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An analysis workflow has been developed to assess energy deposition and material damage for ITER vertical displacement events (VDEs) and major disruptions (MD). This paper describes the use of this workflow to assess the melt damage to be expected during unmitigated current quench (CQ) phases of VDEs and MDs at different points in the ITER research plan. The plasma scenarios are modeled using the DINA code with variations in plasma current I p, disruption direction (upwards or downwards), Be impurity density n Be, and diffusion coefficient χ. Magnetic field line tracing using SMITER calculates time-dependent, 3D maps of surface power density q ⊥ on the Be-armored first wall panels (FWPs) throughout the CQ. MEMOS-U determines the temperature response, macroscopic melt motion, and final surface topology of each FWP. Effects of Be vapor shielding are included. Scenarios at the baseline combination of I p and toroidal field (15 MA/5.3 T) show the most extreme melt damage, with the assumed n Be having a strong impact on the disruption duration, peak q ⊥ and total energy deposition to the first wall. The worst-cases are upward 15 MA VDEs and MDs at lower values of n Be, with q ⊥,max = 307 MW m−2 and maximum erosion losses of ∼2 mm after timespans of ∼400–500 ms. All scenarios at 5 MA avoided melt damage, and only one 7.5 MA scenario yields a notable erosion depth of 0.25 mm. These results imply that disruptions during 5 MA, and some 7.5 MA, operating scenarios will be acceptable during the pre-fusion power operation phases of ITER. Preliminary analysis shows that localized melt damage for the worst-case disruption should have a limited impact on subsequent stationary power handling capability.

Astrocytic endfeet cover the brain surface and form a sheath around the cerebral vasculature. An emerging concept is that endfeet control blood–brain water transport and drainage of interstitial fluid and waste along paravascular pathways. Little is known about the signaling mechanisms that regulate endfoot volume and hence the width of these drainage pathways. Here, we used the genetically encoded fluorescent Ca2+ indicator GCaMP6f to study Ca2+ signaling within astrocytic somata, processes, and endfeet in response to an osmotic challenge known to induce cell swelling. Acute cortical slices were subjected to artificial cerebrospinal fluid with 20% reduction in osmolarity while GCaMP6f fluorescence was imaged with two‐photon microscopy. Ca2+ signals induced by hypoosmotic conditions were observed in all astrocytic compartments except the soma. The Ca2+ response was most prominent in subpial and perivascular endfeet and included spikes with single peaks, plateau‐type elevations, and rapid oscillations, the latter restricted to subpial endfeet. Genetic removal of the type 2 inositol 1,4,5‐triphosphate receptor (IP3R2) severely suppressed the Ca2+ responses in endfeet but failed to affect brain water accumulation in vivo after water intoxication. Furthermore, the increase in endfoot Ca2+ spike rate during hypoosmotic conditions was attenuated in mutant mice lacking the aquaporin‐4 anchoring molecule dystrophin and after blockage of transient receptor potential vanilloid 4 channels. We conclude that the characteristics and underpinning of Ca2+ responses to hypoosmotic stress differ within the astrocytic territory and that IP3R2 is essential for the Ca2+ signals only in subpial and perivascular endfeet.

The beryllium (Be) main chamber wall interaction during a 5 MA/1.8 T upward, unmitigated VDE scenario, first analysed in [J. Coburn et al., Phys. Scr. T171 (2020) 014076] for ITER, has been re-evaluated using the latest energy deposition analysis software. Updates to the DINA disruption model are summarized, including an improved numerical convergence for the 0D power balance, limitations on the safety factor within the plasma core, and the choice to maintain a constant plasma + halo poloidal cross-section. Such updates result in a broad halo region and higher radiated power fractions compared to previous models. The new scenario lasts for ~75 ms and deposits ~29 MJ of energy, with the radial distribution of parallel heat flux q ‖ r resembling an exponential falloff with an effective λ q = 75 - 198 mm. A maximum halo width w h of 0.52 m at the outboard midplane is observed. SMITER field line tracing and energy deposition simulations calculate a q ⊥ , m a x of ~83 MW/m2 on the upper first wall panels (FWP). Heat transfer calculations with the MEMOS-U code show that the FWP surface temperature reaches ~1000 K, well below the Be melt threshold. Variations of this 5 MA scenario with Be impurity densities from 0 to 3∙1019 m−3 also remain below the melt threshold despite differences in energy deposition and duration. These results are in contrast to the early study which predicted melt damage to the first wall [J. Coburn et al., Phys. Scr. T171 (2020) 014076], and emphasize the importance of accurate models for the halo width w h and the heat flux distribution q ‖ r within that halo width. The 2020 halo model in DINA has been compared with halo current experiments on COMPASS, JET, and Alcator C-Mod, and the preliminary results build confidence in the broad halo width predictions. Results for the 5 MA VDE are compared with those for a 15 MA equivalent, generated using the new DINA model. At the higher current, significant melting of the upper FWP is to be expected.

The MEMOS-U code, a significantly upgraded version of MEMOS-3D, has been developed to address macroscopic metallic melt motion in large-deformation long-displacement regimes, where melts spill onto progressively colder solid surfaces, that are ubiquitous in contemporary tokamaks and expected to be realized in ITER. The modelling of plasma effects, appearing via the free-surface boundary conditions, is discussed along with the sensitivity to external input. The crucial roles of convective and thermionic cooling are exemplified by simulations of ELM-induced tungsten leading edge melting. Key melt characteristics, revealed by previous MEMOS-U modelling of grounded sample exposures, are confirmed in new simulations of the recent floating sample exposures in ASDEX-Upgrade.

BackgroundPrevious studies have reported associations between obesity, chronic pain and increased pain sensitivity. The adipokine leptin has been suggested to be involved in the osteoarthritis process as well as in pain sensitisation.ObjectivesThe aim was to study associations between chronic widespread pain, pain sensitivity and leptin in individuals with knee pain.MethodsIn all, 306 individuals with knee pain were included in the Halland osteoarthritis cohort, ClinicalTrials.gov NCT04928170. Of those, 265 were included in this cross-sectional baseline study. The mean age (sd) was 51.6 (8.8) years, and 71% was women. The participants marked their painful areas on a pain figure with 18 predefined areas. They were categorised in three different pain groups according to the modified WP2019 definition (1), with knees excluded (due to highest goodness of fit): Chronic widespread pain (CWP), chronic regional pain (ChRP) if CWP was not met, and no chronic pain (NCP). The group with CWP were compared with those reporting no CWP (ChRP and NCP). The pressure pain thresholds (PPT) were measured using a computerised pressure algometry (AlgoMed, Medoc) on eight predefined tender points (trapezius (bilateral), right second rib, right lateral epicondyle, knees, gluteal (bilateral)) (2). Increased pain sensitivity was defined as having PPT in the lowest third in all tender points. Obesity was measured via waistline measurement and a bioimpedance (InBody 770) measuring BMI and visceral fat area (VFA). Serum-Leptin were analysed with an ELISA method (Alpco). Knee Injury and Osteoarthritis Outcome Score (KOOS) was used to describe the groups.ResultsIn this baseline study, 16% reported CWP, and 15% had low pain pressure thresholds at baseline in the study. Those fulfilling CWP were more often women, had higher BMI, VFA, and increased leptin levels and worse KOOS in four of five subscores, see Table 1A. The age and gender-adjusted leptin levels were 21.6 ng/ml (95% CI 18.2-25.0) in the group with no CWP vs. 35.5 ng/ml (95% CI 27.6-43.4) in the CWP group, p=0.002. In a logistic regression adjusting for age and gender, leptin was associated with reporting CWP OR 1.015 (95% CI 1.004-1.027, p= 0.008).Table 1.A Comparisons between those without CWP and those fulfilling CWP and table 1B comparisons between those not having low PPT and those with low PPT.ABNo CWPMean (sd)CWPMean (sd)p-valueNot Low PPTMean (sd)Low PPTMean (sd)p-valuen2104022639Age51.8 (8.7)52.8 (7.6)0.46552.1 (8.5)48.8 (9.9)0.030Gender, female n(%)67900.00472670.524BMI (kg/m2)26.2 (4.6)28.0 (5.0)0.02226.4 (4.9)27.5 (4.3)0.213VFA (cm2)107 (50)137 (56)0.001110 (54)127 (49)0.088Leptin (ng/ml)21.0 (23.9)39.0 (36.6)23.0 (26.0)31.8 (31.6)0.061CRP (mg/L)1.9 (2.7)2.2 (2.3)0.6022.0 (2.7)1.9 (1.8)0.825KOOSPain (0-100, worst to best)74 (15)61 (17)73 (15)65 (18)0.002Symptom (0-100, worst to best)72 (17)64 (18)0.01671 (17)67 (19)0.188ADL (0-100, worst to best)84 (13)69 (19)84 (14)72 (21)Sport/rec (0-100, worst to best)49 (26)34 (27)0.00149 (26)36 (25)0.009QoL (0-100, worst to best)53 (18)46 (20)0.05053 (18)45 (21)0.017BMI, body mass index; VFA, visceral fat area; CRP, C-reactive protein; KOOS, knee injury and osteoarthritis outcome score; ADL; function in daily living; sport/Rec, Function in sport and recreation; QOL, knee-related Quality of lifeThe participants with low PPT were younger and had a mean (sd) leptin 31.8 ng/ml (31.6) vs 23.0 (26.0), p=0.061 in the group not having low PPT, Table 1B. In a logistic regression adjusting for age and gender, leptin was associated with low PPT OR 1.016 (95% CI 1.004-1.029, p= 0.012).ConclusionThe pathophysiological mechanism causing widespread pain is probably multifactorial, involving both biological and physical factors. The adipokine leptin could be involved in some of these mechanisms, but longitudinal studies are needed to be able to study causal relationships.References[1]Wolfe F, et al. Scand J Pain. 2019;20:77-86.[2]Wolfe F, et al. Arthritis and rheumatism. 1990;33:160-72.Disclosure of InterestsNone declared

The first MEMOS 3D simulations of liquid metal motion on an inclined bulk tungsten sample transiently molten by edge-localized modes (ELMs) are reported. The exposures took place at the outer ASDEX-Upgrade divertor with the tungsten surface tangent intersecting the magnetic field at ∼ 18°. Simulations confirm that the observed poloidal melt motion is caused by the volumetric J × B force with J the bulk replacement current triggered by thermionic emission. The final erosion profile and total melt build up are reproduced by employing the escaping thermionic current dependence on the incident heat flux derived from dedicated particle-in-cell simulations. Modelling reveals that melt dynamics is governed by the volumetric Lorentz force, capillary flows due to thermal surface tension gradients and viscous deceleration. The effect of the evolving surface deformation, that locally alters the field-line inclination modifying the absorbed power flux and the escaping thermionic current, in the final surface morphology is demonstrated to be significant. Keywords: Melting, Tungsten, Divertor, Melt layer motion, MEMOS, Thermionic emission

The consequences of tungsten (W) melting on divertor lifetime and plasma operation are high priority issues for ITER. Sustained and controlled W-melting experiment has been achieved for the first time in WEST on a poloidal sharp leading edge of an actively cooled ITER-like plasma facing unit (PFU). A series of dedicated high power steady state plasma discharges were performed to reach the melting point of tungsten. The leading edge was exposed to a parallel heat flux of about 100 MW.m−2 for up to 5 s providing a melt phase of about 2 s without noticeable impact of melting on plasma operation (radiated power and tungsten impurity content remained stable at constant input power) and no melt ejection were observed. The surface temperature of the MB was monitored by a high spatial resolution (0.1 mm/pixel) infrared camera viewing the melt zone from the top of the machine. The melting discharge was repeated three times resulting in about 6 s accumulated melting duration leading to material displacement from three similar pools. Cumulated on the overall sustained melting periods, this leads to excavation depth of about 230 μm followed by a re-solidified tungsten bump of 200 μm in the JxB direction.

Introduction During brain edema (BE), elevated intracranial pressure (ICP) compresses capillaries and reduces cerebral blood flow (CBF) by decreasing perfusion pressure. The reduction in CBF and th...

Studies of macroscopic melt motion induced by fast transient power loads and the ensuing damage to plasma-facing components are critical for ITER. Based on state-of-the-art experiments, heat transfer is argued to be strongly entangled with fluid dynamics. The physics model of the MEMOS-U code is introduced. Simulations are reported of recent tokamak experiments concerning deliberate transient melting of beryllium main chamber tiles (JET) and tungsten divertor components (ASDEX Upgrade, JET). MEMOS-U is demonstrated to capture the main physics responsible for melt dynamics and to reproduce the observed surface deformation. The intricate role of resolidification is elucidated.

Within the EUROfusion MST1 work package, a series of experiments has been conducted on AUG and TCV devices to disentangle the role of plasma fueling and plasma shape for the onset of small ELM regimes. On both devices, small ELM regimes with high confinement are achieved if and only if two conditions are fulfilled at the same time. Firstly, the plasma density at the separatrix must be large enough (), leading to a pressure profile flattening at the separatrix, which stabilizes type-I ELMs. Secondly, the magnetic configuration has to be close to a double null (DN), leading to a reduction of the magnetic shear in the extreme vicinity of the separatrix. As a consequence, its stabilizing effect on ballooning modes is weakened. Peer Reviewed Article escrit per 365 autors/autores: Labit, B.; Eich, T.; Harrer, G. F.; Wolfrum, E.; Bernert, M.; Dunne, M. G.; Frassinetti, L.; Hennequin, P.; Maurizio, R.; Merle, A.; Meyer, H.; Saarelma, S.; Sheikh, U.; Adamek, J.; Agostini, M.; Aguiam, D.; Akers, R.; Albanese, R.; Albert, C.; Alessi, E.; Ambrosino, R.; Andr be, Y.; Angioni, C.; Apruzzese, G.; Aradi, M.; Arnichand, H.; Auriemma, F.; Avdeeva, G.; Ayllon-Guerola, J. M.; Bagnato, F.; Bandaru, V. K.; Barnes, M.; Barrera-Orte, L.; Bettini, P.; Bilato, R.; Biletskyi, O.; Bilkova, P.; Bin, W.; Blanchard, P.; Blanken, T.; Bobkov, V.; Bock, A.; Boeyaert, D.; Bogar, K.; Bogar, O.; Bohm, P.; Bolzonella, T.; Bombarda, F.; Boncagni, L.; Bouquey, F.; Bowman, C.; Brezinsek, S.; Brida, D.; Brunetti, D.; Bucalossi, J.; Buchanan, J.; Buermans, J.; Bufferand, H.; Buller, S.; Buratti, P.; Burckhart, A.; Calabr, G.; Calacci, L.; Camenen, Y.; Cannas, B.; Cano Megías, P.; Carnevale, D.; Carpanese, F.; Carr, M.; Carralero, D.; Carraro, L.; Casolari, A.; Cathey, A.; Causa, F.; Cavedon, M.; Cecconello, M.; Ceccuzzi, S.; Cerovsky, J.; Chapman, S.; Chmielewski, P.; Choi, D.; Cianfarani, C.; Ciraolo, G.; Coda, S.; Coelho, R.; Colas, L.; Colette, D.; Cordaro, L.; Cordella, F.; Costea, S.; Coster, D.; Cruz Zabala, D. J.; Cseh, G.; Czarnecka, A.; Cziegler, I.; D’Arcangelo, O.; Dal Molin, A.; David, P.; De Carolis, G.; De Oliveira, H.; Decker, J.; Dejarnac, R.; Delogu, R.; Den Harder, N.; Dimitrova, M.; Dolizy, F.; Domínguez-Palacios Durán, J. J.; Douai, D.; Drenik, A.; Dreval, M.; Dudson, B.; Dunai, D.; Duval, B. P.; Dux, R.; Elmore, S.; Embréus, O.; Erds, B.; Fable, E.; Faitsch, M.; Fanni, A.; Farnik, M.; Faust, I.; Faustin, J.; Fedorczak, N.; Felici, F.; Feng, S.; Feng, X.; Ferreira, J.; Ferr, G.; Février, O.; Ficker, O.; Figini, L.; Figueiredo, A.; Fil, A.; Fontana, M.; Francesco, M.; Fuchs, C.; Futatani, S.; Gabellieri, L.; Gadariya, D.; Gahle, D.; Galassi, D.; Gałązka, K.; Galdon-Quiroga, J.; Galeani, S.; Gallart, D.; Gallo, A.; Galperti, C.; Garavaglia, S.; Garcia, J.; Garcia-Lopez, J.; Garcia-Mu oz, M.; Garzotti, L.; Gath, J.; Geiger, B.; Giacomelli, L.; Giannone, L.; Gibson, S.; Gil, L.; Giovannozzi, E.; Giruzzi, G.; Gobbin, M.; Gonzalez-Martin, J.; Goodman, T. P.; Gorini, G.; Gospodarczyk, M.; Granucci, G.; Grekov, D. 1; Grenfell, G.; Griener, M.; Groth, M.; Grover, O.; Gruca, M.; Gude, A.; Guimarais, L.; Gyergyek, T.; Hacek, P.; Hakola, A.; Ham, C.; Happel, T.; Harrison, J.; Havranek, A.; Hawke, J.; Henderson, S.; Hesslow, L.; Hitzler, F.; Hnat, B.; Hobirk, J.; Hoelzl, M.; Hogeweij, D.; Hopf, C.; Hoppe, M.; Horacek, J.; Hron, M.; Huang, Z.; Iantchenko, A.; Iglesias, D.; Igochine, V.; Innocente, P.; Ionita-Schrittwieser, C.; Isliker, H.; Ivanova-Stanik, I.; Jacobsen, A.; Jakubowski, M.; Janky, F.; Jardin, A.; Jaulmes, F.; Jensen, T.; Jonsson, T.; Kallenbach, A.; Kappatou, A.; Karpushov, A.; Kasilov, S.; Kazakov, Y.; Kazantzidis, P. V.; Keeling, D.; Kelemen, M.; Kendl, A.; Kernbichler, W.; Kirk, A.; Kocsis, G.; Komm, M.; Kong, M.; Korovin, V.; Koubiti, M.; Kovacic, J.; Krawczyk, N.; Krieger, K.; Kripner, L.; Křivská, A.; Kudlacek, O.; Kulyk, Y.; Kurki-Suonio, T.; Kwiatkowski, R.; Laggner, F.; Laguardia, L.; Lahtinen, A.; Lang, P.; Likonen, J.; Lipschultz, B.; Liu, F.; Lombroni, R.; Lorenzini, R.; Loschiavo, V. P.; Lunt, T.; MacUsova, E.; Madsen, J.; Maggiora, R.; Maljaars, B.; Manas, P.; Mantica, P.; Mantsinen, M. J.; Manz, P.; Maraschek, M.; Marchenko, V.; Marchetto, C.; Mariani, A.; Marini, C.; Markovic, T.; Marrelli, L.; Martin, P.; Martín Solís, J. R.; Martitsch, A.; Mastrostefano, S.; Matos, F.; Matthews, G.; Mayoral, M.-L.; Mazon, D.; Mazzotta, C.; Mc Carthy, P.; McClements, K.; McDermott, R.; McMillan, B.; Meineri, C.; Menkovski, V.; Meshcheriakov, D.; Messmer, M.; Micheletti, D.; Milanesio, D.; Militello, F.; Miron, I. G.; Mlynar, J.; Moiseenko, V.; Molina Cabrera, P. 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F.; Rocchi, G.; Rodriguez-Ramos, M.; Romano, A.; Rosato, J.; Rubinacci, G.; Rubino, G.; Ryan, D. A.; Salewski, M.; Salmi, A.; Samaddar, D.; Sanchis-Sanchez, L.; Santos, J.; Särkimäki, K.; Sassano, M.; Sauter, O.; Scannell, R.; Scheffer, M.; Schneider, B. S.; Schneider, P.; Schrittwieser, R.; Schubert, M.; Seidl, J.; Seliunin, E.; Sharapov, S.; Sheeba, R. R.; Sias, G.; Sieglin, B.; Silva, C.; Sipilä, S.; Smith, S.; Snicker, A.; Solano, E. R.; Hansen, S. K.; Soria-Hoyo, C.; Sorokovoy, E.; Sozzi, C.; Sperduti, A.; Spizzo, G.; Spolaore, M.; Stejner, M.; Stipani, L.; Stober, J.; Strand, P.; Sun, H.; Suttrop, W.; Sytnykov, D.; Szepesi, T.; Tál, B.; Tala, T.; Tardini, G.; Tardocchi, M.; Teplukhina, A.; Terranova, D.; Testa, D.; Theiler, C.; Thorén, E.; Thornton, A.; Tilia, B.; Tolias, P.; Tomes, M.; Toscano-Jimenez, M.; Tsironis, C.; Tsui, C.; Tudisco, O.; Urban, J.; Valisa, M.; Vallar, M.; Vallejos Olivares, P.; Valovic, M.; Van Vugt, D.; Vanovac, B.; Varje, J.; Varju, J.; Varoutis, S. 1; Vartanian, S.; Vasilovici, O.; Vega, J.; Verdoolaege, G.; Verhaegh, K.; Vermare, L.; Vianello, N.; Vicente, J.; Viezzer, E.; Villone, F.; Voitsekhovitch, I.; Voltolina, D.; Vondracek, P.; Vu, N. M. T.; Walkden, N.; Wauters, T.; Weiland, M.; Weinzettl, V.; Wensing, M.; Wiesen, S.; Wiesenberger, M.; Wilkie, G.; Willensdorfer, M.; Wischmeier, M.; Wu, K.; Xiang, L.; Zagorski, R.; Zaloga, D.; Zanca, P.; Zaplotnik, R.; Zebrowski, J.; Zhang, W.; Zisis, A.; Zoletnik, S.; Zuin, M.

The bulk replacement current density triggered by surface charge loss owing to thermionic emission leads to a volumetric Lorentz force which has been observed to drive macroscopic melt layer motion ...

International audience; The first comparison of dust radius and surface temperature estimates, obtained from spectroscopic measurements of thermal radiation, with simulations of dust heating and vaporization by the MIGRAINe dust dynamics code is reported. The measurements were performed during controlled tungsten dust injection experiments in the cold and dense plasmas of Pilot-PSI, reproducing ITER divertor conditions. The comparison has allowed us to single out the dominating role of the work function contribution to the dust heating budget. However, in the plasmas of interest, dust was found to enter the strong vaporization regime, in which its temperature is practically insensitive to plasma properties and the various uncertainties in modelling. This makes the dust temperature a poor figure of merit for model validation purposes. On the other hand, simple numerical scalings obtained from orbital-motion-limited estimates were found to be remarkably robust and sufficient to understand the main physics at play in such cold and dense plasmas. Validating heat balance models for tungsten dust in cold dense plasmas 2

The ASDEX Upgrade (AUG) programme, jointly run with the EUROfusion MST1 task force, continues to significantly enhance the physics base of ITER and DEMO. Here, the full tungsten wall is a key asset for extrapolating to future devices. The high overall heating power, flexible heating mix and comprehensive diagnostic set allows studies ranging from mimicking the scrape-off-layer and divertor conditions of ITER and DEMO at high density to fully non-inductive operation (q95 = 5.5, ) at low density. Higher installed electron cyclotron resonance heating power 6 MW, new diagnostics and improved analysis techniques have further enhanced the capabilities of AUG. Stable high-density H-modes with MW m−1 with fully detached strike-points have been demonstrated. The ballooning instability close to the separatrix has been identified as a potential cause leading to the H-mode density limit and is also found to play an important role for the access to small edge-localized modes (ELMs). Density limit disruptions have been successfully avoided using a path-oriented approach to disruption handling and progress has been made in understanding the dissipation and avoidance of runaway electron beams. ELM suppression with resonant magnetic perturbations is now routinely achieved reaching transiently . This gives new insight into the field penetration physics, in particular with respect to plasma flows. Modelling agrees well with plasma response measurements and a helically localised ballooning structure observed prior to the ELM is evidence for the changed edge stability due to the magnetic perturbations. The impact of 3D perturbations on heat load patterns and fast-ion losses have been further elaborated. Progress has also been made in understanding the ELM cycle itself. Here, new fast measurements of and Er allow for inter ELM transport analysis confirming that Er is dominated by the diamagnetic term even for fast timescales. New analysis techniques allow detailed comparison of the ELM crash and are in good agreement with nonlinear MHD modelling. The observation of accelerated ions during the ELM crash can be seen as evidence for the reconnection during the ELM. As type-I ELMs (even mitigated) are likely not a viable operational regime in DEMO studies of 'natural' no ELM regimes have been extended. Stable I-modes up to have been characterised using -feedback. Core physics has been advanced by more detailed characterisation of the turbulence with new measurements such as the eddy tilt angle—measured for the first time—or the cross-phase angle of and fluctuations. These new data put strong constraints on gyro-kinetic turbulence modelling. In addition, carefully executed studies in different main species (H, D and He) and with different heating mixes highlight the importance of the collisional energy exchange for interpreting energy confinement. A new regime with a hollow profile now gives access to regimes mimicking aspects of burning plasma conditions and lead to nonlinear interactions of energetic particle modes despite the sub-Alfvénic beam energy. This will help to validate the fast-ion codes for predicting ITER and DEMO. This work has been carried out within the framework of the EUROfusion Consortium and has received funding from the Euratom research and training programme 2014–2018 and 2019–2020 under grant agreement No. 633053. The views and opinions expressed herein do not necessarily reflect those of the European Commission. "Article signat per més de 100 autors/es: H. Meyer, for the AUG Team: D. Aguiam, C. Angioni, C.G. Albert, N. Arden, R. Arredondo Parra, O. Asunta, M. de Baar, M. Balden, V. Bandaru, K. Behler, A. Bergmann, J. Bernardo, M. Bernert, A. Biancalani, R. Bilato, G. Birkenmeier, T.C. Blanken, V. Bobkov, A. Bock, T. Bolzonella, A. Bortolon, B. Böswirth, C. Bottereau, A. Bottino, H. van den Brand, S. Brezinsek, D. Brida, F. Brochard, C. Bruhn, J. Buchanan, A. Buhler, A. Burckhart, Y. Camenen, D. Carlton, M. Carr, D. Carralero, C. Castaldo, M. Cavedon, C. Cazzaniga, S. Ceccuzzi, C. Challis, A. Chankin, S. Chapman, C. Cianfarani, F. Clairet, S. Coda, R. Coelho, J.W. Coenen, L. Colas, G.D. Conway, S. Costea, D.P. Coster, T.B. Cote, A. Creely, G. Croci, G. Cseh, A. Czarnecka, I. Cziegler, O. D'Arcangelo, P. David, C. Day, R. Delogu, P. de Marné, S.S. Denk, P. Denner, M. Dibon, A. Di Siena, D. Douai, A. Drenik, R. Drube, M. Dunne, B.P. Duval, R. Dux, T. Eich, S. Elgeti, K. Engelhardt, B. Erdös, I. Erofeev, B. Esposito, E. Fable, M. Faitsch, U. Fantz, H. Faugel, I. Faust, F. Felici, J. Ferreira, S. Fietz, A. Figuereido, R. Fischer, O. Ford, L. Frassinetti, S. Freethy, M. Fröschle, G. Fuchert, J.C. Fuchs, H. Fünfgelder, K. Galazka, J. Galdon-Quiroga, A. Gallo, Y. Gao, S. Garavaglia, A. Garcia-Carrasco, M. Garcia-Muñoz, B. Geiger, L. Giannone, L. Gil, E. Giovannozzi, C. Gleason-González, S. Glöggler, M. Gobbin, T. Görler, I. Gomez Ortiz, J. Gonzalez Martin, T. Goodman, G. Gorini, D. Gradic, A. Gräter, G. Granucci, H. Greuner, M. Griener, M. Groth, A. Gude, S. Günter, L. Guimarais, G. Haas, A.H. Hakola, C. Ham, T. Happel, N. den Harder, G.F. Harrer, J. Harrison, V. Hauer, T. Hayward-Schneider, C.C. Hegna, B. Heinemann, S. Heinzel, T. Hellsten, S. Henderson, P. Hennequin, A. Herrmann, M.F. Heyn, E. Heyn, F. Hitzler, J. Hobirk, K. Höfler, M. Hölzl, T. Höschen, J.H. Holm, C. Hopf, W.A. Hornsby, L. Horvath, A. Houben, A. Huber, V. Igochine, T. Ilkei, I. Ivanova-Stanik, W. Jacob, A.S. Jacobsen, F. Janky, A. Jansen van Vuuren, A. Jardin, F. Jaulmes, F. Jenko, T. Jensen, E. Joffrin, C.-P. Käsemann, A. Kallenbach, S. Kálvin, M. Kantor, A. Kappatou, O. Kardaun, J. Karhunen, S. Kasilov,, Y. Kazakov, W. Kernbichler, A. Kirk, S. Kjer Hansen, V. Klevarova, G. Kocsis, A. Köhn, M. Koubiti, K. Krieger, A. Krivska, A. Krämer-Flecken, O. Kudlacek, T. Kurki-Suonio, B. Kurzan, B. Labit, K. Lackner, F. Laggner, P.T. Lang, P. Lauber, A. Lebschy, N. Leuthold, M. Li, O. Linder, B. Lipschultz, F. Liu, Y. Liu, A. Lohs, Z. Lu, T. Luda di Cortemiglia, N.C. Luhmann, R. Lunsford, T. Lunt, A. Lyssoivan, T. Maceina, J. Madsen, R. Maggiora, H. Maier, O. Maj, J. Mailloux, R. Maingi, E. Maljaars, P. Manas, A. Mancini, A. Manhard, M.-E. Manso, P. Mantica, M. Mantsinen, P. Manz, M. Maraschek, C. Martens, P. Martin, L. Marrelli, A. Martitsch, M. Mayer, D. Mazon, P.J. McCarthy, R. McDermott, H. Meister, A. Medvedeva, R. Merkel, A. Merle, V. Mertens, D. Meshcheriakov, O. Meyer, J. Miettunen, D. Milanesio, F. Mink, A. Mlynek, F. Monaco, C. Moon, F. Nabais, A. Nemes-Czopf, G. Neu, R. Neu, A.H. Nielsen, S.K. Nielsen, V. Nikolaeva, M. Nocente, J.-M. Noterdaeme, I. Novikau, S. Nowak, M. Oberkofler, M. Oberparleiter, R. Ochoukov, T. Odstrcil, J. Olsen, F. Orain, F. Palermo, O. Pan, G. Papp, I. Paradela Perez, A. Pau, G. Pautasso, F. Penzel, P. Petersson, J. Pinzón Acosta, P. Piovesan, C. Piron, R. Pitts, U. Plank, B. Plaum, B. Ploeckl, V. Plyusnin, G. Pokol, E. Poli, L. Porte, S. Potzel, D. Prisiazhniuk, T. Pütterich, M. Ramisch, J. Rasmussen, G.A. Rattá, S. Ratynskaia, G. Raupp, G.L. Ravera, D. Réfy, M. Reich, F. Reimold, D. Reiser, T. Ribeiro, J. Riesch, R. Riedl, D. Rittich, J.F. Rivero-Rodriguez, G. Rocchi, M. Rodriguez-Ramos, V. Rohde, A. Ross1, M. Rott, M. Rubel, D. Ryan, F. Ryter, S. Saarelma, M. Salewski, A. Salmi, L. Sanchis-Sanchez, J. Santos, O. Sauter, A. Scarabosio, G. Schall, K. Schmid, O. Schmitz, P.A. Schneider, R. Schrittwieser, M. Schubert, T. Schwarz-Selinger, J. Schweinzer, B. Scott, T. Semer, E. Seliunin, M. Sertoli, A. Shabbir, A. Shalpegin, L. Shao, S. Sharapov, G. Sias, M. Siccinio, B. Sieglin, A. Sigalov, A. Silva, C. Silva, D. Silvagni, P. Simon, J. Simpson, E. Smigelskis, A. Snicker, C. Sommariva, C. Sozzi, M. Spolaore, A. Stegmeir, M. Stejner, J. Stober, U. Stroth, E. Strumberger, G. Suarez, H.-J. Sun, W. Suttrop, E. Sytova, T. Szepesi, B. Tál, T. Tala, G. Tardini, M. Tardocchi, M. Teschke, D. Terranova, W. Tierens, E. Thorén, D. Told, P. Tolias, O. Tudisco, W. Treutterer, E. Trier, M. Tripský, M. Valisa, M. Valovic, B. Vanovac, D. van Vugt, S. Varoutis, G. Verdoolaege, N. Vianello, J. Vicente, T. Vierle, E. Viezzer, U. von Toussaint, D. Wagner, N. Wang, X. Wang, M. Weiland, A.E. White, S. Wiesen, M. Willensdorfer, B. Wiringer, M. Wischmeier, R. Wolf, E. Wolfrum, L. Xiang, Q. Yang, Z. Yang, Q. Yu, R. Zagórski, I. Zammuto, W. Zhang, M. van Zeeland, T. Zehetbauer, M. Zilker, S. Zoletnik, H. Zohm and the EUROfusion MST1 Team55

Repetitive melting of tungsten by power transients originating from edge localized modes (ELMs) has been studied in the tokamak experiment ASDEX Upgrade. Tungsten samples were exposed to H-mode dis ...

The first aim of this study was to determine how complete or perivascular loss of aquaporin-4 (AQP4) water channels affects membrane permeability for water in the mouse brain grey matter in the steady state. Time-dependent diffusion magnetic resonance imaging was performed on global Aqp4 knock out (KO) and α-syntrophin (α-syn) KO mice, in the latter perivascular AQP4 are mislocalized, but still functioning. Control animals were corresponding wild type (WT) mice. By combining in vivo diffusion measurements with the effective medium theory and previously measured extra-cellular volume fractions, the effects of membrane permeability and extracellular volume fraction were uncoupled for Aqp4 and α-syn KO. The second aim was to assess the effect of α-syn KO on cortical intermediary metabolism combining in vivo [1-13C]glucose and [1,2-13C]acetate injection with ex vivo 13C MR spectroscopy. Aqp4 KO increased the effective diffusion coefficient at long diffusion times by 5%, and a 14% decrease in membrane water permeability was estimated for Aqp4 KO compared with WT mice. α-syn KO did not affect the measured diffusion parameters. In the metabolic analyses, significantly lower amounts of [4-13C]glutamate and [4-13C]glutamine, and percent enrichment in [4-13C]glutamate were detected in the α-syn KO mice. [1,2-13C]acetate metabolism was unaffected in α-syn KO, but the contribution of astrocyte derived metabolites to GABA synthesis was significantly increased. Taken together, α-syn KO mice appeared to have decreased neuronal glucose metabolism, partly compensated for by utilization of astrocyte derived metabolites. This is the authors' accepted and refereed manuscript to the article. Locked until 30 December 2017 due to copyright restrictions. The final publication is available at link.springer.com via https://link.springer.com/article/10.1007%2Fs11064-016-2139-y

Melt motion simulations of recent ASDEX Upgrade experiments on transient-induced melting of a tungsten leading edge during ELMing H-mode are performed with the incompressible fluid dynamics code ME ...

Remobilization is one of the most prominent unresolved fusion dust-relevant issues, strongly related to the lifetime of dust in plasma-wetted regions, the survivability of dust on hot plasma-facing surfaces and the formation of dust accumulation sites. A systematic cross-machine study has been initiated to investigate the remobilization of tungsten micron-size dust from tungsten surfaces implementing a newly developed technique based on controlled pre-adhesion by gas dynamics methods. It has been utilized in a number of devices and has provided new insights on remobilization under steady-state and transient conditions. The experiments are interpreted with contact mechanics theory and heat conduction models.

There is a constitutive production of water in brain. The efflux routes of this excess water remain to be identified. We used basal brain water content as a proxy for the capacity of water exit routes. Basal brain water content was increased in mice with a complete loss of aquaporin-4 (AQP4) water channels (global Aqp4-/- mice), but not in mice with a selective removal of perivascular AQP4 or in a novel mouse line with a selective deletion of ependymal AQP4 (Foxj1-Cre:Aqp4flox/flox mice). Unique for the global Aqp4-/- mice is the loss of the AQP4 pool subjacent to the pial membrane. Our data suggest that water accumulates in brain when subpial AQP4 is missing, pointing to a critical role of this pool of water channels in brain water exit.

Expression of the water channel aquaporin-4 (AQP4) at the blood-brain interface is dependent upon the dystrophin associated protein complex. Here we investigated whether deletion of the Aqp4 gene affects the molecular composition of this protein scaffold and the integrity of the blood-brain barrier. High-resolution immunogold cytochemistry revealed that perivascular expression of α-syntrophin was reduced by 60% in Aqp4(-/-) mice. Additionally, perivascular AQP4 expression was reduced by 88% in α-syn(-/-) mice, in accordance with earlier reports. Immunofluorescence showed that Aqp4 deletion also caused a modest reduction in perivascular dystrophin, whereas β-dystroglycan labeling was unaltered. Perivascular microglia were devoid of AQP4 immunoreactivity. Deletion of Aqp4 did not alter the ultrastructure of capillary endothelial cells, the expression of tight junction proteins (claudin-5, occludin, and zonula occludens 1), or the vascular permeability to horseradish peroxidase and Evans blue albumin dye. We conclude that Aqp4 deletion reduces the expression of perivascular glial scaffolding proteins without affecting the endothelial barrier. Our data also indicate that AQP4 and α-syntrophin are mutually dependent upon each other for proper perivascular expression.

Tissue- and cell-specific deletion of the Aqp4 gene is required to differentiate between the numerous pools of aquaporin-4 (AQP4) water channels. A glial-conditional Aqp4 knockout mouse line was generated to resolve whether astroglial AQP4 controls water exchange across the blood–brain interface. The conditional knockout was driven by the glial fibrillary acidic protein promoter. Brains from conditional Aqp4 knockouts were devoid of AQP4 as assessed by Western blots, ruling out the presence of a significant endothelial pool of AQP4. In agreement, immunofluorescence analysis of cryostate sections and quantitative immunogold analysis of ultrathin sections revealed no AQP4 signals in capillary endothelia. Compared with litter controls, glial-conditional Aqp4 knockout mice showed a 31% reduction in brain water uptake after systemic hypoosmotic stress and a delayed postnatal resorption of brain water. Deletion of astroglial Aqp4 did not affect the barrier function to macromolecules. Our data suggest that the blood–brain barrier (BBB) is more complex than anticipated. Notably, under certain conditions, the astrocyte covering of brain microvessels is rate limiting to water movement.

Castellated substrates with adhered micron dust have been exposed in the outer ASDEX-Upgrade divertor to ELMy H-mode discharges. Beryllium proxy (chromium, copper) and refractory metal (tungsten, molybdenum) dust has been deposited on the plasma-facing and plasma-shadowed sides of the monoblocks as well as the bottom of the gaps. Interaction with time-averaged transient heat loads up to 5 MWm(-2) led to dust remobilization, clustering, melting and wetting-induced coagulation. The amount of dust released in the vessel has been quantified and remobilized dust trajectories inferred. Gaps can efficiently trap locally adhered dust, but dust detaching from adjacent monoblocks does not preferentially move inside the gaps implying that they do not constitute a dust accumulation site. Heat transfer simulations of melting events are also reported taking into account heat constriction due to the finite contact area and the presence of surface roughness.

International audience; Genetic correlations were computed for show jumping competition traits from national estimated breeding values (EBV) of stallions of five countries: Belgium, Denmark, France, Ireland and Sweden. Data involved 24,390 horses, i.e. 8993 stallions with EBV and their ancestors. There were 617 stallions with several EBVs in more than one country. Method involved MACE (Multi-Trait Across Country Evaluation) methodology based on deregressed proofs adapted to the existence of own performance for stallions and to missing EBVs for some ancestors. ASREML was used to estimate covariance with an equivalent multiple trait model described as a random regression model. Within country sire variances were considered as known. The estimated genetic correlations were high (0.86 to 0.88) especially for reliable estimates between Belgium, France, Sweden and between Sweden and Denmark, and relatively high (0.70 to 0.91) for other pairs. These results open perspectives for the international evaluation of sporthorses.

To provide insights into the effects of temporary focal ischemia on the function of neurons and astrocytes in vivo, we measured the incorporation of radiolabel from [U-14C]glucose into both glutamate and glutamine in brain subregions at 1 h of reperfusion following occlusion of the middle cerebral artery for 2 or 3 h. Under the experimental conditions used, 14C-glutamate is mainly produced in neurons whereas 14C-glutamine is generated in astrocytes from 14C-glutamate of both neuronal and astrocytic origin. Radiolabel incorporation into both amino acids was greatly decreased. The change in 14C-glutamate accumulation provides strong evidence for substantial reductions in neuronal glucose metabolism. The resulting decrease in delivery of 14C-glutamate from the neurons to astrocytes was probably also the major contributor to the change in 14C-glutamine content. These alterations probably result in part from a marked depression of glycolytic activity in the neurons, as suggested by previous studies assessing deoxyglucose utilization. Alterations in 14C-glucose metabolism were not restricted to tissue that would subsequently become infarcted. Thus, these changes did not inevitably lead to death of the affected cells. The ATP : ADP ratio and phosphocreatine content were essentially preserved during recirculation following 2 h of ischemia and showed at most only moderate losses in some subregions following 3 h of ischemia. This retention of energy reserves despite the decreases in 14C-glucose metabolism in neurons suggests that energy needs were substantially reduced in the post-ischemic brain. Marked increases in tissue lactate accumulation during recirculation, particularly following 3 h of ischemia, provided evidence that impaired pyruvate oxidation probably also contributed to the altered 14C-glucose metabolism. These findings indicate the presence of complex changes in energy metabolism that are likely to greatly influence the responses of neurons and astrocytes to temporary focal ischemia.

Stroke is one of the leading causes of disability and death. Most often, stroke results from blockage of an artery in the brain leading to tissue infarction within the perfusion territory of the affected vessel. Despite the severity of the insult, many cells are not irreversibly damaged within the first few hours and can be rescued by early restoration of blood flow or other interventions. Astrocytes, the most numerous cells in the brain, normally perform many functions that are essential for neuronal viability. Thus, stimulation of key astrocytic properties in ischemic or post-ischemic brain could potentially contribute to neuroprotection. However, at present, there is very little understanding of either the response of astrocytes to cerebral ischemia or the extent to which these cells can recover function if blood flow is restored. The main aim of the project was to assess key metabolic properties in astrocytes during early reperfusion following unilateral occlusion of the middle cerebral artery (MCA) in rats. Astrocytic oxidative metabolism was assessed from the incorporation of radiolabel from [1- 14 C]acetate into glutamine, an activity that is essentially specific for these cells. Striatal tissue from the hemisphere subjected to ischemia showed substantial decreases in 14 C-glutamine production at 1 hour of reperfusion following either 2 or 3 hours of ischemia. In contrast, this activity was almost fully preserved for at least 4 hours in parts of the cerebral cortex that had been subjected to more moderate ischemia, even when the duration of ischemia was sufficient to induce infarction in this region. The production of 14 C-glutamine was also not significantly affected in cortical tissue exposed to more severe ischemia but this measure was much more variable between animals. These findings demonstrate regional differences in the response of astrocytes to focal ischemia and provide evidence that most cortical astrocytes remain viable and metabolically active for many hours, even in tissue destined to become infarcted. To further evaluate metabolic recovery in the post-ischemic brain, the production of 14 C-glutamate and 14 C-glutamine from [U- 14 C]glucose was assessed. Neurons are responsible for most of the 14 Cglutamate generation whereas 14 C-glutamine is produced in astrocytes from glutamate of neuronal and astrocytic origin. Marked reductions in the labeling of both amino acids were observed in all regions of the MCA territory during early reperfusion after either 2 or 3 h ischemia irrespective of whether the tissue would become infarcted. These results provide evidence for widespread depression of glucose metabolism in neurons and altered metabolic interactions with astrocytes. Interestingly, this reduction in glucose metabolism was not associated with substantial changes in tissue phosphocreatine content and ATP:ADP ratio suggesting that energy requirements were reduced by the ischemia-reperfusion. Increases in lactate content were detected during early reperfusion in tissue regions that would develop infarcts. This finding coupled with previous evidence for deleterious effects of lactic acid suggests that accumulation of this metabolite might promote cell death. An impairment of pyruvate oxidation or reduced clearance of lactate could contribute to the increased lactate. The mechanisms by which excess lactate is cleared from the brain are not known. We hypothesized that MCT4 is involved in the removal of lactate as this transporter isoform is responsible for lactate export from other tissues. Using immunogold cytochemistry, MCT4 was found to be densely expressed in the endfeet of glial cells facing blood capillaries and pial surface of the brain, suggesting an important role in the removal of excess lactate from the CNS. In future studies, the expression of MCT4 will be examined following ischemia to resolve whether an altered expression of this transporter may be one reason for the elevated lactate levels in the brain.

A role for astroglia in epileptogenesis has been hypothesised but is not established. Low doses of fluorocitrate specifically and reversibly disrupt astroglial metabolism by blocking aconitase, an enzyme integral to the tricarboxylic acid cycle. We used cerebral cortex injections of fluorocitrate, at a dose that we demonstrated to inhibit astroglial metabolism selectively, to determine whether astroglial disturbances lead to seizures. Rats were halothane-anesthetized, and 0.8 nmol of sodium fluorocitrate was injected into the cerebral cortex. Extradural electroencephalogram (EEG) electrodes were implanted, after which the anesthesia was ceased and the animals were observed. In all experiments, 14 of 15 fluorocitrate-treated animals exhibited epileptiform EEG discharges, with some animals exhibiting convulsive seizures. Discharges commenced as early as 30 min postfluorocitrate injection. Intraperitoneal octanol, but not halothane by inhalation, given to test the possible participation of gap junctions in EEG discharge generation, blocked or delayed the occurrence of discharges after fluorocitrate. These results indicate that focal cerebrocortical astroglial dysfunction leads to focal epileptiform discharges and sometimes to convulsive seizures and that the process possibly depends on effects mediated by gap junctions.

Five palliative home care teams participated in a prospective Swedish study that included 221 palliative cancer patients. All patients with incurable malignant disease that were admitted and died during 1999 were included. On admission, demographic data were recorded. When patients, despite ongoing home care, were referred to institutional care, doctors and nurses involved were interviewed about the reasons for this. After the patients' death next of kin involved in the care were interviewed according to a questionnaire. Approximately half of the patients died at home. The reasons for referral showed a wide diversity and included both social and psychosocial factors, medical emergencies and problems related to symptom control. A preference for dying at home and not living alone were shown to be the strongest predictors of home death (p = 0.001). However, 35% of patients living alone died at home. Interestingly enough, Karnofsky performance index (KPI) at admission was significantly lower for those dying at home, despite similar mean time of care. The understanding of impending death was significantly more common among the families of those patients dying at home.

Recent experimental data in mice have shown that the inwardly rectifying K+ channel Kir4.1 mediates K+ spatial buffering in the hippocampus. Here we used immunohistochemistry to examine the distribution of Kir4.1 in hippocampi from patients with medication refractory temporal lobe epilepsy. The selectivity of the antibody was confirmed in mice with a glial conditional deletion of the gene encoding Kir4.1. These mice showed a complete loss of labeled cells, indicating that Kir4.1 is restricted to glia. In the human cases, Kir4.1 immunoreactivity observed in cells morphological consistent with astrocytes was significantly reduced in 12 patients with hippocampal sclerosis vs. 11 patients without sclerosis and 4 normal autopsy controls. Loss of astrocytic Kir4.1 immunoreactivity was most pronounced around vessels and was restricted to gliotic areas. Loss of Kir4.1 expression was associated with loss of dystrophin and α-syntrophin, but not with loss of β-dystroglycan, suggesting partial disruption of the dystrophin-associated protein complex. The changes identified in patients with hippocampal sclerosis likely interfere with K+ homeostasis and may contribute to the epileptogenicity of the sclerotic hippocampus.

Until its final revision by Longomontanus in 1600, Tycho's lunar theory was fundamentally Copernican: Tycho (or Longomontanus) had been able to represent the Variation by simply putting an extra circle, AB in Figure A.3.1, into the center of Copernicus's theory. By making the center of the deferent ( B ) revolve around the earth ( A ) at twice the synodic velocity of the moon, he produced displacements that mounted to ±45' 20′ when the moon was in the octants and yet vanished in syzygy and quadrature. But the Variation was not the only extra circle grafted onto the traditional theory. The center of the large epicycle also moved on a new circle, CD , producing a periodic displacement up to ±11'. This correction appears without a prior hint of any kind in either Tycho's log notes or his letters and would therefore be unknown if Tycho had not allowed Jostel to “prepublish” his theory in 1599. What it represented, although somewhat imperfectly, was a phenomenon called the annual equation . When it finally attained recognition as a legitimate lunar phenomenon and was explained by Newton a hundred years later, it was seen as an annual variation of the speed of the moon in its orbit, owing to the annual fluctuation of the sun's distance from (and hence influence on) the earth–moon system. That Tycho also associated the phenomenon with the sun in some sense is obvious from the fact that his period for it was a year.

To provide insights into the effects of temporary focal ischemia on the function of neurons and astrocytes in vivo, we measured the incorporation of radiolabel from [U-14C]glucose into both glutamate and glutamine in brain subregions at 1 h of reperfusion following occlusion of the middle cerebral artery for 2 or 3 h. Under the experimental conditions used, 14C-glutamate is mainly produced in neurons whereas 14C-glutamine is generated in astrocytes from 14C-glutamate of both neuronal and astrocytic origin. Radiolabel incorporation into both amino acids was greatly decreased. The change in 14C-glutamate accumulation provides strong evidence for substantial reductions in neuronal glucose metabolism. The resulting decrease in delivery of 14C-glutamate from the neurons to astrocytes was probably also the major contributor to the change in 14C-glutamine content. These alterations probably result in part from a marked depression of glycolytic activity in the neurons, as suggested by previous studies assessing deoxyglucose utilization. Alterations in 14C-glucose metabolism were not restricted to tissue that would subsequently become infarcted. Thus, these changes did not inevitably lead to death of the affected cells. The ATP : ADP ratio and phosphocreatine content were essentially preserved during recirculation following 2 h of ischemia and showed at most only moderate losses in some subregions following 3 h of ischemia. This retention of energy reserves despite the decreases in 14C-glucose metabolism in neurons suggests that energy needs were substantially reduced in the post-ischemic brain. Marked increases in tissue lactate accumulation during recirculation, particularly following 3 h of ischemia, provided evidence that impaired pyruvate oxidation probably also contributed to the altered 14C-glucose metabolism. These findings indicate the presence of complex changes in energy metabolism that are likely to greatly influence the responses of neurons and astrocytes to temporary focal ischemia.

The gas turbine development history of Sweden is exciting. By international comparison Sweden and its gas turbine manufacturers are small but can nevertheless claim periods with the worlds highest output, or highest efficiency large industrial gas turbine respectively. Sweden has always created its own military aircraft and fitting, high performance engines are developed in Sweden in license cooperation with large international manufacturers. The Swedish Air Force ranked number four in the world during the 60s. Pioneering contributions were also made with small gas turbines, such as high speed turbogenerators in hybrid propulsion systems for cars and trucks. Professionals know that gas turbine development success does not come easy. A lot of setbacks have to be mastered. The size of the crew is not always significant in the process.

The Lord of Uraniborg is a comprehensive biography of Tycho Brahe, father of modern astronomy, famed alchemist and littérateur of the sixteenth-century Danish Renaissance. Written in a lively and engaging style, Victor Thoren's biography offers interesting perspectives on Tycho's life and presents alternative analyses of virtually every aspect of his scientific work. A range of readers interested in astronomy, history of astronomy and the history of science will find this book fascinating.