19 research outputs found
The Inviscid Limit and Boundary Layers for Navier-Stokes Flows
The validity of the vanishing viscosity limit, that is, whether solutions of
the Navier-Stokes equations modeling viscous incompressible flows converge to
solutions of the Euler equations modeling inviscid incompressible flows as
viscosity approaches zero, is one of the most fundamental issues in
mathematical fluid mechanics. The problem is classified into two categories:
the case when the physical boundary is absent, and the case when the physical
boundary is present and the effect of the boundary layer becomes significant.
The aim of this article is to review recent progress on the mathematical
analysis of this problem in each category.Comment: To appear in "Handbook of Mathematical Analysis in Mechanics of
Viscous Fluids", Y. Giga and A. Novotn\'y Ed., Springer. The final
publication is available at http://www.springerlink.co
The Mitochondrial Targets of Neuroprotective Drug Vinpocetine on Primary Neuron Cultures, Brain Capillary Endothelial Cells, Synaptosomes, and Brain Mitochondria
Vinpocetine is considered as neuroprotectant drug and used for treatment of brain ischemia and cognitive deficiencies for decades. A number of enzymes, channels and receptors can bind vinpocetine, however the mechanisms of many effects' are still not clear. The present study investigated the effects of vinpocetine from the mitochondrial bioenergetic aspects. In primary brain capillary endothelial cells the purinergic receptor-stimulated mitochondrial Ca2+ uptake and efflux were studied. Vinpocetine exerted a partial inhibition on the mitochondrial calcium efflux. In rodent brain synaptosomes vinpocetine (30 ÎĽM) inhibited respiration in uncoupler stimulated synaptosomes and decreased H2O2 release from the nerve terminals in resting and in complex I inhibited conditions, respectively. In isolated rat brain mitochondria using either complex I or complex II substrates leak respiration was stimulated, but ADP-induced respiration was inhibited by vinpocetine. The stimulation of oxidation was associated with a small extent of membrane depolarization. Mitochondrial H2O2 production was inhibited by vinpocetine under all conditions investigated. The most pronounced effects were detected with the complex II substrate succinate. Vinpocetine also mitigated both Ca2+-induced mitochondrial Ca2+-release and Ca2+-induced mitochondrial swelling. It lowered the rate of mitochondrial ATP synthesis, while increasing ATPase activity. These results indicate more than a single mitochondrial target of this vinca alkaloid. The relevance of the affected mitochondrial mechanisms in the anti ischemic effect of vinpocetine is discussed