Optimizing the antitumor selectivity of PVP-Hypericin re A549 cancer cells and HLF normal cells through pulsed blue light.

Photodynamic therapy (PDT) is based on the preferential accumulation of photosensitizer in cancer cells with subsequent cytotoxicity mediated by singlet oxygen production after light excitation. As photosensitizers accumulate also in the surrounding non-cancer cells, the risk of damaging them by photosensitization is a limitation of PDT. Thus, minimizing the side-effects of PDT on normal cells is one of the challenging problems in medical practice.

Modifying excitation light dose of novel photosensitizer PVP-Hypericin for photodynamic diagnosis and therapy.

Conventional photodynamic diagnosis (PDD) and therapy (PDT) makes use of photosensitizers that are excited by continuous light irradiation of specific wavelengths. In the case of PDT, the overdose of continuous excitation may lead to an expansion of necrosis in cancer cells or morbidity in healthy surroundings. The present study involves 5-h fluorescence imaging of living human lung epithelial carcinoma cells (A549) in the presence of a novel photosensitizer, PVP-Hypericin (PVP: polyvinylpyrrolidone) to optimize the excitation light doses for PDD and PDT.

Light-induced vasodilation of coronary arteries and its possible clinical implication.

Background: Low-level laser therapy and light-emitting diodes (LED) are increasingly used in phototherapy. Their therapeutic effects are at least partly mediated by light-induced vasodilation. The aim of this study was to determine the effect of different light sources on coronary arteries.

Long-term monitoring of live cell proliferation in presence of PVP-Hypericin: a new strategy using ms pulses of LED and the fluorescent dye CFSE.

During fluorescent live cell imaging it is critical to keep excitation light dose as low as possible, especially in the presence of photosensitizer drugs, which generate free radicals upon photobleaching. During fluorescent imaging, stress by excitation and free radicals induces serious cell damages that may arrest the cell cycle. This limits the usefulness of the technique for drug discovery, when prolonged live cell imaging is necessary.

Pinacidil-primed ATP-sensitive potassium channels mediate feedback control of mechanical power output in isolated myocardium of rats and guinea pigs.

We tested the hypothesis, that ATP-sensitive potassium (K(ATP)) channels limit cardiac energy demand by a feedback control of mean power output at increased cardiac rates. We analysed the interrelationships between rising energy demand of adult rat and guinea pig left ventricular papillary muscle and down-regulatory electromechanical effects mediated by K(ATP) channels. Using the K(ATP)-opener pinacidil the stimulation frequency was increased stepwise and the mechanical parameters and action potentials were recorded.