[The diastolic gradient of pressure and the effective area of section artifical mitral valve in aspect of its dysfunction].

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.

Activation of DNA damage response signaling in mouse embryonic stem cells.

Mouse 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.

[Signaling pathways regulating proliferation of murine embryonic stem cells].

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.

Phosphoinositide 3-kinase inhibitor LY294002 but not serum withdrawal suppresses proliferation of murine embryonic stem cells.

Mouse 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.

[Anti-proliferative effect of histone deacetylase inhibitors on murine embryonic stem cells].

The effect of histone deacetylase (HDAC) inhibitors trichostatin A (TSA) and sodium butirate (NaBut) on the proliferation of murine embryonic stem cells (MESC) was studied. Both agents suppressed the population growth and clonability of MESC. Flow cytometry analysis showed a decrease in the amount of S-phase cells upon treatment with HDAC inhibitors.

[PI3-kinase inhibitors LY294002 and wortmannin have different effects on proliferation of murine embryonic stem cells].

Murine embryonic stem (mES) cells can proliferate independently of the presence of growth factors in the medium. It is yet unknown what intrinsic activity triggers cell cycle events in mES cells. Here we investigated the contribution of the PI3-kinase cascade to autonomous proliferation of mES cell using PI3-kinase inhibitors wortmannin and LY294002.

[Transcription of c-fos gene and DNA binding activity of transcription factor AP-1 increase upon differentiation of mouse F9 teratocarcinoma cells].

Retinoic acid (RA) causes differentiation of mouse F9 embryonic carcinoma cell line into primitive and parietal (with dibutiril-cAMP) endoderm. The role of AP-1 transcription factor during RA-induced differentiation was studied in F9 cell line. It was shown that differentiated cells acquired protein complexes, which are specifically bound to well characterized AP-1 32P-labeled binding sites from collagenase (Col-AP-1) and c-jun (Jun2-AP-1) promoters.

[PI 3-kinase activity is necessary for F9 mouse embryonic carcinoma cell proliferation].

Embryonic carcinoma (EC) cells and embryonic stem (ES) cells have short cell cycles and, accordingly, proliferate very fast. Serum starvation does not suppress proliferation of EC and ES cells that allows to assume independence of their proliferation from the activity of cascades induced by serum. In the present work, we used flow cytometry to investigate how specific MAP-kinase and PI3-kinase inhibitors may influence proliferation and cell cycle of EC F9 cells.

[Noninduced single-stranded breaks in DNA in murine F9 teratocarcinoma cells].

Our previous study demonstrated the high incidence of non-induced DNA single strand breaks (SSB) in preimplantation mouse embryo genom (Patkin et al., 1994). F9 mouse teratocarcinoma cell line is an in vitro model for early embryonal differentiation, since F9 cells remind in many respects the inner cell mass cells of mouse blastocyst and are capable of differentiation under retinoic acid (RA) and dibutyryl cAMP (db-cAMP) treatment.

[Differentiated murine F9 teratocarcinoma cells are susceptible to apoptosis upon contact with substrate].

Epithelial and endothelial cells are susceptible to a subset of apoptosis known as anoikis. This type of programmed cell death is activated upon disruption of cell-substrate contacts. Here we demonstrate that mouse F9 embryonal carcinoma cell line acquires susceptibility to anoikis upon retinoic acid-induced differentiation towards non-malignant pariental endoderm-like cells.