Non-ideal magnetohydrodynamics versus turbulence II : which is the dominant process in stellar core formation?

Funding: JW acknowledges support from the European Research Council under the European Community’s Seventh Framework Programme (FP7/2007- 2013 grant agreement no. 339248), and from the University of St Andrews. BTL acknowledges the support of the National Aeronautics and Space Administration (NASA) through grant NN17AK90G and from the National Science Foundation (NSF) through grants no. 1517488 and PHY-1748958.Non-ideal magnetohydrodynamics (MHD) is the dominant process. We investigate the effect of magnetic fields (ideal and non-ideal) and turbulence (sub- and transsonic) on the formation of protostars by following the gravitational collapse of 1 M☉ gas clouds through the first hydrostatic core to stellar densities. The clouds are imposed with both rotational and turbulent velocities, and are threaded with a magnetic field that is parallel/antiparallel or perpendicular to the rotation axis; we investigate two rotation rates and four Mach numbers. The initial radius and mass of the stellar core are only weakly dependent on the initial parameters. In the models that include ideal MHD, the magnetic field strength implanted in the protostar at birth is much higher than observed, independent of the initial level of turbulence; only non-ideal MHD can reduce this strength to near or below the observed levels. This suggests that not only is ideal MHD an incomplete picture of star formation, but that the magnetic fields in low mass stars are implanted later in life by a dynamo process. Non-ideal MHD suppresses magnetically launched stellar core outflows, but turbulence permits thermally launched outflows to form a few years after stellar core formation.Publisher PDFPeer reviewe

Non-ideal magnetohydrodynamics versus turbulence – I. Which is the dominant process in protostellar disc formation?

Funding: European Research Council under the European Community’s Seventh Framework Programme (FP7/2007-2013 grant agreement no. 339248); University of St Andrews (JW). National Aeronautics and Space Administration (NASA) through grant NN17AK90G and from the National Science Foundation (NSF) through grants no 1517488 and PHY-1748958 (BTL).Non-ideal magnetohydrodynamics (MHD) is the dominant process. We investigate the effect of magnetic fields (ideal and non-ideal) and turbulence (sub- and transsonic) on the formation of circumstellar discs that form nearly simultaneously with the formation of the protostar. This is done by modelling the gravitational collapse of a 1 M☉ gas cloud that is threaded with a magnetic field and imposed with both rotational and turbulent velocities. We investigate magnetic fields that are parallel/antiparallel and perpendicular to the rotation axis, two rotation rates, and four Mach numbers. Disc formation occurs preferentially in the models that include non-ideal MHD where the magnetic field is antiparallel or perpendicular to the rotation axis. This is independent of the initial rotation rate and level of turbulence, suggesting that subsonic turbulence plays a minimal role in influencing the formation of discs. Aside from first core outflows that are influenced by the initial level of turbulence, non-ideal MHD processes are more important than turbulent processes during the formation of discs around low-mass stars.Publisher PDFPeer reviewe

Component-aware Orchestration of Cloud-based Enterprise Applications, from TOSCA to Docker and Kubernetes

Enterprise IT is currently facing the challenge of coordinating the management of complex, multi-component applications across heterogeneous cloud platforms. Containers and container orchestrators provide a valuable solution to deploy multi-component applications over cloud platforms, by coupling the lifecycle of each application component to that of its hosting container. We hereby propose a solution for going beyond such a coupling, based on the OASIS standard TOSCA and on Docker. We indeed propose a novel approach for deploying multi-component applications on top of existing container orchestrators, which allows to manage each component independently from the container used to run it. We also present prototype tools implementing our approach, and we show how we effectively exploited them to carry out a concrete case study

Intercellular signaling as a cause of cell death in cyclically impacted cartilage explants

AbstractRecently, in vitro cartilage studies have shown that impact loading can produce structural damage and osteoarthritis-like changes, including tissue swelling, collagen denaturation, and cell death.Objective This study was to determine whether a signal for cell death moves through the cartilage matrix, resulting in the spread of cell death over time from impacted to unimpacted regions.Design Cyclic impacts were applied to the 2mm core of 4mm cartilage discs. Post-impact culturing extended for 3, 6 or 21 days and occurred in one of two ways. In one, discs were cultured intact. In the second, cores were removed immediately after cessation of impact and cores and rings cultured separately. Cells in apoptosis and later stage necrosis were monitored using the TUNEL assay.Results The extent of cell death in impacted samples increased with increased duration of post-impact culturing. At the early time, the majority of cell death was located in the regions of direct impact whereas after extended culture, the extent of cell death was similar in the surrounding unimpacted regions and in the impacted core region. However, the physical separation of the impacted core from the surrounding, non-impacted ring regions immediately after impact, and prior to independent culture, kept the level of cell death in the surrounding ring close to control levels, even after 21 days of incubation.Discussion These findings indicate that soluble intercellular signalling is involved in the spreading of cell death through the cartilage matrix, and that its effects can be prevented by physical isolation of the surrounding ring from the impacted core

Performance engineering for microservices and serverless applications: the RADON approach

Microservices and serverless are becoming integral parts of mod-ern cloud-based applications. Tailored performance engineering isneeded for assuring that the applications meet their requirementsfor quality attributes such as timeliness, resource efficiency, andelasticity. A novel DevOps-based framework for developing mi-croservices and serverless applications is being developed in theRADON project. RADON contributes to performance engineeringby including novel approaches for modeling, deployment optimiza-tion, testing, and runtime management. This paper summarizes thecontents of our tutorial presented at the 11th ACM/SPEC Interna-tional Conference on Performance Engineering (ICPE)

Tungsten fibre-reinforced composites for advanced plasma facing components

AbstractThe European Fusion Roadmap foresees water cooled plasma facing components in a first DEMO design in order to provide enough margin for the cooling capacity and to only moderately extrapolate the technology which was developed and tested for ITER. In order to make best use of the water cooling concept copper (Cu) and copper-chromium-zirconium alloy (CuCrZr) are envisaged as heat sink whereas as armour tungsten (W) based materials will be used. Combining both materials in a high heat flux component asks for an increase of their operational range towards higher temperature in case of Cu/CuCrZr and lower temperatures for W. A remedy for both issues- brittleness of W and degrading strength of CuCrZr- could be the use of W fibres (Wf) in W and Cu based composites. Fibre preforms could be manufactured with industrially viable textile techniques. Flat textiles with a combination of 150/70 µm W wires have been chosen for layered deposition of tungsten-fibre reinforced tungsten (Wf/W) samples and tubular multi-layered braidings with W wire thickness of 50 µm were produced as a preform for tungsten-fibre reinforced copper (Wf /Cu) tubes. Cu melt infiltration was performed together with an industrial partner resulting in sample tubes without any blowholes. Property estimation by mean field homogenisation predicts strongly enhanced strength of the Wf/CuCrZr composite compared to its pure CuCrZr counterpart. Wf /W composites show very high toughness and damage tolerance even at room temperature. Cyclic load tests reveal that the extrinsic toughening mechanisms counteracting the crack growth are active and stable. FEM simulations of the Wf/W composite suggest that the influence of fibre debonding, which is an integral part of the toughening mechanisms, and reduced thermal conductivity of the fibre due to the necessary interlayers do not strongly influence the thermal properties of future components

Deletion of TRPC6 attenuates NMDA receptor-mediated Ca\u3csup\u3e2+\u3c/sup\u3e Entry and Ca\u3csup\u3e2+\u3c/sup\u3e-induced neurotoxicity following cerebral ischemia and oxygen-glucose deprivation

Transient receptor potential canonical 6 (TRPC6) channels are permeable to Na+ and Ca2+ and are widely expressed in the brain. In this study, the role of TRPC6 was investigated following ischemia/reperfusion (I/R) and oxygen-glucose deprivation (OGD). We found that TRPC6 expression was increased in wild-type (WT) mice cortical neurons following I/R and in primary neurons with OGD, and that deletion of TRPC6 reduced the I/R-induced brain infarct in mice and the OGD- /neurotoxin-induced neuronal death. Using live-cell imaging to examine intracellular Ca2+ levels ([Ca2+]i), we found that OGD induced a significant higher increase in glutamate-evoked Ca2+ influx compared to untreated control and such an increase was reduced by TRPC6 deletion. Enhancement of TRPC6 expression using AdCMV-TRPC6-GFP infection in WT neurons increased [Ca2+]i in response to glutamate application compared to AdCMV-GFP control. Inhibition of N-methyl-d-aspartic acid receptor (NMDAR) with MK801 decreased TRPC6-dependent increase of [Ca2+]i in TRPC6 infected cells, indicating that such a Ca2+ influx was NMDAR dependent. Furthermore, TRPC6-dependent Ca2+ influx was blunted by blockade of Na+ entry in TRPC6 infected cells. Finally, OGD-enhanced Ca2+ influx was reduced, but not completely blocked, in the presence of voltage-dependent Na+ channel blocker tetrodotoxin (TTX) and dl-α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) blocker CNQX. Altogether, we concluded that I/R-induced brain damage was, in part, due to upregulation of TRPC6 in cortical neurons. We postulate that overexpression of TRPC6 following I/R may induce neuronal death partially through TRPC6-dependent Na+ entry which activated NMDAR, thus leading to a damaging Ca2+ overload. These findings may provide a potential target for future intervention in stroke-induced brain damage

Deletion of TRPC6 attenuates NMDA receptor-mediated Ca\u3csup\u3e2+\u3c/sup\u3e Entry and Ca\u3csup\u3e2+\u3c/sup\u3e-induced neurotoxicity following cerebral ischemia and oxygen-glucose deprivation

Transient receptor potential canonical 6 (TRPC6) channels are permeable to Na+ and Ca2+ and are widely expressed in the brain. In this study, the role of TRPC6 was investigated following ischemia/reperfusion (I/R) and oxygen-glucose deprivation (OGD). We found that TRPC6 expression was increased in wild-type (WT) mice cortical neurons following I/R and in primary neurons with OGD, and that deletion of TRPC6 reduced the I/R-induced brain infarct in mice and the OGD- /neurotoxin-induced neuronal death. Using live-cell imaging to examine intracellular Ca2+ levels ([Ca2+]i), we found that OGD induced a significant higher increase in glutamate-evoked Ca2+ influx compared to untreated control and such an increase was reduced by TRPC6 deletion. Enhancement of TRPC6 expression using AdCMV-TRPC6-GFP infection in WT neurons increased [Ca2+]i in response to glutamate application compared to AdCMV-GFP control. Inhibition of N-methyl-d-aspartic acid receptor (NMDAR) with MK801 decreased TRPC6-dependent increase of [Ca2+]i in TRPC6 infected cells, indicating that such a Ca2+ influx was NMDAR dependent. Furthermore, TRPC6-dependent Ca2+ influx was blunted by blockade of Na+ entry in TRPC6 infected cells. Finally, OGD-enhanced Ca2+ influx was reduced, but not completely blocked, in the presence of voltage-dependent Na+ channel blocker tetrodotoxin (TTX) and dl-α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) blocker CNQX. Altogether, we concluded that I/R-induced brain damage was, in part, due to upregulation of TRPC6 in cortical neurons. We postulate that overexpression of TRPC6 following I/R may induce neuronal death partially through TRPC6-dependent Na+ entry which activated NMDAR, thus leading to a damaging Ca2+ overload. These findings may provide a potential target for future intervention in stroke-induced brain damage