Array-based disease diagnostics using lipid/polydiacetylene vesicles encapsulated in a sol-gel matrix.

We demonstrate a novel array-based diagnostic platform comprising lipid/polydiacetylene (PDA) vesicles embedded within a transparent silica-gel matrix. The diagnostic scheme is based upon the unique chromatic properties of PDA, which undergoes blue-red transformations induced by interactions with amphiphilic or membrane-active analytes. We show that constructing a gel matrix array hosting PDA vesicles with different lipid compositions and applying to blood plasma obtained from healthy individuals and from patients suffering from disease, respectively, allow distinguishing among the disease conditions through application of a simple machine-learning algorithm, using the colorimetric response of the lipid/PDA/gel matrix as the input. Importantly, the new colorimetric diagnostic approach does not require a priori knowledge on the exact metabolite compositions of the blood plasma, since the concept relies only on identifying statistically significant changes in overall disease-induced chromatic response. The chromatic lipid/PDA/gel array-based "fingerprinting" concept is generic, easy to apply, and could be implemented for varied diagnostic and screening applications.

Staurosporine suppresses replicon initiation in mammalian cells.

Replication in cellular replicons of mouse Ehrlich ascites, human CCRF-CEM and hamster BHK-21 cells was analyzed, after exposition of the cells to staurosporine, by measuring the overall DNA synthesis rate, by alkaline sedimentation analysis of length distributions of growing daughter strand DNA and by DNA fibre autoradiography. The results consistently indicated that micromolar concentrations of staurosporine caused, in all three cell lines, a fast suppression of replicon initiation which was reversible if the drug treatment did not exceed about 2 h. The inhibition of initiation was accompanied by a slight reduction of rates of propagation of replication forks. The data are interpreted in terms of the existence of a so far unknown factor which seems to be involved relatively directly in the initiation process of cellular replicons and has to be activated, like the large T antigen of SV 40 for the replication initiation in the viral genome, by a specific phosphorylation event. Unlike several other protein phosphorylations of cellular regulation, the kinase concerned here seems to be inhibited only by relatively high staurosporine concentrations.