187 research outputs found

    Energy-aware video streaming on smartphones

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    Abstract—Video streaming on smartphone consumes lots of energy. One common solution is to download and buffer future video data for playback so that the wireless interface can be turned off most of time and then save energy. However, this may waste energy and bandwidth if the user skips or quits before the end of the video. Using a small buffer can reduce the bandwidth wastage, but may consume more energy and introduce rebuffering delay. In this paper, we analyze the power consumption during video streaming considering user skip and early quit scenarios. We first propose an offline method to compute the minimum power consumption, and then introduce an online solution to save energy based on whether the user tends to watch video for a long time or tends to skip. We have implemented the online solution on Android based smartphones. Experimental results and trace-driven simulation results show that that our method can save energy while achieving a better tradeoff between delay and bandwidth compared to existing methods. I

    Energy optimization through traffic aggregation in wireless networks

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    Abstract—Cellular networks can provide pervasive data ac-cess for smartphones, but also consume lots of energy, because the cellular interface has to stay in high power state for a long time (called long tail problem) after a data transmission. In this paper, we propose to reduce the tail energy by aggregating the data traffic of multiple nodes using their P2P interfaces. This traffic aggregation problem is formalized as finding the best task schedule to minimize energy. We first propose an A search algorithm, which can reduce the search space for finding the optimal schedule offline, and then introduce an online traffic aggregation algorithm. We have implemented the online traffic aggregation algorithm on Android smartphones, and have built a small testbed. Trace-driven simulations and Experimental results show that our traffic aggregation algorithm can significantly reduce the energy and delay. I

    Compromise-resilient anti-jamming communication in wireless sensor networks

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    A highly sensitive and specific system for large-scale gene expression profiling

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    <p>Abstract</p> <p>Background</p> <p>Rapid progress in the field of gene expression-based molecular network integration has generated strong demand on enhancing the sensitivity and data accuracy of experimental systems. To meet the need, a high-throughput gene profiling system of high specificity and sensitivity has been developed.</p> <p>Results</p> <p>By using specially designed primers, the new system amplifies sequences in neighboring exons separated by big introns so that mRNA sequences may be effectively discriminated from other highly related sequences including their genes, unprocessed transcripts, pseudogenes and pseudogene transcripts. Probes used for microarray detection consist of sequences in the two neighboring exons amplified by the primers. In conjunction with a newly developed high-throughput multiplex amplification system and highly simplified experimental procedures, the system can be used to analyze >1,000 mRNA species in a single assay. It may also be used for gene expression profiling of very few (<it>n </it>= 100) or single cells. Highly reproducible results were obtained from duplicate samples with the same number of cells, and from those with a small number (100) and a large number (10,000) of cells. The specificity of the system was demonstrated by comparing results from a breast cancer cell line, MCF-7, and an ovarian cancer cell line, NCI/ADR-RES, and by using genomic DNA as starting material.</p> <p>Conclusion</p> <p>Our approach may greatly facilitate the analysis of combinatorial expression of known genes in many important applications, especially when the amount of RNA is limited.</p

    Trajectories of Self-Rated Health of Chinese Elders: A Piecewise Growth Model Analysis

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    This study used piecewise growth modeling to describe the developmental trajectories of self-rated health (SRH) in the elderly and longitudinal associations with activities of daily living (ADL), educational level, economic status, age, and gender. Data were drawn from the Chinese Longitudinal Healthy Longevity Survey (CLHLS), collected over 12 years (from 2002 to 2014) at five waves. A total of 16,064 Chinese elders (57.4% females) were analyzed. Results showed two phases of development for SRH; specifically, the decreasing trend of SRH was from slow (in the first phase, waves 1 to 3) to fast (in the second phase, waves 3 to 5). Descriptives showed that the turning point age was at the age of 83.69 (range = 68 to 116, median age = 82 years old). ADL were positively associated with SRH within each time point (wave of data). Female elders had a higher initial state (i.e., worse) of SRH than did male elders, and poorer economic status was associated with worse initial status of SRH

    Pharmaco-transcriptomic correlation analysis reveals novel responsive signatures to HDAC inhibitors and identifies Dasatinib as a synergistic interactor in small-cell lung cancer.

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    BACKGROUND Histone acetylation/deacetylase process is one of the most studied epigenetic modifications. Histone deacetylase inhibitors (HDACis) have shown clinical benefits in haematological malignancies but failed in solid tumours due to the lack of biomarker-driven stratification. METHODS We perform integrative pharmaco-transcriptomic analysis by correlating drug response profiles of five pan-HDACis with transcriptomes of solid cancer cell lines (n=659) to systematically identify generalizable gene signatures associated with HDACis sensitivity and resistance. The established signatures are then applied to identify cancer subtypes that are potentially sensitive or resistant to HDACis, and drugs that enhance the efficacy of HDACis. Finally, the reproductivity of the established HDACis signatures is evaluated by multiple independent drug response datasets and experimental assays. FINDINGS We successfully delineate generalizable gene signatures predicting sensitivity (containing 46 genes) and resistance (containing 53 genes) to all five HDACis, with their reproductivity confirmed by multiple external sources and independent internal assays. Using the gene signatures, we identify low-grade glioma harbouring isocitrate dehydrogenase 1/2 (IDH1/2) mutation and non-YAP1-driven subsets of small-cell lung cancer (SCLC) that particularly benefit from HDACis monotherapy. Further, based on the resistance gene signature, we identify clinically-approved Dasatinib as a synthetic lethal drug with HDACi, synergizing in inducing apoptosis and reactive oxygen species on a panel of SCLC. Finally, Dasatinib significantly enhances the therapeutic efficacy of Vorinostat in SCLC xenografts. INTERPRETATION Our work establishes robust gene signatures predicting HDACis sensitivity/resistance in solid cancer and uncovers combined Dasatinib/HDACi as a synthetic lethal combination therapy for SCLC

    Lipopolysaccharide (LPS) potentiates hydrogen peroxide toxicity in T98G astrocytoma cells by suppression of anti-oxidative and growth factor gene expression

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    <p>Abstract</p> <p>Background</p> <p>Lipopolysaccharide (LPS) is a cell wall component of Gram-negative bacteria with proved role in pathogenesis of sepsis. Brain injury was observed with both patients dead from sepsis and animal septic models. However, <it>in vitro </it>administration of LPS has not shown obvious cell damage to astrocytes and other relative cell lines while it does cause endothelial cell death <it>in vitro</it>. These observations make it difficult to understand the role of LPS in brain parenchymal injury.</p> <p>Results</p> <p>To test the hypothesis that LPS may cause biological changes in astrocytes and make the cells to become vulnerable to reactive oxygen species, a recently developed highly sensitive and highly specific system for large-scale gene expression profiling was used to examine the gene expression profile of a group of 1,135 selected genes in a cell line, T98G, a derivative of human glioblastoma of astrocytic origin. By pre-treating T98G cells with different dose of LPS, it was found that LPS treatment caused a broad alteration in gene expression profile, but did not cause obvious cell death. However, after short exposure to H<sub>2</sub>O<sub>2</sub>, cell death was dramatically increased in the LPS pretreated samples. Interestingly, cell death was highly correlated with down-regulated expression of antioxidant genes such as cytochrome b561, glutathione s-transferase a4 and protein kinase C-epsilon. On the other hand, expression of genes encoding growth factors was significantly suppressed. These changes indicate that LPS treatment may suppress the anti-oxidative machinery, decrease the viability of the T98G cells and make the cells more sensitive to H<sub>2</sub>O<sub>2 </sub>stress.</p> <p>Conclusion</p> <p>These results provide very meaningful clue for further exploring and understanding the mechanism underlying astrocyte injury in sepsis <it>in vivo</it>, and insight for why LPS could cause astrocyte injury <it>in vivo</it>, but not <it>in vitro</it>. It will also shed light on the therapeutic strategy of sepsis.</p
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