CCL

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1.

001-es BibID:BIBFORM004070
Első szerző:Bányász Tamás (élettanász)
Cím:Transformation of adult rat cardiac myocytes in primary culture / Bányász T., Lozinskiy I., Payne C. E., Edelmann S., Norton B., Chen B., Chen-Izu Y., Izu L.T., Balke C. W.
Dátum:2008
Megjegyzések:We characterized the morphological, electrical and mechanical alterations of cardiomyocytes in long-term cell culture. Morphometric parameters, sarcomere length, T-tubule density, cell capacitance, L-type calcium current (I(Ca,L)), inward rectifier potassium current (I(K1)), cytosolic calcium transients, action potential and contractile parameters of adult rat ventricular myocytes were determined on each day of 5 days in culture. We also analysed the health of the myocytes using an apoptotic/necrotic viability assay. The data show that myocytes undergo profound morphological and functional changes during culture. We observed a progressive reduction in the cell area (from 2502 +/- 70 microm(2) on day 0 to 1432 +/- 50 microm(2) on day 5), T-tubule density, systolic shortening (from 0.11 +/- 0.02 to 0.05 +/- 0.01 microm) and amplitude of calcium transients (from 1.54 +/- 0.19 to 0.67 +/- 0.19) over 5 days of culture. The negative force-frequency relationship, characteristic of rat myocardium, was maintained during the first 2 days but diminished thereafter. Cell capacitance (from 156 +/- 8 to 105 +/- 11 pF) and membrane currents were also reduced (I(Ca,L), from 3.98 +/- 0.39 to 2.12 +/- 0.37 pA pF; and I(K1), from 34.34p +/- 2.31 to 18.00 +/- 5.97 pA pF(-1)). We observed progressive depolarization of the resting membrane potential during culture (from 77.3 +/- 2.5 to 34.2 +/- 5.9 mV) and, consequently, action potential morphology was profoundly altered as well. The results of the viability assays indicate that these alterations could not be attributed to either apoptosis or necrosis but are rather an adaptation to the culture conditions over time.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Experimental Physiology 93 : 3 (2008), p. 370-382. -
További szerzők:Lozinskiy, Ilya Payne, Charles E. Edelmann, Stephanie Norton, Byron Chen, Biyi Chen-Izu, Ye Izu, Leighton T. Balke, C. William
Internet cím:elektronikus változat
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2.

001-es BibID:BIBFORM001017
Első szerző:Bányász Tamás (élettanász)
Cím:A new approach to the detection and statistical classification of Ca2+ sparks / Bányász T., Chen-Izu Y., Balke C. W., Izu L. T.
Dátum:2007
Megjegyzések:The availability of high-speed, two-dimensional (2-D) confocal microscopes and the expanding armamentarium of fluorescent probes presents unprecedented opportunities and new challenges for studying the spatial and temporal dynamics of cellular processes. The need to remove subjectivity from the detection process, the difficulty of the human eye to detect subtle changes in fluorescence in these 2-D images, and the large volume of data produced by these confocal microscopes call for the need to develop algorithms to automatically mark the changes in fluorescence. These fluorescence signal changes are often subtle, so the statistical estimate of the likelihood that the detected signal is not noise is an integral part of the detection algorithm. This statistical estimation is fundamental to our new approach to detection; in earlier Ca(2+) spark detectors, this statistical assessment was incidental to detection. Importantly, the use of the statistical properties of the signal local to the spark, instead of over the whole image, reduces the false positive and false negative rates. We developed an automatic spark detection algorithm based on these principles and used it to detect sparks on an inhomogeneous background of transverse tubule-labeled rat ventricular cells. Because of the large region of the cell surveyed by the confocal microscope, we can detect a large enough number of sparks to measure the dynamic changes in spark frequency in individual cells. We also found, in contrast to earlier results, that cardiac sparks are spatially symmetric. This new approach puts the detection of fluorescent signals on a firm statistical foundation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Biophysical Journal 92 (2007), p. 4458-4465. -
További szerzők:Chen-Izu, Ye Balke, C. William Izu, Leighton T.
Internet cím:elektronikus változat
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3.

001-es BibID:BIBFORM001086
Első szerző:Chen-Izu, Ye
Cím:Hypertension-induced remodeling of cardiac excitation-contraction coupling in ventricular myocytes occurs prior to hypertrophy development / Chen-Izu Y., Chen L., Bányász T., McCulle S. L., Norton B., Scharf S. M., Agarwal A., Patwardhan A., Izu L. T., Balke C. W.
Dátum:2007
ISSN:0363-6135 (Print)
Megjegyzések:Hypertension is a major risk factor for developing cardiac hypertrophy and heart failure. Previous studies show that hypertrophied and failing hearts display alterations in excitation-contraction (E-C) coupling. However, it is unclear whether remodeling of the E-C coupling system occurs before or after heart disease development. We hypothesized that hypertension might cause changes in the E-C coupling system that, in turn, induce hypertrophy. Here we tested this hypothesis by utilizing the progressive development of hypertensive heart disease in the spontaneously hypertensive rat (SHR) to identify a window period when SHR had just developed hypertension but had not yet developed hypertrophy. We found the following major changes in cardiac E-C coupling during this window period. 1) Using echocardiography and hemodynamics measurements, we found a decrease of left ventricular ejection fraction and cardiac output after the onset of hypertension. 2) Studies in isolated ventricular myocytes showed that myocardial contraction was also enhanced at the same time. 3) The action potential became prolonged. 4) The E-C coupling gain was increased. 5) The systolic Ca(2+) transient was augmented. These data show that profound changes in E-C coupling already occur at the onset of hypertension and precede hypertrophy development. Prolonged action potential and increased E-C coupling gain synergistically increase the Ca(2+) transient. Functionally, augmented Ca(2+) transient causes enhancement of myocardial contraction that can partially compensate for the greater workload to maintain cardiac output. The increased Ca(2+) signaling cascade as a molecular mechanism linking hypertension to cardiac hypertrophy development is also discussed.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal of Physiology. Heart and Circulatory Physiology 293 (2007), p. 3301-3310. -
További szerzők:Chen, L. Bányász Tamás (1960-) (élettanász) McCulle, S. L. Norton, Byron Scharf, S. M. Agarwal, Anupam Patwardhan, A. Izu, Leighton T. Balke, C. William
Internet cím:Elektronikus változat
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4.

001-es BibID:BIBFORM001084
Első szerző:Chen-Izu, Ye
Cím:Phosphorylation of RyR2 and shortening of RyR2 cluster spacing in spontaneously hypertensive rat with heart failure / Chen-Izu Y., Ward C. W., Stark W., Bányász T., Sumandea M. P., Balke W., Izu L. T., Wehrens X. H. T.
Dátum:2007
ISSN:0363-6135 (Print)
Megjegyzések:As a critical step toward understanding the role of abnormal intracellular Ca(2+) release via the ryanodine receptor (RyR(2)) during the development of hypertension-induced cardiac hypertrophy and heart failure, this study examines two questions: 1) At what stage, if ever, in the development of hypertrophy and heart failure is RyR(2) hyperphosphorylated at Ser(2808)? 2) Does the spatial distribution of RyR(2) clusters change in failing hearts? Using a newly developed semiquantitative immunohistochemistry method and Western blotting, we measured phosphorylation of RyR(2) at Ser(2808) in the spontaneously hypertensive rat (SHR) at four distinct disease stages. A major finding is that hyperphosphorylation of RyR(2) at Ser(2808) occurred only at late-stage heart failure in SHR, but not in age-matched controls. Furthermore, the spacing between RyR(2) clusters was shortened in failing hearts, as predicted by quantitative model simulation to increase spontaneous Ca(2+) wave generation and arrhythmias.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal of Physiology. Heart and Circulatory Physiology 293 (2007), p. 2409-2417. -
További szerzők:Ward, C. W. Stark, W. Bányász Tamás (1960-) (élettanász) Sumandea, M. P. Balke, C. William Izu, Leighton T. Wehrens, X. H. T.
Internet cím:elektronikus változat
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5.

001-es BibID:BIBFORM001018
Első szerző:Izu, Leighton T.
Cím:Eavesdropping on the social lives of Ca2+ sparks / Izu L. T., Bányász T., Balke C. W., Chen-Izu Y.
Dátum:2007
ISSN:0006-3495 (Print)
Megjegyzések:Ca(2+) sparks arise from the stochastic opening of spatially discrete clusters of ryanodine receptors called a Ca(2+) release unit (CRU). If the RyR clusters were not spatially separated, then Ca(2+) released from one RyR would immediately diffuse to its neighbor and lead to uncontrolled, runaway Ca(2+) release throughout the cell. While physical separation provides some isolation from neighbors, CRUs are not incommunicado. When inter-neighbor interactions become large enough, Ca(2+) waves spontaneously emerge. A more circumscribed interaction shows up in high-speed two-dimensional confocal images as jumping Ca(2+) sparks that seem to be sequentially activated along the Z-line and across Z-lines. However, since Ca(2+) sparks are stochastic events how can we tell whether two sparks occurring close together in space and time are causally related or appeared simply by coincidence? Here we develop a mathematical method to disentangle cause and coincidence in a statistical sense. From our analysis we derive three fundamental properties of Ca(2+) spark generation: 1), the "intrinsic" spark frequency, the spark frequency one would observe if the CRUs were incommunicado; 2), the coupling strength, which measures how strongly one CRU affects another; and 3), the range over which the communication occurs. These parameters allow us to measure the effect RyR regulators have on the intrinsic activity of CRUs and on the coupling between them.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Biophysical Journal 93 (2007), p. 3408-3420. -
További szerzők:Bányász Tamás (1960-) (élettanász) Balke, C. William Chen-Izu, Ye
Internet cím:elektronikus valtozat
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