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It is believed that broadcast is an efficient way to transmit data in an asymmetric communication system. Most of the previous work focused on either pull-based or push-based scheduling. However, for systems with a very large number of data items, none of these schemes is efficient individually. We propose a novel hybrid scheduling algorithm which uses both pull- and push-based schemes. In our approach, data items are divided, by a suitable cut-off point, into two disjoint sets: one consisting of more-popular items and the other of less-popular items. The items in the former set are broadcast by a push-based schedule, while those in the latter set by a pull-based schedule. A cut-off point is said to be optimal when it minimizes the expected access time in the system. The optimal cut-off point is derived analytically and validated by simulation experiments. Results show that the proposed hybrid push- and pull-based scheduling performs always better than a pure push-based scheduling and improves on the expected access time of an existing hybrid scheduling scheme.

Aims: Several recent reports have shown irisin protects the heart against ischemia/ reperfusion injury. However, the effect of irisin on I/R injury in diabetic mice has not been described. The present study was designed to investigate the role of irisin in myocardial ischemia-reperfusion (MI/R) injury in diabetic mice. Methods: A mouse model of diabetes was established by feeding wild type or genemanipulated adult male mice with a high-fat diet. All the mice received intraperitoneal injection of irisin or PBS. Thirty minutes after injection, mice were subjected to 30 min of myocardial ischemia followed by 3h (for cell apoptosis and protein determination), 24 h (for infarct size and cardiac function). Results: Knockout of gene FNDC5 augmented MI/R injury in diabetic mice, while irisin treatment attenuated MI/R injury, improved cardiac function, cellular ATP biogenetics, mitochondria potential, and impaired mitochondrion-related cell death. More severely impaired AMPK pathway was observed in diabetic FNDC5-/mice received MI/R. Knockout of gene AMPK blocks the beneficial effects of irisin on MI/R injury, cardiac function, cellular ATP biogenetics, mitochondria potential, and mitochondrion-related cell death. Conclusions: Our present study demonstrated that irisin improves the mitochondria function and attenuates MI/R injury in diabetic mice through AMPK pathway.