3,272 research outputs found

    Secure Communication in Wireless Multimedia Sensor Networks using Watermarking

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    Wireless multimedia sensor networks (WMSNs) are an emerging type of sensor networks which contain sensor nodes equipped with microphones, cameras, and other sensors that producing multimedia content. These networks have the potential to enable a large class of applications ranging from military to modern healthcare. Since in WMSNs information is multimedia by nature and it uses wireless link as mode of communication so this posse?s serious security threat to this network. Thereby, the security mechanisms to protect WMSNs communication have found importance lately. However given the fact that WMSN nodes are resources constrained, so the traditionally intensive security algorithm is not well suited for WMSNs. Hence in this research, we aim to a develop lightweight digital watermarking enabled techniques as a security approach to ensure secure wireless communication. Finally aim is to provide a secure communication framework for WMSNs by developing new

    Model-enhanced Vector Index

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    Embedding-based retrieval methods construct vector indices to search for document representations that are most similar to the query representations. They are widely used in document retrieval due to low latency and decent recall performance. Recent research indicates that deep retrieval solutions offer better model quality, but are hindered by unacceptable serving latency and the inability to support document updates. In this paper, we aim to enhance the vector index with end-to-end deep generative models, leveraging the differentiable advantages of deep retrieval models while maintaining desirable serving efficiency. We propose Model-enhanced Vector Index (MEVI), a differentiable model-enhanced index empowered by a twin-tower representation model. MEVI leverages a Residual Quantization (RQ) codebook to bridge the sequence-to-sequence deep retrieval and embedding-based models. To substantially reduce the inference time, instead of decoding the unique document ids in long sequential steps, we first generate some semantic virtual cluster ids of candidate documents in a small number of steps, and then leverage the well-adapted embedding vectors to further perform a fine-grained search for the relevant documents in the candidate virtual clusters. We empirically show that our model achieves better performance on the commonly used academic benchmarks MSMARCO Passage and Natural Questions, with comparable serving latency to dense retrieval solutions

    A simulation study on the measurement of D0-D0bar mixing parameter y at BES-III

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    We established a method on measuring the \dzdzb mixing parameter yy for BESIII experiment at the BEPCII e+e−e^+e^- collider. In this method, the doubly tagged ψ(3770)→D0D0‾\psi(3770) \to D^0 \overline{D^0} events, with one DD decays to CP-eigenstates and the other DD decays semileptonically, are used to reconstruct the signals. Since this analysis requires good e/πe/\pi separation, a likelihood approach, which combines the dE/dxdE/dx, time of flight and the electromagnetic shower detectors information, is used for particle identification. We estimate the sensitivity of the measurement of yy to be 0.007 based on a 20fb−120fb^{-1} fully simulated MC sample.Comment: 6 pages, 7 figure

    Effects of excluding grazing on the vegetation and soils of degraded sparse-elm grassland in the Horqin Sandy Land, China

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    Livestock grazing is a crucial cause of vegetation degradation and desertification in sandy lands. The sparse-elm grassland of Horqin Sandy Land, China has suffered severe degradation of biodiversity and ecosystem services. Management to exclude grazing is often necessary for ecological restoration, especially in arid and semi-arid regions. We report effects on vegetation and soils in a 10-year experiment to exclude livestock, completely or seasonally, in comparison with a continuously grazed area in Horqin. Complete exclusion of grazing and restriction of grazing to summer both led to significantly increased plant cover and density relative to the grazed control. Species richness increased, reflected in higher Shannon-Wiener indices; only complete exclusion increased the Simpson diversity index, whereas Pielou evenness was significantly lowest under seasonal grazing. Exclosure treatments were also associated with improved soil texture, and increased water retention, available nitrogen, total nitrogen, total carbon and total phosphorus. Soil pH and C/N ratio were highest under the seasonal grazing regime. The results indicated that exclosure management indeed improved biodiversity and ecosystem services in an erosion-prone region. Although total exclosure was most effective in restoration of degraded sparse-elm grassland, seasonal grazing management was highly beneficial and represented a good compromise with resource utilization and economic development

    Metformin improves polycystic ovary syndrome in mice by inhibiting ovarian ferroptosis

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    Background and objectivePCOS is a common metabolic disorder in women of reproductive age, which pathogenesis is very complex. The role of ferroptosis in PCOS is a novel finding, and the mechanistic studies are not clear. Metformin is a commonly used drug of PCOS but few studies on whether metformin can improve the follicle development and ovarian function in PCOS. We aims to use PCOS mouse model to study the effect of metformin on PCOS based on the ovarian function and explored the regulation of metformin in PCOS mice by intervening in ferroptosis pathway.Materials and methodsC57 BL/6J female mice aged 4-5 weeks were purchased and gavaged with letrozole (1 mg/kg/day) combined with high-fat diet for 21days to establish PCOS model, and control group was set up. After modeling, the mice were divided into PCOS model group and metformin treatment group (Met) (n=6).The Met group were gavaged metformin (200 mg/kg/day) for 28 days. The body weight, estrous cycle, glucose tolerance test (OGTT)and insulin resistance test (ITT) were monitored. Then, The mice were euthanized to collect serum and ovaries. Elisa was used to detect changes in related serum hormones (E2, LH, FSH, TP). Ovaries used for molecular biology experiments to detect changes in GPX4, SIRT3, AMPK/p-AMPK, and mTOR/p-mTOR by Western blot and qPCR.ResultsCompared with the model group mice, body weight was significantly reduced, and their estrous cycle was restored in Met group. The results of OGTT and ITT showed an improvment of glucose tolerance and insulin resistance. Morphological results showed that after metformin treatment, polycystic lesions in ovaries were reduced, the ovarian function was restored, and the expressions of SIRT3 and GPX4 were elevated. WB results demonstrated that the expressions of p-mTOR and p-AMPK in ovaries were significantly reduced in Model group, but reversed in MET group.ConclusionOur study confirmed metformin could not only improve body weight and metabolism disorders, but also improve ovarian dysfunction in PCOS mice.In addition, we explored metformin could regulate ferroptosis to improve PCOS via the SIRT3/AMPK/mTOR pathway. Our study complements the mechanisms by which metformin improves PCOS

    Toll-Like Receptor 9 Is Required for Opioid-Induced Microglia Apoptosis

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    Opioids have been widely applied in clinics as one of the most potent pain relievers for centuries, but their abuse has deleterious physiological effects beyond addiction. However, the underlying mechanism by which microglia in response to opioids remains largely unknown. Here we show that morphine induces the expression of Toll-like receptor 9 (TLR9), a key mediator of innate immunity and inflammation. Interestingly, TLR9 deficiency significantly inhibited morphine-induced apoptosis in microglia. Similar results were obtained when endogenous TLR9 expression was suppressed by the TLR9 inhibitor CpGODN. Inhibition of p38 MAPK by its specific inhibitor SB203580 attenuated morphine-induced microglia apoptosis in wild type microglia. Morphine caused a dramatic decrease in Bcl-2 level but increase in Bax level in wild type microglia, but not in TLR9 deficient microglia. In addition, morphine treatment failed to induce an increased levels of phosphorylated p38 MAPK and MAP kinase kinase 3/6 (MKK3/6), the upstream MAPK kinase of p38 MAPK, in either TLR9 deficient or µ-opioid receptor (µOR) deficient primary microglia, suggesting an involvement of MAPK and µOR in morphine-mediated TLR9 signaling. Moreover, morphine-induced TLR9 expression and microglia apoptosis appears to require μOR. Collectively, these results reveal that opioids prime microglia to undergo apoptosis through TLR9 and µOR as well. Taken together, our data suggest that inhibition of TLR9 and/or blockage of µOR is capable of preventing opioid-induced brain damage
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