We describe a new image coding approach in which a 4-ary arithmetic coder is used to represent signi cant coe cient values and the lengths of zero runs between coe cients. This algorithm works by raster scanning within subbands, and therefore involves much lower addressing complexity than other algorithms such as zerotree coding that require the creation and maintenance of lists of dependencies across di erent decomposition levels. Despite its simplicity, and the fact that these dependencies are not explicitly utilized, the algorithm presented here is competitive with the best enhancements of zerotree coding. In addition, it performs comparably with adaptive subband splitting approaches that involve much higher implementation complexity. Finally, although this technique is described here in the context of a wavelet coding system, it can also be applied in a block DCT framework.
Recent studies have demonstrated a relative deficiency in voltage-gated Ca2+ currents (ICa) in immature myocardium. We hypothesized that contraction in developing heart results in part from Ca2+ influx via "reverse" Na+/Ca2+ exchange current (INa/Ca). Accordingly, INa/Ca and cell contraction amplitude were measured in single neonatal and adult rabbit ventricular myocytes. INa/Ca was dependent on Ca2+ concentration, Na+ concentration, and membrane potential and was blocked by 5 mM Ni2+ but not by the Ca(2+)-channel blocker nifedipine. In neonatal cells, contraction amplitude reached a plateau for depolarizations positive to 0 mV. In adult myocytes, contraction amplitude was maximal at 0 mV and decreased at positive membrane potentials. Inhibition of ICa with nifedipine did not affect maximal contraction amplitude in neonatal myocytes but almost completely suppressed contraction of adult cells. These data suggest that Ca2+ influx via ICa is not required for contraction of neonatal rabbit cardiac myocytes. Moreover, Ca2+ influx via reversal of the Na+/Ca2+ exchange mechanism may provide a significant portion of the Ca2+ regulating cell contraction, especially during depolarization to positive membrane potentials.
The Na+/Ca2+ exchanger is a major pathway for transmembrane flux of Ca2+ in cardiac cells. Immunolabeling in adult rabbit myocytes showed localization of the Na+/Ca2+ exchanger to the peripheral sarcolemma and especially in the T tubules. Previous studies have also demonstrated higher Na+/Ca2+ exchanger activity in fetal and newborn rabbit hearts in which the T tubular system is not completely developed. Indirect immunofluorescent studies were performed to localize the Na+/Ca2+ exchanger in isolated myocytes from immature (5, 11, 17, and 30 days) and adult rabbits. Cells were incubated with a monoclonal antibody to the exchanger followed by fluorescein-labeled goat anti-mouse antibody. It is found that at 5 days of age the immunofluorescent labeling was very intense and confined to the peripheral sarcolemma. After 11 days of age, localization of labeling followed the development of the T tubules. The exchanger appeared in the T tubules as soon as they were formed. The Na+/Ca2+ exchange protein is abundantly localized to the peripheral sarcolemma before and during the development of T tubule system.
The subcellular localization of dystrophin was examined in adult rabbit and rat cardiac myocytes with immunofluorescence and at higher resolution with immunogold. The aim was to resolve the conflicting reports on the presence of dystrophin in the transverse tubules (T tubules) of cardiac muscle and to determine its distribution in neonatal myocytes before and during the development of the T tubules. Dystrophin was localized to the peripheral sarcolemma and the T-tubular membrane and was absent from the intercalated disk membranes. In addition, dystrophin localization was followed with immunofluorescence in developing rabbit myocytes at 4 days, 1 wk, and 1 mo after birth. At 4 days of age, T tubules are absent and dystrophin was localized only in the peripheral sarcolemma. Dystrophin was present in the developing T tubules at 1 wk and 1 mo. These results imply that dystrophin is expressed in the T tubules as soon as they develop and confirm the different distribution of dystrophin in the T tubules of cardiac and skeletal muscle.
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