Non-line-of-sight Node Localization based on Semi-Definite Programming in Wireless Sensor Networks

An unknown-position sensor can be localized if there are three or more anchors making time-of-arrival (TOA) measurements of a signal from it. However, the location errors can be very large due to the fact that some of the measurements are from non-line-of-sight (NLOS) paths. In this paper, we propose a semi-definite programming (SDP) based node localization algorithm in NLOS environment for ultra-wideband (UWB) wireless sensor networks. The positions of sensors can be estimated using the distance estimates from location-aware anchors as well as other sensors. However, in the absence of LOS paths, e.g., in indoor networks, the NLOS range estimates can be significantly biased. As a result, the NLOS error can remarkably decrease the location accuracy. And it is not easy to efficiently distinguish LOS from NLOS measurements. In this paper, an algorithm is proposed that achieves high location accuracy without the need of identifying NLOS and LOS measurement.Comment: submitted to IEEE ICC'1

Identification of novel components of Trypanosoma brucei editosomes

The editosome is a multiprotein complex that catalyzes the insertion and deletion of uridylates that occurs during RNA editing in trypanosomatids. We report the identification of nine novel editosome proteins in Trypanosoma brucei. They were identified by mass spectrometric analysis of functional editosomes that were purified by serial ion exchange/gel permeation chromatography, immunoaffinity chromatography specific to the TbMP63 editosome protein, or tandem affinity purification based on a tagged RNA editing ligase. The newly identified proteins have ribonuclease and/or RNA binding motifs suggesting nuclease function for at least some of these. Five of the proteins are interrelated, as are two others, and one is related to four previously identified editosome proteins. The implications of these findings are discussed

Bimetallic Cooperativity in Proton Reduction with an Amido‐Bridged Cobalt Catalyst

The bimetallic catalyst [CoII2(L1)(bpy)2]ClO4 (1), in which L1 is an [NN′2O2] fused ligand, efficiently reduced H+ to H2 in CH3CN in the presence of 100 equiv of HOAc with a turnover number of 18 and a Faradaic efficiency of 94 % after 3 h of bulk electrolysis at −1.6 V (vs. Ag/AgCl). This observation allowed the proposal that this bimetallic cooperativity is associated with distance, angle, and orbital alignment of the two Co centers, as promoted by the unique Co−Namido−Co environment offered by L1. Experimental results revealed that the parent [CoIICoII] complex undergoes two successive metal‐based 1 e− reductions to generate the catalytically active species [CoICoI], and DFT calculations suggested that addition of a proton to one CoI triggers a cooperative 1 e− transfer by each of these CoI centers. This 2 e− transfer is an alternative route to generate a more reactive [CoII(CoII−H−)] hydride, thus avoiding the CoIII−H− required in monometallic species. This [CoII(CoII−H−)] species then accepts another H+ to release H2

Adiponectin as a key player in inflammation

Chronic inflammation has recently been proposed to be a key mediator linking obesity to a cluster of cardiometabolic disorders. Obese adipose tissue, infiltrated with activated macrophages and mast cells, is an important source of systemic inflammation, by secreting dozens of the pro-inflammatory adipokines into the blood stream. One the other hand, adiponectin, an abundant adipokine secreted predominantly from adipocytes, is markedly decreased in obesity and associated inflammatory diseases. Adiponectin exerts its anti-inflammatory actions in several target cells by inhibiting the production and activities of tumor necrosis factor-alpha, preventing the activation of nuclear factor-kappa B, and inducing expression of anti-inflammatory cytokines. In animal models, adiponectin treatment alleviates several obesity-associated inflammatory diseases, such as atherosclerosis, nonalcoholic steatohepatitis, asthma and acute myocardial infarction. In humans, circulating levels of adiponectin are inversely correlated with several well-established markers of inflammation, including C-reactive protein and interleukin-6. Furthermore, anti-inflammatory drugs, such as peroxisome proliferator-activated receptor-gamma agonists, can elevate plasma levels of adiponectin. While the majority of clinical and animal data support the role of adiponectin as an anti-inflammatory, anti-atheroscerotic and anti-diabetic adipokine, a number of recent studies have reported its pro-inflammatory actions in certain conditions. Here, we summarize the pathophysiological roles of adiponectin in inflammation-related disorders, and discuss the potential mechanisms involved, also their implications in adiponectin-targeted pharmacotherapy.Biomedical Reviews 2006, 17: 11-22

MM Algorithms for Geometric and Signomial Programming

This paper derives new algorithms for signomial programming, a generalization of geometric programming. The algorithms are based on a generic principle for optimization called the MM algorithm. In this setting, one can apply the geometric-arithmetic mean inequality and a supporting hyperplane inequality to create a surrogate function with parameters separated. Thus, unconstrained signomial programming reduces to a sequence of one-dimensional minimization problems. Simple examples demonstrate that the MM algorithm derived can converge to a boundary point or to one point of a continuum of minimum points. Conditions under which the minimum point is unique or occurs in the interior of parameter space are proved for geometric programming. Convergence to an interior point occurs at a linear rate. Finally, the MM framework easily accommodates equality and inequality constraints of signomial type. For the most important special case, constrained quadratic programming, the MM algorithm involves very simple updates.Comment: 16 pages, 1 figur

Photodynamic priming with triple-receptor targeted nanoconjugates that trigger T cell-mediated immune responses in a 3D in vitro heterocellular model of pancreatic cancer

Photodynamic priming (PDP), a collateral effect of photodynamic therapy, can transiently alter the tumor microenvironment (TME) beyond the cytotoxic zone. Studies have demonstrated that PDP increases tumor permeability and modulates immune-stimulatory effects by inducing immunogenic cell death, via the release of damage-associated molecular patterns and tumor-associated antigens. Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest of cancers with a stubborn immunosuppressive TME and a dense stroma, representing a challenge for current molecular targeted therapies often involving macromolecules. We, therefore, tested the hypothesis that PDP\u27s TME modulation will enable targeted therapy and result in immune stimulation. Using triple-receptor-targeted photoimmuno-nanoconjugate (TR-PINs)-mediated PDP, targeting epidermal growth factor receptor, transferrin receptor, and human epidermal growth factor receptor 2 we show light dose-dependent TR-PINs mediated cytotoxicity in human PDAC cells (MIA PaCa-2), co-cultured with human pancreatic cancer-associated fibroblasts (PCAFs) in spheroids. Furthermore, TR-PINs induced the expression of heat shock proteins (Hsp60, Hsp70), Calreticulin, and high mobility group box 1 in a light dose and time-dependent manner. TR-PINs-mediated T cell activation was observed in co-cultures of immune cells with the MIA PaCa-2-PCAF spheroids. Both CD4+ T and CD8+ T cells showed light dose and time-dependant antitumor reactivity by upregulating degranulation marker CD107a and interferon-gamma post-PDP. Substantial tumor cell death in immune cell-spheroid co-cultures by day 3 shows the augmentation by antitumor T cell activation and their ability to recognize tumors for a light dose-dependent kill. These data confirm enhanced destruction of heterogeneous pancreatic spheroids mediated by PDP-induced phototoxicity, TME modulation and increased immunogenicity with targeted nanoconstructs