111 research outputs found

    FIBS: A Generic Framework for Classifying Interval-based Temporal Sequences

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    We study the problem of classifying interval-based temporal sequences (IBTSs). Since common classification algorithms cannot be directly applied to IBTSs, the main challenge is to define a set of features that effectively represents the data such that classifiers can be applied. Most prior work utilizes frequent pattern mining to define a feature set based on discovered patterns. However, frequent pattern mining is computationally expensive and often discovers many irrelevant patterns. To address this shortcoming, we propose the FIBS framework for classifying IBTSs. FIBS extracts features relevant to classification from IBTSs based on relative frequency and temporal relations. To avoid selecting irrelevant features, a filter-based selection strategy is incorporated into FIBS. Our empirical evaluation on eight real-world datasets demonstrates the effectiveness of our methods in practice. The results provide evidence that FIBS effectively represents IBTSs for classification algorithms, which contributes to similar or significantly better accuracy compared to state-of-the-art competitors. It also suggests that the feature selection strategy is beneficial to FIBS's performance.Comment: In: Big Data Analytics and Knowledge Discovery. DaWaK 2020. Springer, Cha

    Allen's Interval Algebra Makes the Difference

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    Allen's Interval Algebra constitutes a framework for reasoning about temporal information in a qualitative manner. In particular, it uses intervals, i.e., pairs of endpoints, on the timeline to represent entities corresponding to actions, events, or tasks, and binary relations such as precedes and overlaps to encode the possible configurations between those entities. Allen's calculus has found its way in many academic and industrial applications that involve, most commonly, planning and scheduling, temporal databases, and healthcare. In this paper, we present a novel encoding of Interval Algebra using answer-set programming (ASP) extended by difference constraints, i.e., the fragment abbreviated as ASP(DL), and demonstrate its performance via a preliminary experimental evaluation. Although our ASP encoding is presented in the case of Allen's calculus for the sake of clarity, we suggest that analogous encodings can be devised for other point-based calculi, too.Comment: Part of DECLARE 19 proceeding

    Neural network equalisation for high-speed eye-safe optical wireless communication with 850 nm SM-VCSELs

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    In this paper, we experimentally illustrate the effectiveness of neural networks (NNs) as non-linear equalisers for multilevel pulse amplitude modulation (PAM-M) transmission over an optical wireless communication (OWC) link. In our study, we compare the bit-error-rate (BER) performances of two decision feedback equalisers (DFEs)—a multilayer-perceptron-based DFE (MLPDFE), which is the NN equaliser, and a transversal DFE (TRDFE)—under two degrees of non-linear distortion using an eye-safe 850 nm single-mode vertical-cavity surface-emitting laser (SM-VCSEL). Our results consistently show that the MLPDFE delivers superior performance in comparison to the TRDFE, particularly in scenarios involving high non-linear distortion and PAM constellations with eight or more levels. At a forward error correction (FEC) threshold BER of 0.0038, we achieve bit rates of ~28 Gbps, ~29 Gbps, ~22.5 Gbps, and ~5 Gbps using PAM schemes with 2, 4, 8, and 16 levels, respectively, with the MLPDFE. Comparably, the TRDFE yields bit rates of ~28 Gbps and ~29 Gbps with PAM-2 and PAM-4, respectively. Higher PAM levels with the TRDFE result in BERs greater than 0.0038 for bit rates above 2 Gbps. These results highlight the effectiveness of the MLPDFE in optimising the performance of SM-VCSEL-based OWC systems across different modulation schemes and non-linear distortion levels

    Canagliflozin attenuates the progression of atherosclerosis and inflammation process in APOE knockout mice

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    Background: Sodium glucose co-transporter2 inhibitors reduce the incidence of cardiovascular events in patients with type 2 diabetes mellitus based on the results of recent cardiovascular outcome studies. Herein, we investigated the efects of long-term treatment with canaglifozin on biochemical and immunohistochemical markers related to atherosclerosis and atherosclerosis development in the aorta of apolipoprotein E knockout (Apo-E(−/−) ) mice. Methods: At the age of 5 weeks, mice were switched from normal to a high-fat diet. After 5 weeks, Apo-E(−/−) mice were divided into control-group (6 mice) treated with 0.5% hydroxypropyl methylcellulose and Cana-group (7 mice) treated with canaglifozin (10 mg/kg per day) per os. After 5 weeks of intervention, animals were sacrifced, and heart and aorta were removed. Sections stained with hematoxylin–eosin (H&E) were used for histomorphometry whereas Masson’s stained tissues were used to quantify the collagen content. Immunohistochemistry to assess MCP-1, CD68, a-smooth muscle actin, MMP-2, MMP-9, TIMP-1 and TIMP-2 expression was carried out and q-PCR experiments were performed to quantify mRNA expression. Results: Canaglifozin-group mice had lower total-cholesterol, triglycerides and glucose levels (P<0.01), while heart rate was signifcantly lower (P<0.05). Histomorphometry revealed that one in seven Cana-group mice versus four in six control mice developed atheromatosis, while aortic root plaque was signifcantly less, and collagen was 1.6 times more intense in canaglifozin-group suggesting increased plaque stability. Immunohistochemistry revealed that MCP-1 was signifcantly less expressed (P<0.05) in the aortic root of canaglifozin-group while reduced expression of a-actin and CD68 was not reaching signifcance (P=0.15). VCAM-1 and MCP-1 mRNA levels were lower (P=0.02 and P=0.07, respectively), while TIMP-1/MMP-2 ratio expression was higher in canaglifozin-group approaching statistical signifcance (P=0.07). Conclusions: Canaglifozin attenuates the progression of atherosclerosis, reducing (1) hyperlipidemia and hyper‑ glycemia, and (2) infammatory process, by lowering the expression of infammatory molecules such as MCP-1 and VCAM-1. Moreover, canaglifozin was found to increase the atherosclerotic plaque stability via increasing TIMP-1/ MMP-2 ratio expression

    Lanthanoid “Bottlebrush” Clusters: Remarkably Elongated Metal-Oxo Core Structures with Controllable Lengths

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    Large metal-oxo clusters consistently assume spherical or regular polyhedral morphologies rather than high-aspect-ratio structures. Access to elongated core structures has now been achieved by the reaction of lanthanoid salts with a tetrazole-functionalized calixarene in the presence of a simple carboxylate coligand.The resulting Ln19 and Ln12 clusters are constructed from apex-fused Ln5O6 trigonal bipyramids and are formed consistently under a range of reaction conditions and reagent ratios. Altering the carboxylate coligandstructure reliably controls the cluster length, giving access to a new class of rod-like clusters of variable length

    History of clinical transplantation

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    The emergence of transplantation has seen the development of increasingly potent immunosuppressive agents, progressively better methods of tissue and organ preservation, refinements in histocompatibility matching, and numerous innovations is surgical techniques. Such efforts in combination ultimately made it possible to successfully engraft all of the organs and bone marrow cells in humans. At a more fundamental level, however, the transplantation enterprise hinged on two seminal turning points. The first was the recognition by Billingham, Brent, and Medawar in 1953 that it was possible to induce chimerism-associated neonatal tolerance deliberately. This discovery escalated over the next 15 years to the first successful bone marrow transplantations in humans in 1968. The second turning point was the demonstration during the early 1960s that canine and human organ allografts could self-induce tolerance with the aid of immunosuppression. By the end of 1962, however, it had been incorrectly concluded that turning points one and two involved different immune mechanisms. The error was not corrected until well into the 1990s. In this historical account, the vast literature that sprang up during the intervening 30 years has been summarized. Although admirably documenting empiric progress in clinical transplantation, its failure to explain organ allograft acceptance predestined organ recipients to lifetime immunosuppression and precluded fundamental changes in the treatment policies. After it was discovered in 1992 that long-surviving organ transplant recipient had persistent microchimerism, it was possible to see the mechanistic commonality of organ and bone marrow transplantation. A clarifying central principle of immunology could then be synthesized with which to guide efforts to induce tolerance systematically to human tissues and perhaps ultimately to xenografts

    History of clinical transplantation

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    How transplantation came to be a clinical discipline can be pieced together by perusing two volumes of reminiscences collected by Paul I. Terasaki in 1991-1992 from many of the persons who were directly involved. One volume was devoted to the discovery of the major histocompatibility complex (MHC), with particular reference to the human leukocyte antigens (HLAs) that are widely used today for tissue matching.1 The other focused on milestones in the development of clinical transplantation.2 All the contributions described in both volumes can be traced back in one way or other to the demonstration in the mid-1940s by Peter Brian Medawar that the rejection of allografts is an immunological phenomenon.3,4 © 2008 Springer New York

    Effect of Systemic Hypertension With Versus Without Left Ventricular Hypertrophy on the Progression of Atrial Fibrillation (from the Euro Heart Survey).

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    Hypertension is a risk factor for both progression of atrial fibrillation (AF) and development of AF-related complications, that is major adverse cardiac and cerebrovascular events (MACCE). It is unknown whether left ventricular hypertrophy (LVH) as a consequence of hypertension is also a risk factor for both these end points. We aimed to assess this in low-risk AF patients, also assessing gender-related differences. We included 799 patients from the Euro Heart Survey with nonvalvular AF and a baseline echocardiogram. Patients with and without hypertension were included. End points after 1 year were occurrence of AF progression, that is paroxysmal AF becoming persistent and/or permanent AF, and MACCE. Echocardiographic LVH was present in 33% of 379 hypertensive patients. AF progression after 1 year occurred in 10.2% of 373 patients with rhythm follow-up. In hypertensive patients with LVH, AF progression occurred more frequently as compared with hypertensive patients without LVH (23.3% vs 8.8%, p = 0.011). In hypertensive AF patients, LVH was the most important multivariably adjusted determinant of AF progression on multivariable logistic regression (odds ratio 4.84, 95% confidence interval 1.70 to 13.78, p = 0.003). This effect was only seen in male patients (27.5% vs 5.8%, p = 0.002), while in female hypertensive patients, no differences were found in AF progression rates regarding the presence or absence of LVH (15.2% vs 15.0%, p = 0.999). No differences were seen in MACCE for hypertensive patients with and without LVH. In conclusion, in men with hypertension, LVH is associated with AF progression. This association seems to be absent in hypertensive women
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