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The anaesthetic, narcotic effect of magnesium has been discussed since the publication of Meltzer-Auger (1906), but its mechanism has not been clarified. Since then, other investigations have also been performed, but none of the publications has explained the issue. We propose a mechanism analogous to the studies made by Feinstein (1964), who examined organic compounds showing anaesthetic effects. Our view is that magnesium abridges two phospholipids of the opposite sides of the membrane through their phosphate groups. This binding results in membrane rigidity, which makes the ion permeability provided by the ion channel and/or carrier decrease or discontinue, thus the halting of the Na+, K+ and Ca2+ ion flow eventually causes an anaesthetic effect. Another possible pathway is that magnesium ions block the activity of N-methyl-D-aspartate (NMDA) receptor to control the ion channel, which also lowers the permeability of the membrane.
It remains unclear whether enhanced ion fluxes occur in the esophageal stratified squamous epithelium upon acid exposure. Rat esophageal tissues devoid of submucosal glands displayed basal short-circuit current (Isc) of 5.03 ± 1.93 µA/cm2 and lumen-negative potential difference (PD) in association with net absorption of Na+ and Cl-, and secretion of HCO3-. Luminal hydrochloric acid (HCl) challenge (pH = 1.6) triggered an acute rise of the Isc and increment of negative PD to seven-fold of baseline, which was diminished in HCO3--free, but not Na+- free buffer. The rise of Isc was inhibited by pretreatment with di-isothiocyanatostilbene-2, 2'-disulphonic acid (DIDS) and 5-(N-ethyl-N-isopropyl)-amiloride (EIPA). Topical carbachol, capsaicin, forskolin or CFTRinh-172 had no effect on basal Isc. CFTRinh-172 did not reduce the acid-increased Isc. Functional ablation of capsaicin-sensitive nerves had no effect on the acid-induced Isc. The phenomenon of enhanced ion fluxes upon acid stimulation was confirmed in human esophageal specimens. Our results demonstrated that the mechanism of acid-induced rapid transepithelial ion fluxes is dependent on the presence of bicarbonate ions as well as functional anion transporters and Na+/H+ exchanger, but independent of cystic fibrosis transmembrane conductance regulator (CFTR). The capsaicin-sensitive and muscarinic-dependent nerve pathways did not play roles in the mechanism.
Syntheses of biomimetic low-molecular weight poly-(R)-3-hydroxybutanoate mediated by three types of supramolecular catalysts are presented. The utility of these synthetic polyesters for preparation of artificial channels in phospholipid bilayers capable of sodium and calcium ion transport across cell membranes, is discussed. Further studies on possible applications of these bio-polymers for manufacturing drugs of prolonged activity are under way.
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Biochemistry of magnesium

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Magnesium is essential for biochemical functions of cells. Since Mg2+ has a relatively low ionic radius in proportion to the size of the nucleus (0.86 versus 1.14 f A for Ca2+), it shows exceptional biochemical activity. Due to its physicochemical properties, intracellular magnesium can bind to the nucleus, ribosomes, cell membranes or macromolecules occurring in the cell’s cytosol. It is indispensable for the nucleus to function as a whole and for the maintenance of physical stability as well as aggregation of rybosomes into polysomes able to initiate protein synthesis. Mg2+ can also act as a cofactor for ribonucleic acid enzymes (ribozymes) capable of specifically recognizing and cleaving the target mRNA. As an essential cofactor in NER, BER, MMR processes, Mg2+ is required for the removal of DNA damage. An activator of over 300 different enzymes, magnesium participates in many metabolic processes, such as glycolysis, Krebs cycle, β-oxidation or ion transport across cell membranes. Mg2+ plays a key role in the regulation of functions of mitochondria, including the control of their volume, composition of ions and ATP production.
Work by Ramsay in the 1950’s established the foundations for our current understanding of primary urine production by Malpighian tubules and we now have detailed knowledge of the epithelial transport processes underlying fluid secretion. Identified neuropeptides and biogenic amines have been shown to stimulate fluid secretion and, for some, detailed information is available on the second messenger pathways and transport processes they activate. There are significant gaps in our knowledge, however, particularly concerning the role of identified diuretics in vivo. The hormonal status of many has yet to be established and it is also unclear whether they are used to control different types of diuresis.
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Ion transport in rabbit caecum at 12 and 36 months of age

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The aim of this study was to investigate the effect of aging on sodium and chloride ions transport in the isolated rabbit coecum. The experiment consisted in measuring PD- transepithelial electrical potential difference mV SM-mechanical stimulation and mechano-sensitivity (dPD) in collected from 12- and 36-month-old rabbits. A modified Ussing system was used for the experiment. Under the incubation in Ringer solution the values of PD and dPD of young rabbit caecum were, respectively, -3.0 ±0.4 mV and -1.2 ±0.3 mV. In 36-month rabbits, on the other hand, the values of these parameters were lower, PD by about 90% whereas dPD by about 83%. Incubation of young rabbits caecum with the presence of amiloride resulted in a reduction of PD by about 17 % and dPD by about 50%, while it did not influence the electrophysiological parameters of caecum in 36-month rabbits. Incubation with bumetanide on young rabbits caecum resulted in PD dropped by about 70% and dPD by about 83%. In the same incubation conditions as those applied for incubation of 36-month rabbits caecum, the level of PD decreased by about 67% while dPD by about 50%. Incubation of young rabbits caecum at the presence of both transport inhibitors resulted in PD decreased by about 87% and dPD by about 83%, whereas that applied for the old rabbits' caecum reduced PD by about 90%, without influencing dPD. Presented data demonstrate that the process of organism ageing inhibits sodium ion transport as well as reduces caecum epithelium sensitivity to mechanical stimuli. Probably, it is a consequence of a reduced with age release of neurotransmitter from sensory terminals; these neurotransmitters modify transepithelial ion transport.
Double-barrelled ion-selective microelectrodes were used to measure Na+, K+ and Cl- activities in the principal cells of cricket Malpighian tubules, allowing electrochemical gradients across apical and basal membranes to be calculated. At the basal membrane, K+ and Cl- gradients support passive exit into the bathing medium. A thermodynamic analysis shows both ions can be taken up by Na+/K+/2Cl- cotransport driven by a favourable Na+ gradient. At the apical membrane, cations are actively transported into the lumen whereas Cl- moves passively. Evidence is presented to show that diuretic kinins open an apical membrane Cl- conductance whereas Achdo-DH acts via cAMP to stimulate the basal membrane NKCC.
The influence of voltage on ionic transport through a high conductance locust K+ channel (BK channel) has been investigated. The nature of ionic flow has been examined by power spectrum, Hurst analysis, generalised entropy and surrogate data sets. The ordering influence of voltage on ionic current behaviour has been found.
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