or
dying from meningococcal disease
Activation of ion transport by combined effects of ionomycin, forskolin and phorbol ester on cultured HT-29cl.19A human colonocytes
The differentiated clone 19A of the HT-29 human colon carcinoma cell line was used as a model to study the intracellular electrophysiological effects of interaction of the cAMP, the protein kinase C (PKC) and the Ca2+ pathways, (a) A synergistic effect between ionomycin and forskolin was observed. From intracellular responses it was concluded that the synergistic effect is caused by activation of an apical Cl- conductance by protein kinase A and a basolateral K+ conductance by Ca2+. (b) A transient synergistic effect of ionomycin and the phorbol ester phorbol dibutyrate (PDB) was found. The decrease of the response appeared to be due to PKC-dependent inactivation of the basolateral K+ conductance. The synergism is caused by PKC-dependent increase of the apical Cl- conductance and Ca2+-dependent increase of the basolateral K+ conductance. (c) The effects of carbachol and PDB were not fully additive presumably because of their convergence on PKC activation, (d) Forskolin and P
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