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1.

001-es BibID:BIBFORM074550
035-os BibID:(WoS)000427631700003 (Scopus)85040654509 (PubMed)29344775
Első szerző:Almássy János (élettanász, biológus, angol-magyar szakfordító)
Cím:New saliva secretion model based on the expression of Na+-K+ pump and K+ channels in the apical membrane of parotid acinar cells / Almássy János, Siguenza Elias, Skaliczki Marianna, Matesz Klara, Sneyd James, Yule David I., Nánási Péter P.
Dátum:2018
ISSN:0031-6768
Megjegyzések:The plasma membrane of parotid acinar cells is functionally divided into apical and basolateral regions. According to the current model, fluid secretion is driven by transepithelial ion gradient, which facilitates water movement by osmosis into the acinar lumen from the interstitium. The osmotic gradient is created by the apical Cl? efflux and the subsequent paracellular Na+ transport. In this model, the Na+-K+ pump is located exclusively in the basolateral membrane and has essential role in salivary secretion, since the driving force for Cl? transport via basolateral Na+?K+?2Cl? cotransport is generated by the Na+-K+ pump. In addition, the continuous electrochemical gradient for Cl? flow during acinar cell stimulation is maintained by the basolateral K+ efflux. However, using a combination of single-cell electrophysiology and Ca2+-imaging, we demonstrate that photolysis of Ca2+ close to the apical membrane of parotid acinar cells triggered significant K+ current, indicating that a substantial amount of K+ is secreted into the lumen during stimulation. Nevertheless, the K+ content of the primary saliva is relatively low, suggesting that K+ might be reabsorbed through the apical membrane. Therefore, we investigated the localization of Na+-K+ pumps in acinar cells. We show that the pumps appear evenly distributed throughout the whole plasma membrane, including the apical pole of the cell. Based on these results, a new mathematical model of salivary fluid secretion is presented, where the pump reabsorbs K+ from and secretes Na+ to the lumen, which can partially supplement the paracellular Na+ pathway.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Parotid acinar cell
Saliva production
Fluid secretion model
Na+-K+ pump
BK channel
maxiK
Gardos channel
Megjelenés:Pflugers Archiv-European Journal Of Physiology. - 470 : 4 (2018), p. 613-621. -
További szerzők:Siguenza, Elias Skaliczki Marianna Matesz Klára (1949-) (anatómus, neurobiológus) Sneyd, James Yule, David I. Nánási Péter Pál (1956-) (élettanász)
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2.

001-es BibID:BIBFORM004134
Első szerző:Almássy János (élettanász, biológus, angol-magyar szakfordító)
Cím:Effects of K-201 on the calcium pump and calcium release channel of rat skeletal muscle / Janos Almassy, Monika Sztretye, Balazs Lukacs, Beatrix Dienes, Laszlo Szabo, Peter Szentesi, Guy Vassort, Laszlo Csernoch, Istvan Jona
Dátum:2008
ISSN:0031-6768
Megjegyzések:The benzothiazepine derivative K-201 has been suggested as a potential therapeutic agent due to its antiarrhythmogenic action. To understand how the drug alters calcium release from the sarcoplasmic reticulum (SR), we investigated its effects on the SR calcium channel and calcium pump by single channel electrophysiology, whole-cell confocal microscopy, and ATPase activity measurements on control and post-myocardial infarcted (PMI) rat skeletal muscle. In bilayers, K-201 induced two subconductance states corresponding to approximately 24% (S(1)) and approximately 13% (S(2)) of the maximum conductance. Dependence of event frequency and of time spent in S(1) and S(2) on the drug concentration was biphasic both in control and in PMI rats, with a maximum at 50 microM. At this concentration, the channel spends 26 +/- 4% and 24 +/- 4%, respectively, of the total time in these subconductance states at positive potentials, while no subconductances are observed at negative potentials. K-201 altered the frequency of elementary calcium release events: spark frequency decreased from 0.039 +/- 0.001 to 0.023 +/- 0.001 s(-1) sarcomere(-1), while the frequency of embers increased from 0.011 +/- 0.001 to 0.023 +/- 0.001 s(-1) sarcomere(-1). Embers with different amplitude levels were observed after the addition of the drug. K-201 inhibited the Ca(2+) ATPase characterized by IC(50,contr) = 119 +/- 21 muM and n (Hill,contr) = 1.84 +/- 0.48 for control and IC(50,PMI) = 122 +/- 18 microM and n (Hill,PMI) = 1.97 +/- 0.24 for PMI animals. These results suggest that although K-201 would increase the appearance of subconductance states, the overall calcium release is reduced by the drug. In addition, the effect of K-201 is identical on calcium release channels from control and PMI rats.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflügers Archiv. - 457 : 1 (2008), p. 171-183. -
További szerzők:Sztretye Mónika (1981-) (élettanász, elektrofiziológus) Lukács Balázs (1978-) (élettanász) Dienes Beatrix (1972-) (élettanász, molekuláris biológus) Szabó László (Románia) Szentesi Péter (1967-) (élettanász) Vassort, Guy Csernoch László (1961-) (élettanász) Jóna István (1948-) (élettanász, fizikus)
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elektronikus változat
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3.

001-es BibID:BIBFORM064954
Első szerző:Balajthy András (általános orvos)
Cím:7DHC-induced changes of Kv1.3 operation contributes to modified T cell function in Smith-Lemli-Opitz syndrome / András Balajthy, Sándor Somodi, Zoltán Pethő, Mária Péter, Zoltán Varga, Gabriella P. Szabó, György Paragh, László Vígh, György Panyi, Péter Hajdu
Dátum:2016
ISSN:0031-6768
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflügers Archiv. - 468 : 8 (2016), p. 1403-1418. -
További szerzők:Somodi Sándor (1977-) (belgyógyász) Pethő Zoltán (1989-) (orvos) Péter Mária Varga Zoltán (1969-) (biofizikus, szakfordító) P. Szabó Gabriella (1975-) (csecsemő- és gyermekgyógyász, klinikai genetikus) Paragh György (1953-) (belgyógyász) Vígh László (orvos Szeged) Panyi György (1966-) (biofizikus) Hajdu Péter (1975-) (biofizikus)
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4.

001-es BibID:BIBFORM073604
Első szerző:Bányász Tamás (élettanász)
Cím:Beta-adrenergic stimulation reverses the I Kr-I Ks dominant pattern during cardiac action potential / Tamas Banyasz, Zhong Jian, Balazs Horvath, Shaden Khabbaz, Leighton T. Izu, Ye Chen-Izu
Dátum:2014
ISSN:0031-6768
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflugers Archiv-European Journal of Physiology. - 466 : 11 (2014), p. 2067-2076. -
További szerzők:Jian, Zhong Horváth Balázs (1981-) (élettanász) Khabbaz, Shaden Izu, Leighton T. Chen-Izu, Ye
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5.

001-es BibID:BIBFORM040778
Első szerző:Batta József Tamás (fül-orr-gégész)
Cím:Active and passive behaviour in the regulation of stiffness of the lateral wall in outer hair cells of the guinea-pig / Batta, T. J., Panyi, G., Gaspar, R., Sziklai, I.
Dátum:2003
ISSN:0031-6768
Megjegyzések:The stiffness of the outer hair cell (OHC) lateral wall, measured by the micropipette aspiration technique, is non-linear, decreasing from the ciliary pole (stiffness parameter Sp 1.83+/-0.13 nN/microm n=10) towards the cell base (Sp 1.14+/-0.16 nN/microm, n=10) irrespective of the cochleoapical or cochleobasal origin of the cells. The length of the aspirated lateral wall segment was related exponentially to the duration of the applied negative pressure (6 cm H2O) in the synaptic region of the OHCs whereas an active, sigmoid component was observed between 30 and 60 s in the supranuclear regions. A significant increase of the midlateral wall stiffness (to 1.91+/-0.23 nN/microm; n=10) was observed in calcium-free medium and the sigmoid component of the response of the lateral wall was abolished. Salicylate (5 mM) had no significant effect on the active sigmoid behaviour of the lateral wall (n=10). Gadolinium (5 mM), a non-specific cation channel blocker, increased the stiffness of the lateral wall and attenuated the active component (n=10). The motor protein prestin thus does not seem to be involved in the active stiffness regulation seen in this study. A role for the cortical cytoskeleton in the regulation of stiffness seems reasonable according to our model. The mechanism may involve calcium-dependent metabolic modification of cytoskeletal or membrane proteins.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflugers Archiv. - 447 : 3 (2003), p. 328-336. -
További szerzők:Panyi György (1966-) (biofizikus) Gáspár Rezső (1944-) (biofizikus) Sziklai István (1954-) (fül-orr-gégész)
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6.

001-es BibID:BIBFORM040112
Első szerző:Collet, Claude
Cím:Effects of extracellular ATP on freshly isolated mouse skeletal muscle cells during pre-natal and post-natal development / Collet Claude, Strube Caroline, Csernoch Laszlo, Mallouk Nora, Ojeda Carlos, Allard Bruno, Jacquemond Vincent
Dátum:2002
ISSN:0031-6768
Megjegyzések:Extracellular adenosine 5'-triphosphate (ATP) has profound effects on membrane conductance and on the intracellular free [Ca(2+)] ([Ca(2+)](i)) in cultured skeletal muscle cells. The aim of the present study was to examine the occurrence and to characterize the properties of such responses during mammalian muscle development in vivo. The effect of ATP (0.2 mM) was tested on membrane current and [Ca(2+)](i) in freshly isolated pre- and post-natal mouse skeletal muscle cells. Pre-natal cells were from 14- to 19-day-old fetuses. In pre- and early post-natal cells, very small elevations of [Ca(2+)](i) (<50 nM) following ATP application could be detected with the fluorescent indicator fura-2. A clear subsarcolemmal rise in [Ca(2+)] was however associated to the presence of ATP, as demonstrated by increased activity of plasma membrane Ca(2+)-activated K(+) channels in cells bathed in a depolarizing, high-calcium-containing solution. In cells voltage-clamped at -80 mV in external Tyrode, ATP induced an inward current associated with an increased membrane conductance. The mean maximal amplitude of the ATP-induced current was -0.84 +/- 0.07 A/F ( n=39). The response to ATP was still present after birth, although its amplitude tended to decrease with post-natal development and was completely absent in muscle cells from 3- to 6-month-old mice. The ATP-induced current could be abolished reversibly by suramin. Our results suggest that, over the range of developmental stages examined, skeletal muscle cells display an ionotropic purinergic signalling pathway with functional properties qualitatively consistent with what is observed in cultured myotubes.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflugers Archiv-European Journal Of Physiology. - 443 : 5-6 (2002), p. 771-778. -
További szerzők:Strube, Caroline Csernoch László (1961-) (élettanász) Mallouk, Nora Ojeda, Carlos Allard, Bruno Jacquemond, Vincent
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7.

001-es BibID:BIBFORM004135
Első szerző:Cseri Julianna (laboratóriumi diagnosztika szakorvos)
Cím:A purinergic signal transduction pathway in mammalian skeletal muscle cells in culture / Julianna Cseri, Henrietta Szappanos, Gyula Péter Szigeti, Zoltán Csernátony, László Kovács, László Csernoch
Dátum:2002
ISSN:0031-6768
Megjegyzések:The effects of adenosine 5'-triphosphate (ATP) on human and mouse skeletal muscle fibres in primary culture were investigated. ATP-evoked changes in intracellular calcium concentration ([Ca(2+)](i)) were measured and compared with those induced by agonists of the nicotinic acetylcholine (Ach)- and P2X purinoreceptors. While ATP was effective on both myoblasts and multi-nucleated myotubes in the micromolar range, Ach failed to induce any change in [Ca(2+)](i) at early stages of development. In contrast, myofibres with peripheral nuclei showed little response to ATP but responded to Ach with a large change in [Ca(2+)](i). The responsiveness of the myotubes to Ach paralleled that to potassium. The removal of external calcium abolished the response to ATP. P2X receptor agonists mimicked the response to ATP with the order of potency being ATP>2',3'- O-(4-benzoyl)-benzoyl-ATP>beta,gamma-methylene-ATP>alpha,beta-methylene-ATP. Under voltage-clamp conditions ATP induced an inward current that showed little inactivation. These results are consistent with the existence of P2X receptor-mediated signal transduction pathway in cultured mammalian skeletal muscle cells.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflügers Archiv. - 443 : 5-6 (2002), p. 731-738. -
További szerzők:Szappanos Henrietta (1976-) (biológus, élettanász) Szigeti Gyula (1969-) (élettanász, elektrofiziológus) Csernátony Zoltán (1959-2023) (ortopéd sebész, traumatológus) Kovács László (1939-) (élettanász) Csernoch László (1961-) (élettanász)
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8.

001-es BibID:BIBFORM001079
Első szerző:Csernoch László (élettanász)
Cím:Sparks and embers of skeletal muscle : the exciting events of contractile activation / László Csernoch
Dátum:2007
ISSN:0031-6768
Megjegyzések:Intracellular calcium concentration ([Ca(2+)](i)) is a key player in a wide range of cellular functions from long-term effects that determine the fate of the cell to immediate responses as secretion and motility. To initiate contraction, calcium ions in skeletal muscle are released into the myoplasm through the calcium channels, the ryanodine receptors, of the sarcoplasmic reticulum. The opening of these channels give rise to localised increases in [Ca(2+)](i), originally termed calcium sparks, that fuse and generate the global calcium transient. Whereas calcium sparks in amphibians are abundant and stereotyped, events in mammalian skeletal muscle are scarce and morphologically diverse. This review compares the different forms of calcium release events, occurring spontaneously or evoked by a depolarising pulse, observed in the different classes of vertebrates. It then addresses the questions whether or not these events can be considered as elementary and how the global calcium transient can be reconstructed from them.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflügers Archiv. - 454 : 6 (2007), p. 869-878. -
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9.

001-es BibID:bibEBI00019167
Első szerző:Deli Tamás (szülész-nőgyógyász, endokrinológus szakorvos)
Cím:Contribution from P2X and P2Y purinoreceptors to ATP-evoked changes in intracellular calcium concentration on cultured myotubes / Tamás Deli, Henrietta Szappanos, Gyula Péter Szigeti, Julianna Cseri, László Kovács, László Csernoch
Dátum:2007
ISSN:0031-6768
Megjegyzések:Although the alteration of purinoreceptor pattern on skeletal muscle is known to accompany physiological muscle differentiation and the pathogenesis of muscle dystrophy, the exact identity of and the relative contribution from the individual receptor subtypes to the purinergic signal have been controversial. To identify these subtypes in cultured myotubes of 5-10 nuclei, changes in intracellular calcium concentration and surface membrane ionic currents were detected and calcium fluxes calculated after the application of the subtype-specific agonists 2'3'-O-(benzoyl-4-benzoyl)-ATP (BzATP), 2-methyltio-ADP and UTP. The effectiveness of these agonists together with positive immunocytochemical staining revealed the presence of P2X(4), P2X(5), P2X(7), P2Y(1) and P2Y(4) receptors. siRNA-reduced protein expression of P2X(5), P2X(7) and P2Y(1) receptors was accompanied by reduction in the ATP-evoked calcium transients. Furthermore, anti-P2X(7) siRNA caused a significant drop in the early peak and delayed steady component of the calculated calcium flux. The use of its antagonist, oxidized ATP, similarly to transfection with anti-P2X(7) siRNA caused significant reduction in the agonist-elicited ionic currents I (ATP) and I (BzATP), with a greater drop in the latter. Our results demonstrate that the activation of ionotropic P2X(4), P2X(5) and P2X(7) and metabotropic P2Y(1) and P2Y(4) purinoreceptors participates in forming the calcium transients of multinucleated myotubes.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflügers Archiv. - 453 : 4 (2007), p. 519-529. -
További szerzők:Szappanos Henrietta (1976-) (biológus, élettanász) Szigeti Gyula (1969-) (élettanász, elektrofiziológus) Cseri Julianna (1949-2022) (laboratóriumi diagnosztika szakorvos) Kovács László (1939-) (élettanász) Csernoch László (1961-) (élettanász)
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Szerző által megadott URL
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10.

001-es BibID:BIBFORM040598
Első szerző:Ebus, J.
Cím:Effects of MgATP on ATP utilization and force under normal and simulated ischaemic conditions in rat cardiac trabeculae / J. Ebus, Z. Papp, R. Zaremba, G. J. Stienen
Dátum:2001
ISSN:0031-6768
Megjegyzések:The dependency of ATP utilization and isometric force on [MgATP] was studied in skinned rat trabeculae under normal (pH 7.0) and simulated ischaemic (pH 6.2, 30 mM added Pi) conditions at 20+/-1 degrees C. At saturating [Ca2+], mean (+/-SEM) ATP utilization at 5 mM MgATP (A0) was 0.48+/-0.03 mM/s and force (F0) was 37+/-2 kN/m2. At 10 microM MgATP under normal conditions ATP utilization decreased gradually to 66+/-3% of A0, and force increased to 169+/-7% of F0. Under ischaemic conditions at 10 microM MgATP, ATP utilization decreased from 30+/-5% to 11+/-2% of A0 whereas force increased eightfold from 12+/-4% to 97+/-7% of F0. The [MgATP] at half-maximal ATP utilization (Km) under ischaemic conditions was 21+/-3 microM. At pH 7.0, Km was estimated to be less than 10 microM. These results show that tension cost decreases markedly with decreasing MgATP. Under ischaemic conditions parallel changes in Ca2+ sensitivity of force and ATP utilization were observed, corresponding to 1.3 pCa units. Reducing [MgATP] from 0.5 to 0.05 mM caused a modest reversal of this change in Ca2+ sensitivity. These changes in Ca2+ sensitivity are consistent with a marked reduction in active force and force-related ATP utilization during ischaemia but are insufficient to explain the ischaemic contracture on the basis of active force development.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflugers Archiv-European Journal Of Physiology. - 443 : 1 (2001), p. 102-111. -
További szerzők:Papp Zoltán (1965-) (kardiológus, élettanász) Zaremba, Ruud Stienen, Ger J. M.
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11.

001-es BibID:BIBFORM062647
Első szerző:Egger, Marcel
Cím:Refractoriness of SR-Calcium release after betaadrenergic stimulation in cardiac myocytes / M. Egger, C. Pignier, P. Szentesi, E. Niggli
Dátum:2003
ISSN:0031-6768
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
Megjelenés:Pflügers Archiv. - 445 : Suppl. 1 (2003), p. S35. -
További szerzők:Pignier, Christophe Szentesi Péter (1967-) (élettanász) Niggli, Ernst
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12.

001-es BibID:BIBFORM057717
Első szerző:González Rodríguez, Estela
Cím:Phosphoinositide substrates of myotubularin affect voltage-activated Ca2+ release in skeletal muscle / Estela González Rodríguez, Romain Lefebvre, Dóra Bodnár, Claude Legrand, Peter Szentesi, János Vincze, Karine Poulard, Justine Bertrand-Michel, Laszlo Csernoch, Anna Buj-Bello, Vincent Jacquemond
Dátum:2014
ISSN:0031-6768
Megjegyzések:Skeletal muscle excitation?contraction (E?C) couplingis altered in several models of phosphatidylinositol phosphate(PtdInsP) phosphatase deficiency and ryanodine receptoractivity measured in vitro was reported to be affected by certainPtdInsPs, thus prompting investigation of the physiologicalrole of PtdInsPs in E?C coupling. We measured intracellularCa2+ transients in voltage-clamped mouse muscle fibresmicroinjected with a solution containing a PtdInsP substrate(PtdIns(3,5)P2 or PtdIns(3)P) or product (PtdIns(5)P orPtdIns) of the myotubularin phosphatase MTM1. No significantchange was observed in the presence of either PtdIns(5)Por PtdIns but peak SR Ca2+ release was depressed by ~30%and50% in fibres injected with PtdIns(3,5)P2 and PtdIns(3)P,respectively, with no concurrent alteration in the membranecurrent signals associated with the DHPR function as well asin the voltage dependence of Ca2+ release inactivation. Inpermeabilized muscle fibres, the frequency of spontaneousCa2+ release events was depressed in the presence of the threetested phosphorylated forms of PtdInsP with PtdIns(3,5)P2being the most effective, leading to an almost complete disappearanceof Ca2+ release events. Results support the possibilitythat pathological accumulation of MTM1 substrates mayacutely depress ryanodine receptor-mediated Ca2+ release.Overexpression of a mCherry-tagged form of MTM1 in musclefibres revealed a striated pattern consistent with the triadicarea. Ca2+ release remained although unaffected by MTM1overexpression and was also unaffected by the PtdIns-3-kinaseinhibitor LY2940002, suggesting that the 3-phosphorylatedPtdIns lipids active on voltage-activated Ca2+ release are inherentlymaintained at a low level, inefficient on Ca2+ releasein normal conditions.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Calcium homeostasis
Excitation-contraction coupling
Ryanodine receptor
Sarcoplasmic reticulum Ca2+ release
Phosphatidylinositol phosphate
Megjelenés:Pflugers Archiv-European Journal Of Physiology. - 466 : 5 (2014), p. 973-985. -
További szerzők:Lefebvre, Romain Bodnár Dóra (1987-) (molekuláris biológus) Legrand, Claude Szentesi Péter (1967-) (élettanász) Vincze János (1988-) (orvos) Poulard, Karine Bertrand-Michel, Justine Csernoch László (1961-) (élettanász) Buj-Bello, Anna Jacquemond, Vincent
Pályázati támogatás:OTKA-K107765
OTKA
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