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The secreted proinflammatory interleukins IL-1, IL-6 and TNF in the course of experimentally-induced pleurisy can be the cause of pathological changes in the ultrastructure of cardiac muscle and of apoptosis. The pleurisy was induced in rats by means of carrageenin. The scraps of cardiac muscle obtained during the inflammatory reaction in the pleura were analysed by means of an electron microscope. The scraps were also stained with the TUNEL method in order to find the apoptotic foci. It was proved by the experiment that the inflammatory process affected mitochondria in the cardiomyocytes, enhanced collagen fibre synthesis and contributed to the formation of apoptotic foci in the cardiac muscle.
1. The evaluation of still more pretentious and complicated methods is accompanied by a decline of methodical knowledge outside of the own technical field. Interpretations or extrapolations are taken as granted without critical examination of the methodical steps applied. An example is given by re-evaluating the ⁴⁵Ca release from isolated cardiac tissue and the possible interpretations. 2. ⁴⁵Ca release and tissue Ca content were measured in isolated guinea-pig left atria during Ca equilibrium and under conditions known to induce net Ca movements. 3. At equilibrium condition (1.8 mM Na²⁺ ₀)3 exponential phase of ⁴⁵Ca release from the atria were observed. The compartments contained 61%, 29% and 10% of total ⁴⁵Ca; the were 2, 12 and 90 min, respectively. 4. The release of ⁴⁵Ca from the slowly exchanging compartment (t½ 90 min) decreased during incubation in nominal Ca-free solution, although a net loss of tissue Ca occurred. Addition of EGTA (5 x 10⁻⁵ M) to the washout medium abolished this retardation of ⁴⁵Ca release. 5. At external Na⁺ concentrations below 40 mM (substituted by sucrose), the ⁴⁵Ca release from the slowly exchanging compartment decreased. Simultaneously, the tissue Ca content increased massively. The ⁴⁵Ca release was further reduced in Na-poor, nominal Ca-free solution. Under both conditions, the presence of EGTA in the washout medium normalized the rate of ⁴⁵Ca release. 6. The results suggest that the apparent decline of ⁴⁵Ca release from intact atria upon reduction of the external Ca and Na concentration does not reflect a decrease of the cellular efflux rate, but is the consequence of an enhanced re-uptake of ⁴⁵Ca from the extracellular space into the myocardial cells. The probability for the released ⁴⁵Ca either to escape into the organ bath or to become reabsorbed depends on the specific radioactivity of ⁴⁵Ca in the extracellular space during the washout phase. Thus, this experimental procedure is not suited to demonstrate a Na-Ca exchange at the cardiac sarcolemma.
Pathological automatism and triggered activity had focal origin. Thus, the treatment has to be aimed at ablation of the arrhythmogenic region. Some arrythmogenic places can be precisely characterized by analysis of ECG patterns. Among them are foci located close to the pulmonary veins, sinus node, ventricular outflow tracts or mitroaortic commissura. Classical ablation of these loci is highly successful. In other types of focal arrhythmias electroanatomical systems make possible to create 3D map, with activation sequence allowing for identification of the place where the arrhythmia could be eliminated. In reentrant mechanism of the arrhythmia the impulse circulates around the loop via the cardiac muscle. In case of the atrioventricular nodal reentrant tachycardia, atrial flutter or bundle branch ventricular tachycardia the loop can be easily outlined. Ablation can be performed using the anatomical method without induction of the tachycardia. In patients with the ventricular tachycardia with multiple forms or hemodynamically unstable it is possible to perform electranatomical map with visualization of the scar and the border zones. In this case the proarrhythmic region in the borderline zone is the aim of linear ablation without induction of tachycardias. In the chaotic tachycardias (atrial or ventricular fibrillation), the arrythmogenic substrate is too much dispersed to destroy them. Therefore, the ablation is aimed at the trigger which is initiating the arrhythmia (for instance the pathological Purkinje fibers). The excitability of the substrate may be also modified by pacemakers (ventricular or atrial resynchronization). In the life-threatening arrhythmias implantable cardioverter-defibrillator is necessary.
Effects of electrode placement on the ECG quality were studied in 200-1500 g individual weight carp. Out of 12 combinations of lead placement relative to the cardiac muscle, 3 were found to produce the most legible, reproducible ECG′s.
In this review the molecular characteristics and reaction mechanisms of different Ca2+ transport systems associated with various membranes in muscle cells will be summarized. The following topics will be discussed in detail: a brief history of early observations concerning maintenance and regulation of cellular Ca2+ homeostasis, characterization of the Ca2+ pumps residing in plasma membranes and sarco(endo)plasmic reticulum, mitochondrial Ca2+ transport, Ca2+ -binding proteins, coordinated expression of Ca2+ transport systems, a general background of muscle excitation-contraction coupling with emphasis to the calcium release channels of plasma membrane and sarcoplasmic reticulum, the structure and function of dihydropyridine and ryanodine receptors of skeletal and cardiac muscles, and finally their disposition in various types of muscles.
This brief review attempts to summarize some of the major phases of muscle research from Leeuwenhoek's description of sarcomeres in 1674, through Galvani's observation of animal electricity in 1791, to the discovery of Ca2+ as the key messenger in the coupling of nerve excitation to muscle contraction. The emerging molecular mechanism of the contraction process is one of the great achievements of biology, reflecting the intimate links between physics, chemistry and the life Sciences in the solution of biological problems.
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Role of adiponectin in the regulation of carbohydrate and lipid metabolism

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Adiponectin, an adipocyte-derived plasma protein, has been shown to play an important role in the regulation of fatty acid and glucose metabolism. Adiponectin enhances fatty acid oxidation both in skeletal and cardiac muscle as well as in the liver, thus reducing triglyceride content in these tissues. Moreover, it stimulates glucose uptake by skeletal and cardiac muscle, and inhibits glucose production by the liver; consequently decreasing blood glucose levels. This review focuses on the molecular mechanisms underlying adiponectin effects on carbohydrate and lipid metabolism in skeletal muscle, cardiac muscle and liver.
In this article the morphology of sarcoplasmic reticulum, classification of Ca2+ -ATPase (SERCA) isoenzymes presented in this membrane system, as well as their topology will be reviewed. The focus is on the structure and interactions of Ca2+ -ATPase determined by electron and X-ray crystallog2r+aphy, lamellar X-ray and neutron diffraction analysis of the profile structure of Ca2+ -ATPase in sarcoplasmic reticulum multilayers. In addition, targeting of the Ca2+ -ATPase to the sarcoplasmic reticulum is discussed.
Sera from 455 patients with diagnosed toxocarosis were examined for the presence of specific IgE by the ε-capture ELISA. Total IgE levels were measured in the sera of 174 patients. Specific IgE was found in 54% of cases, with a high level in 30%. Total IgE level was elevated in 67% of patients. A similar pattern was found in patients with ocular and visceral forms of toxocarosis. There was no statistically significant difference in levels of specific IgE between patients with these forms of the disease. However, we observed significantly higher concentrations of specific IgE among patients who showed high specific IgG activity (titre equal to or higher than 1 : 20,000).
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