Chronic sojourn in hypoxic environment results in the structural remodeling of peripheral pulmonary arteries and pulmonary hypertension. We hypothesize that the pathogenesis of changes in pulmonary vascular structure is related to the increase of radical production induced by lung tissue hypoxia. Hypoxia primes alveolar macrophages to produce more hydrogen peroxide. Furthermore, the increased release of oxygen radicals by other hypoxic lung cells cannot be excluded. Several recent reports demonstrate the oxidant damage of lungs exposed to chronic hypoxia. The production of nitric oxide is high in animals with hypoxic pulmonary hypertension and the serum concentration of nitrotyrosine (radical product of nitric oxide and superoxide interaction) is also increased in chronically hypoxic rats. Antioxidants were shown to be effective in the prevention of hypoxia induced pulmonary hypertension. We suppose that the mechanism by which the radicals stimulate of the vascular remodeling is due to their effect on the metabolism of vascular wall matrix proteins. Non-enzymatic protein alterations and/or activation of collagenolytic matrix metalloproteinases may also participate. The presence of low-molecular weight cleavage products of matrix proteins stimulates the mesenchymal proliferation in the wall of distal pulmonary arteries. Thickened and less compliant peripheral pulmonary vasculature is then more resistant to the blood flow and the hypoxic pulmonary hypertension is developed., J. Herget, J. Wilhelm, J. Novotná, A. Eckhardt, R. Vytášek, L. Mrázková, M. Ošťádal., and Obsahuje bibliografii
In this paper is proved a weighted inequality for Riesz potential similar to the classical one by D. Adams. Here the gain of integrability is not always algebraic, as in the classical case, but depends on the growth properties of a certain function measuring some local potential of the weight.
This paper presents a novel error-feedback practical solution for real-time implementation of nonlinear output regulation. Sufficient and necessary conditions for both state- and error-feedback output regulation have been established for linear and nonlinear systems several decades ago. In their most general form, these solutions require solving a set of nonlinear partial differential equations, which may be hard or even impossible to solve analytically. In recent years, a methodology for dynamic calculation of the mappings required for state-feedback regulation has been put forward; following the latter, an error-feedback extension is hereby provided which, when combined with design conditions in the form of linear matrix inequalities, becomes suitable for real-time setups. Real-time results are presented for a nonlinear twin rotor MIMO system. Issues concerning the implementation as well as the solutions adopted, are discussed.
Tzv. teorie optimality patří к nejnovějším směrům současného lingvistického bádání. Nejdříve nalezla uplatnění ve fonologii, později v syntaxi a nejnověji i v sémantice. Naše stať naznačuje možnosti a meze uplatnění tohoto pohledu na oblast aktuálního členění věty.
The existence of a positive solution for the generalized predator-prey model for two species $$ \begin{gathered} \Delta u + u(a + g(u,v)) = 0\quad \mbox {in}\ \Omega ,\\ \Delta v + v(d + h(u,v)) = 0\quad \mbox {in} \ \Omega ,\\ u = v = 0\quad \mbox {on}\ \partial \Omega , \end{gathered} $$ are investigated. The techniques used in the paper are the elliptic theory, upper-lower solutions, maximum principles and spectrum estimates. The arguments also rely on some detailed properties of the solution of logistic equations.
This study was directed to use the genetically developed isoprenaline-sensitive (S), isoprenaline-resistant (R) and spontaneous hypertensive rats (SHR) as standard diseased animal models for in vitro liver function evaluation of drug biotransformation. Hepatic hexobarbital hydroxylase and glutathione transferase (GST) were evaluated by using hexobarbital and l-chloro-2,4-dinitrobenzene (CDNB) as substrates, at concentrations of 0.21 mmol/l and 1 mmol/l, respectively. The assay was conducted by using isolated hepatocytes in suspension and hepatocytes in a bioreactor configuration. The data demonstrate that there are certain cellular pharmacokinetic differénces in hexobarbital hydroxylase and GST activities in hepatocytes obtained from Wistar, SHR, R and S strains which can be better demonstrated, when using the model of perfused and immobilized hepatocytes.
The purpose of the present study was to examine the role of the T-786C endothelial nitric oxide synthase (eNOS) gene polymorphism on changes in renal hemodynamics and blood pressure due to Na+ loading. Twenty-eight older (63±1 years), moderately obese (39±2 % fat) hypertensives had th eir glomerular filtration rate (GFR), renal plasma flow (RPF), blood pressure (BP) and plasma nitric oxide (NOx) levels determined after eight days of low (20 mEq) and high (200 mEq) Na+ diets. The two Na+ diets were separated by a 1-week washout period. Subjects were genotyped for the eNOS-786 site and were grouped on whether they were homozygous or heterozygous for the C allele (TC+CC, n=13) or only homozygous for the T allele (TT, n=15). The TC+CC genotype group had a significantly greater increase in diastolic (P=0.021) and mean arterial (P=0.018) BP and a significant decline in both RPF (P=0.007) and GFR (P=0.029) compared to the TT genotype group with Na+ loading. Furthermore, Na+ loading resulted in a significant (P=0.036) increase in plasma NOx in the TT, but not in the TC+CC genotype group as well as a trend (P=0.051) for an increase in urine NOx in TC+CC, but not in the TT genotype group. The increase in BP during Na+ loading in older hypertensives was associated with the eNOS genotype and may be related to changes in renal hemodynamics due to changes in NO metabolism., D. R. Dengel, M. D. Brown, R. E. Ferrell, T. H. Reynolds, M. A. Supiano., and Obsahuje bibliografii a bibliografické odkazy