Recent studies focused on epicardial fat, formerly relatively neglected component of the heart, have elucidated some of its key roles. It possesses several properties that can distinguish it from other adipose tissue depots. Its unique anatomical location in the heart predisposes the epicardial fat to be an important player in the physiological and biochemical regulation o f cardiac homeostasis. Obesity is associated with an increase in epicardial fat mass. Excess of cardiac fat can contribute to greater left ventricular mass and work, diastolic dysfunction and attenuated septal wall thickening. Imbalance in adipokines levels secreted in autocrine or paracrine fashion by epicardial fat can contribute to the activation of the key atherogenic pathways in the setting of metabolic syndrome. Epicardial fat has also been identified as an important source of pro-inflammatory mediato rs worsening endothelial dysfunction, eventually leading to coronary artery disease. Increased production of pro-inflammatory factors by epicardial fat can also contribute to systemic insulin resistance in patients undergoing cardiac surgery. Here we revie w the most important roles of epicardial fat with respect to heart disease in the context of other underlying pathologies such as obesity and type 2 diabetes mellitus., Z. Matloch, T. Kotulák, M. Haluzík., and Obsahuje bibliografii
Gastrointestinal hormones play an important role in the neuroendocrine regulation of food intake and postprandial satiety. Ghrelin is a 28-amino acid orexigenic peptide produced mainly by the stomach that is involved in both the long-term regulation of body weight and the short-term regulation of postprandial satiety. Impairments in ghrelin secretion may in concert with other factors play an important role in the development of both obesity and anorexia nervosa. Despite an intensive research the critical factors regulating physiological postprandial ghrelin response in healthy individuals and its modification by the presence of obesity and anorexia nervosa are only partially understood. The potential contribution of ghrelin to the differences of diet- vs. surgical-induced weight losses in morbidly obese patients is now also being recognized. The aim of this review is to summarize the current knowledge about the physiology and pathophysiology of ghrelin and to discuss its potential in the prevention and/or treatment of obesity and anorexia nervosa., I. Dostálová, M. Haluzík., and Obsahuje seznam literatury
Ferritin and increased iron stores first appea red on the list of cardiovascular risk factors more than 30 years ago and their causal role in the pathogenesis of atherosclerosis has been heavily discussed since the early 1990s. It seems that besides traditional factors such as hyperlipoprotein emia, hyp ertension, diabetes mellitus, obesity, physical inactivity, smoking and family history, high iron stores represent an additional parameter that could modify individual cardiovascular risk. The role of iron in the pathogenesis of atherosclerosis was origina lly primarily associated with its ability to cataly ze the formation of highly reactive free oxygen radicals and the oxidation of atherogenic lipoproteins. Later, it became clear that the mechanism is more complex. Atherosclerosis is a chronic fibroprolife rative inflammatory process and iron, through increased oxidation stress as well as directly, can control both native and adaptive immune responses. Within the arterial wall, iron affects all of the cell types that participate in the atherosclerotic proces s (monocytes/macrophages, endothelial cells, vascular smooth muscle cells and platelets). Most intracellular iron is bound in ferritin, whereas redox-active iron forms labile iron pool. Pro-inflammatory and anti-inflammatory macrophages within arterial plaque differ with regard to the amount of intracellular iron and most probably with regard to their labile iron pool. Yet, the relation between plasma ferritin and intracellular labile iro n pool has not been fully clarified. Data from population studies document that the consumption of meat and lack of physical activity contribute to increased iron stores. Patients with hereditary h emochromatosis, despite extreme iron storage, do not show i ncreased manifestation of atherosclerosis probably due to the low expression of hepcidin in macrophages., P. Kraml., and Obsahuje bibliografii
This review focuses on current knowledge of leptin biology and the role of leptin in various physiological and pathophysiological states. Leptin is involved in the regulation of body weight. Serum leptin can probably be considered as one of the best biological markers reflecting total body fat in both animals and humans. Obesity in man is accompanied by increased circulating leptin concentrations. Gender differences clearly exist. Leptin is not only correlated to a series of endocrine parameters such as insulin, glucocorticoids, thyroid hormones, testosterone, but it also seems to be involved in mediating some endocrine mechanisms (onset of puberty, insulin secretion) and diseases (obesity, polycystic ovary syndrome). It has also been suggested that leptin can act as a growth factor in the fetus and the neonate., R. Janečková., and Obsahuje bibliografii
Lipid peroxidation of rat cerebral cortex membranes was induced by Fe2+/ADP and ascorbate. The rate of Na+/K+-ATPase inhibition was correlated with the increase of thiobarbituric acid-reactive substances (TBARS) and conjugated dienes (CD) and with membrane fluidity changes. Our data showed that membrane fluidity changes (evaluated by fluorescence steady-state anisotropy measurements) can participate in Na+/K+-ATPase inhibition during the initial period of lipid peroxidation process, whereas during the following period the enzyme inhibition correlates only with TBARS and CD production., H. Rauchová, Z. Drahota, J. Koudelová., and Obsahuje bibliografii
Endothelial dysfunction may be considered as the interstage between risk factors and cardiovascular pathology. An imbalance between the production of vasorelaxing and vasoconstricting factors plays a decisive role in the development of hypertension, atherosclerosis and target organ damage. Except vasorelaxing and antiproliferative properties per se, nitric oxide participates in antagonizing vasoconstrictive and growth promoting effects of angiotensin II, endothelins and reactive oxygen species. Angiotensin II is a potent activator of NAD(P)H oxidase contributing to the production of reactive oxygen species. Numerous signaling pathways activated in response to angiotensin II and endothelin-1 are mediated through the increased level of oxidative stress, which seems to be in casual relation to a number of cardiovascular disturbances including hypertension. With respect to the oxidative stress, the NO molecule seems to be of ambivalent nature. On the one hand, NO is able to reduce generation of reactive oxygen species by inhibiting association of NAD(P)H oxidase subunits. On the other hand, when excessively produced, NO reacts with superoxides resulting in the formation of peroxynitrite, which is a free radical deteriorating endothelial function. The balance between vasorelaxing and vasoconstricting substances appears to be the principal issue for the physiological functioning of the vascular bed., O. Pecháňová, F. Šimko., and Obsahuje bibliografii
Dihydrotestosterone (DHT) originates via irreversible reduction of testosterone by catalytic activity of 5α-reductase enzyme and it is demonstratively the most effective androgen. Androgens influence adipose tissue in men either directly by stimulation of the androgen receptor or indirectly, after aromatization, by acting at the estrogen receptor. DHT as a non-aromatizable androgen could be responsible for a male type fat distribution. The theory of non-aromatizable androgens as a potential cause of a male type obesity development has been studied intensively. However, physiological levels of DHT inhibit growth of mature adipocytes. In animal models, substitution of DHT in males after gonadectomy has a positive effect on body composition as a testosterone therapy. Thus, DHT within physiological range positively influences body composition. However, there are pathological conditions with an abundance of DHT, e.g. androgenic alopecia and benign prostatic hyperplasia. These diseases are considered as ri sk factors for development of metabolic syndrome or atherosclerosis. In obese people, DHT metabolism in adipose tissue is altered. Local abundance of non- aromatizable androgen has a nega tive effect on adipose tissue and it could be involved in pathogenesis of metabolic and cardiovascular diseases. Increased DHT levels, compared to physiological levels, have negati ve effect on development of cardiovascular diseases. Difference between the effect of physiological and increased level brings about certain paradox., M. Dušková, H. Pospíšilová., and Obsahuje bibliografii a bibliografické odkazy
Oxygen can afFect the photosynthetic processes in two antagonistic (protective and destructive) ways. The protection is represented by draining off of the electron transport systém, by utilisation of NADPH and ATP, and production of carbon dioxide in the process of photorespiration, oxygen reduction in the Mehler reaction, and also by regeneration of monodehydroascorbate, one of the fmal products of the Mehler-peroxidase reaction. The subsequent building up of the proton gradient in the Mehler and Mehler-peroxidase reactions also helps protéct the photosynthetic apparatus. The production of harmful oxygen radicals is accompanied by the Mehler reaction. This is in contrast to the fact that the Mehler reaction can also protéct the photosynthetic apparatus. Nevertheless, the scavenging mechanisms in plants are efficient enough for protection against the active oxygen species. In some cases the disproportion between the production and scavenging of active oxygen can result in the destruction of thylakoid membrane. Singlet oxygen, another toxic form of oxygen, can also significantly increase the inhibition of photosynthesis in the presence of oxygen. None of these processes works alone or independently, they are in a dynamic equilibrium and each of them contributes to the regulation of photosynthesis.
Protease-activated receptors (PARs) belong to the G-proteincoupled receptor family, that are expressed in many body tissues especially in different epithelial cells, mast cells and also in neurons and astrocytes. PARs play different physiological roles according to the location of their expression. Increased evidence supports the importance of PARs activation during nociceptive signaling and in the development of chronic pain states. This short review focuses on the role of PAR2 receptors in nociceptive transmission with the emphasis on the modulation at the spinal cord level. PAR2 are cleaved and subsequently activated by endogenous proteases such as tryptase and trypsin. In vivo, peripheral and intrathecal administration of PAR2 agonists induces thermal and mechanical hypersensitivity that is thought to be mediated by PAR2-induced release of pronociceptive neuropeptides and modulation of different receptors. PAR2 activation leads also to sensitization of transient receptor potential channels (TRP) that are crucial for nociceptive signaling and modulation. PAR2 receptors may play an important modulatory role in the development and maintenance of different pathological pain states and could represent a potential target for new analgesic treatments., P. Mrozkova, J. Palecek, D. Spicarova., and Obsahuje bibliografii
Podle knihy Petera Harrisona The Bible, Protestantism and the Rise of Natural Science z roku 1998 vznikla moderní věda jako výsledek důrazu protestantů na doslovný smysl Písma, jejich odmítnutí dřívějšího symbolického či alegorického výkladu a jejich snahy o fi xaci významu biblického textu, v němž každá pasáž měla mít jediný a jedinečný význam. Tento článek se pokouší o shrnutí nejvýznamnějších kritik Harrisonovy hypotézy (od Kennetha Howella, Jitse van der Meera a Richarda Oosterhoff a) a uznává jejich oprávněnost. Nicméně ani alternativní vysvětlení vzestupu moderní vědy jakožto výsledku neshod ve výkladu Písma a následného objevu nejednoznačné povahy běžného verbálního jazyka není zcela uspokojivé., According to Peter Harrison’s book The Bible, Protestantism and the Rise of Natural Science (1998) modern science came into existence as a result of the emphasis of Protestants on the literal sense of the Scripture, their refusal of the earlier symbolic or allegorical interpretation, and their efforts at fixing the meaning of the biblical text in which each passage was to be ascribed a single and unique meaning. This article tries to summarize the most significant critiques of Harrison’s hypothesis (by Kenneth Howell, Jiste van der Meer and Richard Oosterhoff) and to acknowledge their legitimacy. However, the alternative explanation of the emergence of modern science as a result of disputes over the biblical interpretation and the subsequent discovery of the ambiguous character of the ordinary verbal language is not fully satisfactory either., and Petr Pavlas.