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

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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.

Electrical communication between the flavin adenine dinucleotlde redox centers of glucose oxidase and a conventional carbon paste electrode has been achieved by using electron-transfer relay systems based on polyslloxanes. Six materials for amperometric biosensors are described In which ferrocene and dlmethylferrocene electron relays are covalently attached to Insoluble slloxane polymers. Sensors containing these polymeric relay systems and glucose oxidase respond rapidly to glucose, with steady-state current responses achieved In less than 10 s. The response to glucose under N2 saturation shows apparent Michaells-Menten constants, *VPP, In the range 16-71 mM and limiting current densities, ymax, of 29-275 µ /cm2. The dependence of the sensor response on the nature of the slloxane polymer and the type of polymer-bound relay Is discussed.

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SummaryWe aimed to determine how age‐associated changes in mechanisms extrinsic and intrinsic to pacemaker cells relate to basal beating interval variability (BIV) reduction in vivo. Beating intervals (BIs) were measured in aged (23–25 months) and adult (3–4 months) C57BL/6 male mice (i) via ECG in vivo during light anesthesia in the basal state, or in the presence of 0.5 mg mL−1 atropine + 1 mg mL−1 propranolol (in vivo intrinsic conditions), and (ii) via a surface electrogram, in intact isolated pacemaker tissue. BIV was quantified in both time and frequency domains using linear and nonlinear indices. Although the average basal BI did not significantly change with age under intrinsic conditions in vivo and in the intact isolated pacemaker tissue, the average BI was prolonged in advanced age. In vivo basal BIV indices were found to be reduced with age, but this reduction diminished in the intrinsic state. However, in pacemaker tissue BIV indices increased in advanced age vs. adults. In the isolated pacemaker tissue, the sensitivity of the average BI and BIV in response to autonomic receptor stimulation or activation of mechanisms intrinsic to pacemaker cells by broad‐spectrum phosphodiesterase inhibition declined in advanced age. Thus, changes in mechanisms intrinsic to pacemaker cells increase the average BIs and BIV in the mice of advanced age. Autonomic neural input to pacemaker tissue compensates for failure of molecular intrinsic mechanisms to preserve average BI. But this compensation reduces the BIV due to both the imbalance of autonomic neural input to the pacemaker cells and altered pacemaker cell responses to neural input.

defined by the remaining five ring atoms. In 2 the corresponding displacement is 0.62 A. This type of distortion is attributed to the presence of the transannular ferrocenyl unit."The coordination of the lithium atom to N(3) in the solid state is consistent with a significant amount of the negative charge in 3 residing on the skeletal nitrogen atoms adjacent to P(3). Interestingly, the N M R spectra for 3 (see above) show that N(3) and N(2) are equivalent, which indicates that the lithium ion either dissociates from N(3) or fluctuates rapidly between N(3) and N(2) in solution at room temperature. These possibilities, together with the reactivity and mechanism of formation of 3, are under investigation.Acknowledgment. W e thank the U.S. Army Research Office for financial support.Supplementary Material Available: An ORTEP drawing of 3 and tables of positional and displacement parameters and bond distances and angles (1 3 pages). Ordering information is given on any current masthead page.

Recent evidence indicates that the spontaneous action potential (AP) of isolated sinoatrial node cells (SANC) is regulated by a system of stochastic mechanisms embodied within two clocks: ryanodine receptors of the “Ca2+ clock” within the sarcoplasmic reticulum, spontaneously activate during diastole and discharge local Ca2+ releases (LCRs) beneath the cell surface membrane; clock crosstalk occurs as LCRs activate an inward Na+/Ca2+ exchanger current (INCX), which together with If and decay of K+ channels prompts the “M clock,” the ensemble of sarcolemmal-electrogenic molecules, to generate APs. Prolongation of the average LCR period accompanies prolongation of the average AP beating interval (BI). Moreover, prolongation of the average AP BI accompanies increased AP BI variability. We hypothesized that both the average AP BI and AP BI variability are dependent upon stochasticity of clock mechanisms reported by the variability of LCR period. We perturbed the coupled-clock system by directly inhibiting the M clock by ivabradine (IVA) or the Ca2+ clock by cyclopiazonic acid (CPA). When either clock is perturbed by IVA (3, 10 and 30μM), which has no direct effect on Ca2+ cycling, or CPA ( 0.5 and 5μM), which has no direct effect on the M clock ion channels, the clock system failed to achieve the basal AP BI and both AP BI and AP BI variability increased. The changes in average LCR period and its variability in response to perturbations of the coupled-clock system were correlated with changes in AP beating interval and AP beating interval variability. We conclude that the stochasticity within the coupled-clock system affects and is affected by the AP BI firing rate and rhythm via modulation of the effectiveness of clock coupling.