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tom 51
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nr 1
55-74
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.
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.
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Content available remote Dysregulation of calcium in Alzheimer's disease
88%
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.
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Content available remote Anticonvulsive effects of nimodipine on penicillin-induced epileptiform activity
88%
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
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.
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Content available remote Sphingolipid derivatives modulate intracellular Ca2+ in rat synaptosomes
88%
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
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
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.
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