ABSTRACTS â ORAL PRESENTATIONS - AMCA, spol. s r.o.

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a very significantly increased γ-H2AX expression was detected in rat B-lymphocytes. Differences between T-lymphocytes and NK cells were evident after a high dose (9 Gy) and revealed the least intensive response in CD161 NK cells. The increase in all subsets was dose-dependent (Zárybnická et al. 2013). In contrary, we found out that it is not possible to detect D ψ decrease in porcine lymphocytes after in vivo irradiation instead of the fact that these changes are connected with very early phases of apoptosis. Hence we analyzed D ψ changes within in vitro irradiated lymphocytes where no significant differences between T-lymphocytes and NK cells were found (B-lymphocytes were not studied). Results show dose dependency upon 0 – 2 Gy. The apoptotic fraction for higher doses is stable nevertheless representation of this fraction increases with in vitro cultivation time. Peripheral blood lymphocytes are generally used as sensitive biodosimetric markers of in vivo irradiation. Different radiosenzitivity of individual lymphocyte subsets propounds the question what are differences between DNA double strand breaks repairing and/ or apoptosis inducing between of these subsets. Analysis of γ-H2AX expression and D ψ changes is only first step in this study. The advanced biodosimetric approach combining lymphocyte surface immunophenotyping with intracellular detection suggests the possibility for exploitation for the future development of a biodosimetry procedure. Acknowledgements This work was supported by the Ministry of Defence of the Czech Republic (The institutional support to a long-term organization development plan 1011, project No. OVUOFVZ200806 and project No. OVUOFVZ200809). References Bogdándi EN, Balogh A, Felgyinszki N, Szatmári T, Persa E, Hildebrandt G, Safrany G, Lumniczky K. Effects of low-dose radiation on the immune system of mice after totalbody irradiation. Radiation Research 174: 480-489. 2010. Girinsky T, Socie G, Cosset JM, Malaise EP. Blood lymphocyte subsets after the first fraction in patients given hyperfractionated total body irradiation for bone marrow transplantation. British Journal of Cancer 63: 646-647. 1991. Rothkamm K, Horn S. Gamma-H2AX as protein biomarker for radiation exposure. Annali Dell Instituto Superiore di Sanita 45: 265-271. 2009. Šinkorova Z, Sinkora J, Zarybnicka L, Vilasova Z, Pejchal J. Radiosensitivity of peripheral blood B cells in pigs. Veterinarni Medicina 54: 223-235. 2009. Zárybnická L, Vávrová J, Havelek R, Tichý A, Pejchal J, Šinkorová Z. Lymphocyte subsets and their H2AX phosphorylation in response to in vivo irradiation in rats. Internatinal Journal of Radiation Biology. 89(2): 110-7. 2013. Analytical Cytometry VII 137
P42. ELUCIDATION OF CROSSTALK BETWEEN SENESCENCE AND APOPTOSIS Zuzana Nahacka, Gita Novakova, Ladislav Anděra Institute of Molecular Genetics of the Academy of Science of Czech Republic, Laboratory of Cell Signaling and Apoptosis, Prague, Czech Republic, nahackaz@img.cas.cz Senescence is irreversible cell-cycle arrest, where senescent cells stay metabolically active and acquire distinctive morphological and biochemical alterations (Bartek et al., 2007). Replicative senescence was described in normal cells as an intrinsic molecular programme that limits cell multiplication (Hayflick and Moorhead, 1961). Apart from aging, senescence in normal human cells can be induced by oncogenes such as activated H-Ras as a protective measure against tumorigenesis. Furthermore stress-induced or premature senescence is one of the major cellular response to chemotherapy and radiotherapy in solid tumors (Mirzayans et al., 2005). The other type of cell protection against tumorigenesis is apoptosis. In our study we are mainly interested in an elucidation of presumed crosstalk between apoptotic signaling and senescence-triggered rewiring the cellular signaling and metabolism. We induced premature senescence in primary (colorectal NCM460) and cancer cell lines (pancreatic PANC and mestohelial H28) with BrdU (20-100uM) treatment for 5-7 days. Then using mainly flow cytometry we analyzed response of senescent cells to different apoptotic stimuli inducing extrinsic (Trail, Fas ligand) or intrinsic (mito-VES, staurosporine, campthotecin) apoptotic signaling and the expression profile of TRAIL-R1 (Death receptor 4), TRAIL-R2 (Death receptor 5), TRAIL-R3 (Decoy receptor 1), TRAIL-R4 (Decoy receptor 2), FAS and TNF receptors. In addition to drug-induced senescence we are currently testing recombinant lentiviruses with inducible (pLVX p16-T2A-p21) or constitutive (pCDH p16-T2A-p21), expression of cell cycle inhibitors p16 and p21 proteins. We found that Fas expression has increased in the drug-induced senescent cells which is in agreement with recently published data (Crescenzi et al., 2011). These cells were also sensitized to FasL-induced apoptosis. Similarly, these senescent cells were sensitized to campthotecin and mito-VES triggered apoptosis. In contrast, DR4 expression and sensitivity to TRAIL dropped in the senescent cells. References Hayflick, L. and Moorhead, P.S. (1961) The serial cultivation of human diploid cell strains. Exp Cell Res, 25, 585-621. Mirzayans, R., Scott, A., Cameron, M. (2005) Induction of accelerated senescence by gamma radiation in human solid tumor-derived cell lines expressing wild-type TP53. Radiat Res, 163, 53-62. Bartek, J., Bartkova, J., Lukas, J. (2007) DNA damage signalling guards against activated oncogenes and tumour progression. Oncogene, 26, 7773-7779. Crescenzi, E., Pacifico, F., Lavorgna, A. et al. (2011) NF-κB-dependent cytokine secretion controls Fas expression on chemotherapy-induced premature senescent tumor cells. Oncogene, 30, 2707-2717. 138 Analytical Cytometry VII
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ABSTRACTS - ORAL PRESENTATIONS 14.
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and (iii) siRNA-mediated knockdown
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25. PROFILING OF CHILDHOOD ACUTE LE
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more dominantly than Th1 and CD4 ce
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29. INFLUENCE OF THE LEVEL OF CD133
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36. B-CELL IMMUNOPHENOTYPING OF LAR
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possible mechanism behind risk alle
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isotype controls and FMO for CD14 a
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NEP developmental stages were disti
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50. THE PROGRESSION OF HIV INFECTIO
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52. PRŮKAZ REGULAČNÍCH T LYMFOCY
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values when analysing paediatric ly
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42,0) vs. 1,5 (0,0-28), p
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for application of proton therapy,
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effects will be also characterized
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Although multiple signalling pathwa
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an ability to recreate the tumour f
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incubated with non-filtered superna
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approaches how to detect and isolat
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progress in development of automate
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Page 43 and 44: kappaB. Beside that, we found OANO
Page 45 and 46: therapy in patients (Calderwood et
Page 47 and 48: difference in the effect caused eit
Page 49 and 50: 4 CIC bioGUNE Technology Park of Bi
Page 51 and 52: P8. PROADIFEN (SKF-525A) ATTENUATES
Page 53 and 54: models. As manifested by compromise
Page 55 and 56: P11. NEW BIOACTIVE AND FLUORESCENT
Page 57 and 58: Acetylation of histones, along with
Page 59 and 60: stimulated cells. The physiological
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Page 63 and 64: chemotherapeutic drug LA-12. These
Page 65 and 66: aberrant expression, localization a
Page 67 and 68: P21. ASSESSMENT OF MITOCHONDRIAL FU
Page 69 and 70: P23. PTEROSTILBENE: COMPARISON OF A
Page 71 and 72: Fam123b. Amer1 has been shown very
Page 73 and 74: In summary, we described different
Page 75 and 76: this process. Combined treatment wi
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Page 81 and 82: was harmful neither alone nor in co
Page 83 and 84: P34. PHARMACOLOGICAL INHIBITION OF
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Page 87 and 88: P38. EVIDENCE OF ABNORMAL PERIPHERA
Page 89 and 90: acid to 5-lipoxygenase. Similarly t
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Page 97 and 98: e used to cultivate endothelial cel
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Page 101 and 102: P49. NEW ANALOGS OF RHODAMINE Jiři
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Page 105 and 106: could be achieved via the activatio
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Page 109 and 110: cells (SFC) using IFN-γ Elispot in
Page 111 and 112: FACSCantoII flow cytometer (Becton
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Page 115 and 116: cross-reacting group (CREG) and sha
Page 117 and 118: the frequency of autoimmune disease
Page 119 and 120: non-covalent bonds. For a solution
Page 121 and 122: P65. OVULATION STIMULATION PROTOCOL
Page 123 and 124: Acknowledgements This work was supp
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Page 127 and 128: triggers a process of normal blood
Page 129 and 130: 3 Department of Internal Medicine -
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Page 141 and 142: LD11015, from GAČR 13-29358S, and
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P83. DIFFERENTIATION OF NEURAL CRES
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given cell type are missing and the
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and HistoPARK (CZ.1.07/2.3.00/20.01
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Our results show that both p38α +/
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P90. TOLL-LIKE RECEPTOR 2 TRACKS TH
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for chemokines in attracting “inf
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in immune organs (Bursa of Fabricii
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