This review article summarizes the problems of metabolic disorders and nutrition imbalances that often occur in chronic kidney failure (CKF) or following regular dialysis treatment. In this survey, we cover the pathogenesis of these disorders, their clinical consequences, and their association with the most severe complications of chronic kidney failure and dialysis treatment. These complications are primarily at herosclerosis, malnutrition, anemia, hyperparathyroidism, and other serious problems that markedly and negatively affect prognosis and the quality of life of uremic patients. Risk factors for cardiovascular disease are discussed in-depth because cardiovascular disease is the leading cause of death in patients with chronic kidney failure. It is important to pay attention to the development of these complications because early diagnosis and therapy can improve the prognosis for these patients and reduce treatment costs., R. Cibulka, J. Racek., and Obsahuje bibliografii a bibliografické odkazy
The miniature excitatory postsynaptic currents (MEPCs) of the muscle cells of the earthworm Lumbricus terrestris were recorded by glass microelectrodes. In a single synaptic zone, three types of MEPC were recorded: a fast single-exponential type that decayed with τ=0.9 ms, a slow single-exponential with τ=9.2 ms and a two-exponential MEPC with τ = 1.3 and 8.5 ms, respectively. The muscle cells of earthworms contain populations of yet-unidentified ionic channels that might be different from the common nicotinic and muscarinic groups of acetylcholine receptors, since these MEPCs are not sensitive to d-tubocurarine, atropine, benzohexonium or proserine. Alternatively, besides ACh receptors, the membrane may contain receptors for an other yet-unidentified excitatory transmitter., E. M. Volkov, L. F. Nurullin, E. Nikolsky, F. Vyskočil., and Obsahuje bibliografii a bibliografické odkazy
The authors aimed to evaluate if the monitoring of serum advanced glycation end-products (s-AGEs) could help to predict a development of diabetic complications. Clinical and biochemical parameters including fructosamine (FAM), glycated hemoglobin (HbA1c) and serum AGEs were investigated in children and adolescents with 1 type diabetes with (+DC) and without (–DC) complications. FAM levels (in mmol/l) were significantly elevated in +DC diabetic group compared to –DC one (3.043±0.459 vs. 2.614±0.430; p<0.001) or to controls (3.043±0.459 vs. 1.620±0.340; p<0.001) as well as in –DC compared to controls (2.614±0.430 vs. 1.620±0.340; p< 0.001). HbA1c (in %) were significantly elevated in +DC diabetic group compared to –DC one (10.48±1.83 vs. 8.41±1.19; p<<0.001) or to controls (10.48±1.83 vs. 5.0±0.38, p<<0.001) and also in –DC compared to controls (8.41±1.19 vs. 5. 0±0.38; p<0.001). Serum AGEs levels (in A. U.) were significantly higher in +DC group than in –DC (73.0±14.09 vs. 65.8±9.05; p< 0.05) and in group +DC than in controls (73.0±14.09 vs. 60.17±13.78; p<0.05), whereas there was no difference between –DC and controls. FAM correlated with HbA1c in both diabetic groups (+DC: r=0.374; p<0.05; –DC: r=0.719; p<0.001), but not in controls. Serum AGEs were correlated with Hb A1c (r=0.478; p=0.003) in +DC, but not in –DC or controls. Enhanced serum AGEs levels show that they could be not only an attendant phenomenon of microangiopathies, but also a predictor of their development., J. Kostolanská, V. Jakuš, Ľ. Barák., and Obsahuje seznam literatury
Earlier this month, the Czech media reported that a highly efficient antiviral drug developed by Czech scientists has been shelved, reportedly for fear it would compete with existing medicines manufactured by pharmaceutical giants. The substance, known as MK-612, was designed at the Academy´s Institute of Organic Chemistry and Biochemistry. Academic Bulletin interviewed Zdeněk Havlas, headmaster of the Institute, about next stage in the future of this efficient substance MK-612. and Marina Hužvárová.
Depression is a complex disorder related to chronic inflammatory processes, chronic stress changes and a hippocampal response. There is a increasing knowledge about the role of glial cells in nutrient supply to neurons, maintenance of synaptic contacts and tissue homeostasis within the CNS. Glial cells, viewed in the past as passive elements with a limited influence on neuronal function, are becoming recognized as active partners of neurons and are starting to be discussed as a possible therapeutic target. Their role in the pathogenesis of depressive disorders is also being reconsidered. Attention is devoted to studies of the different types of antidepressants and their effects on transmembrane signaling, including levels of α subunits of G proteins in C6 glioma cells in vitro as a model of postsynaptic changes in vivo. These models indicate similarities in antidepressant effects on G proteins of brain cells and effector cells of natural immunity, natural killers and granulocytes. Thus, an antidepressant response can exhibit certain common characteristics in functionally different systems which also participate in disease pathogenesis. There are, however, differences in the astrocyte G-protein responses to antidepressant treatment, indicating that antidepressants differ in their effect on glial signalization. Today mainstream approach to neurobiological basis of depressive disorders and other mood illnesses is linked to abnormalities in transmembrane signal transduction via G-protein coupled receptors. Intracellular signalization cascade modulation results in the activation of transcription factors with subsequent increased production of a wide array of products including growth factors and to changes in cellular activity and reactivity., M. Páv, H. Kovářů, A. Fišerová, E. Havrdová, V. Lisá., and Obsahuje bibliografii a bibliografické odkazy
Rhythmic daily changes in the Na,K-ATPase activity have been previously described for rat kidney cortex, showing two peaks: at 0900 h and 2100 h, and two valleys: at 1500 h and 0100 h - 0300 h. The oscillations in Na,K-ATPase activity are produced by an inhibitor, which binds the enzyme and is present in the rat blood plasma at valley times and absent or at very low concentrations at peak times. Since it has been demonstrated that active Na+ extrusion from the cells of several tissues depends not only on the Na,K-ATPase but also on the ouabain-insensitive Na-ATPase, we studied the activity of this latter enzyme of several rat tissues, i.e., kidney cortex, small intestine, liver, heart and red blood cells along the day. None of these tissues showed any variation of their Na-ATPase activity along the day. Preincubation of kidney cortex homogenates obtained at 0900 h, with blood plasma drawn at 0900 h and 1500 h, did not modify the Na-ATPase activity. Our results indicate that the Na-ATPase activity does not oscillate along the day. These results are in agreement with the idea that the Na-ATPase could partially compensate the Na+ transport affected by oscillations of the Na,K-ATPase activity., A. Reyes ... [et al.]., and Obsahuje seznam literatury
Functional C(-260)→T polymorphism in the promoter of the CD14 gene has been reported to be associated with coronary heart disease (CHD). The functional role of the polymorphism, however, is still a matter of debate, since several studies have not proved its effect on clinical outcomes associated with atherosclerosis. Cardiovascular-related morbidity and mortality was assessed in a post-hoc approach four years after baseline characterization of patients (male/female n = 36/32) with angiographically proven coronary heart disease. CD14 C(-260)→T promoter genotype was determined at baseline. Seventeen out of 20 CHD patients with non-lethal cardiovascular events carried at least one T-allele. CD14 T-260 allele carriers have a 3.59-fold (95 % confidence interval: 1.11-6.75) increased risk for non-lethal cardiovascular events (Kaplan-Meier plot: log rank test p = 0. 029). All patients with lethal outcomes (n = 6) were also T-allele carriers. Multivariate logistic regression analysis among CHD patients including age, established risk factors and the C(-260)→T polymorphism as covariates and non-lethal events as a dependent variable confirmed the independent prospective effect of the T-allele on cardiovascular outcomes in this subset. Further evidence is provided for the role of CD14 C(-260)→T promoter polymorphism as a genetic susceptibility marker of atherosclerosis in patients with an advanced clinical course of the disease. Due to the small sample size and post-hoc character of the study large-scale prospective studies that monitor patients with proven CHD are needed to confirm these findings., M. Porsch-Öucürümez, J.Hucke, S. Westphal, J. A. Hubáček, G. Schmitz, C. Luley., and Obsahuje bibliografii a bibliografické odkazy