The activity of lipoprotein lipase (LPL) is increased after alcohol consumption and can contribute to an increased level of HDL-cholesterol, which is considered to play a key role in the ethanol-mediated protective effect against cardiovascular disease. The increase in HDL-cholesterol concentration can be also due to an ethanol-enhanced synthesis and secretion of apolipoprotein A-I (apo A-I) from hepatocytes. Therefore, the hypothesis that ethanol consumption affects the LPL and apo A-I gene (LPL and APOA1, respectively) expression was tested in male C57BL/6 mice drinking 5 % ethanol or water and fed a standard chow or high-fat (HF) diet for 4 weeks. The LPL expression was determined in the heart, epididymal and dorsolumbal adipose tissues, the APOA1 expression in the liver. Alcohol consumption did not affect lipid and lipoprotein concentrations in the serum. The LPL expression was increased in the heart of mice given ethanol and HF diet compared to mice on chow and ethanol (p<0.001) and was also increased in epididymal fat in mice given ethanol and HF diet compared to mice on water and HF diet (p<0.05). Neither LPL expression in dorsolumbal fat nor APOA1 expression in the liver were affected by ethanol consumption. Our data suggest that ethanol consumption upregulate LPL expression in a tissue- and diet-dependent manner., E. Mudráková, J. Kovář., and Obsahuje bibiografii a bibliografické odkazy
Reliable diagnosis of congenital heart defects and arrhythmias in utero has been possible since the introduction of fetal echocardiography. The nation-wide prenatal ultrasound screening program in the Czech Republic enabled detection of cardiac abnormities in 1/3 of patients born with any congenital heart disease and up to 83 % of those with critical forms. Prenatal frequency of individual heart anomalies significantly differed from the postnatal frequency. Fetal isolated complete atrioventricular block and supraventricular tachycardia may lead to heart failure and are important causes of fetal mortality. The regression of heart failure was achieved by a conversion to the sinus rhythm in the supraventricular tachycardia and by increase of ventricular rate in the complete atrioventricular block., V. Tomek ... [et al.]., and Obsahuje seznam literatury
Type 1 diabetes mellitus (DM 1A) is an autoimmune disease belonging to the most frequent chronic diseases of the childhood and young adults. DM 1A results from immune-mediated destruction of the insulin-producing beta cells of the pancreas. It is a genetically determined disease and many genes or genetic regions were found to be associated with its induction. In addition to the insulin-dependent diabetes mellitus 1 (IDDM1) gene, which marks the HLA region, and IDDM2 which marks the insulin gene, significant associations of DM 1A to other IDMM genes or genetic regions we reported. We shortly review recent achievements in the field, and the state of current knowledge., D. Kantárová, M. Buc., and Obsahuje bibliografii a bibliografické odkazy
I. Band, Enthaltend: Die Abnormitäten des Zellgewebes, der serösen und Schleim-Häute im Allgemeinen, der äussern Haut, des fibrösen, des Knochen-, Muskel-, Gefäss- und Nerven-Systemes, and von Carl Rokitansky
The aim of the study was to evaluate skin microvascular reactivity (MVR) and possible influencing factors (fibrinolysis, oxidative stress, and endothelial function) in patients with Cushing’s syndrome. Twenty-nine patients with active Cushing’s syndrome (ten of them also examined after a successful operation) and 16 control subjects were studied. Skin MVR was measured by laser Doppler flowmetry during post-occlusive (PORH) and thermal hyperemia (TH). Malondialdehyde and Cu,Zn-superoxide dismutase were used as markers of oxidative stress. Fibrinolysis was estimated by tissue plasminogen activator (tPA) and its inhibitor (PAI-1). N-acetyl-β-glucosaminidase, E-selectin, P-selectin, and ICAM-1 were used as markers of endothelial function. Oxidative stress and endothelial dysfunction was present in patients with hypercortisolism, however, increased concentration of ICAM-1 was also found in patients after the operation as compared to controls (290.8±74.2 vs. 210.9±56.3 ng.ml-1, p<0.05). Maximal perfusion was significantly lower in patients with arterial hypertension during PORH and TH (36.3±13.0 vs. 63.3±32.4 PU, p<0.01, and 90.4±36.6 vs. 159.2±95.3 PU, p<0.05, respectively ) and similarly the velocity of perfusion increase during PORH and TH was lower (3.2±1.5 vs. 5.2±3.4 PU.s-1, p<0.05, and 0.95±0.6 vs. 1.8±1.1 PU.s-1, p<0.05, respectively). The most pronounced impairment of microvascular reactivity was present in patients with combination of arterial hypertension and diabetes mellitus., M. Prázný, J. Ježková, E. Horová, V. Lazárová, V. Hána, J. Kvasnička, L. Pecen, J. Marek, J. Škrha, M. Kršek., and Obsahuje bibliografii a bibliografické odkazy
In healthy subjects, the right ventricular filling pattern estimated from tricuspid valve inflow is highly load-dependent. This can be clearly demonstrated by changes of Doppler inflow tracings recorded during tidal breathing at rest. The aim of our study was to test the magnitude of tricuspid inflow changes during more pronounced load changes induced by specific maneuvers. In 31 apparently healthy subjects (16 men and 15 women, mean age 36±16 years) we recorded pulsed Doppler tracings of tricuspid inflow during forced inspiration, elevation of lower extremities (increased preload) and handgrip exercise (increased afterload). The obtained values were compared with end-expiratory phase of tidal breathing at rest. We found a significantly larger increase in the early and late filling velocities (for E and A p<0.001) under the conditions of increasing preload (elevation of legs) and less pronounced, but still significant changes with isometric exercise (for E p<0.001 and for A p<0.01). We conclude that the right ventricular filling pattern in healthy humans is highly load-sensitive and for this reason the effect of any intervention (e.g. pharmacological) must be studied under strict and well-defined resting conditions., E. Mandysová, P. Niederle., and Obsahuje bibliografii a bibliografické odkazy
Photothrombotic model of ischemia (PT) is based on free radical-mediated endothelial dysfunction followed by thrombosis. Free radicals are also involved in hypoxic preconditioning. We tested the sensitivity of PT to preconditioning with hypobaric hypoxia and to pretreatment with melatonin. In adult Wistar rats, after intravenous application of Rose Bengal, a stereo-tactically defined spot on the denuded skull was irradiated by a laser for 9 min. The first experimental group underwent hypobaric hypoxia three days before irradiation. In the second experimental group, melatonin was applied intraperitoneally one hour before irradiation. Three days after irradiation, animals were sacrificed, the brains perfused, and stained with TTC. Ischemic lesions were divided into grades (I, II, III). In the control group (where no manipulation preceded photothrombosis), most animals displayed deep damage involving the striatum (grade III). The group pre-exposed to hypoxia showed similar results. Only 28.57 % of the melatonin pretreated animals exhibited grade III lesions, and in 57.14 % no signs of lesions were detected. Pre-exposure to hypoxia was not protective in our model. Pretreatment with melatonin lead to a significant reduction of the number of large ischemic lesions. This result is probably caused by protection of endothelial cells by melatonin., I. Matějovská, K. Bernášková, D. Krýsl, J. Mareš., and Obsahuje bibliografii a bibliografické odkazy