240 research outputs found

    On generalized processor sharing and objective functions: analytical framework

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    Today, telecommunication networks host a wide range of heterogeneous services. Some demand strict delay minima, while others only need a best-effort kind of service. To achieve service differentiation, network traffic is partitioned in several classes which is then transmitted according to a flexible and fair scheduling mechanism. Telecommunication networks can, for instance, use an implementation of Generalized Processor Sharing (GPS) in its internal nodes to supply an adequate Quality of Service to each class. GPS is flexible and fair, but also notoriously hard to study analytically. As a result, one has to resort to simulation or approximation techniques to optimize GPS for some given objective function. In this paper, we set up an analytical framework for two-class discrete-time probabilistic GPS which allows to optimize the scheduling for a generic objective function in terms of the mean unfinished work of both classes without the need for exact results or estimations/approximations for these performance characteristics. This framework is based on results of strict priority scheduling, which can be regarded as a special case of GPS, and some specific unfinished-work properties in two-class GPS. We also apply our framework on a popular type of objective functions, i.e., convex combinations of functions of the mean unfinished work. Lastly, we incorporate the framework in an algorithm to yield a faster and less computation-intensive result for the optimum of an objective function

    Local filtering operations on two qubits

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    We consider one single copy of a mixed state of two qubits and investigate how its entanglement changes under local quantum operations and classical communications (LQCC) of the type ρ(AB)ρ(AB)\rho'\sim (A\otimes B)\rho(A\otimes B)^{\dagger}. We consider a real matrix parameterization of the set of density matrices and show that these LQCC operations correspond to left and right multiplication by a Lorentz matrix, followed by normalization. A constructive way of bringing this matrix into a normal form is derived. This allows us to calculate explicitly the optimal local filterin operations for concentrating entanglement. Furthermore we give a complete characterization of the mixed states that can be purified arbitrary close to a Bell state. Finally we obtain a new way of calculating the entanglement of formation.Comment: 4 page

    Improvement of the chondrocyte-specific phenotype upon equine bone marrow mesenchymal stem cell differentiation. Influence of TGF-ß1 or TGF-ß3, associated with BMP-2 and type I collagen siRNAs

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    International audienceArticular cartilage is a tissue characterized by its poor intrinsic capacity for self-repair. This tissue is frequently altered upon trauma or in osteoarthritis (OA), a degenerative disease that is currently incurable. Consequently, cartilage markers, such as type II collagen, are degraded whereas atypic molecules, such as type I collagen, are newly synthetized. Another essential phenomenon occurring in OA is the upregulation of HtrA1, a serine protease targeting upstream receptors of signalling pathways involved in the synthesis of articular cartilage markers. OA incurs considerable economic loss for the equine sector. In the view to develop new therapies for humans and horses, significant progress in tissue engineering has led to the emergence of new generations of cartilage therapy. Matrix-associated autologous chondrocyte implantation is an advanced 3D cell-based therapy that holds promise for cartilage repair. The aim of this study is to improve the autologous chondrocyte implantation strategy by enhancing the chondrogenic differentiation of mesenchymal stem cells (MSCs) in order to increase the type II collagen/ type I collagen ratio

    Subsequent female breast cancer risk associated with anthracycline chemotherapy for childhood cancer.

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    Anthracycline-based chemotherapy is associated with increased subsequent breast cancer (SBC) risk in female childhood cancer survivors, but the current evidence is insufficient to support early breast cancer screening recommendations for survivors treated with anthracyclines. In this study, we pooled individual patient data of 17,903 survivors from six well-established studies, of whom 782 (4.4%) developed a SBC, and analyzed dose-dependent effects of individual anthracycline agents on developing SBC and interactions with chest radiotherapy. A dose-dependent increased SBC risk was seen for doxorubicin (hazard ratio (HR) per 100 mg m-2: 1.24, 95% confidence interval (CI): 1.18-1.31), with more than twofold increased risk for survivors treated with ≥200 mg m-2 cumulative doxorubicin dose versus no doxorubicin (HR: 2.50 for 200-299 mg m-2, HR: 2.33 for 300-399 mg m-2 and HR: 2.78 for ≥400 mg m-2). For daunorubicin, the associations were not statistically significant. Epirubicin was associated with increased SBC risk (yes/no, HR: 3.25, 95% CI: 1.59-6.63). For patients treated with or without chest irradiation, HRs per 100 mg m-2 of doxorubicin were 1.11 (95% CI: 1.02-1.21) and 1.26 (95% CI: 1.17-1.36), respectively. Our findings support that early initiation of SBC surveillance may be reasonable for survivors who received ≥200 mg m-2 cumulative doxorubicin dose and should be considered in SBC surveillance guidelines for survivors and future treatment protocols

    Subsequent Female Breast Cancer Risk Associated With Anthracycline Chemotherapy for Childhood Cancer

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    Anthracycline-based chemotherapy is associated with increased subsequent breast cancer (SBC) risk in female childhood cancer survivors, but the current evidence is insufficient to support early breast cancer screening recommendations for survivors treated with anthracyclines. In this study, we pooled individual patient data of 17,903 survivors from six well-established studies, of whom 782 (4.4%) developed a SBC, and analyzed dose-dependent effects of individual anthracycline agents on developing SBC and interactions with chest radiotherapy. A dose-dependent increased SBC risk was seen for doxorubicin (hazard ratio (HR) per 100 mg 

    Smad gene expression in pulmonary fibroblasts: indications for defective ECM repair in COPD

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    Background: Chronic Obstructive Pulmonary Disease ( COPD) is characterized by defective extracellular matrix (ECM) turnover as a result of prolonged cigarette smoking. Fibroblasts have a central role in ECM turnover. The TGF beta induced Smad pathway provides intracellular signals to regulate ECM production. We address the following hypothesis: fibroblasts have abnormal expression of genes in the Smad pathway in COPD, resulting in abnormal proteoglycan modulation, the ground substance of ECM. Methods: We compared gene expression of the Smad pathway at different time points after stimulation with TGF beta, TNF or cigarette smoke extract (CSE) in pulmonary fibroblasts of GOLD stage II and IV COPD patients, and controls. Results: Without stimulation, all genes were similarly expressed in control and COPD fibroblasts. TGF beta stimulation: downregulation of Smad3 and upregulation of Smad7 occurred in COPD and control fibroblasts, indicating a negative feedback loop upon TGF beta stimulation. CSE hardly influenced gene expression of the TGF beta-Smad pathway in control fibroblasts, whereas it reduced Smad3 and enhanced Smad7 gene expression in COPD fibroblasts. Furthermore, decorin gene expression decreased by all stimulations in COPD but not in control fibroblasts. Conclusion: Fibroblasts of COPD patients and controls differ in their regulation of the Smad pathway, the contrast being most pronounced under CSE exposure. This aberrant responsiveness of COPD fibroblasts to CSE might result in an impaired tissue repair capability and is likely important with regard to the question why only a subset of smokers demonstrates an excess ECM destruction under influence of cigarette smoking
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