Sparse complex FxLMS for active noise cancellation over spatial regions

In this paper, we investigate active noise control over large 2D spatial regions when the noise source is sparsely distributed. The l1 relaxation technique originated from compressive sensing is adopted and based on that we develop the algorithm for two cases: multipoint noise cancellation and wave domain noise cancellation. This results in two new variants (i) zero-attracting multi-point complex FxLMS and (ii) zero-attracting wave domain complex FxLMS. Both approaches use a feedback control system, where a microphone array is distributed over the boundary of the control region to measure the residual noise signals and a loudspeaker array is placed outside the microphone array to generate the anti-noise signals. Simulation results demonstrate the performance and advantages of the proposed methods in terms of convergence rate and spatial noise reduction levels.This work is supported by Australian Research Council (ARC) Discovery Projects funding scheme (project no. DP140103412). The work of J. Zhang was sponsored by the China Scholarship Council with the Australian National University

Active Noise Control Over Space: A Wave Domain Approach

Noise control and cancellation over a spatial region is a fundamental problem in acoustic signal processing. In this paper, we utilize wave-domain adaptive algorithms to iteratively calculate the secondary source driving signals and to cancel the primary noise field over the control region. We propose wave-domain active noise control algorithms based on two minimization problems: first, minimizing the wave-domain residual signal coefficients, and second, minimizing the acoustic potential energy over the region, and derive the update equations with respect to two variables, the loudspeaker weights and wave-domain secondary source coefficients. Simulation results demonstrate the effectiveness of the proposed algorithms, more specifically the convergence speed and the noise cancellation performance in terms of the noise reduction level and acoustic potential energy reduction level over the entire spatial region.DP14010341

Multichannel active noise control for spatially sparse noise fields

Multi-channel active noise control (ANC) is currently an attractive solution for the attenuation of low-frequency noise fields, in three-dimensional space. This paper develops a controller for the case when the noise source components are sparsely distributed in space. The anti-noise signals are designed as in conventional ANC to minimize the residual errors but with an additional term containing an ℓl norm regularization applied to the signal magnitude. This results in that only secondary sources close to the noise sources are required to be active for cancellation of sparse noise fields. Adaptive algorithms with low computational complexity and faster convergence speeds are propose

Renyi Differential Privacy of Propose-Test-Release and Applications to Private and Robust Machine Learning

Propose-Test-Release (PTR) is a differential privacy framework that works with local sensitivity of functions, instead of their global sensitivity. This framework is typically used for releasing robust statistics such as median or trimmed mean in a differentially private manner. While PTR is a common framework introduced over a decade ago, using it in applications such as robust SGD where we need many adaptive robust queries is challenging. This is mainly due to the lack of Renyi Differential Privacy (RDP) analysis, an essential ingredient underlying the moments accountant approach for differentially private deep learning. In this work, we generalize the standard PTR and derive the first RDP bound for it when the target function has bounded global sensitivity. We show that our RDP bound for PTR yields tighter DP guarantees than the directly analyzed (\eps, \delta)-DP. We also derive the algorithm-specific privacy amplification bound of PTR under subsampling. We show that our bound is much tighter than the general upper bound and close to the lower bound. Our RDP bounds enable tighter privacy loss calculation for the composition of many adaptive runs of PTR. As an application of our analysis, we show that PTR and our theoretical results can be used to design differentially private variants for byzantine robust training algorithms that use robust statistics for gradients aggregation. We conduct experiments on the settings of label, feature, and gradient corruption across different datasets and architectures. We show that PTR-based private and robust training algorithm significantly improves the utility compared with the baseline.Comment: NeurIPS 202

A Model to Describe Transport Properties in Bi2Sr2(CazPr1−z)Cu2O8+yBi_2Sr_2(Ca_zPr_{1-z})Cu_2O_{8+y}

A pseudo-spin model is proposed, as a means to describe some transport properties (resistivity and Hall mobility) in $Bi_2Sr_2(Ca_zPr_{1-z})Cu_2O_{8+y}$. Our model is based in a double-well potential where tunneling in a given site and interaction between different lattice sites are allowed only through the excited states. Doping of the pure system by the addition of $Pr$ increases the ratio between the activation energy and the tunneling constant. The model Hamiltonian displays some features which are present in the hydrogen-bonded ferroelectrics. Its dynamics is treated in the random phase approximation and the characteristic frequency (time) is used in a Drude formula in order to obtain some transport properties of the system, namely the electric resistivity and the Hall mobility. The quantities calculated in this work are compared with the experimental data of B. Beschoten, S. Sadewasser, G. G\"{u}ntherodt and C. Quitmann [Phys. Rev. Lett.77, 1837(1996)].Comment: 14 pages, 4 figure

Pravastatin Prevents Aortic Atherosclerosis via Modulation of Signal Transduction and Activation of Transcription 3 (STAT3) to Attenuate Interleukin-6 (IL-6) Action in ApoE Knockout Mice

The purpose of this study was to determine whether pravastatin’s prevention of aortic atherosclerosis via attenuation of IL-6 action depends on modulation of STAT3 activity. Male apoE knockout (apoE-/-) mice fed on a diet containing 1.25% cholesterol (wt/wt) were divided into pravastatin group provided with pravastatin (80 mg kg-1 per day) and atherosclerosis group. After eight weeks, pravastatin significantly prevented atherosclerotic lesion and reduced levels of IL-6 in serum and lesion, and significantly decreased expressions of phosphorylated STAT3 (pSTAT3) and increased suppressor of cytokine signaling 3 (SOCS3) expressions in lesions. Our results suggested that pravastatin’s aortic atherosclerosis preventing action via attenuation of IL-6 action may partially depend on modulation of STAT3 activity

Mammalian innate resistance to highly pathogenic avian influenza H5N1 virus infection is mediated through reduced proinflammation and infectious virus release

Respiratory epithelial cells and macrophages are the key innate immune cells that play an important role in the pathogenesis of influenza A virus infection. We found that these two cell types from both human and pig showed comparable susceptibilities to initial infection with a highly pathogenic avian influenza (HPAI) H5N1 virus (A/turkey/Turkey/1/05) and a moderately pathogenic human influenza H1N1 virus (A/USSR/77), but there were contrasting differences in host innate immune responses. Human cells mounted vigorous cytokine (tumor necrosis factor alpha [TNF-α] and interleukin-6 [IL-6]) and chemokine (CXCL9, CXCL10, and CXCL11) responses to H5N1 virus infection. However, pig epithelial cells and macrophages showed weak or no TNF-α and chemokine induction with the same infections. The apparent lack of a strong proinflammatory response, corroborated by the absence of TNF-α induction in H5N1 virus-challenged pigs, coincided with greater cell death and the reduced release of infectious virus from infected pig epithelial cells. Suppressor of cytokine signaling 3 (SOCS3), a protein suppressor of the JAK-STAT pathway, was constitutively highly expressed and transcriptionally upregulated in H5N1 virus-infected pig epithelial cells and macrophages, in contrast to the corresponding human cells. The overexpression of SOCS3 in infected human macrophages dampened TNF-α induction. In summary, we found that the reported low susceptibility of pigs to contemporary Eurasian HPAI H5N1 virus infections coincides at the level of innate immunity of respiratory epithelial cells and macrophages with a reduced output of viable virus and an attenuated proinflammatory response, possibly mediated in part by SOCS3, which could serve as a target in the treatment or prevention of virus-induced hypercytokinemia, as observed for humans

Expression of Toll-like receptor 2 is up-regulated in monocytes from patients with chronic obstructive pulmonary disease

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is characterised by pulmonary and systemic inflammation which flare-up during episodes of acute exacerbation (AECOPD). Given the role of Toll-like receptors (TLRs) in the induction of inflammatory responses we investigated the involvement of TLRs in COPD pathogenesis. METHODS: The expression of TLR-2, TLR-4 and CD14 in monocytes was analyzed by flow cytometry. To study the functional responses of these receptors, monocytes were stimulated with peptidoglycan or lipopolysaccharide and the amounts of TNFα and IL-6 secreted were determined by ELISA. RESULTS: We found that the expression of TLR-2 was up-regulated in peripheral blood monocytes from COPD patients, either clinically stable or during AECOPD, as compared to never smokers or smokers with normal lung function. Upon stimulation with TLR-2 ligand monocytes from COPD patients secreted increased amounts of cytokines than similarly stimulated monocytes from never smokers and smokers. In contrast, the expressions of TLR-4 and CD14 were not significantly different between groups, and the response to lipopolysaccharide (a TLR-4 ligand) stimulation was not significantly different either. At discharge from hospital TLR-2 expression was down-regulated in peripheral blood monocytes from AECOPD patients. This could be due to the treatment with systemic steroids because, in vitro, steroids down-regulated TLR-2 expression in a dose-dependent manner. Finally, we demonstrated that IL-6, whose plasma levels are elevated in patients, up-regulated in vitro TLR-2 expression in monocytes from never smokers. CONCLUSION: Our results reveal abnormalities in TLRs expression in COPD patients and highlight its potential relationship with systemic inflammation in these patients

Immunohistochemical expression of promyelocytic leukemia body in soft tissue sarcomas

<p>Abstract</p> <p>Background</p> <p>The function of promyelocytic leukemia (PML) bodies is not well known but plays an important role in controlling cell proliferation, apoptosis and senescence. This study was undertaken to analyze the clinical significance of PML body expression in primary tumor samples from malignant fibrous histiocytoma (MFH) and liposarcoma patients.</p> <p>Methods</p> <p>We studied MFH and liposarcoma samples from 55 patients for PML bodies. Fluorescent immunostaining of PML bodies was performed in the paraffin-embedded tumor sections.</p> <p>Results</p> <p>PML body immunostaining was identified in 63.9% of MFH and 63.2% of liposarcoma samples. PML body expression rates of all sarcoma cells were 1.5 ± 1.8% (range: 0–7.0) in MFH and 1.3 ± 1.4% (0–5.2) in liposarcoma samples. PML body expression (p = 0.0053) and a high rate of PML body expression (p = 0.0012) were significantly greater prognostic risk factors for death than the other clinical factors in MFH patients. All liposarcoma patients without expression of PML were disease free at the end of the study.</p> <p>Conclusion</p> <p>Our study suggests that the presence of PML bodies may indicate a poor prognosis for MFH and liposarcoma patients.</p

Are Th17 Cells an Appropriate New Target in the Treatment of Rheumatoid Arthritis?

Th17 cells play crucial roles not only in host defense but also in many human autoimmune diseases and corresponding animal models. Although many of the fundamental principles regarding Th17 biology have been rapidly elucidated in mice, there remain numerous controversies regarding the differentiation, plasticity, and pathogenicity of human Th17 cells. In this review, we consider these open questions in comparison to what has already been clarified in mice, and discuss the potential impact of discoveries related to the Th17 pathway on the development of new therapeutic strategies in Th17 driven autoimmune diseases, specifically rheumatoid arthritis. Clin Trans Sci 2010; Volume 3: 319–326Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/79296/1/j.1752-8062.2010.00233.x.pd