[Effects of diphenyl derivatives on electrophoretic mobility of murine T lymphocytes].

The early changes of electrophoretic mobility (EPM) of murine T lymphocytes induced by structural analogues of amixine-dihydrochloryde 4,4'-bis-[2(diethylamino)ethoxy]diphenyl (compound 1) and dihydrochloryde 2-methoxycarbonil-4,4'-bis-[2(diethylamino)ethoxy]diphenyl (compound 2) were studied by electrophoresis technique. During the interval 0-2 hours all compounds increased the absolute values of EPM in comparison with control. These changes were of the same kind--distinctions were quantitative. Amixine and compound 1 during the interval 2-4 hours additionally increased the EPM. The compound 2, on the contrary, decreased the EPM. It was shown that the opposite effects of the aforementioned compounds were caused by the fact that amixine and compound 1 induce, and compound 2 does not induce IFN production in T lymphocytes in vitro. The results of our experiments are important for understanding of the mechanisms of immunomodulating effect of amixine and its structural analogues.

Signal function of potassium channels--clinical aspects.

Potassium (K+) channels are the most diverse class of ion channels, and are important for regulating neuronal excitability and signaling activity in a variety of ways. They are major determinants of membrane excitability, influencing the resting potential of membranes, wave forms and frequencies of action potentials, and thresholds of excitation. Voltage-gated K+ cannels exist not as independent units merely responding to changes in transmembrane potential but as macromolecular complexes able to integrate a plethora of cellular signals that fine tune channel activities. There are a wide variety of therapeutic agents that are targeted to non-K+ channels, but result in unintended block of K+ channels. This K+ channel block can result in potentially serious and sometimes even fatal side effects.