2,116 research outputs found

    Reconstructing diffusion fields sampled with a network of arbitrarily distributed sensors

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    Sensor networks are becoming increasingly prevalent for monitoring physical phenomena of interest. For such wireless sensor network applications, knowledge of node location is important. Although a uniform sensor distribution is common in the literature, it is normally difficult to achieve in reality. Thus we propose a robust algorithm for reconstructing two-dimensional diffusion fields, sampled with a network of arbitrarily placed sensors. The two-step method proposed here is based on source parameter estimation: in the first step, by properly combining the field sensed through well-chosen test functions, we show how Prony's method can reveal locations and intensities of the sources inducing the field. The second step then uses a modification of the Cauchy-Schwarz inequality to estimate the activation time in the single source field. We combine these steps to give a multi-source field estimation algorithm and carry out extensive numerical simulations to evaluate its performance

    Estimating localized sources of diffusion fields using spatiotemporal sensor measurements

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    We consider diffusion fields induced by a finite number of spatially localized sources and address the problem of estimating these sources using spatiotemporal samples of the field obtained with a sensor network. Within this framework, we consider two different time evolutions: the case where the sources are instantaneous, as well as, the case where the sources decay exponentially in time after activation. We first derive novel exact inversion formulas, for both source distributions, through the use of Green's second theorem and a family of sensing functions to compute generalized field samples. These generalized samples can then be inverted using variations of existing algebraic methods such as Prony's method. Next, we develop a novel and robust reconstruction method for diffusion fields by properly extending these formulas to operate on the spatiotemporal samples of the field. Finally, we present numerical results using both synthetic and real data to verify the algorithms proposed herein

    Spatiotemporal Sampling Trade-off for Inverse Diffusion Source Problems

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    We consider the spatiotemporal sampling of diffusion fields induced by M point sources, and study the associated inverse problem of recovering the initial parameters of the unknown sources. In particular, we focus on characterising qualitatively the error of the obtained source estimates. To achieve this, we obtain an expression with which we can trade the sensor density for performance accuracy. In other words, by evaluating the optimal sampling instant for a given sensor density-and using the corresponding field samples at that instant-we can expect to obtain an improvement in the estimation performance when compared to an arbitrary sampling instant. Finally, several numerical simulations are presented, to support the theoretical results obtained

    Attempts to detect retrotransposition and de novo deletion of Alus and other dispersed repeats at specific loci in the human genome

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    Dispersed repeat elements contribute to genome instability by de novo insertion and unequal recombination between repeats. To study the dynamics of these processes, we have developed single DNA molecule approaches to detect de novo insertions at a single locus and Alu-mediated deletions at two different loci in human genomic DNA. Validation experiments showed these approaches could detect insertions and deletions at frequencies below 10(-6) per cell. However, bulk analysis of germline (sperm) and somatic DNA showed no evidence for genuine mutant molecules, placing an upper limit of insertion and deletion rates of 2 x 10(-7) and 3 x 10(-7), respectively, in the individuals tested. Such re-arrangements at these loci therefore occur at a rate lower than that detectable by the most sensitive methods currently available

    Epithelial senescence in idiopathic pulmonary fibrosis is propagated by small extracellular vesicles

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    BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease that affects 3 million people worldwide. Senescence and small extracellular vesicles (sEVs) have been implicated in the pathogenesis of IPF, although how sEVs promote disease remains unclear. Here, we profile sEVs from bronchial epithelial cells and determine small RNA (smRNA) content. METHODS: Conditioned media was collected and sEVs were isolated from normal human bronchial epithelial cells (NHBEs) and IPF-diseased human bronchial epithelial cells (DHBEs). RESULTS: Increased sEV release from DHBEs compared to NHBEs (n = 4; p < 0.05) was detected by nanoparticle tracking analysis. NHBEs co-cultured with DHBE-derived sEVs for 72 h expressed higher levels of SA-β-Gal and γH2AX protein, p16 and p21 RNA and increased secretion of IL6 and IL8 proteins (all n = 6-8; p < 0.05). sEVs were also co-cultured with healthy air-liquid interface (ALI) cultures and similar results were observed, with increases in p21 and p16 gene expression and IL6 and IL8 (basal and apical) secretion (n = 6; p < 0.05). Transepithelial electrical resistance (TEER) measurements, a reflection of epithelial barrier integrity, were decreased upon the addition of DHBE-derived sEVs (n = 6; p < 0.05). smRNA-sequencing identified nineteen significantly differentially expressed miRNA in DHBE-derived sEVs compared to NHBE-derived sEVs, with candidate miRNAs validated by qPCR (all n = 5; p < 0.05). Four of these miRNAs were upregulated in NHBEs co-cultured with DHBE-derived sEVs and three in healthy ALI cultures co-cultured with DHBE-derived sEVs (n = 3-4; p < 0.05). CONCLUSIONS: This data demonstrates that DHBE-derived sEVs transfer senescence to neighbouring healthy cells, promoting the disease state in IPF

    Sample size calculations for cluster randomised controlled trials with a fixed number of clusters

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    Background\ud Cluster randomised controlled trials (CRCTs) are frequently used in health service evaluation. Assuming an average cluster size, required sample sizes are readily computed for both binary and continuous outcomes, by estimating a design effect or inflation factor. However, where the number of clusters are fixed in advance, but where it is possible to increase the number of individuals within each cluster, as is frequently the case in health service evaluation, sample size formulae have been less well studied. \ud \ud Methods\ud We systematically outline sample size formulae (including required number of randomisation units, detectable difference and power) for CRCTs with a fixed number of clusters, to provide a concise summary for both binary and continuous outcomes. Extensions to the case of unequal cluster sizes are provided. \ud \ud Results\ud For trials with a fixed number of equal sized clusters (k), the trial will be feasible provided the number of clusters is greater than the product of the number of individuals required under individual randomisation (nin_i) and the estimated intra-cluster correlation (ρ\rho). So, a simple rule is that the number of clusters (κ\kappa) will be sufficient provided: \ud \ud κ\kappa > nin_i x ρ\rho\ud \ud Where this is not the case, investigators can determine the maximum available power to detect the pre-specified difference, or the minimum detectable difference under the pre-specified value for power. \ud \ud Conclusions\ud Designing a CRCT with a fixed number of clusters might mean that the study will not be feasible, leading to the notion of a minimum detectable difference (or a maximum achievable power), irrespective of how many individuals are included within each cluster. \ud \u

    Offspring Production among the Extended Relatives of Samoan Men and Fa'afafine

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    Androphilia refers to sexual attraction to adult males, whereas gynephilia refers to sexual attraction to adult females. Male androphilia is an evolutionary paradox. Its development is at least partially influenced by genetic factors, yet male androphiles exhibit lower reproductive output, thus raising the question of how genetic factors underlying its development persist. The sexual antagonism hypothesis posits that the fitness costs associated with genetic factors underlying male androphilia are offset because these same factors lead to elevated reproduction on the part of the female relatives of androphilic males. Western samples drawn from low fertility populations have yielded inconsistent results when testing this hypothesis. Some studies documented elevated reproduction among the matrilineal female kin of androphilic males, whereas others found such effects in the paternal line. Samoa is a high-fertility population in which individuals reproduce closer to their maximum capacities. This study compared the reproductive output of the paternal and maternal line grandmothers, aunts, and uncles of 86 Samoan androphilic males, known locally as fa'afafine, and 86 Samoan gynephilic males. Reproductive output was elevated in the paternal and maternal line grandmothers, but not aunts or uncles, of fa'afafine. These findings are consistent with the sexual antagonism hypothesis and suggest that male androphilia is associated with elevated reproduction among extended relatives in both the maternal and paternal line. Discussion focuses on how this study, in conjunction with the broader literature, informs various models for the evolution of male androphilia via elevated reproduction on the part of female kin

    Economic Impact of Cystic Echinococcosis in Peru

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    Cystic echinococcosis (CE), caused by infection with the larval stage of the cestode Echinococcus granulosus, constitutes an important public health problem in Peru. Despite its high prevalence in endemic communities no studies have attempted to estimate the economic impact of CE in Peruvian society. We used official and published sources of epidemiological and economic information to estimate direct and indirect costs associated with livestock production losses and human disease. We also used disability adjusted life years (DALYs) which is an overall measure of disease burden, expressed as number of years lost due to ill-health, disability or early death due to CE. We found that the total estimated cost of human CE in Peru was U.S.2,420,348peryear.TotalestimatedlivestockassociatedcostsduetoCErangedfromU.S.2,420,348 per year. Total estimated livestock-associated costs due to CE ranged from U.S.196,681 to U.S.$3,846,754. An estimated 1,139 DALYs were also lost due to surgical cases of CE which is comparable to DALY losses from Amebiasis or Malaria in Peru. This conservative assessment found significant economic losses caused by this CE in Peruvian society. The findings of this study are important as these data can serve to prioritize those areas that may need to be targeted in a control program
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