Optimise web browsing on heterogeneous mobile platforms:a machine learning based approach

Web browsing is an activity that billions of mobile users perform on a daily basis. Battery life is a primary concern to many mobile users who often find their phone has died at most inconvenient times. The heterogeneous mobile architecture is a solution for energy-efficient mobile web browsing. However, the current mobile web browsers rely on the operating system to exploit the underlying architecture, which has no knowledge of the individual web workload and often leads to poor energy efficiency. This paper describes an automatic approach to render mobile web workloads for performance and energy efficiency. It achieves this by developing a machine learning based approach to predict which processor to use to run the web browser rendering engine and at what frequencies the processor cores of the system should operate. Our predictor learns offline from a set of training web workloads. The built predictor is then integrated into the browser to predict the optimal processor configuration at runtime, taking into account the web workload characteristics and the optimisation goal: whether it is load time, energy consumption or a trade-off between them. We evaluate our approach on a representative ARM big.LITTLE mobile architecture using the hottest 500 webpages. Our approach achieves 80% of the performance delivered by an ideal predictor. We obtain, on average, 45%, 63.5% and 81% improvement respectively for load time, energy consumption and the energy delay product, when compared to the Linux governo

Inhibitory Effects of Baicalin on the Expression and Activity of CYP3A Induce the Pharmacokinetic Changes of Midazolam in Rats

Baicalin, a flavonoid compound isolated from Scutellaria baicalensis, has been shown to possess antiinflammatory, antiviral, antitumour, and immune regulatory properties. The present study evaluated the potential herb-drug interaction between baicalin and midazolam in rats. Coadministration of a single dose of baicalin (0.225, 0.45, and 0.90 g/kg, i.v.) with midazolam (10 mg/kg, i.v.) in rats resulted in a dose-dependent decrease in clearance (CL) from 25%  (P<0.05) to 34%  (P<0.001) with an increase in AUC0−∞ from 47%  (P<0.05) to 53%  (P<0.01). Pretreatment of baicalin (0.90 g/kg, i.v., once daily for 7 days) also reduced midazolam CL by 43%  (P<0.001), with an increase in AUC0−∞ by 87%  (P<0.01). Multiple doses of baicalin decreased the expression of hepatic CYP3A2 by approximately 58%  (P<0.01) and reduced midazolam 1′-hydroxylation by 23%  (P<0.001) and 4′-hydroxylation by 21%  (P<0.01) in the liver. In addition, baicalin competitively inhibited midazolam metabolism in rat liver microsomes in a concentration-dependent manner. Our data demonstrated that baicalin induced changes in the pharmacokinetics of midazolam in rats, which might be due to its inhibition of the hydroxylation activity and expression of CYP3A in the liver