Cardiovascular disease (CVD) and depressive disorders (DD) are two of the most prevalent health problems in the world. Although CVD and depression have different origin, they share some common pathophysiological characteristics and risk factors, such as the increased production of proinflammatory cytokines, endothelial dysfunction, blood flow abnormalities, decreased glucose metabolism, elevated plasma homocysteine levels, oxidative stress and disorder in vitamin D metabolism. Current findings confirm the common underlying factors for both pathologies, which are related to dramatic dietary changes in the mid-19th century. By changing dietary ratio of omega-6 to omega-3 fatty acids from 1:1 to 15-20:1 some changes in metabolism were induced, such as increased pro-inflammatory mediators and m odulations of different signaling pathways following pathophysiological response related to both, cardiovascular diseases and depressive disorders., J. Trebatická, A. Dukát, Z. Ďuračková, J. Muchová., and Obsahuje bibliografii
In this study we set out to understand is sleep fragmentation affects the cardiovascular regulation and circadian variability of core body temperature more or less than sleep deprivation. 50 healthy men (age 29.0±3.1 years; BMI 24.3±2.1 kg/m2) participated in a 3-day study that included one adaptative night and one experimental night involving randomization to: sleep deprivation (SD) and sleep fragmentation (SF). The evaluation included hemodynamic parameters, measures of the spectral analysis of heart rate and blood pressure variability, and the sensitivity of arterial baroreflex function. Core body temperature (CBT) was measured with a telemetric system. SF affects heart rate (61.9±5.6 vs. 56.2±7.6, p<0.01) and stroke index (52.7±11.1 vs. 59.8±12.2, p<0.05) with significant changes in the activity of the ANS (LF-sBP: 6.0±5.3 vs. 3.4±3.7, p<0.05; HF-sBP: 1.8±1.8 vs. 1.0±0.7, p<0.05; LF-dBP: 5.9±4.7 vs. 3.5±3.2, p<0.05) more than SD. Post hoc analysis revealed that after SD mean value of CBT from 21:30 to 06:30 was significantly higher compared to normal night’s sleep and SF. In healthy men SF affects the hemodynamic and autonomic changes more than SD. Sympathetic overactivity is the proposed underlying mechanism., J. Słomko, M. Zawadka-Kunikowska, J. J. Klawe, M. Tafil-Klawe, J. Newton, P. Zalewski., and Obsahuje bibliografii
The altered regulation of autonomic response to mental stress can result in increased cardiovascular risk. The laboratory tests used to simulate the autonomic responses to real-life stressors do not necessarily induce generalized sympathetic activation; therefore, the assessment of regulatory outputs to different effector organs could be important. We aimed to study the cardiovascular sympathetic arousal in response to different mental stressors (Stroop test, mental arithmetic test) in 20 healthy students. The conceivable sympathetic vascular index - spectral power of low frequency band of systolic arterial pressure variability (LF-SAP) and novel potential cardiosympathetic index - symbolic dynamics heart rate variability index 0V% were evaluated. The heart and vessels responded differently to mental stress - while Stroop test induced increase of both 0V% and LF-SAP indices suggesting complex sympathetic arousal, mental arithmetic test evoked only 0V% increase compared to baseline (p<0.01, p<0.001, p<0.01, respectively). Significantly greater reactivity of LF-SAP, 0V%, heart rate (HR) and mean arterial pressure (MAP) were found in response to Stroop test compared to mental arithmetic test potentially indicating the effect of different central processing (0V%, LF-SAP: p<0.001; HR, MAP: p<0.01). The different effectors’ sympathetic responses to cognitive stressors could provide novel important information regarding potential pathomechanisms of stress-related diseases., M. Mestanik, A. Mestanikova, Z. Visnovcova, A. Calkovska, I. Tonhajzerova., and Obsahuje bibliografii
a1_The question was addressed of how nitric oxide synthase (NO synthase) inhibition-induced hypertension in rat parents would affect the cardiovascular system in their offsprings. Two experimental groups were set up: Group I - offsprings of parents who had both been administered NO synthase inhibitor L-nitro-arginine methyl ester (L-NAME 40 mg/kg/day) for 5 weeks, the treatment of dams continued till week 12. Group II - offsprings fed by dams administered L-NAME after delivery only for a period of 4 weeks. Control age-matched offsprings formed the third group. Blood pressure and heart rate in parents and in 3-week-old offsprings were determined noninvasively. In the offsprings, body and heart weight were measured and the heart/body weight ratio (HW/BW) was calculated. The NO synthase activity, and also ornithine decarboxylase activity as a marker of polyamine production, were determined in the heart. The acetylcholine-induced relaxation of aortic rings was also followed. A marked blood pressure increase with a tendency to a decreased heart rate was found in the offsprings of Group I. A significant decrease in heart weight and body weight with a decreased HW/BW ratio indicated cardiac hypotrophy that contrasted with the decrease in NO synthase activity and increase in ornithine decarboxylase activity in the heart. Noteworthy was also the finding of completely preserved relaxation of the aorta to acetylcholine. Offsprings of Group II were similarly characterized by significantly higher blood pressure, a tendency to decreased heart rate, a decrease in heart weight, but not of the HW/BW ratio. The contrasting findings of heart weight decrease on the one hand and NO synthase activity decrease and ornithine decarboxylase increase on the other, were also found in this group. Full relaxation of the aorta to acetylcholine was preserved., a2_It can be concluded that remarkable alterations in the cardiovascular system were found in offsprings of hypertensive NO compromised parents., M. Gerová, I. Bernátová, J. Török, M. Juráni., and Obsahuje bibliografii
CARM1 i nteracts with numerous transcription factors to mediate cellular processes, especially gene expression. This is important for the maintenance of ESC pluripotency or intervention to tumorigenesis. Here, we studied epigenomic effects of two potential CARM1 m odulators: an activator (EML159) and an inhibitor (ellagic acid dihydrate, EA). We examined nuclear morphology in human and mouse embryonic stem cells (hESCs, mESCs), as well as in iPS cells. The CARM1 modulators did not function similarly in all cell type s. EA decreased the levels of the pluripotency markers, OCT4 and NANOG, particularly in iPSCs, whereas the levels of these proteins increased after EML159 treatment. EML159 treatment of mouse ESCs led to decreased levels of OCT4 and NANOG, which was accomp anied by an increased level of Endo -A. The same trend was observed for NANOG and Endo -A in hESCs affected by EML159. Interestingly, EA mainly changed epigenetic features of nucleoli because a high level of arginine asymmetric di- methylation in the nucleoli of hESCs was reduced after EA treatment. ChIP -PCR of ribosomal genes confirmed significantly reduced levels of H3R17me2a, in both the promoter region of ribosomal genes and rDNA encoding 28S rRNA, after EA addition. Moreover, EA treatment changed the nuclear pattern of AgNORs (silver -stained nucleolus organizer regions) in all cell types studied. In EA -treated ESCs, AgNOR pattern was similar to the pattern of AgNORs after inhibition of RNA pol I by actinomycin D. Together, inhibitory effect of EA on arginine methylation and effect on related morphological parameters was especially observed in compartment of nucleoli., M. Franek, S. Legartová, J. Suchánková, C. Milite, S. Castellano, G. Sbardella, S. Kozubek, E. Bártová., and Obsahuje bibliografii