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EN
An adequate calcium intake is important to attain peak bone mass and to oppose that component of age-related bone loss. Calcium deficiency is one of the risk factors for osteoporosis. Calcium supplements is particularly important for preventing bone loss and fractures.
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vol. 55
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issue 1
157-175
EN
Ca 2+ is involved in the regulation of many events in the nucleus, such as gene expression, DNA replication, DNA repair, chromatin fragmentation in apoptosis, modulation of an intranuclear contractile system. In some cases, the function of Ca 2+ is mediated by calmodulin. However, the regulation of nucleoplasmic Ca 2+ concentration has not been explored throughly. The data discussed in this review show that the [Ca 2+]n may be regulated independently of that of cytosolic Ca 2+. IP3 and acid ADP-ribose are the major factors responsible for Ca 2+ release into the nucleus from perinuclear space.
EN
The effect of calcium upon embryonic growth was studied using cultured mouse preimplantation embryos. Both morphological development of the embryos and embryo DNA synthesis were shown to be dependent on the in the medium in which the embryos were grown. Reduction of the calcium concentration completely blocked cell division and blastocyst formation in the cultured embryos, but only moderately inhibited embryo DNA synthesis. Trifluoperazine, a calmodulin antagonist, strongly inhibited the calcium - dependent DNA synthesis in the embryos. On the other hand, the drug only slightly affected the morphological development of the embryos. These results demonstrate that calcium independently affects two different aspects of the embryo development, i.e. DNA synthesis and cell division. It is suggested that the former effect is calmodulin-dependent, while the latter involves the calcium-dependence of metabolite transport through the cell membranes.
EN
The common features of all types of epilepsy are synchronized and uncontrolled discharges of nerve cell assemblies. It is believed that calcium ions play an important role in the generation of epileptic activity. Excessive calcium influx into neurons is the first step toward a seizure. The aim of the present study is to investigate whether the calcium channel blocker nimodipine has anticonvulsive effects. The left cerebral cortex was exposed by craniotomy in anaesthetized rats. An epileptic focus was produced by injection of penicillin G potassium (500 units) into the somatomotor cortex. After the epileptiform activity reached maximum frequency and amplitude; nimodipine was injected into the same area. Application of nimodipine caused an inhibition in the electrocorticograms (ECoG). Solvent alone did not affect the epileptiform activity. The results of this study indicate that nimodipine may have anticonvulsant effects.
EN
Sphingosylphosphorylcholine (SPC) induces a rapid increase of intracellular Ca2+ concentration in isolated synaptosomes. This effect is dose-dependent and is also dependent on extracellular Ca2+. Sphingosine (SPH) has a smaller effect and treatment with psychosine (PSY) is ineffective, which suggests that phosphorylation of the 1-carbon of SPH is required for the SPC to act as a Ca2+ release agonist in synaptosomes. Experiments performed in the presence of heparin or ryanodine indicate that SPC-elicited Ca2+ release is not mediated by IP3 or ryanodine receptors. Finally, our results show that the effect of SPC on Ca2+ concentration is nimodipine-sensitive, suggesting that SPC possibly activates a specific sphingolipid-gated Ca2+ channel in synaptosomes.
EN
This review focuses on the influence of well-known intracellular second messengers on the activity of potassium channels expressed in human T lymphocytes. Basic biophysical properties of the channels are briefly presented. Available data on the regulatory role of intracellular calcium and cyclic AMP is reviewed. Finally, a possible influence of lipid compounds, especially high-density lipoproteins, lysophospholipids and sphingolipids, on the expression and activity of potassium channels in human T lymphocytes is discussed.
Biotechnologia
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2009
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issue 3
85-110
EN
In the somatic cell cloning of pigs, nuclear transfer-derived oocytes are artificially stimulated with the use one of the three experimental protocols: 1) electrical, chemical or physicochemical delayed activation (i.e., post-activation); 2) simultaneous fusion and electrical activation (SF-EA) or simultaneous electrofusion and physicochemical activation, as well as 3) chemical sequential (combined) electrical and chemical activation. In the first activation protocol, somatic cell nuclei at G0/G1 or G2/M stages are introduced into enucleated Metaphase II oocytes (ooplasts), which are activated 30 minutes to several hours after nuclear transfer. In the second activation protocol, somatic cell nuclei at G1 or G0 stage are introduced into non-activated Metaphase II ooplasts and simultaneously obtained clonal nuclear-cytoplasmic hybrids are activated. In turn, the third activation protocol includes the SF-EA followed by an additional treatment of the reconstituted oocytes with chemical factors, which is initiated after a 1.5-2-h delay. The concentration of calcium cations in the fusion/activation medium affects not only the transition from meiotic to mitotic control of cell cycle of clonal cybrids, but also the degree of ploidy of reconstructed zygotes as a result of both emission of second polar body and formation of pseudopronucleus/pseudopronuclei. The artificial stimulation of reconstituted oocytes also determines the processes of architectural remodeling and epigenetic reprogramming of donor cell nuclei in nuclear-transferred embryos. Moreover, the transcriptional and translational activity of genes (eg Oct-3/Oct-4) that are crucial for preimplantation development of porcine cloned embryos is dependent on physicochemical parameters of calcium oscillations induced by activation of clonal nuclear-cytoplasmic hybrids.
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Dysregulation of calcium in Alzheimer's disease

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EN
Multiple efforts has underlined importance of calcium dependent cellular processes in the biochemical characterisation of Alzheimer?s disease (AD), suggesting that abnormalities in calcium (Ca2+) homeostasis might be involved in the pathophysiology of the disease. Studies of the pathogenic mutations in presenilins 1 and 2 (PS1 and PS2) and amyloid precursor protein (APP) responsible for early onset familial AD have estabilished central roles for perturbed cellular Ca2+ homeostasis. Studies of apolipoprotein E (ApoE) neurotoxic effects in AD confirmed involvement of Ca2+-mediated mechanisms. Futher consequences of Ca2+ alterations in AD underline the importance of the ER and mitochondria as the regulatory sites involved in the pathogenesis of neuronal degeneration. Alterations of Ca2+ homeostasis include cells from peripheral tissues, including lymphocytes and fibroblasts from AD donors.
EN
Previous ex vivo experiments by others suggest that elevated body temperature can prime the respiratory burst of human neutrophils. The mechanism of the priming phenomenon induced by temperature has not been addressed so far. Furthermore, the priming temperature range was not defined. In the present study we explored, under in vitro conditions, the influence of febrile.range temperatures on reactive oxygen species (ROS) generation by human peripheral blood neutrophils. ROS production was measured using whole.blood luminol.dependent chemiluminescence. Two elements of signal transduction pathways, calcium and p38 mitogen.activated protein kinase alpha (p38MAPK alpha), frequently underlying neutrophil priming were also examined. Calcium levels in the cytosol of resting and fMLP.stimulated isolated neutrophils were measured with the Fura.2AM spectrofluorimetric method. The activity of p38MAPK alpha was assessed indirectly with a specific inhibitor of the kinase, SB 203580. The study revealed a priming effect at 38?C toward human peripheral blood neutrophil ROS production. Any con. comitant effect on calcium response was not observed. Instead, experiments with SB 203580, a specific inhibitor of p38MAPK alpha, pointed to an increased activity of the kinase as a molecular background of temperature.induced priming. However, the priming effect of temperature was confined to 38?C, while higher temperatures proved to exert no effect (39 and 40?C) or even inhibited ROS generation by neutrophils (43?C). Our study suggests a heterogeneous influence of temperature on human neutrophil functioning, including the prim. ing of the cells by a low.febrile.range temperature. It also suggests a p38MAPK alpha dependent molecular background of the priming phenomenon.
EN
The aim of the study was to identify the causes underlying overgrowth of incisors in chinchillas through an analysis of selected plasma electrolyte concentrations, with particular consideration of minerals involved in the formation of osseous tissue, i.e. Ca,Mg, and P. The analysis involved 40 female standard chinchillasmanaged in a commercial farmsystem, aged 2 to 4 years, divided into two groups of 20 individuals each: D . chinchillas with incisor overgrowth and C . controls with normal dentition. Concentrations of Ca, Mg, and P were measured in blood plasma. The analysis was carried out using ICP OES (inductively coupled plasma optical emission spectrometry) by means of the Optima 2000 DV instrument (Perkin Elmer). The resulting data were analysed statistically using one-way ANOVA with Duncan.s range test. The results show that abnormal metabolism of dental tissue minerals, especially Ca and P, cannot be excluded as the cause of tooth overgrowth in chinchilla.
EN
The aims of this study were (1) to characterize calcium signaling in rat cortex induced by repeated in vitro application of the glutamatergic agonists L-glutamate, NMDA, AMPA and DHPG, (2) to analyze the influence of transient severe hypobaric hypoxia (180 Torr) administered in vivo on calcium responses to stimulation of glutamate receptors by their agonists, and (3) to evaluate the effects of preconditioning with intermittent mild hypobaric hypoxia (360 Torr), 24 h before the severe hypoxia, on these Ca2+ responses. Intracellular Ca2+ dynamics was studied using the fluorescent probes fura-2 and chlortetracycline to monitor free and bound calcium (Cai and Cab), respectively. In control cortical slices, application of L-glutamate, NMDA and AMPA induced concomitant increases in Cai and Cab, reflecting Ca2+ influx and its intracellular accumulation in neurons. DHPG, an agonist of group I mGlu receptors induced a decrease in Cab accompanied by a rise in Cai levels, indicating Ca2+ mobilization. In cortical slices collected 24 h after severe hypoxia, the responses of Cab to glutamate administration were increased, DHPG-induced shifts were reversed, the increase in Cab after the first application of AMPA was reduced, while after the second, Cab rises were potentiated, and the increases in Cab evoked by NMDA application were slightly suppressed. The alterations of responses in Cab to the selective agonists were completely prevented by preconditioning with mild hypoxia. Our results suggest that protection of normal glutamatergic calcium signaling contributes to tolerance to hypoxia induced by preconditioning.
EN
Depolarization of cultured astrocytes by KCl stimulated gamma-aminobutyric acid (GABA) release in a dose-dependent manner. At 60 mM KCl, the stimulatory effect was calcium- and sodium- independent, and was not altered by the presence of beta- alanine. The potassium-evoked GABA release was inhibited by furosemide and 4-acetamido-4'-isothiocyano- -2,2'-stilbene disulfonic acid (SITS), blockers of the chloride transporter across the plasma membrane, as well by chloride ion replacement with glucuronate. Other depolarizing agents, such as veratridine and ouabain, decreased basal GABA release; ouabain also inhibited the stimulatory effect of 60 mM KCl. The high K^+-induced GABA release may affect CNS excitability and may represent an important aspect of glial-neuronal interactions.
EN
One of the most important factors that affect the developmental competences of mammalian somatic cell nuclear transfer (SCNT) embryos is artificial activation of reconstructed oocytes (clonal cybrids). However, calcium signal transduction in a cytosol of such oocytes that has been initiated incorrectly by physical or chemical activating factors (electric pulses or specific ionophore antibiotics) can stimulate not only the development of cloned embryos. It can also induce apoptotic cell death following considerable elevation in intracellular calcium concentration and thereby excitotoxicity of Ca2+ ions. Therefore, the basic objective of this paper is to present the current knowledge on the mechanisms regulating biochemical and biophysical proapoptotic changes within SCNT embryos via the process of excitotoxic calcium signal transmission resulting from an improper artificial activation of clonal cybrid.
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