WiFi Sensing at the Edge Towards Scalable On-Device Wireless Sensing Systems

WiFi sensing offers a powerful method for tracking physical activities using the radio-frequency signals already found throughout our homes and offices. This novel sensing modality offers continuous and non-intrusive activity tracking since sensing can be performed (i) without requiring wearable sensors, (ii) outside the line-of-sight, and even (iii) through the wall. Furthermore, WiFi has become a ubiquitous technology in our computers, our smartphones, and even in low-cost Internet of Things devices. In this work, we consider how the ubiquity of these low-cost WiFi devices offer an unparalleled opportunity for improving the scalability of wireless sensing systems. Thus far, WiFi sensing research assumes costly offline computing resources and hardware for training machine learning models and for performing model inference. To improve the scalability of WiFi sensing systems, this dissertation introduces techniques for improving machine learning at the edge by thoroughly surveying and evaluating signal preprocessing and edge machine learning techniques. Additionally, we introduce the use of federated learning for collaboratively training machine learning models with WiFi data only available on edge devices. We then consider privacy and security concerns of WiFi sensing by demonstrating possible adversarial surveillance attacks. To combat these attacks, we propose a method for leveraging spatially distributed antennas to prevent eavesdroppers from performing adversarial surveillance while still enabling and even improving the sensing capabilities of allowed WiFi sensing devices within our environments. The overall goal throughout this work is to demonstrate that WiFi sensing can become a ubiquitous and secure sensing option through the use of on-device computation on low-cost edge devices

Women, Health and Aging: Building a Statewide Movement

Provides an overview of current policy and program environments that affect the state's most vulnerable elder population, and considers some effective strategies to address the growing needs of older persons in California

Resveratrol augments ER stress and the cytotoxic effects of glycolytic inhibition in neuroblastoma by downregulating Akt in a mechanism independent of SIRT1

Cancer cells typically display increased rates of aerobic glycolysis that are correlated with tumor aggressiveness and a poor prognosis. Targeting the glycolytic pathway has emerged as an attractive therapeutic route mainly because it should spare normal cells. Here, we evaluate the effects of combining the inhibition of glycolysis with application of the polyphenolic compound resveratrol (RSV) in neuroblastoma (NB) cancer cell lines. Inhibiting glycolysis with 2-deoxy-D-glucose (2-DG) significantly reduced NB cell viability and was associated with increased endoplasmic reticulum (ER) stress and Akt activity. Administration of 2-DG increased the expression of the ER molecular chaperones GRP78 and GRP94, the prodeath protein C/EBP homology protein (CHOP) and the phosphorylation of Akt at S473, T450 and T308. Combined treatment with both RSV and 2-DG reduced GRP78, GRP94 and Akt phosphorylation but increased CHOP and NB cell death when compared with the administration of 2-DG alone. The selective inhibition of Akt activity also decreased 2-DG-induced GRP78 and GRP94 expression and increased CHOP expression, suggesting that Akt can modulate ER stress. Protein phosphatase 1 alpha (PP1 alpha) was activated by RSV, as indicated by a reduction in PP1 alpha phosphorylation at T320. Pretreatment of cells with tautomycin, a selective PP1 alpha inhibitor, prevented the RSV-mediated decrease in Akt phosphorylation, suggesting that RSV enhances 2-DG-induced cell death by activating PP1 and downregulating Akt. The RSV-mediated inhibition of Akt in the presence of 2-DG was not prevented by the selective inhibition of SIRT1, a known target of RSV, indicating that the effects of RSV on this pathway are independent of SIRT1. We propose that RSV inhibits Akt activity by increasing PP1 alpha activity, thereby potentiating 2-DG-induced ER stress and NB cell death

Heavy-light decay constants---MILC results with the Wilson action

We present the current status of our ongoing calculations of pseudoscalar meson decay constants for mesons that contain one light and one heavy quark (f_B, f_{B_s}, f_D, f_{D_s}). We are currently generating new gauge configurations that include dynamical quarks and calculating the decay constants. In addition, we have several new results for the static approximation. Those results, as well as several refinements to the analysis, are new since Lattice '96. Our current (still preliminary) value for f_B is 156 +- 11 +- 30 +- 14 MeV, where the first error is from statistical and fitting errors, the second error is an estimate of other systematic errors within the quenched approximation and the third error is an estimate of the quenching error. For the ratio f_{B_s}/f_B, we get 1.11 +- 0.02 +- 0.03 +- 0.07.Comment: 8 pages, 9 figures, LaTeX, uses espcrs2, epsf, Invited talk presented by S. Gottlieb at Lattice QCD on Parallel Computers, University of Tsukuba, March, 1997, to appear in the proceeding

Mapping The Interstellar Medium With Near-Infrared Diffuse Interstellar Bands

We map the distribution and properties of the Milky Way's interstellar medium as traced by diffuse interstellar bands (DIBs) detected in near-infrared stellar spectra from the SDSS-III/APOGEE survey. Focusing exclusively on the strongest DIB in the H band, at lambda similar to 1.527 mu m, we present a projected map of the DIB absorption field in the Galactic plane, using a set of about 60,000 sightlines that reach up to 15 kpc from the Sun and probe up to 30 mag of visual extinction. The strength of this DIB is linearly correlated with dust reddening over three orders of magnitude in both DIB equivalent width (Wpm) and extinction, with a power law index of 1.01 +/- 0.01, a mean relationship of W-DIB/A(v) = 0.1 angstrom mag(-1) and a dispersion of similar to 0.05 angstrom mag(-1) at extinctions characteristic of the Galactic midplane. These properties establish this DIB as a powerful, independent probe of dust extinction over a wide range of Av values. The subset of about 14,000 robustly detected DIB features have a W-DIB distribution that follows an exponential trend. We empirically determine the intrinsic rest wavelength of this transition to be lambda(0) = 15 272.42 angstrom and use it to calculate absolute radial velocities of the carrier, which display the kinematical signature of the rotating Galactic disk. We probe the DIB carrier distribution in three dimensions and show that it can be characterized by an exponential disk model with a scale height of about 100 pc and a scale length of about 5 kpc. Finally, we show that the DIB distribution also traces large-scale Galactic structures, including the Galactic long bar and the warp of the outer disk.NSF Astronomy & Astrophysics Postdoctoral Fellowship AST-1203017NSF AST-1109665Alfred P. Sloan FoundationNational Science FoundationU.S. Department of Energy Office of ScienceUniversity of ArizonaBrazilian Participation GroupBrookhaven National LaboratoryUniversity of CambridgeCarnegie Mellon UniversityUniversity of FloridaFrench Participation GroupGerman Participation GroupHarvard UniversityInstituto de Astrofisica de CanariasMichigan State/Notre Dame/JINA Participation GroupJohns Hopkins UniversityLawrence Berkeley National LaboratoryMax Planck Institute for AstrophysicsMax Planck Institute for Extraterrestrial PhysicsNew Mexico State UniversityNew York UniversityOhio State UniversityPennsylvania State UniversityUniversity of PortsmouthPrinceton UniversitySpanish Participation GroupUniversity of TokyoUniversity of UtahVanderbilt UniversityUniversity of VirginiaUniversity of WashingtonYale UniversitySpanish Ministry of Economy and Competitiveness AYA-2011-27754McDonald Observator

Lattice results for the decay constant of heavy-light vector mesons

We compute the leptonic decay constants of heavy-light vector mesons in the quenched approximation. The reliability of lattice computations for heavy quarks is checked by comparing the ratio of vector to pseudoscalar decay constant with the prediction of Heavy Quark Effective Theory in the limit of infinitely heavy quark mass. Good agreement is found. We then calculate the decay constant ratio for B mesons: $f_{B^*}/f_B= 1.01(0.01)(^{+0.04}_{-0.01})$. We also quote quenched $f_{B^*}=177(6)(17)$ MeV.Comment: 11 pages, 3 postscript figs., revtex; two references adde

Genomic imprinting variations in the mouse type 3 deiodinase gene between tissues and brain regions.

The Dio3 gene, which encodes for the type 3 deiodinase (D3), controls thyroid hormone (TH) availability. The lack of D3 in mice results in tissue overexposure to TH and a broad neuroendocrine phenotype. Dio3 is an imprinted gene, preferentially expressed from the paternally inherited allele in the mouse fetus. However, heterozygous mice with paternal inheritance of the inactivating Dio3 mutation exhibit an attenuated phenotype when compared with that of Dio3 null mice. To investigate this milder phenotype, the allelic expression of Dio3 was evaluated in different mouse tissues. Preferential allelic expression of Dio3 from the paternal allele was observed in fetal tissues and neonatal brain regions, whereas the biallelic Dio3 expression occurred in the developing eye, testes, and cerebellum and in the postnatal brain neocortex, which expresses a larger Dio3 mRNA transcript. The newborn hypothalamus manifests the highest degree of Dio3 expression from the paternal allele, compared with other brain regions, and preferential allelic expression of Dio3 in the brain relaxed in late neonatal life. A methylation analysis of two regulatory regions of the Dio3 imprinted domain revealed modest but significant differences between tissues, but these did not consistently correlate with the observed patterns of Dio3 allelic expression. Deletion of the Dio3 gene and promoter did not result in significant changes in the tissue-specific patterns of Dio3 allelic expression. These results suggest the existence of unidentified epigenetic determinants of tissue-specific Dio3 imprinting. The resulting variation in the Dio3 allelic expression between tissues likely explains the phenotypic variation that results from paternal Dio3 haploinsufficiency.This is the final version of the article. It is available from the Endocrine Society in Molecular Endocrinology here: http://press.endocrine.org/doi/pdf/10.1210/me.2014-1210

Effect of Oral Iron Repletion on Exercise Capacity in Patients With Heart Failure With Reduced Ejection Fraction and Iron Deficiency: The IRONOUT HF Randomized Clinical Trial.

Importance: Iron deficiency is present in approximately 50% of patients with heart failure with reduced left ventricular ejection fraction (HFrEF) and is an independent predictor of reduced functional capacity and mortality. However, the efficacy of inexpensive readily available oral iron supplementation in heart failure is unknown. Objective: To test whether therapy with oral iron improves peak exercise capacity in patients with HFrEF and iron deficiency. Design, Setting, and Participants: Phase 2, double-blind, placebo-controlled randomized clinical trial of patients with HFrEF ( Interventions: Oral iron polysaccharide (n = 111) or placebo (n = 114), 150 mg twice daily for 16 weeks. Main Outcomes and Measures: The primary end point was a change in peak oxygen uptake (V̇o2) from baseline to 16 weeks. Secondary end points were change in 6-minute walk distance, plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels, and health status as assessed by Kansas City Cardiomyopathy Questionnaire (KCCQ, range 0-100, higher scores reflect better quality of life). Results: Among 225 randomized participants (median age, 63 years; 36% women) 203 completed the study. The median baseline peak V̇o2 was 1196 mL/min (interquartile range [IQR], 887-1448 mL/min) in the oral iron group and 1167 mL/min (IQR, 887-1449 mL/min) in the placebo group. The primary end point, change in peak V̇o2 at 16 weeks, did not significantly differ between the oral iron and placebo groups (+23 mL/min vs -2 mL/min; difference, 21 mL/min [95% CI, -34 to +76 mL/min]; P = .46). Similarly, at 16 weeks, there were no significant differences between treatment groups in changes in 6-minute walk distance (-13 m; 95% CI, -32 to 6 m), NT-proBNP levels (159; 95% CI, -280 to 599 pg/mL), or KCCQ score (1; 95% CI, -2.4 to 4.4), all P \u3e .05. Conclusions and Relevance: Among participants with HFrEF with iron deficiency, high-dose oral iron did not improve exercise capacity over 16 weeks. These results do not support use of oral iron supplementation in patients with HFrEF. Trial Registration: clinicaltrials.gov Identifier: NCT02188784

Arginase I in myeloid suppressor cells is induced by COX-2 in lung carcinoma

Myeloid suppressor cells (MSCs) producing high levels of arginase I block T cell function by depleting l-arginine in cancer, chronic infections, and trauma patients. In cancer, MSCs infiltrating tumors and in circulation are an important mechanism for tumor evasion and impair the therapeutic potential of cancer immunotherapies. However, the mechanisms that induce arginase I in MSCs in cancer are unknown. Using the 3LL mouse lung carcinoma, we aimed to characterize these mechanisms. Arginase I expression was independent of T cell–produced cytokines. Instead, tumor-derived soluble factors resistant to proteases induced and maintained arginase I expression in MSCs. 3LL tumor cells constitutively express cyclooxygenase (COX)-1 and COX-2 and produce high levels of PGE2. Genetic and pharmacological inhibition of COX-2, but not COX-1, blocked arginase I induction in vitro and in vivo. Signaling through the PGE2 receptor E-prostanoid 4 expressed in MSCs induced arginase I. Furthermore, blocking arginase I expression using COX-2 inhibitors elicited a lymphocyte-mediated antitumor response. These results demonstrate a new pathway of prostaglandin-induced immune dysfunction and provide a novel mechanism that can help explain the cancer prevention effects of COX-2 inhibitors. Furthermore, an addition of arginase I represents a clinical approach to enhance the therapeutic potential of cancer immunotherapies