Network-aware design-space exploration of a power-efficient embedded application

The paper presents the design and multi-parameter optimization of a networked embedded application for the health-care domain. Several hardware, software, and application parameters, such as clock frequency, sensor sampling rate, data packet rate, are tuned at design- and run-time according to application specifications and operating conditions to optimize hardware requirements, packet loss, power consumption. Experimental results show that further power efficiency can be achieved by considering also communication aspects during design space exploratio

Fluctuations and scaling in creep deformation

The spatial fluctuations of deformation are studied in creep in the Andrade's power-law and the logarithmic phases, using paper samples. Measurements by the Digital Image Correlation technique show that the relative strength of the strain rate fluctuations increases with time, in both creep regimes. In the Andrade creep phase characterized by a power law decay of the strain rate $\epsilon_t \sim t^{-\theta}$, with $\theta \approx 0.7$, the fluctuations obey $\Delta \epsilon_t \sim t^{-\gamma}$, with $\gamma \approx 0.5$. The local deformation follows a data collapse appropriate for an absorbing state/depinning transition. Similar behavior is found in a crystal plasticity model, with a jamming or yielding phase transition

Group memory rehabilitation for people with multiple sclerosis: a feasibility randomized controlled trial

Objective: To assess the feasibility and effectiveness of a group memory rehabilitation programme combining compensation and restitution strategies. Design: Randomized controlled trial. Setting: Community. Participants: People with multiple sclerosis who reported memory difficulties were recruited. Interventions: A group memory rehabilitation programme, comprising ten 1.5-hour sessions, was compared with a waiting list control. Main measures: The primary outcome was the Everyday Memory Questionnaire. Secondary outcomes included the General Health Questionnaire 28 and MS Impact Scale administered four and eight months after randomization. In addition, those in the intervention group gave feedback about the intervention. Results: Forty-eight participants were recruited. They were aged 34–72 years (mean 54.3, SD 11.0) and 33 (69%) were women. There were no significant differences between the two groups on the Everyday Memory Questionnaire or MS Impact Scale (P > 0.05) at four or eight months after randomization. However, the intervention group reported significantly better mood than controls on the GHQ-28 at eight months (P = 0.04). Participants showed minimal benefit from the memory rehabilitation programme on quantitative measures but the intervention was well received, as indicated by positive feedback at the end of the intervention. Conclusions: There was no significant effect of the intervention on memory but there was a significant effect on mood. The results suggest a larger scale study is justified

An interface capturing method for liquid-gas flows at low-Mach number

Multiphase, compressible and viscous flows are of crucial importance in a wide range of scientific and engineering problems. Despite the large effort paid in the last decades to develop accurate and efficient numerical techniques to address this kind of problems, current models need to be further improved to address realistic applications. In this context, we propose a numerical approach to the simulation of multiphase, viscous flows where a compressible and an incompressible phase interact in the low-Mach number regime. In this frame, acoustics is neglected but large density variations of the compressible phase can be accounted for as well as heat transfer, convection and diffusion processes. The problem is addressed in a fully Eulerian framework exploiting a low-Mach number asymptotic expansion of the Navier-Stokes equations. A Volume of Fluid approach (VOF) is used to capture the liquid-gas interface, built on top of a massive parallel solver, second order accurate both in time and space. The second-order-pressure term is treated implicitly and the resulting pressure equation is solved with the eigenexpansion method employing a robust and novel formulation. We provide a detailed and complete description of the theoretical approach together with information about the numerical technique and implementation details. Results of benchmarking tests are provided for five different test cases

Circulating endothelial progenitor cells from patients with renal cell carcinoma display aberrant VEGF regulation, reduced apoptosis and altered ultrastructure

Endothelial colony forming cells (ECFCs) are the only endothelial progenitor cells (EPCs) subtype belonging to the endothelial phenotype and capable of forming neovessels in vivo. We have recently shown that the intracellular Ca2+ machinery plays a key role in ECFC activation and is remodeled in ECFCs isolated from patients suffering from renal cellular carcinoma (RCC-ECFCs). More specifically, ECFCs upregulate the store-operated Ca2+ entry (SOCE) machinery, while they seemingly show a reduction in the Ca2+ concentration within the endoplasmic reticulum ([Ca2+]ER). Metastatic RCC patients are commonly treated with an anti-vascular endothelial growth factor (VEGF) therapy, but they show either intrinsic or adaptive refractoriness, which ultimately leads to their death. Herein, we assessed whether and how the rearrangement of the Ca2+ machinery impacts on the pro-angiogenic Ca2+ response to VEGF, which stimulates normal ECFCs (N-ECFCs) through an oscillatory Ca2+ response. We found that VEGF stimulates the nuclear translocation of p65/RelA, a major component of the Ca2+-dependent transcription fac- tor NF-kB, in N-ECFCs. This process is blocked by the pharmacological abrogation of VEGF-induced Ca2+ oscillations. We further showed that NF-kB controls VEGF-induced protein expression of E-selectin, VCAM-1 and MMP9. Likewise, VEGF-induced expression was also inhibited by the pharmacological suppression of the accompanying Ca2+ spikes. Thus, VEGF induces a Ca2+-dependent, NF-kB-mediated protein expression in N-ECFCs. VEGF did not trigger protein expression in RCC-ECFCs despite the fact that VEGFR-2 was normally expressed and auto-phosphorylated. Our subsequent studies employed the tar- geted recombinant Ca2+-sensitive photoprotein aequorin to confirm that [Ca2+]ER is lower in RCC-ECFCs; surprisingly, electron microscopy analysis revealed that the endoplasmic reticulum cisternae are enlarged rather than shrinked in these cells. These results show for the first time that VEGF fails to stimulate tumor-derived ECFCs: these findings could therefore help to understand the relative failure of anti-VEGF treatment in RCC patients. Reference

FluTAS: A GPU-accelerated finite difference code for multiphase flows

We present the Fluid Transport Accelerated Solver, FluTAS, a scalable GPU code for multiphase flows with thermal effects. The code solves the incompressible Navier-Stokes equation for two-fluid systems, with a direct FFT-based Poisson solver for the pressure equation. The interface between the two fluids is represented with the Volume of Fluid (VoF) method, which is mass conserving and well suited for complex flows thanks to its capacity of handling topological changes. The energy equation is explicitly solved and coupled with the momentum equation through the Boussinesq approximation. The code is conceived in a modular fashion so that different numerical methods can be used independently, the existing routines can be modified, and new ones can be included in a straightforward and sustainable manner. FluTAS is written in modern Fortran and parallelized using hybrid MPI/OpenMP in the CPU-only version and accelerated with OpenACC directives in the GPU implementation. We present different benchmarks to validate the code, and two large-scale simulations of fundamental interest in turbulent multiphase flows: isothermal emulsions in HIT and two-layer Rayleigh-B\'enard convection. FluTAS is distributed through a MIT license and arises from a collaborative effort of several scientists, aiming to become a flexible tool to study complex multiphase flows

Arachidonic acid-evoked Ca^{2+} signals promote nitric oxide release and proliferation in human endothelial colony forming cells

Arachidonic acid (AA) stimulates endothelial cell (EC) proliferation through an increase in intracellular Ca^{2+} concentration ([Ca^{2+}]_{i}), that, in turn, promotes nitric oxide (NO) release. AA-evoked Ca^{2+} signals are mainly mediated by Transient Receptor Potential Vanilloid 4 (TRPV4) channels. Circulating endothelial colony forming cells (ECFCs) represent the only established precursors of ECs. In the present study, we, therefore, sought to elucidate whether AA promotes human ECFC (hECFC) proliferation through an increase in [Ca^{2+}]_{i} and the following activation of the endothelial NO synthase (eNOS). AA induced a dose-dependent [Ca^{2+}]_{i} raise that was mimicked by its non-metabolizable analogue eicosatetraynoic acid. AA-evoked Ca^{2+} signals required both intracellular Ca^{2+} release and external Ca^{2+} inflow. AA-induced Ca^{2+} release was mediated by inositol-1,4,5-trisphosphate receptors from the endoplasmic reticulum and by two pore channel 1 from the acidic stores of the endolysosomal system. AA-evoked Ca^{2+} entry was, in turn, mediated by TRPV4, while it did not involve store-operated Ca^{2+} entry. Moreover, AA caused an increase in NO levels which was blocked by preventing the concomitant increase in [Ca^{2+}]_{i} and by inhibiting eNOS activity with NG-nitro-l-arginine methyl ester (l-NAME). Finally, AA per se did not stimulate hECFC growth, but potentiated growth factors-induced hECFC proliferation in a Ca^{2+} - and NO-dependent manner. Therefore, AA-evoked Ca^{2+} signals emerge as an additional target to prevent cancer vascularisation, which may be sustained by ECFC recruitment

Spatial fluctuations in transient creep deformation

We study the spatial fluctuations of transient creep deformation of materials as a function of time, both by Digital Image Correlation (DIC) measurements of paper samples and by numerical simulations of a crystal plasticity or discrete dislocation dynamics model. This model has a jamming or yielding phase transition, around which power-law or Andrade creep is found. During primary creep, the relative strength of the strain rate fluctuations increases with time in both cases - the spatially averaged creep rate obeys the Andrade law $\epsilon_t \sim t^{-0.7}$, while the time dependence of the spatial fluctuations of the local creep rates is given by $\Delta \epsilon_t \sim t^{-0.5}$. A similar scaling for the fluctuations is found in the logarithmic creep regime that is typically observed for lower applied stresses. We review briefly some classical theories of Andrade creep from the point of view of such spatial fluctuations. We consider these phenomenological, time-dependent creep laws in terms of a description based on a non-equilibrium phase transition separating evolving and frozen states of the system when the externally applied load is varied. Such an interpretation is discussed further by the data collapse of the local deformations in the spirit of absorbing state/depinning phase transitions, as well as deformation-deformation correlations and the width of the cumulative strain distributions. The results are also compared with the order parameter fluctuations observed close to the depinning transition of the 2$d$ Linear Interface Model or the quenched Edwards-Wilkinson equation.Comment: 27 pages, 18 figure