Optimized Data Switching for Opportunistic Data DSDS Devices

Dual SIM Dual Standby (DSDS) wireless devices are configured with a primary subscriber identity module (SIM) card providing both voice and data connections on a primary network and a secondary SIM card for providing data-only access on a secondary network. The utilization of wireless network resources by a DSDS wireless device can be enhanced by accounting for congestion on each of the associated networks and data usage of the device to determine whether a switch between networks would be beneficial for device performance

INTELLIGENT SIM SWITCHING IN A MULTI-SIM COMPUTING DEVICE

A system is described that enables a computing device (e.g., a mobile phone, a tablet computer, a laptop computer, etc.) to intelligently determine whether to move a data connection from a default data subscriber identity module (DDS) to a non-default data subscriber identity module (non-DDS) when initiating a voice call or during an on-going voice call on the non-DDS in a multiple subscriber identity module (multi-SIM) computing device based on a current state of the computing device. The current state of the computing device may be determined based on various contextual signals, including data usage for each application on the device, the number of foreground applications, the number of background applications, data tethering state, voice call characteristics, connected peripherals, computing device screen state, and/or sensor data generated by one or more sensors (e.g., proximity sensors, near-field microwave sensors, radar, capacitive sensors, etc.) of the computing device. The computing device may analyze these contextual signals to determine a current state of the device and may selectively move the data connection from the DDS to the non-DDS based on this state information

Link Capacity Estimation for Devices in Idle State

In order to estimate throughput between a user device and a radio access network (RAN), a modem of the user device may estimate the link capacity of the link between the user device and the RAN. When the user device is in a connected state, the modem can determine link capacity estimation (LCE) values directly, based on signal strength parameter values measured by the modem from signals received by the user device from a given RAN. In order to estimate the link capacity for a user device that is in an idle mode, the modem of the user device may maintain, in memory, one or more look-up tables (LUTs) in which historical, aggregate LCE values are stored and organized into various buckets according to signal strength parameter type and signal strength measurement value range. The modem may obtain signal strength parameter measurements while the user device is in a connected state, calculate an LCE value for each signal strength parameter measurement, and update a moving average or weighted average of LCE values for a corresponding bucket. When the user device enters the idle mode from the connected mode, the modem receives signal strength parameter measurements (e.g., from paging signals received by the user device from a RAN), determines new LCE values (one for each signal strength parameter type) based on those signal strength parameter measurements, identifies the buckets to which each new LCE value correspond, calculates an average of the historical, aggregate LCE values for each identified bucket, then uses the average of the historical, aggregate LCE values to estimate what the throughput will be between the RAN and the user device when the user device transitions back to the connected state

MARK4 controls ischaemic heart failure through microtubule detyrosination.

Myocardial infarction is a major cause of premature death in adults. Compromised cardiac function after myocardial infarction leads to chronic heart failure with systemic health complications and a high mortality rate1. Effective therapeutic strategies are needed to improve the recovery of cardiac function after myocardial infarction. More specifically, there is a major unmet need for a new class of drugs that can improve cardiomyocyte contractility, because inotropic therapies that are currently available have been associated with high morbidity and mortality in patients with systolic heart failure2,3 or have shown a very modest reduction of risk of heart failure4. Microtubule detyrosination is emerging as an important mechanism for the regulation of cardiomyocyte contractility5. Here we show that deficiency of microtubule-affinity regulating kinase 4 (MARK4) substantially limits the reduction in the left ventricular ejection fraction after acute myocardial infarction in mice, without affecting infarct size or cardiac remodelling. Mechanistically, we provide evidence that MARK4 regulates cardiomyocyte contractility by promoting phosphorylation of microtubule-associated protein 4 (MAP4), which facilitates the access of vasohibin 2 (VASH2)-a tubulin carboxypeptidase-to microtubules for the detyrosination of α-tubulin. Our results show how the detyrosination of microtubules in cardiomyocytes is finely tuned by MARK4 to regulate cardiac inotropy, and identify MARK4 as a promising therapeutic target for improving cardiac function after myocardial infarction.BHF fellowship grant (FS/14/28/30713), Issac Newton Trust Grant (18.40u), and Cambridge BHF Centre of Research Excellence grants (RE/13/6/30180 and RE/18/1/34212)

Thermal and Mechanical Behavior of Hybrid Polymer Nanocomposite Reinforced with Graphene Nanoplatelets

In the present investigation, we successfully fabricate a hybrid polymer nanocomposite containing epoxy/polyester blend resin and graphene nanoplatelets (GNPs) by a novel technique. A high intensity ultrasonicator is used to obtain a homogeneous mixture of epoxy/polyester resin and graphene nanoplatelets. This mixture is then mixed with a hardener using a high-speed mechanical stirrer. The trapped air and reaction volatiles are removed from the mixture using high vacuum. The hot press casting method is used to make the nanocomposite specimens. Tensile tests, dynamic mechanical analysis (DMA) and thermogravimetric analysis (TGA) are performed on neat, 0.2 wt %, 0.5 wt %, 1 wt %, 1.5 wt % and 2 wt % GNP-reinforced epoxy/polyester blend resin to investigate the reinforcement effect on the thermal and mechanical properties of the nanocomposites. The results of this research indicate that the tensile strength of the novel nanocomposite material increases to 86.8% with the addition of a ratio of graphene nanoplatelets as low as 0.2 wt %. DMA results indicate that the 1 wt % GNP-reinforced epoxy/polyester nanocomposite possesses the highest storage modulus and glass transition temperature (Tg), as compared to neat epoxy/polyester or the other nanocomposite specimens. In addition, TGA results verify thethermal stability of the experimental specimens, regardless of the weight percentage of GNPs

Suppression of angiotensin II-induced pathological changes in heart and kidney by the caveolin-1 scaffolding domain peptide.

Dysregulation of the renin-angiotensin system leads to systemic hypertension and maladaptive fibrosis in various organs. We showed recently that myocardial fibrosis and the loss of cardiac function in mice with transverse aortic constriction (TAC) could be averted by treatment with the caveolin-1 scaffolding domain (CSD) peptide. Here, we used angiotensin II (AngII) infusion (2.1 mg/kg/day for 2 wk) in mice as a second model to confirm and extend our observations on the beneficial effects of CSD on heart and kidney disease. AngII caused cardiac hypertrophy (increased heart weight to body weight ratio (HW/BW) and cardiomyocyte cross-sectional area); fibrosis in heart and kidney (increased levels of collagen I and heat shock protein-47 (HSP47)); and vascular leakage (increased levels of IgG in heart and kidney). Echocardiograms of AngII-infused mice showed increased left ventricular posterior wall thickness (pWTh) and isovolumic relaxation time (IVRT), and decreased ejection fraction (EF), stroke volume (SV), and cardiac output (CO). CSD treatment (i.p. injections, 50 μg/mouse/day) of AngII-infused mice significantly suppressed all of these pathological changes in fibrosis, hypertrophy, vascular leakage, and ventricular function. AngII infusion increased β1 and β3 integrin levels and activated Pyk2 in both heart and kidney. These changes were also suppressed by CSD. Finally, bone marrow cell (BMC) isolated from AngII-infused mice showed hyper-migration toward SDF1. When AngII-infused mice were treated with CSD, BMC migration was reduced to the basal level observed in cells from control mice. Importantly, CSD did not affect the AngII-induced increase in blood pressure (BP), indicating that the beneficial effects of CSD were not mediated via normalization of BP. These results strongly indicate that CSD suppresses AngII-induced pathological changes in mice, suggesting that CSD can be developed as a treatment for patients with hypertension and pressure overload-induced heart failure