Hypoxia stimulates ventilation, but when it is sustained, a decline in the ventilatory response is seen. The mechanism responsible for this decline lies within the CNS, but still remains unknown. In this study, we attempted to elucidate the possible role of hypoxia-induced depression of respiratory neurons by comparing the ventilatory response to hypoxia in intact rats and those with denervated carotid bodies. A whole-body plethysmograph was used to measure tidal volume, frequency of breathing and minute ventilation (VE) in awake and anesthetized intact rats and rats after carotid body denervation during exposure to hypoxia (FIO2 0.1). Fifteen-minute hypoxia induced an initial increase of VE in intact rats (to 248 % of control ventilation in awake and to 227 % in anesthetized rats) followed by a consistent decline (to 207 % and 196 % of control VE, respectively). Rats with denervated carotid bodies responded with a smaller increase in VE (to 134 % in awake and 114 % in anesthetized animals), but without a secondary decline (145 % and 129 % of control VE in the 15th min of hypoxia). These results suggest that afferentation from the carotid bodies and/or the substantial increase in ventilation are crucial for the biphasicity of the ventilatory response to sustained hypoxia and that a central hypoxic depression cannot fully explain the secondary decline in VE., H. Maxová, M. Vízek., and Obsahuje bibliografii
Aims of the study were to compare the development of electrocardiographic responses of the ischemia-induced heterogeneities of activation and repolarization in the ventricular myocardium of normal and diabetic animals. Body surface ECGs and unipolar electrograms in 64 epicardial leads were recorded before and during 20 min after the ligation of the left anterior descending artery in diabetic (alloxan model, 4 weeks, n=8) and control (n=8) rabbits. Activation times (ATs), end of repolarization times (RTs) and repolarization durations (activation-recovery intervals, ARIs) were determined in ischemic and periischemic zones. In contrast to the controls, the diabetic rabbits demonstrated the significant prolongation of ATs and shortening of ARIs (P<0.05) during ischemia in the affected region resulting in the development and progressive increase of the ARI and RT gradients across the ischemic zone boundary. The alterations of global and local dispersions of the RTs in diabetics correlated with the Tpeak-Tend interval changes in the limb leads ECGs. In the ischemic conditions, the diabetic animals differed from the controls by the activation delay, significant repolarization duration shortening, and the increase of local repolarization dispersion; the latter could be assessed by the Tpeak-Tend interval measurements in the body surface ECGs., K. A. Sedova, M. A. Vaykshnorayte, A. O. Ovechkin, P. Kneppo, O. G. Bernikova, V. A. Vityazev, J. E. Azarov., and Obsahuje bibliografii
Frontal auditory evoked potentials (FAEPs) obtained as a response to the warning auditory stimulus of a contingent negative variation task from depth electrodes were investigated. The second, imperative stimulus was visual. Thirteen epileptic patients participated in the study. Records from 20 electrodes of 10 patients exhibited signs of local generation. They were localized in the motor cortices (7 cases), in the superior, medial, and inferior frontal gyri (7 cases), in the cingulate gyrus (5 cases), and in the nucleus caudatus (1 case). A typical FAEP from these generators consisted of three components: (i) first negative wave peaking at 99±13 ms; (ii) positive wave peaking at 181±21 ms; (iii) second negative wave peaking at 324±63 ms. In 11 generators no evoked activity to visual stimulus was observed; in the remaining 9 generators both auditory and visual stimuli evoked a response. FAEPs with very early onsets (onset latency below 20 ms) were found in three sites in the precentral gyrus., M. Kukleta, B. Turak, J. Louvel., and Obsahuje bibliografii
Mechanical behavior of biological structures under dynamic loading generally depends on elastic as well as viscous properties of biological materials. The significance of “viscous” parameters in real situations remains to be elucidated. Behavior of rheological models consisting of a combination of inertial body and two Voigt’s bodies were described mathematically with respect to inverse problem solution, and behavior in impulse and harmonic loadings was analyzed. Samples of walls of porcine and human aorta thoracica in transverse direction and samples of human bone (caput femoris, substantia compacta) were measured. Deformation responses of human skin in vivo were also measured. Values of elastic moduli of porcine aorta walls were in the interval from 102 kPa to 103 kPa, values of viscous coefficients were in the interval from 102 Pa.s to 103 Pa.s. The value of shear stress moduli of human caput femoris, substantia compacta range from 52.7 to 161.1 MPa, and viscous coefficients were in the interval from 27.3 to 98.9 kPa.s. The role of viscous coefficients is significant for relatively high loading frequencies - in our materials above 8 Hz in aorta walls and 5 Hz for bones. In bones, the viscosity reduced maximum deformation corresponding to short rectangular stress., M. Kuchařová, S. Ďoubal, P. Klemera, P. Rejchrt, M. Navrátil., and Obsahuje bibliografii
Visfatin is a multi-functional molecule that can act intracellularly and extracellularly as an adipokine, cytokine and enzyme. One of the main questions concerning visfatin is the mechanism of its secretion; whether, how and from which cells visfatin is released. The objective of this in vitro study was to observe the active secretion of visfatin from 3T3-L1 preadipocytes and adipocytes, HepG2 hepatocytes, U-937, THP-1 and HL-60 monocytes and macrophages. The amount of visfatin in media and cell lysate was always related to the intracellular enzyme, glyceraldehyde-3- phosphate dehydrogenase (GAPDH), to exclude the passive release of visfatin. Visfatin was not found in media of 3T3-L1 preadipocytes. In media of 3T3-L1 adipocytes and HepG2 hepatocytes, the ratio of visfatin to the amount of GAPDH was identical to cell lysates. Hence, it is likely that these cells do not actively secrete visfatin in a significant manner. However, we found that significant producers of visfatin are differentiated macrophages and that the amount of secreted visfatin depends on used cell line and it is affected by the mode of differentiation. Results show that 3T3-L1 adipocytes and HepG2 hepatocytes released visfatin only passively during the cell death. U-937 macrophages secrete visfatin in the greatest level from all of the tested cell lines., P. Svoboda, E. Křížová, K. Čeňková, K. Vápenková, J. Zídková, V. Zídek, V. Škop., and Obsahuje bibliografii
In this review we summarize recent opinions on the possible role of vitamin D in the risk of thyroid diseases development. It may be concluded from the available data that vitamin D deficiency, particularly levels below 12.5 ng/ml should be considered as an additional, but important risk factor for development of thyroid autoimmunity, both chronic autoimmune thyroiditis and Graves´ disease. A higher risk of Graves´ disease development is also associated with several polymorphisms in the gene encoding for vitamin D binding protein and for the specific receptor of active form of vitamin D - 1,25-(OH)2D3 in the respective target cells. Important for development of thyroid cancer appeared polymorphisms of genes encoding for vitamin D receptors and of genes encoding for the participating hydroxylating enzymes in thyroid tissue, leading to a diminished local 1,25-(OH)2D3 formation capacity with following alteration of antiproliferatory, antiapoptotic and prodifferentiating efficacy of the latter. Whether supplementation with high doses of vitamin D or its analogues possesses preventive or therapeutic effect is an object of intensive studies., K. Vondra, L. Stárka, R. Hampl., and Obsahuje bibliografii
Reduced levels of vitamin or its metabolites have been reported in various psychiatric disorders. Insufficient levels of vitamin D in depressive patients have been confirmed by many authors, but there have been conflicting results in subjects with anxiety disorders. In the present cross-sectional study, levels of calcidiol were determined in groups of depressive men and women and in men and women with anxiety disorders and compared with age matched controls. Significantly lower levels of calcidiol were found in men and women with depression as well as in age matched patients with anxiety disorders., M. Bičíková, M. Dušková, J. Vítků, B. Kalvachová, D. Řípová, P. Mohr, L. Stárka., and Obsahuje bibliografii
In women with chronic autoimmune thyroiditis and vitamin D deficiency we have found reference levels of relevant metabolichormonal parameters except for parathormone and total calcium. Three months supplementation with vitamin D (4300 IU/day, cholekalciferol) did not lead to significant changes of investigated hormonal parameters, while the levels of parathormone and calcium reached normal levels. However, a correlation analysis revealed marked changes in mutual relations. First, an inverse correlation of vitamin D with parathormone, insulin secretion (C peptide, insulin) and its efficiency (HOMA IR) disappeared. Relationships of vitamin D to hepatic insulin resistance (insulin/C peptide), to DHEA (both negative), and to DHEAS/DHEA ratio (positive) were newly found. Second, a positive correlation of CRP with insulin secretion remained, while its relation to insulin efficiency (HOMA IR, insulin/ C peptide) was newly observed. Analogical positive correlations appeared also among anti TPO and insulinemia, insulin/C peptide, HOMA IR, and anti Tg to C peptide. A relationship of the CRP with anti TPO became significant (+). Third, out of glucose metabolism parameters only insulin/C peptide and glycemia did not correlate with vitamin D during its deficiency, while after supplementation insulin/ C peptide alone correlated positively with both DHEAS and DHEA, and negatively with vitamin D., K. Vondra, R. Bílek, P. Matucha, M. Salátová, M. Vosátková, L. Stárka, R. Hampl., and Obsahuje bibliografii
Vitamin D had been for a long time investigated for its effects on bone metabolism. Recently has been observed that the incidence of some neurodevelopmental disorders (including autism) increases hand in hand with vitamin D deficiency. Indeed, vitamin D was reported to modulate the biosynthesis of neurotransmitters and neurotrophic factors; moreover, its receptor was found in the central nervous system. Vitamin D deficiency was therefore assessed as a risk factor for autism, however the biological mechanism has not yet been revealed. In our review we focused on potential connections among vitamin D, steroids and autism. Potential mechanisms of vitamin D action are also discussed., L. Máčová, M. Bičíková, D. Ostatníková, M. Hill, L. Stárka., and Obsahuje bibliografii