In article seven-year experience of treatment 126 sick mitral heart diseases to which have been implanted domestic monofolding the MIKS and folding MEDING-2 and ROSCARDIKS artificial mitral valve. At a comparative estimation of a haemodynamic efficiency and the analysis of frequency of occurrence of dysfunctions of the specified mechanical artificial valve it is revealed, that till three years the postimlantsperiod implant the MIKS and MEDING-2 possess advantage over ROSCARDIKS on haemodynamic properties, despite priority ROSCARDIKS on a standard size. It is shown, that initially low diastolic pressure gradient on mitral artificial valve and initially big area effective apertures mitral artificial valve have crucial importance in aspect of preventive maintenance of formation valve complications and reduction of number of repeated operations by open heart.
View Article and Find Full Text PDFMouse embryonic stem cells (mESC) are characterized by high proliferation activity. mESC are highly sensitive to genotoxic stresses and do not undergo G(1)/S checkpoint upon DNA-damage. mESC are supposed to develop sensitive mechanisms to maintain genomic integrity provided by either DNA damage repair or elimination of defected cells by apoptosis.
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September 2007
Murine embryonic stem cells (mESC) are capable of unlimiting proliferation with maintenance of pluripotency during long-term cultivation. Signaling pathways regulating the cell cycle of mESC are of the great interest for further investigation. This review concerns to the cell cycle regulation of mESC through different signaling pathways (LIF-STAT3, PI3K-Akt, Wnt-beta-catenin) and to the mechanisms of unlimited proliferation of mESC and their inability to undergo long-term block of proliferation in response to DNA-damaging and stress factors.
View Article and Find Full Text PDFMouse embryonic stem (mES) cells have short duration of their cell cycle and are capable of proliferating in the absence of growth factors. To find out which signaling pathways contribute to the regulation of the mES cell cycle, we used pharmacological inhibitors of MAP and PI3 kinase cascades. The MAP kinase inhibitors as well as serum withdrawal did not affect mES cell cycle distribution, whereas the inhibitor of PI3K activity, LY294002, induced accumulation of cells in G(1) phase followed by apoptotic cell death.
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