I. Introduction 2357 II. Organic Electroluminescent Devices 2357 III. Lanthanide Metal Ions Complexes as the Emitting Layer 2359 IV. Eu (III) and Tb (III) Complexes as Emitting Materials 2359 V. Nd(III), Er(III), and Yb(III) Complexes as Emitting Materials 2365 VI. Tm(III) and Eu(II) Complexes as Emitting Materials 2366 VII. Conclusion 2367 VIII. References 2367 Junji Kido has received his B.S. degree (1984) from

No abstract

Background A reduction of complexity of heart-beat interval variability (BIV) that is associated with an increased morbidity and mortality in cardiovascular disease states is thought to derive from the balance of sympathetic and parasympathetic neural impulses to the heart. But rhythmic clock-like behavior intrinsic to pacemaker cells within the sinoatrial node (SAN) drives their beating, even in the absence of autonomic neural input. Objective To test how this rhythmic clock-like behavior intrinsic to pacemaker cells interacts with autonomic impulses to the heart-beat interval variability in vivo. Methods We analyzed BIV in the time and frequency domains and by fractal and entropy analyses: i) in vivo, when the brain input to the SAN is intact; ii) during autonomic denervation in vivo; iii) in isolated SAN tissue (i.e., in which the autonomic-neural input is completely absent); iv) in single pacemaker cells isolated from the SAN; and v) following autonomic receptor stimulation of these cells. Results Spontaneous-beating intervals of pacemaker cells residing within the isolated SAN tissue exhibit fractal-like behavior and have lower approximate entropy than in the intact heart. Isolation of pacemaker cells from SAN tissue, however, leads to a loss in the beating-interval order and fractal-like behavior. β adrenergic receptor stimulation of isolated pacemaker cells increases intrinsic clock synchronization, decreases their action potential period and increases system complexity. Conclusions Both the average-beating interval in vivo and beating interval complexity are conferred by the combined effects of clock periodicity intrinsic to pacemaker cells and their response to autonomic-neural input.