In order to evaluate the influence of the respiratory cycle on the EEG, we compared the power spectral analysis of the EEG performed by fast Fourier transformation during inspirium and exspirium in 10 healthy subjects. The measurement was performed during spontaneous breathing and then during eupnoe (0.25 Hz), bradypnoe (0.1 Hz) and tachypnoe (0.5 Hz) paced by a metronome. In the course of spontaneous breathing and bradypnoe, there was an increase in the delta power and in the total power in the anterior temporal region during inspirium in comparison with exspirium. The eupnoe was characterized by an inspiratory decrease in the delta power in the parietal region and in the total power in the frontal region. The tachypnoe resulted in a decrease of the beta power in the central region and a decrease of the theta power in the posterior temporal and in the occipital region during inspirium. In comparison of the EEG in eupnoe, bradypnoe and tachypnoe, a decrease of spectral power of all spectral bands was found except for delta during faster breathing frequencies and vice versa with a significant difference which wa
s found mostly between bradypnoe and tachypnoe, less frequently between eupnoe and tachypnoe.
Metabolism of palmitate-14C was studied in the rat liver and muscle incubated with 1 mmol.1-1 tolbutamide in vitro experiments: Tolbutamide reduces the utilization of free fatty acids in the liver by inhibiting their uptake, incorporation into total lipids, and oxidation to 14CC>2. Tolbutamide stimulates the incorporation into the triacylglycerol fraction in individual liver lipid fractions and inhibits the incorporation into the free fatty acid fraction. As in the liver, tolbutamide inhibits the uptake, incorporation into total lipids, and oxidation to 14C02 in the muscle. In individual lipid fractions, tolbutamide only inhibits the incorporation of palmitate into cholesterol esters. It can be concluded that tolbutamide directly interferes with fatty acid metabolism and thus improves glucose utilization and insulin resistance.
In normal practice, during the estimation of reservoir storage uncertainties affecting the values of mean monthly discharge series are not normally considered, and usually no estimates of these are known. Therefore, the question arises as to whether the results of the estimation of the capacity of storage reservoirs may be affected by uncertainties in the discharge series. The aim of this article is the suggestion of a possible approach to estimating the level of uncertainties affecting the elements of mean monthly discharge series. These discharge series are subsequently integrated into water reservoir storage capacity calculations, and the significance of the proposed approach is explored. and Nejistoty členů řad průměrných měsíčních průtoků nejsou v běžné praxi udávány, není ani znám odhad jejích velikostí. Otázkou rovněž je, zda nejistotami zatížené průtokové řady mohou ovlivnit výsledky vodohospodářského řešení zásobní funkce vodní nádrže. Cílem článku je naznačení možného postupu odhadu míry nejistot zatěžujících členy průtokové řady průměrných měsíčních průtoků a následné začlenění uvedené řady do výpočtů zásobního objemu vodní nádrže a posouzení významu uvedeného postupu.
The aim of our study was to determine whether adipocyte-derived hormones leptin, adiponectin and resistin contribute to the improvement of insulin sensitivity after very-low calorie diet (VLCD). Therefore, serum levels of these hormones were measured in fourteen obese females before and after three weeks VLCD and in seventeen age- and sex-matched healthy controls. Body mass index, HOMA index, serum insulin and leptin levels in obese women before VLCD were significantly higher than in control group (BMI 48.01±2.02 vs. 21.38±0.42 kg/m2, HOMA 10.72±2.03 vs. 4.69±0.42, insulin 38.63±5.10 vs. 18.76±1.90 μIU/ml, leptin 77.87±8.98 vs. 8.82±1.52 ng/ml). In contrast, serum adiponectin and soluble leptin receptors levels were significantly lower in obese women before VLCD than in the control group. No differences were found in serum glucose and resistin levels between the obese group before VLCD and the control group. VLCD significantly decreased BMI, HOMA index, serum glucose, insulin and leptin levels and increased soluble leptin receptor levels. The changes in serum adiponectin and resistin levels in obese women after VLCD did not reach statistical significance. We conclude that leptin and soluble leptin receptor levels were affected by VLCD while adiponectin and resistin concentrations were not. Therefore, other mechanisms rather than changes in the endocrine function of the adipose tissue are probably involved in the VLCD-induced improvement of insulin sensitivity.
In Phaseolus and Robinia leaves, direct light reaction (de-epoxidatíon of violaxanthín) was inhibited during 7-9 h as an aftereffect of y-radiation (167 mGy s'*). Complete suppression of the light reaction by the de-epoxidation was reached after 12-14 h. The suppression of xanthophyll de-epoxidation reflects the inhibitíon of photosynthetic electron transport chain and may be ušed for testing deleterious efifects on plants.
The effect of chronic administration of angiotensin converting enzyme inhibitor on the development of hypoxic pulmonary hypertension was studied in rats. Male Wistar rats were exposed for 3 weeks to isobaric hypoxia (10 % O2) and treated with 10 mg/kg b.w. of Ramipril daily. The haemodynamic properties of the pulmonary vasculature were then measured in isolated blood-perfused lung preparation. Ramipril administration during the sojourn in hypoxia resulted in lower baseline perfusion pressure and lower slope of perfusion pressure-flow relationship compared to non-treated hypoxic rats. Partitioning of the distribution of pulmonary vascular resistance across the vascular bed by the occlusion technique showed that it was mainly due to a decrease of arterial and venous vascular resistances to blood flow. It is suggested that Ramipril attenuates the process of morphological reconstruction of pulmonary vasculature by chronic hypoxia rather than the level of vascular smooth muscle tone.
We investigated the actions of dantrolene Ca2+-induced on Ca2+-release (CICR) evoked by action potentials in cultured rat sensory neurons. The effect of dantrolene on action potential after-depolarization and voltage-activated calcium currents was studied in cultured neonatal rat dorsal root ganglion cells (DRG) using the whole-cell patch-clamp technique. Depolarizing current injection evoked action potentials and depolarizing after-potentials, which are activated as a result of CICR following a single action potential in some cells. The type of after-potentials was determined by inducing action potentials from the resting membrane potential. Extracellular application of dantrolene (10 mM) abolished after-depolarizations without affecting action potential properties. Furthermore, dantrolene significantly reduced repetitive action potentials after depolarizing current injection into these neurons, but had no significant effect on the steady-state current voltage relationship of calcium currents in these neurons. We conclude that dantrolene inhibits the induction of action potential after depolarizations by inhibiting CICR in cultured rat sensory neurons., A. Ayar, H. Kelestimur., and Obsahuje bibliografii
We studied the effect of herbicide and nitrogen supply on photosynthesis in Perilla frutescens L. Britt. Plants were exposed to combined treatment of urea and herbicide, fenoxaprop-P-ethyl (FPE), in various concentrations. FPE reduced significantly chlorophyll (Chl) content, photosynthetic rate, and stomatal conductance, but increased significantly intercellular CO2 concentration; thus, FPE inhibited significantly the photosynthetic capacity. In addition, FPE also decreased significantly the PSII photochemical efficiency, effective quantum yield of photochemical energy conversion in PSII, PSII potential activity, and photochemical quenching of variable Chl fluorescence. It also decreased nonphotochemical quenching. It indicated that FPE impaired PSII and blocked the electron transport in light reaction. The urea treatment at moderate concentration (1-4 g L-1) could antagonize the negative effect of FPE, while the high urea concentration (8 g L-1) aggravated this effect. The treatment with urea (4 g L-1) and then with FPE (1.33 mL L-1) enhanced Chl content index, photosynthetic rate, and stomatal conductance by 12.5, 36.1, and 28.5% compared to FPE treatment alone. Thus, we suggested to treat plants first with urea (4 g L-1) and then by FPE (1.33 mL L-1) as the best and the safest method to balance the fertilization and weeding., J. H. Zhang, S. J. Guo, P. Y. Guo, X. Wang., and Obsahuje bibliografii
ncreased systemic vascular resistance is responsible for blood pressure (BP) elevation in most forms of human or experimental hypertension. The enhanced contractility of structurally remodeled resistance arterioles is mediated by enhanced calcium entry (through L type voltagedependent calcium channels - L-VDCC) and/or augmented calcium sensitization (mediated by RhoA/Rho kinase pathway). It is rather difficult to evaluate separately the role of these two pathways in BP control because BP response to the blockade of either pathway is always dependent on the concomitant activity of the complementary pathway. Moreover, vasoconstrictor systems enhance the activity of both pathways, while vasodilators attenuate them. The basal fasudil-sensitive calcium sensitization determined in rats deprived of endogenous renin-angiotensi n system (RAS) and sympathetic nervous system (SNS) in wh ich calcium entry was dose- dependently increased by L-VDCC opener BAY K8644, is smaller in spontaneously hypertensive rats (SHR) than in normotensive Wistar-Kyoto (WKY) rats. In co ntrast, if endogenous RAS and SNS were present in intact rats, fasudil caused a greater BP fall in SHR than WKY rats. Our in vivo experiments indicated that the endogenous pressor systems (RAS and SNS) augment calcium sensitization mediated by RhoA/Rho kinase pathway, whereas the endogenous vasodilator systems (such as nitric oxide) attenuate this pathway. However, the modulation of calcium entry and calcium sensitization by nitric oxide is strain-dependent because NO deficiency significan tly augments low calcium entry in WKY and low calcium sensitization in SHR. Further in vivo and in vitro experiments should clarify the interrelationships between endogenous vasoactive systems an d the contribution of calcium entry and/or calcium sensitization to BP maintenance in various forms of experimental hypertension., J. Zicha ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy