REM sleep behaviour disorder (RBD) is a parasomnia characterized by the loss of normal skeletal muscle atonia during REM sleep with prominent motor activity accompanying dreaming. The terminology relating to RBD, and mechanisms underlying REM sleep without atonia and RBD based on data in cat and rat are presented. Neuroimaging data from the few published human cases with RBD associated with structural lesions in the brainstem are presented, in which the dorsal midbrain and pons are implicated. Pharmacological manipulations which alter RBD frequency and severity are reviewed, and the data from human neuropathological studies are presented. An anatomic framework and new schema for the pathophysiology of RBD are proposed based on recent data in rat regarding the putative flip-flop switch for REM sleep control. The structure in man analogous to the subcoeruleus region in cat and sublaterodorsal nucleus in rat is proposed as the nucleus (and its associated efferent and afferent pathways) crucial to RBD pathophysiology. The association of RBD with neurological disease ('secondary RBD') is presented, with emphasis on RBD associated with neurodegenerative disease, particularly the synucleinopathies. The hypothesized pathophysiology of RBD is presented in relation to the Braak staging system for Parkinson's disease, in which the topography and temporal sequence of synuclein pathology in the brain could explain the evolution of parkinsonism and/or dementia well after the onset of RBD. These data suggest that many patients with 'idiopathic' RBD are actually exhibiting an early clinical manifestation of an evolving neurodegenerative disorder. Such patients may be appropriate for future drug therapies that affect synuclein pathophysiology, in which the development of parkinsonism and/or dementia could be delayed or prevented. We suggest that additional clinicopathological studies be performed in patients with dementia or parkinsonism, with and without RBD, as well as in patients with idiopathic RBD, to further elucidate the pathophysiology and also characterize the clinical and pathophysiological relevance of RBD in neurodegenerative disease. Furthermore, longitudinal studies in patients with idiopathic RBD are warranted to characterize the natural history of such patients and prepare for future therapeutic trials.

Obesity and the magnitude of nocturnal oxygen desaturation, which is an important pathophysiological consequence of OSA, are independent risk factors for incident AF in individuals <65 years of age.

We describe demographic, clinical, laboratory and aetiological findings in 93 consecutive patients with rapid eye movement (REM) sleep behaviour disorder (RBD), which consists of excessive motor activity during dreaming in association with loss of skeletal muscle atonia of REM sleep. The patients were seen at the Mayo Sleep Disorders Center between January 1, 1991 and July 31, 1995. Eighty-one patients (87%) were male. The mean age of RBD onset was 60.9 years (range 36-84 years) and the mean age at presentation was 64.4 years (37-85 years). Thirty-two per cent of patients had injured themselves and 64% had assaulted their spouses. Subdural haematomas occurred in two patients. Dream content was altered and involved defence of the sleeper against attack in 87%. The frequency of nocturnal events decreased with time in seven untreated patients with neurodegenerative disease. MRI or CT head scans were performed in 56% of patients. Although four scans showed brainstem pathology, all of these patients had apparently unrelated neurodegenerative diseases known to be associated with RBD. Neurological disorders were present in 57% of patients; Parkinson's disease, dementia without parkinsonism and multiple system atrophy accounted for all but 14% of these. RBD developed before parkinsonism in 52% of the patients with Parkinson's disease. Five of the 14 patients with multiple system atrophy were female, and thus the strong male predominance in RBD is less evident in this condition. Psychiatric disorders, drug use or drug withdrawal were rarely causally related to RBD. Clonazepam treatment of RBD was completely or partially successful in 87% of the patients who used the drug. We conclude that RBD is a well-defined condition and that descriptions from different centres are fairly consistent. It is commonest in elderly males and may result in serious morbidity to patients and bed partners. There is a strong relationship to neurodegenerative disease, especially Parkinson's disease, multiple system atrophy and dementia, and neurologists should explore the possibility of RBD in patients with these conditions. RBD symptoms may be the first manifestations of these disorders and careful follow-up is needed. Neuroimaging is unlikely to reveal underlying disorders not suspected clinically. We confirm the effectiveness of clonazepam, but note that attention to the safety of the bed environment may be sufficient for patients with contraindications to the drug.

People with obstructive sleep apnea have a peak in sudden death from cardiac causes during the sleeping hours, which contrasts strikingly with the nadir of sudden death from cardiac causes during this period in people without obstructive sleep apnea and in the general population.

[Ru(phen)2dppz]2+ (phen = 1,10-phenanthroline, dppz = dipyridophenazine) and closely related complexes have previously been observed to have an undetectably small quantum yield of photoluminescence in water but a moderate emission yield when bound to DNA. This so-called “light-switch” effect is a critical factor in the utility of these complexes as spectroscopic probes for DNA. Here we describe a detailed investigation of the photophysics of [Ru(phen)2dppz]2+ in aqueous solution, and in mixtures of acetonitrile and water, by time-resolved absorption and emission spectroscopies. The emission of the complex in water has been measured for the first time. A prompt initial emission, derived from a metal-to-ligand charge-transfer (MLCT) excited state typical for polypyridyl−ruthenium complexes, is observed along with a delayed emission attributed to a novel MLCT species. The small quantum yield of photoluminescence for [Ru(phen)2dppz]2+ in water, and in water/acetonitrile, depends upon efficient formation of a novel MLCT species, followed by its rapid radiationless decay. The MLCT interconversion is assigned to an intramolecular charge-transfer process that is induced by the polarity and proton donating ability of the solvent.

We present a new continuous data assimilation algorithm based on ideas that have been developed for designing finite-dimensional feedback controls for dissipative dynamical systems, in particular, in the context of the incompressible two-dimensional Navier--Stokes equations. These ideas are motivated by the fact that dissipative dynamical systems possess finite numbers of determining parameters (degrees of freedom) such as modes, nodes and local spatial averages which govern their long-term behavior. Therefore, our algorithm allows the use of any type of measurement data for which a general type of approximation interpolation operator exists. Our main result provides conditions, on the finite-dimensional spatial resolution of the collected data, sufficient to guarantee that the approximating solution, obtained by our algorithm from the measurement data, converges to the unknown reference solution over time. Our algorithm is also applicable in the context of signal synchronization in which one can recover, asymptotically in time, the solution (signal) of the underlying dissipative system that is corresponding to a continuously transmitted partial data

We propose the viscous Camassa-Holm equations as a closure approximation for the Reynoldsaveraged equations of the incompressible Navier-Stokes fluid. This approximation is tested on turbulent channel flows with steady mean. Analytical solutions for the mean velocity and the Reynolds shear stress across the entire channel are obtained, showing good agreement with experimental measurements and direct numerical simulations. As Reynolds number varies, these analytical mean velocity profiles form a family of curves whose envelopes are shown to have either power law, or logarithmic behavior, depending on the choice of drag law.

Ultrafast emission and absorption spectroscopies were used to measure the kinetics of DNA-mediated electron transfer reactions between metal complexes intercalated into DNA. In the presence of rhodium(III) acceptor, a substantial fraction of photoexcited donor exhibits fast oxidative quenching (>3 x 10(10) per second). Transient-absorption experiments indicate that, for a series of donors, the majority of back electron transfer is also very fast (approximately 10(10) per second). This rate is independent of the loading of acceptors on the helix, but is sensitive to sequence and pi stacking. The cooperative binding of donor and acceptor is considered unlikely on the basis of structural models and DNA photocleavage studies of binding. These data show that the DNA double helix differs significantly from proteins as a bridge for electron transfer.