The present study proposed procedure for predicting an optimal left and right ventricular pacing interval delay (V-V interval). In 16 patients (heart failure, left bundle branch block, biventricular pacing) two methods (A and B) identifying optimal V-V interval were tested. Method A: predicted optimal V-V interval A (POVV-A) = electromechanical delay of the segment paced by left ventricle lead minus electromechanical delay of the segment paced by right ventricle lead. Method B: predicted optimal V-V interval B (POVV-B) = difference in the onset of aortic and pulmonary flows. Both methods were validated using echocardiography and right-sided heart catheterization. Cardiac output during POVV-A (4.6 l.min-1 ) was significantly better than that during POVV-A minus 20 ms (4.3 l.min-1, p<0.01) and POVV-A plus 20 ms (4.3 l.min-1 , p<0.01), and than that during POVV-B (4.4 l.min-1, p<0.05). LV dP/dt during POVV-A (818 mm Hg.s-1 ) exceeded that during POVV-A plus 20 ms (717 mm Hg.s-1 , p<0.05) and POVV-A minus 20 ms (681 mm Hg.s-1, p<0.05), and that during POVV-B (727 mm Hg.s-1 , p<0.01). The time difference in onsets of myocardial deformation of left ventricle segment paced by the left ventricle and right ventricle lead allows identifying the optimal V-V interval and improves left ventricle performance., M. Novák, J. Lipoldová, J. Meluzín, J. Krejčí, P. Hude, V. Feitová, L. Dušek, P. Kamarýt, J. Vítovec., and Obsahuje bibliografii a bibliografické odkazy
The present studies investigated changes in expression of mRNA for adenosine A1, A2a, A2b, and A3 receptors in samples of HL-60 promyelocytic cells differing in the actual presence of cells in various phases of the cell cycle induced by the double thymidine block method. Real-time PCR technique was used for obtaining data on mRNA expression. Statistical analysis of the data revealed that the mRNA ex pression of adenosine A1, A2a, and A3 receptors is dependent on the cell cycle phase. G0/G1 and G2/M phases were characterized by a higher mRNA expression of adenosine A1 receptors and a lower one of adenosine A2a and A3 receptors whereas the opposite was true for the S phase. Interestingly, expression of mRNA of the adenosine A2b receptors was independent on the cell cycle phase. The results indicate the plasticity of mRNA expression of adenosine receptors in the investigated promyelocytic cells and its interaction with physiological mechanisms of the cell cycle., M. Hofer ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
Several members of the TGF-ß family are known to effectively regulate the fate of hematopoietic progenitor cells in a complex and context-dependent manner. Growth differentiation factor-15 (GDF15) is a divergent member of the TGF-ß family. This stress-induced cytokine has been proposed to possess immunomodulatory functions and its high expression is often associated with progression of a variety of pathological conditions. GDF15 is also induced by chemotherapy and irradiation. Very few fundamental studies have been published regarding the effect of GDF15 in hematopoiesis. In this study, we analyzed the hematological status of untreated and γ-irradiated mice deficient for GDF15 as a result of genetic knock-out (KO), in order to clarify the regulatory role of GDF15 in hematopoiesis. Significant differences between GDF15 KO mice and their pertinent WT controls were found in the parameters of blood monocyte numbers, blood platelet size, and distribution width, as well as in the values of bone marrow granulocyte/macrophage progenitor cells. Different tendencies of some hematological parameters in the GDF15 KO mice in normal conditions and those under exposure of the mice to ionizing radiation were registered. These findings are discussed in the context of the GDF15 gene function and its lack under conditions of radiation-induced damage., M. Hofer, Z. Hoferová, J. Remšík, M. Nováková, J. Procházková, R. Fedr, J. Kohoutek, L. Dušek, A. Hampl, K. Souček., and Obsahuje bibliografii
We investigated hematopoiesis in untreated and ionizing radiation-exposed cyclooxygenase-2-deficient (COX-2 KO) mice. We performed a complex hematological analysis of 16 parameters in untreated COX-2 KO male mice or COX-2 KO male mice irradiated with the dose of 4 Gy of γ-rays and their wildtype littermates. At baseline, hematopoiesis was increased in COX-2-deficient mice, but attenuated by irradation in COX-2- deficient mice compared to wildtype. To conclude, the antiinflammatory action of the COX-2 genetic disruption plays a positive role in hematopoiesis under basal conditions but is detrimental following radiation exposure., M. Hofer, Z. Hoferová L. Dušek, K. Souček, A. Gruzdev., and Obsahuje bibliografii