Latest Publications

@article{jirik_blind_2019,

title = {Blind deconvolution estimation of an arterial input function for small animal DCE-MRI.},

author = {Radovan Jiřík and Torfinn Taxt and Ondřej Macíček and Michal Bartoš and Jiří Kratochvíla and Karel Souček and Eva Dražanová and Lucie Krátká and Aleš Hampl and Zenon Jr Starčuk},

doi = {10.1016/j.mri.2019.05.024},

issn = {1873-5894 0730-725X},

year  = {2019},

date = {2019-10-01},

journal = {Magnetic resonance imaging},

volume = {62},

pages = {46–56},

abstract = {PURPOSE: One of the main obstacles for reliable quantitative dynamic contrast-enhanced (DCE) MRI is the need for accurate knowledge of the arterial input function (AIF). This is a special challenge for preclinical small animal applications where it is very difficult to measure the AIF without partial volume and flow artifacts. Furthermore, using advanced pharmacokinetic models (allowing estimation of blood flow and permeability-surface area product in addition to the classical perfusion parameters) poses stricter requirements on the accuracy and precision of AIF estimation. This paper addresses small animal DCE-MRI with advanced pharmacokinetic models and presents a method for estimation of the AIF based on blind deconvolution. METHODS: A parametric AIF model designed for small animal physiology and use of advanced pharmacokinetic models is proposed. The parameters of the AIF are estimated using multichannel blind deconvolution. RESULTS: Evaluation on simulated data show that for realistic signal to noise ratios blind deconvolution AIF estimation leads to comparable results as the use of the true AIF. Evaluation on real data based on DCE-MRI with two contrast agents of different molecular weights showed a consistence with the known effects of the molecular weight. CONCLUSION: Multi-channel blind deconvolution using the proposed AIF model specific for small animal DCE-MRI provides reliable perfusion parameter estimates under realistic signal to noise conditions.},

note = {Place: Netherlands},

keywords = {*Magnetic Resonance Imaging, Algorithms, Animals, Arterial input function, Arteries/*diagnostic imaging, Blind deconvolution, Computer Simulation, Computer-Assisted/*methods, Contrast Media/*pharmacokinetics, DCE-MRI, Humans, Image Processing, Inbred BALB C, Mice, Necrosis/pathology, Perfusion, Pharmacokinetics, Regression Analysis, Reproducibility of Results, Signal-To-Noise Ratio},

pubstate = {published},

tppubtype = {article}

}

@article{steinmetz_oncogene_2014,

title = {The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid.},

author = {Birgit Steinmetz and Hubert Hackl and Eva Slabáková and Ilse Schwarzinger and Monika Smějová and Andreas Spittler and Itziar Arbesu and Medhat Shehata and Karel Souček and Rotraud Wieser},

doi = {10.4161/15384101.2014.946869},

issn = {1551-4005 1538-4101},

year  = {2014},

date = {2014-01-01},

journal = {Cell cycle (Georgetown, Tex.)},

volume = {13},

number = {18},

pages = {2931–2943},

abstract = {The product of the ecotropic virus integration site 1 (EVI1) gene, whose overexpression is associated with a poor prognosis in myeloid leukemias and some epithelial tumors, regulates gene transcription both through direct DNA binding and through modulation of the activity of other sequence specific transcription factors. Previous results from our laboratory have shown that EVI1 influenced transcription regulation in response to the myeloid differentiation inducing agent, all-trans retinoic acid (ATRA), in a dual manner: it enhanced ATRA induced transcription of the RARβ gene, but repressed the ATRA induction of the EVI1 gene itself. In the present study, we asked whether EVI1 would modulate the ATRA regulation of a larger number of genes, as well as biological responses to this agent, in human myeloid cells. U937 and HL-60 cells ectopically expressing EVI1 through retroviral transduction were subjected to microarray based gene expression analysis, and to assays measuring cellular proliferation, differentiation, and apoptosis. These experiments showed that EVI1 modulated the ATRA response of several dozens of genes, and in fact reinforced it in the vast majority of cases. A particularly strong synergy between EVI1 and ATRA was observed for GDF15, which codes for a member of the TGF-β superfamily of cytokines. In line with the gene expression results, EVI1 enhanced cell cycle arrest, differentiation, and apoptosis in response to ATRA, and knockdown of GDF15 counteracted some of these effects. The potential clinical implications of these findings are discussed.},

note = {Place: United States},

keywords = {*Oncogenes, acute myeloid leukemia, acute promyelocytic leukemia, all-trans retinoic acid, AML, APL, Apoptosis, Apoptosis/drug effects, Ar, ATRA, ATRA regulation, Cell Cycle, Cell Cycle Checkpoints/drug effects, Cell Differentiation/drug effects, dimethyl sulfoxide, DMSO, DNA-Binding Proteins/genetics/*metabolism, Down-Regulation/drug effects, Em, Epithelial Cells/drug effects/metabolism, Er, EVI1, EVI1 modulation, EVI1 regulation, false discovery rate, FBS, FC, FDR, fetal bovine serum, fold change, GDF15, Gene Expression Profiling, Gene Knockdown Techniques, Genetic/*drug effects, GFP, green fluorescent protein, Growth Differentiation Factor 15/genetics/metabolism, HL-60 Cells, Humans, mcoEvi1, MDS, MDS1 and EVI1 Complex Locus Protein, murine codon optimized Evi1, myelodysplastic syndrome, Myeloid Cells/drug effects/*metabolism, myeloid differentiation, penicillin streptomycin glutamine, Proto-Oncogenes/genetics, PSG, RAR, RARE, Real-Time Polymerase Chain Reaction, Reproducibility of Results, retinoic acid receptor, retinoic acid response element, SE, standard error, Transcription, Transcription Factors/genetics/*metabolism, Tretinoin/*pharmacology},

pubstate = {published},

tppubtype = {article}

}