We conducted an experimental study to evaluate the presence of coordinated left ventricular mechanical myocardial activity (LVMA) in two types of experimentally induced cardiac arrest: ventricular fibrillation (VF) and pulseless electrical activity (PEA). Twenty anesthetized domestic pigs were randomized 1:1 either to induction of VF or PEA. They were left in nonresuscitated cardiac arrest until the cessation of LVMA and microcirculation. Surface ECG, presence of LVMA by transthoracic echocardiography and sublingual microcirculation were recorded. One minute after induction of cardiac arrest, LVMA was identified in all experimental animals. In the PEA group, rate of LVMA was of 106±12/min. In the VF group, we identified two patterns of LVMA. Six animals exhibited contractions of high frequency (VFhigh group), four of low frequency (VFlow group) (334±12 vs. 125±32/min, p<0.001). A time from cardiac arrest induction to asystole (19.2±7.2 vs. 7.3±2.2 vs. 8.3±5.5 min, p=0.003), cessation of LVMA (11.3±5.6 vs. 4.4±0.4 vs. 7.4±2.9 min, p=0.027) and cessation of microcirculation (25.3±12.6 vs. 13.4±2.4 vs. 23.2±8.7 min, p=0.050) was significantly longer in VFlow group than in VFhigh and PEA group, respectively. Thus, LVMA is present in both VF and PEA type of induced cardiac arrest and moreover, VF may exhibit various patterns of LVMA., R. Skulec, D. Astapenko, R. Cerna Parizkova, B. Furst, M. Bilska, T. Parizek, T. Hovanec, N. Pinterova, J. Knor, J. Dudakova, A. Truhlar, V. Radochova, Z. Zadak, V. Cerny., and Obsahuje bibliografii
The oxidative stress plays an important role in the development of cardiovascular diseases (CVD). In CVD progression an aberrant redox regulation was observed. In this regulation levels of reactive oxygen species (ROS) play an important role in cellular signaling, where Nrf2 is the key regulator of redox homeostasis. Keap1-Nrf2-ARE system regulates a great set of detoxificant and antioxidant enzymes in cells after ROS and electrophiles exposure. In this review we focus on radical-generating systems in cardiovascular system as well as on Nrf2 as a target against oxidative stress and a key player of redox regulation in cardiovascular diseases. We also summarize the current knowledge about the role of Nrf2 in pathophysiology of several CVD (hypertension, cardiac hypertrophy, cardiomyopathies) as well as in cardioprotection against myocardial ischemia/ reperfusion injury., M. Barančík, L. Grešová, M. Barteková, I. Dovinová., and Obsahuje bibliografii
Disorders of ATP synthase, the key enzyme of mitochondrial energy provision belong to the most severe metabolic diseases presenting as early- onset mitochondrial encephalo- cardiomyopathies. Up to now, mutations in four nuclear genes were associated with isolated deficiency of ATP synthase. Two of them, ATP5A1 and ATP5E encode enzyme’s st ructural subunits α and ε , respectively, while the other two ATPAF2 and TMEM70 encode specific ancillary factors that facilitate the biogenesis of ATP synthase. All these defects share a similar biochemical phenotype with pronounced decrease in the content of fully assembled and functional ATP synthase complex. However, substantial differences can be found in their frequency, molecular mechanism of pathogenesis, clinical manifestation as well as the course of the disease progression. While for TMEM70 the number of reported patients as well as spectrum of the mutations is steadily increasing, mutations in ATP5A1, ATP5E and ATPAF2 genes are very rare. Apparently, TMEM70 gene is highly prone to mutagenesis and this type of a rare mitochondrial disease has a rather frequent incidence. Here we present overview of individual reported cases of nuclear mutations in ATP synthase and discuss, how their analysis can improve our understanding of the enzyme biogenesis., K. Hejzlarová ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
Multiple sclerosis (MS) is a chronic inflammatory and demyelinating disease of the central nervous system. In addition to the genetic, epigenetic and immunological components, various other factors, e.g. unhealthy dietary habits, play a role in the MS pathogenesis. Dietary intervention is a highly appealing approach, as it presents a simple and relatively low risk method to potentially improve outcomes in patients with brain disorders in order to achieve remission and improvement of clinical status, well-being and life expectancy of patients with MS. The importance of saturated fat intake restriction for the clinical status improvement of MS patients was pointed for the first time in 1950s. Recently, decreased risk of first clinical diagnosis of CNS demyelination associated with higher intake of omega-3 polyunsaturated fatty acids particularly originating from fish was reported. Only few clinical trials have been performed to address the question of the role of dietary intervention, such is e.g. low saturated fat diet in MS treatment. This review summarizes current knowledge about the effect of different dietary approaches (diets low in saturated fat and dietary supplements such as fish oil, lipoic acid, omega-3 polyunsaturated fatty acids, seeds oils, high fiber diet, vitamin D, etc.) on neurological signs, patient’s well-being, physical and inflammatory status. So far the results are not conclusive, therefore much more research is needed to confirm and to understand the effectiveness of these dietary interventions in the long term and well defined studies., A. Penesová, Z. Dean, B. Kollár, A. Havranová, R. Imrich, M. Vlček, Ž. Rádiková., and Obsahuje bibliografii
Associations between different infectious agents and obesity have been reported in humans for over thirty years. In many cases, as in nosocomial infections, this relationship reflects the greater susceptibility of obese individuals to infection due to impaired immunity. In such cases, the infection is not related to obesity as a causal factor but represents a complication of obesity. In contrast, several infections have been suggested as potential causal factors in human obesity. However, evidence of a causal linkage to human obesity has only been provided for adenovirus 36 (Adv36). This virus activates lipogenic and proinflammatory pathways in adipose tissue, improves insulin sensitivity, lipid profile and hepatic steatosis. The E4orf1 gene of Adv36 exerts insulin senzitizing effects, but is devoid of its pro-inflammatory modalities. The development of a vaccine to prevent Adv36- induced obesity or the use of E4orf1 as a ligand for novel antidiabetic drugs could open new horizons in the prophylaxis and treatment of obesity and diabetes. More experimental and clinical studies are needed to elucidate the mutual relations between infection and obesity, identify additional infectious agents causing human obesity, as well as define the conditions that predispose obese individuals to specific infections., V. Hainer, H. Zamrazilová, M. Kunešová, B. Bendlová, I. Aldhoon-Hainerová., and Obsahuje bibliografii
The functional antagonism between obestatin and ghrelin in the testis is under investigation. We investigated the ability of obestatin to counteract the inhibitory effect of ghrelin on basal and stimulated testosterone (T) secretion in vitro. Testicular strips from adult rats were incubated with 10 ng/ml and 100 ng /ml of obestatin alone, ghrelin alone and obestatin + ghrelin. Obestatin modulation of stimulated T secretion was evaluated by incubation of testicular samples with 10 ng/ml and 100 ng/ml obestatin, ghrelin and obestatin + ghrelin in the absence and presen ce of 10 IU of human chorionic gonadotrophin (hCG). T concentrations in the hCG treated groups were significantly (P<0.0001) higher than those in the control groups. Obestatin caused a significant increase in basal T secretion in a dose-dependent manner; however, obestatin at the both 10 ng /ml and 100 ng/ml significantly (P<0.0001) in creased hCG-stimulated T secretion. In contrast, ghrelin in a dose-dependent manner significantly (P<0.001) decreased both basal and hCG-induced T secretion by testicular slices. Obestatin opposed the inhibitory effect of ghrelin on T secretion under both basal and hCG-stimulated conditions at all doses tested. In conclusions, administration of obestatin was able to antagonize the inhibitory effect of ghrelin on testosterone secretion in vitro ., T. Afsar, S. Jahan, S. Razak, A. Almajwal, M. Abulmeaty, H. Wazir, A. Majeed., and Obsahuje bibliografii