The 3G/LTE wireless interface is a significant contributor to battery drain on mobile devices. A large portion of the energy is consumed by unnecessarily keeping the mobile device's radio in its "Active" mode even when there is no traffic. This paper describes the design of methods to reduce this portion of energy consumption by learning the traffic patterns and predicting when a burst of traffic will start or end. We develop a technique to determine when to change the radio's state from Active to Idle, and another to change the radio's state from Idle to Active. In evaluating the methods on real usage data from 9 users over 28 total days on four different carriers, we find that the energy savings range between 51% and 66% across the carriers for 3G, and is 67% on the Verizon LTE network. When allowing for delays of a few seconds (acceptable for background applications), the energy savings increase to between 62% and 75% for 3G, and 71% for LTE. The increased delays reduce the number of state switches to be the same as in current networks with existing inactivity timers.

Despite the fact that there is a significant difference of the cage subsidence rate between the two groups no clinical outcome, nor sagittal alignment or fusion rate differences among groups was observed in elderly CSM patients.

The recurrence of colorectal cancer after chemotherapy is the leading cause of its high mortality. We propose that elucidating the mechanisms of tumor regrowth after chemotherapy in tumor-bearing mice may provide new insights into tumor relapse in cancer patients. We firstly report the identification of a chemokine, CXCL4, that plays an important role in the molecular mechanism of cancer regrowth after chemotherapy. A syngenic transplantation tumor model was established with murine colon cancer CT26 cells and treated with 5-FU. Genome-wide gene expression analysis determined that CXCL4 was transiently upregulated in the tumor model. Systemic overexpression of CXCL4 accelerated cancer growth in vivo, but not in vitro. Conversely, the anti-CXCL4 monoclonal antibody (CXCL4-mab) retarded tumor-regrowth after 5-FU treatment in immune-competent mice, but not nude mice. The CXCL4-mab treatment increased the local expression levels of IFN-γ and Gran-b genes in the tumor-bed, and elevated the function of CTLs against CT26 cells. Thus, the colon cancer cells in responding to the cytotoxic stress of 5-FU produce a high level of CXCL4, which suppresses antitumor immunity to confer the residual cancer cells an advantage for regrowth after chemotherapy. Our findings provide a novel target for developing therapeutics aiming to increase antitumor immunity after chemotherapy.

Icariin is a flavonoid derived from Epimedium sagittatum , and has a wide range of biological and pharmacological effects; however, little is known regarding its effect on drug-resistant ovarian cancer and the signal transduction pathways underlying the regulation of apoptosis and autophagy. The present study aimed to investigate the re-sensitization effects of icariin exerted on an ovarian cancer cell line. Autophagy was analyzed in a SKVCR cell line that had been treated with icariin. We investigated the sensitivity of SKVCR cells to cisplatin, as well as the effects of an autophagy agonist (rapamycin) on autophagy, apoptosis, and the protein kinase B (AKT) signaling pathway. Finally, the mechanism underlying the effects of autophagy-related (ATG) protein ATG5 overexpression on autophagy, apoptosis and AKT signaling in SKVCR cells were determined. The results revealed that treatment with icariin inhibited cell viability and autophagy, but promoted G0/G1 phase cell cycle arrest and apoptosis as determined by Cell Counting Kit-8, immunofluorescence and flow cytometry assays, respectively. Icariin reduced the resistance of SKVCR cells to cisplatin in vitro by inducing G1/S cell cycle transition, apoptosis and inhibiting autophagy. Furthermore, enhanced autophagy induced by rapamycin treatment or overexpression of ATG5 partially reversed the effect of icariin on cisplatin resistance and autophagy in SKVCR cells. At the molecular level, rapamycin treatment or overexpression of ATG5 reversed the effects of icariin on the expression of autophagy-associated proteins, including microtubule-associated protein 1 light chain 3β, Beclin-1, ATG5 and p62, and the AKT/mammalian target of rapamycin (mTOR) pathway. Collectively, our results suggested that icariin enhances the chemosensitivity of SKVCR cells by suppressing autophagy via activation of the AKT/mTOR signaling pathway.