We find that the interplay between the dispersal directionality NVP-BSK805 in vivo and network topology has important consequences on relative species abundance patterns and the distribution of alpha diversity. (C) 2008 Elsevier Ltd. All rights reserved.”
“Background Sudden death can occur as a consequence of cardiac- conduction abnormalities in the neuromuscular disease myotonic dystrophy type 1. The determinants of the risk of sudden death remain imprecise.

Methods We assessed whether the electrocardiogram (ECG) was useful in predicting sudden death in 406 adult patients with genetically

confirmed myotonic dystrophy type 1. A patient was characterized as having a severe abnormality if the ECG had at least one of the following features: rhythm other than sinus, PR interval of 240 msec or more, QRS duration of 120 msec or more, or second-degree or third-degree atrioventricular block.

Results Patients with severe abnormalities according to the entry ECG were older

than patients without severe abnormalities, had more severe skeletal-muscle impairment, and were more likely to have heart failure, left ventricular systolic dysfunction, or atrial tachyarrhythmia. Such patients were more likely to receive a pacemaker MK-4827 molecular weight or an implantable cardioverter-defibrillator during the follow-up period. During a mean follow-up period of 5.7 years, 81 patients died; there were 27 sudden deaths, 32 deaths from progressive neuromuscular respiratory failure, 5 nonsudden deaths from cardiac

causes, and 17 deaths from other causes. Among the 17 patients who died suddenly in whom postcollapse rhythm was evaluated, a ventricular tachyarrhythmia was observed in 9. A severe ECG abnormality (relative risk, 3.30; 95% confidence interval [CI], 1.24 to 8.78) and a clinical diagnosis of atrial tachyarrhythmia (relative risk, 5.18; 95% CI, 2.28 to 11.77) were independent risk factors for sudden death.

Conclusions Patients with adult myotonic dystrophy type 1 are at high risk for arrhythmias and sudden death. A severe abnormality on the 4EGI-1 nmr ECG and a diagnosis of an atrial tachyarrhythmia predict sudden death.”
“Phenomenological computational models of tissue regeneration and bone healing have been only partially successful in predicting experimental observations. This may be a result of simplistic modeling of cellular activity. Furthermore, phenomenological models are limited when considering the effects of combined physical and biological interventions. In this study, a new model of cell and tissue differentiation, using a more mechanistic approach, is presented and applied to fracture repair. The model directly couples cellular mechanisms to mechanical stimulation during bone healing and is based on the belief that the cells act as transducers during tissue regeneration.