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1.

001-es BibID:BIBFORM049412
Első szerző:Almássy János (élettanász, biológus, angol-magyar szakfordító)
Cím:Miocardial infarct induced changes of skeletal type SR calcium channel (RyR1) / J. Almássy, G. Vassort, I. Jóna
Dátum:2006
Megjegyzések:In heart failure (HF) skeletal muscle weakness and fatigue develop that could be explained by decreased Ca2+ content of the sarcoplasmic reticulum (SR) concomitant reduction of calcium transients' amplitude, indicating the impaired balance of calcium transport mechanisms. The aim of the present study was to identify putative functional RyR1 changes contributing to the reduced Ca2+ content of the SR.Single RyR1 Ca2+-release channels from rats with HF were reconstituted into planar lipid bilayer and gating behaviour of incorporated channels was studied under voltage-clamp conditions. 1/3 of these channels showed 40% higher conductance compared to RyRs from control rats and the voltage dependency of channel conductance altered, showing still ohmic but polarity dependent conductance characterized by 785 ? 28 pS for positive and 575 ? 31 pS for negative polarity. Altered Ca2+-dependency of channel activity was also observed on RyRs from HFafflicted rats, such as enhanced calcium activation and reduced calcium inhibition.
Tárgyszavak:Természettudományok Biológiai tudományok idézhető absztrakt
calcium release
Megjelenés:Journal of Muscle Research and Cell Motility. - 27 (2006), p. 521. -
További szerzők:Vassort, Guy Jóna István (1948-) (élettanász, fizikus)
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2.

001-es BibID:BIBFORM070675
Első szerző:Fodor János (élettanász, biotechnológus)
Cím:Follistatin treatment suppresses SERCA1b levels independently of other players of calcium homeostasis in C2C12 myotubes / Fodor János, Gomba-Tóth Adrienn, Oláh Tamás, Almássy János, Zádor Ernő, Csernoch László
Dátum:2017
ISSN:0142-4319
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Muscle Research And Cell Motility 1 (2017), p. 1-15. -
További szerzők:Gomba-Tóth Adrienn Oláh Tamás (1983-) (élettanász) Almássy János (1981-) (élettanász, biológus, angol-magyar szakfordító) Zádor Ernő (1954-) Csernoch László (1961-) (élettanász)
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3.

001-es BibID:BIBFORM049410
Első szerző:Sárközi Sándor (élettanász)
Cím:Effects of a calcium chelator TPEN on sarcoplasmic reticulum calcium release ryanodine receptor channel / S. Sarkozi, J. Almassy, C. Szegedi, I. Jona
Dátum:2005
Megjegyzések:The aim of the study was to determine the effects of a widely used calcium and zinc chelator TPEN (N,N,N?,N?-Tetrakis (2-pyridylmethyl) ethylendiamine) on skeletal muscle sarcoplasmic reticulum (SR) Ca2+ release channel (RyR). Investigations of TPEN-buffered glioblastoma cells resulted in controversial consequences raised the question if TPEN has any influence on the Ca2+ transport mechanisms of the SR. To clarify if RyRs are concerned in the putative action of TPEN isolated Ca2+ release channels were reconstituted into planar lipid bilayers and the gating behaviour of incorporated channels was studied. TPEN altered the RyR gating in a dose-, polarity- and voltage-dependent manners. These effects were proved to be dual:if the applied holding potential induced current was opposite of the direction occurring physiologically through the RyR TPEN closed the channel in potential dependent way. This result suggests that positively charged TPEN works as a plug and acting so directly blocks RyR's pore. Oppositely, when the direction of the current flowing through the incorporated RyR was of the same during Ca2+ release from SR TPEN slightly activated RyR by increasing the open probability of the channel.
Tárgyszavak:Természettudományok Biológiai tudományok idézhető absztrakt
calcium release
Megjelenés:Journal of Muscle Research and Cell Motility. - 26 (2005), p. 62. -
További szerzők:Almássy János (1981-) (élettanász, biológus, angol-magyar szakfordító) Szegedi Csaba Jóna István (1948-) (élettanász, fizikus)
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4.

001-es BibID:BIBFORM001050
Első szerző:Sárközi Sándor (élettanász)
Cím:Effect of natural phenol derivatives on skeletal type sarcoplasmic reticulum Ca2+ -ATPase and ryanodine receptor / Sárközi S., Almássy J., Lukács B., Dobrosi N., Nagy G., Jóna I.
Dátum:2007
Megjegyzések:The effect of natural phenol derivatives was studied on skeletal type sarcoplasmic reticulum Ca2+-ATPase and ryanodine receptor. The majority of the tested derivatives exerted inhibitory effect on the Ca2+-ATPase with an ascending sequence in regard to their effectiveness (IC50): cineole (3.33 mM) < ortho-vanillin (IC50 =1.13 mM) < 4-methyl-2-nitrophenol (1104 mu M) < vanillin (525 mu M) < thymol (224 mu M) < carvacrol (162 mu M). In two cases biphasic characteristic was observed: trans-anethole and meta-anisaldehyde first caused activation followed by inhibition (with IC50-s of 141 and 1903 mu M respectively) as their concentration was increased. In some cases (cineole, ortho-vanillin, meta-anisaldehyde) total inhibition of Ca2+-ATPase could not be reached as the result of the limited solubility of these drugs. Para-anisaldehyde and 6-amino-meta-cresol did not show any effect up to 3 mM. In Ca2+ release experiments drugs were applied on heavy sarcoplasmic reticulum vesicles isolated from skeletal muscle and actively loaded with calcium. Only thymol and carvacrol were able to evoke Ca2+ release with EC50 values of 158 +/- 16 and 211 +/- 55 mu M respectively. Futhermore the effect of thymol and carvacrol was tested on the isolated ryanodine receptor incorporated into artificial lipid bilayer. Both drugs activated the RyR when applied in concentrations identical to their EC50 values. These observations show that small differences in the structure of phenol derivatives sometimes have little impact on their effect on the sarcoplasmic reticulum Ca2+-ATPase or ryanodine receptor (thymol and carvacrol) whereas in certain cases they can completely abolish a particular effect (para- and meta-anysaldehide).
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Journal of Muscle Research and Cell Motility 28 (2007), p. 167-174. -
További szerzők:Almássy János (1981-) (élettanász, biológus, angol-magyar szakfordító) Lukács Balázs (1978-) (élettanász) Dobrosi Nóra (1981-) (molekuláris biológus) Nagy Georgina (1980-) (orvosbiológus) Jóna István (1948-) (élettanász, fizikus)
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5.

001-es BibID:BIBFORM049411
Első szerző:Szentesi Péter (élettanász)
Cím:Mutations in the scorpion toxin maurocalcine alter its ability to modify the calcium release events in frog skeletal muscle / P. Szentesi, J. Almássy, M. Fehér, B. Dienes, C. A. Simut, I. Jona, M. Ronjat, L. Csernoch
Dátum:2006
Megjegyzések:Maurocalcine (MCa), a 33 amino acid toxin obtained from the venom of Scorpio Maurus Palmatus, has been shown to interact with the isolated skeletal-type ryanodine receptor (RyR1) and to strongly modify its calcium channel gating. In this study, we explored the effects of MCa and its mutants (Lys8Ala, Lys19Ala and Lys22Ala) on elementary calcium release events in frog skeletal muscle fibers.Fibers were mechanically dissected, chemically skinned with saponin and imaged by a laser scanning confocal microscope in line scan mode in the presence of MCa and its mutants.Long lasting spontaneous calcium release events (embers), were observed after the addition of the toxins which were never seen under control conditions. Two typical forms of embers: with or without a classical spark were identified. The length of the embers correlated well with the duration of the long lasting sub-conductance states seen on MCa-modified RyR1-s incorporated into planar lipid bilayers. In particular, the Lys8Ala and Lys19Ala mutants had similar effects as the wild type MCa and produced long (430.9 ? 42.9, 442.6 ? 19.4 ms), while the Lys22Ala mutant induced shorter (65.3 ? 7.5 ms) events. Our observations indicate that the results from artificial lipid bilayer experiments mimic the in situ effects of MCa on RyR. We propose that an ember reflects the calcium release from a single release unit modified by the toxin.
Tárgyszavak:Természettudományok Biológiai tudományok idézhető absztrakt
calcium release
Megjelenés:Journal of Muscle Research and Cell Motility. - 27 (2006), p. 516. -
További szerzők:Almássy János (1981-) (élettanász, biológus, angol-magyar szakfordító) Fehér Miklós Dienes Beatrix (1972-) (élettanász, molekuláris biológus) Simut, Cecilia Jóna István (1948-) (élettanász, fizikus) Ronjat, Michel Csernoch László (1961-) (élettanász)
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6.

001-es BibID:BIBFORM060298
Első szerző:Vincze János (orvos)
Cím:Effects of fluvastatin and coenzyme Q10 on skeletal muscle in normo- and hypercholesterolaemic rats / J. Vincze, Á. Jenes, M. Fűzi, J. Almássy, R. Németh, G. Szigeti, B. Dienes, Z. Gaál, P. Szentesi, I. Jóna, P. Kertai, G. Paragh, L. Csernoch
Dátum:2015
ISSN:0142-4319
Megjegyzések:Myalgia and muscle weakness may appreciably contribute to the poor adherence to statin therapy. Although the pathomechanism of statin-induced myopathy is not completely understood, changes in calcium homeostasis and reduced coenzyme Q10 levels are hypothesized to play important roles. In our experiments, fluvastatin and/or coenzyme Q10 was administered chronically to normocholesterolaemic or hypercholaestherolaemic rats, and the modifications of the calcium homeostasis and the strength of their muscles were investigated. While hypercholesterolaemia did not change the frequency of sparks, fluvastatin increased it on muscles both from normocholesterolaemic and from hypercholesterolaemic rats. This effect, however, was not mediated by a chronic modification of the ryanodine receptor as shown by the unchanged ryanodine binding in the latter group. While coenzyme Q10 supplementation significantly reduced the frequency of the spontaneous calcium release events, it did not affect their amplitude and spatial spread in muscles from fluvastatin-treated rats. This indicates that coenzyme Q10 supplementation prevented the spark frequency increasing effect of fluvastatin without having a major effect on the amount of calcium released during individual sparks. In conclusion, we have found that fluvastatin, independently of the cholesterol level in the blood, consistently and specifically increased the frequency of calcium sparks in skeletal muscle cells, an effect which could be prevented by the addition of coenzyme Q10 to the diet. These results support theories favouring the role of calcium handling in the pathophysiology of statin-induced myopathy and provide a possible pathway for the protective effect of coenzyme Q10 in statin treated patients symptomatic of this condition.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Skeletal muscle
Calcium homeostase
Force
Spark
Statin
Q10
Myopathy Intr
Megjelenés:Journal Of Muscle Research And Cell Motility 36 : 3 (2015), p. 263-274. -
További szerzők:Jenes Ágnes (1980-) (élettanász) Füzi Márta (1980-) (élettanász) Almássy János (1981-) (élettanász, biológus, angol-magyar szakfordító) Németh Renáta Szigeti Gyula (1969-) (élettanász, elektrofiziológus) Dienes Beatrix (1972-) (élettanász, molekuláris biológus) Gaál Zsuzsanna (1990-) (csecsemő-és gyermekgyógyász központi gyakornok) Szentesi Péter (1967-) (élettanász) Jóna István (1948-) (élettanász, fizikus) Kertai Pál (1927-2016) (népegészségügyi szakember) Paragh György (1953-) (belgyógyász) Csernoch László (1961-) (élettanász)
Pályázati támogatás:OTKA-K81923
OTKA
TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
TÁMOP- 4.2.2.A-11/1/KONV-2012-0025
TÁMOP
TÁMOP-4.2.4.A/2-11/1-2012-0001
TÁMOP
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