Browsing by Author "Zekovic, Janko (57209805540)"

Atrial fibrillation (AF) is a disorder in which heart rhythm becomes irregular and has an influence on the respiratory rhythm as well as on cardiopulmonary coupling. We applied detrended fluctuation analysis (DFA) method to find correlation properties of heart and respiratory rhythm in order to clarify behavioral pattern of cardiopulmonary coupling in AF. Scaling exponents: α1 (short-range correlations) and α2 (long-range correlations) were calculated on RR intervals and respiratory signal (Resp). Their relationship with heart/respiratory frequency was examined by regression analysis. In comparison to the control group, there was a significant reduction of α1 and α2 of the heart rhythm in AF group, while a2(Resp) was significantly increased in AF group. In regression analysis, there were significant intrasystemic relationships. In AF, our results imply a compensatory mechanism in regulation of the respiratory rhythm which was not noticed in regulation of the heart rhythm. We can conclude there is a cardiopulmonary coupling in direction heart-respiratory system in AF, but not in the opposite direction because of impaired vagal stimulation of sinoatrial node (SA). © 2018 Creative Commons Attribution.

Atrial fibrillation (AF) is a disorder in which heart rhythm becomes irregular and has an influence on the respiratory rhythm as well as on cardiopulmonary coupling. We applied detrended fluctuation analysis (DFA) method to find correlation properties of heart and respiratory rhythm in order to clarify behavioral pattern of cardiopulmonary coupling in AF. Scaling exponents: α1 (short-range correlations) and α2 (long-range correlations) were calculated on RR intervals and respiratory signal (Resp). Their relationship with heart/respiratory frequency was examined by regression analysis. In comparison to the control group, there was a significant reduction of α1 and α2 of the heart rhythm in AF group, while a2(Resp) was significantly increased in AF group. In regression analysis, there were significant intrasystemic relationships. In AF, our results imply a compensatory mechanism in regulation of the respiratory rhythm which was not noticed in regulation of the heart rhythm. We can conclude there is a cardiopulmonary coupling in direction heart-respiratory system in AF, but not in the opposite direction because of impaired vagal stimulation of sinoatrial node (SA). © 2018 Creative Commons Attribution.

Glioblastomas are aggressive and usually incurable high-grade gliomas without adequate treatment. In this study, we aimed to investigate the potential of desloratadine to induce apoptosis/autophagy as genetically regulated processes that can seal cancer cell fates. All experiments were performed on U251 human glioblastoma cell line and primary human glioblastoma cell culture. Cytotoxic effect of desloratadine was investigated using MTT and CV assays, while oxidative stress, apoptosis, and autophagy were detected by flow cytometry and immunoblot. Desloratadine treatment decreased cell viability of U251 human glioblastoma cell line and primary human glioblastoma cell culture (IC50 value 50 µM) by an increase of intracellular reactive oxygen species and caspase activity. Also, desloratadine decreased the expression of main autophagy repressor mTOR and its upstream activator Akt and increased the expression of AMPK. Desloratadine exerted dual cytotoxic effect inducing both apoptosis- and mTOR/AMPK-dependent cytotoxic autophagy in glioblastoma cells and primary glioblastoma cell culture. © 2023, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

Glioblastomas are aggressive and usually incurable high-grade gliomas without adequate treatment. In this study, we aimed to investigate the potential of desloratadine to induce apoptosis/autophagy as genetically regulated processes that can seal cancer cell fates. All experiments were performed on U251 human glioblastoma cell line and primary human glioblastoma cell culture. Cytotoxic effect of desloratadine was investigated using MTT and CV assays, while oxidative stress, apoptosis, and autophagy were detected by flow cytometry and immunoblot. Desloratadine treatment decreased cell viability of U251 human glioblastoma cell line and primary human glioblastoma cell culture (IC50 value 50 µM) by an increase of intracellular reactive oxygen species and caspase activity. Also, desloratadine decreased the expression of main autophagy repressor mTOR and its upstream activator Akt and increased the expression of AMPK. Desloratadine exerted dual cytotoxic effect inducing both apoptosis- and mTOR/AMPK-dependent cytotoxic autophagy in glioblastoma cells and primary glioblastoma cell culture. © 2023, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.