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At least 19 records

Kinetic equilibrium reconstructions of plasmas in the MAST database and preparation for reconstruction of the first plasmas in MAST upgrade

Reconstructions of plasma equilibria using magnetic sensors were routine during operation of the Mega Ampere Spherical Tokamak (MAST) device, but reconstructions using kinetic profiles were not. These are necessary for stability and disruption analysis of the MAST database, as well as for operation in the upgrade to the device, MAST-U. The three-dimensional (3D) code VALEN is used to determine eddy currents in the 3D vessel structures for vacuum coil test shots, which are then mapped to effective resistances in the two-dimensional vessel groupings in the EFIT equilibrium reconstruction code to be used in conjunction with nearby loop voltage measurements for estimated currents in the structures during reconstruction. Kinetic equilibrium reconstructions with EFIT, using all available magnetic sensors as well as Thomson scattering measurements of electron temperature and density, charge exchange recombination spectroscopy measurements of ion temperature, and internal magnetic field pitch angle measurements from a motional Stark effect (MSE) diagnostic are performed for a large database of MAST discharges. Excellent convergence errors are obtained for the portions of the discharges where the stored energy was not too low, and it is found that reconstructions performed with temperature and density measurements but without MSE data usually already match the pitch angle measurements well. A database of 275 kinetic equilibria is used to test the ideal MHD stability calculation capability for MAST. In conclusion, the necessary changes to conducting structure in VALEN, and diagnostic setup in EFIT have been completed for the upgrade from MAST to MAST-U, enabling kinetic reconstructions to commence from the first plasma discharges of the upgraded device.

70 PLASMA PHYSICS AND FUSION TECHNOLOGY↗

Overview of new MAST physics in anticipation of first results from MAST Upgrade

We report that the mega amp spherical tokamak (MAST) was a low aspect ratio device (R/a = 0.85/0.65 ~ 1.3) with similar poloidal cross-section to other medium-size tokamaks. The physics programme concentrates on addressing key physics issues for the operation of ITER, design of DEMO and future spherical tokamaks by utilising high resolution diagnostic measurements closely coupled with theory and modelling to significantly advance our understanding. An empirical scaling of the energy confinement time that favours higher power, lower collisionality devices is consistent with gyrokinetic modelling of electron scale turbulence. Measurements of ion scale turbulence with beam emission spectroscopy and gyrokinetic modelling in up-down symmetric plasmas find that the symmetry of the turbulence is broken by flow shear. Near the non-linear stability threshold, flow shear tilts the density fluctuation correlation function and skews the fluctuation amplitude distribution. Results from fast particle physics studies include the observation that sawteeth are found to redistribute passing and trapped fast particles injected from neutral beam injectors in equal measure, suggesting that resonances between the m = 1 perturbation and the fast ion orbits may be playing a dominant role in the fast ion transport. Measured D–D fusion products from a neutron camera and a charged fusion product detector are 40% lower than predictions from TRANSP/NUBEAM, highlighting possible deficiencies in the guiding centre approximation. Modelling of fast ion losses in the presence of resonant magnetic perturbations (RMPs) can reproduce trends observed in experiments when the plasma response and charge-exchange losses are accounted for. Measurements with a neutral particle analyser during merging-compression start-up indicate the acceleration of ions and electrons. Transport at the plasma edge has been improved through reciprocating probe measurements that have characterised a geodesic acoustic mode at the edge of an ohmic L-mode plasma and particle-in-cell modelling has improved the interpretation of plasma potential estimates from ball-pen probes. The application of RMPs leads to a reduction in particle confinement in L-mode and H-mode and an increase in the core ionization source. The ejection of secondary filaments following type-I ELMs correlates with interactions with surfaces near the X-point. Simulations of the interaction between pairs of filaments in the scrape-off layer suggest this results in modest changes to their velocity, and in most cases can be treated as moving independently. A stochastic model of scrape-off layer profile formation based on the superposition of non-interacting filaments is in good agreement with measured time-average profiles. Transport in the divertor has been improved through fast camera imaging, indicating the presence of a quiescent region devoid of filament near the X-point, extending from the separatrix to $ψ_n$ ~ 1.02. Simulations of turbulent transport in the divertor show that the angle between the divertor leg on the curvature vector strongly influences transport into the private flux region via the interchange mechanism. Coherence imaging measurements show counter-streaming flows of impurities due to gas puffing increasing the pressure on field lines where the gas is ionised. MAST Upgrade is based on the original MAST device, with substantially improved capabilities to operate with a Super-X divertor to test extended divertor leg concepts. SOLPS-ITER modelling predicts the detachment threshold will be reduced by more than a factor of 2, in terms of upstream density, in the Super-X compared with a conventional configuration and that the radiation front movement is passively stabilised before it reaches the X-point. 1D fluid modelling reveals the key role of momentum and power loss mechanisms in governing detachment onset and evolution. Analytic modelling indicates that long legs placed at large major radius, or equivalently low at the target compared with the X-point are more amenable to external control. With MAST Upgrade experiments expected in 2019, a thorough characterisation of the sources of the intrinsic error field has been carried out and a mitigation strategy developed.

70 PLASMA PHYSICS AND FUSION TECHNOLOGY↗

Pedestal stability analysis on MAST in preparation for MAST-U

In preparation for the upcoming MAST-U campaign, pedestal stability of spherical tokamaks is revisited by investigating standard H-mode discharges on MAST. As a step beyond previous studies, both ion and electron profiles are used for obtaining equilibria and a diverse set of pedestals is evaluated. Stability analysis with the ELITE and CGYRO codes shows that MAST pedestals are constrained by kinetic ballooning modes and medium toroidal mode number peeling-ballooning modes, with most unstable modes ranging from n = 25 to n = 45. In discharges with a steep q profile at the edge a larger number of poloidal harmonics is excited for each toroidal mode. In conclusion, a comparison with discharges on DIII-D with matched shape and similar non-dimensional parameters indicates that the increased shear at lower aspect ratio stabilizes low n peeling modes.

70 PLASMA PHYSICS AND FUSION TECHNOLOGY↗

Anti-allergic activity of 2,4,6-trihydroxy-3-geranylacetophenone (tHGA) via attenuation of IgE-mediated mast cell activation and inhibition of passive systemic anaphylaxis

tHGA, a geranyl acetophenone compound originally isolated from a local shrub called Melicope ptelefolia, has been previously reported to prevent ovalbumin-induced allergic airway inflammation in a murine model of allergic asthma by targeting cysteinyl leukotriene synthesis. Mast cells are immune effector cells involved in the pathogenesis of allergic diseases including asthma by releasing cysteinyl leukotrienes. The anti-asthmatic properties of tHGA could be attributed to its inhibitory effect on mast cell degranulation. As mast cell degranulation is an important event in allergic responses, this study aimed to investigate the anti-allergic effects of tHGA in cellular and animal models of IgE-mediated mast cell degranulation. For in vitro model of IgE-mediated mast cell degranulation, DNP-IgE-sensitized RBL-2H3 cells were pre-treated with tHGA before challenged with DNP-BSA to induce degranulation. For IgE-mediated passive systemic anaphylaxis, Sprague Dawley rats were sensitized by intraperitoneal injection of DNP-IgE before challenged with DNP-BSA. Both in vitro and in vivo models showed that tHGA significantly inhibited the release of preformed mediators (β-hexosaminidase and histamine) as well as de novo mediators (interleukin-4, tumour necrosis factor-α, prostaglandin D{sub 2} and leukotriene C{sub 4}). Pre-treatment of tHGA also prevented IgE-challenged RBL-2H3 cells and peritoneal mast cells from undergoing morphological changes associated with mast cell degranulation. These findings indicate that tHGA possesses potent anti-allergic activity via attenuation of IgE-mediated mast cell degranulation and inhibition of IgE-mediated passive systemic anaphylaxis. Thus, tHGA may have the potential to be developed as a mast cell stabilizer for the treatment of allergic diseases in the future. - Highlights: • The in vitro and in vivo mast cell stabilizing effects of tHGA were examined. • tHGA counteracts the plasma membrane deformation in degranulating mast cells. • tHGA attenuates preformed and de novo mediators released by degranulating mast cells. • tHGA prevents in vivo mast cell activation and passive systemic anaphylaxis in rats. • tHGA could be a potential mast cell stabilizer for the treatment of allergic diseases.

60 APPLIED LIFE SCIENCES↗

An indoxyl compound 5-bromo-4-chloro-3-indolyl 1,3-diacetate, CAC-0982, suppresses activation of Fyn kinase in mast cells and IgE-mediated allergic responses in mice

Mast cells, constituents of virtually all organs and tissues, are critical cells in IgE-mediated allergic responses. The aim of this study was to investigate the effect and mechanism of an indoxyl chromogenic compound, 5-bromo-4-chloro-3-indolyl 1,3-diacetate, CAC-0982, on IgE-mediated mast cell activation and allergic responses in mice. CAC-0982 reversibly suppressed antigen-stimulated degranulation in murine mast cells (IC{sub 50}, ~ 3.8 μM) and human mast cells (IC{sub 50}, ~ 3.0 μM). CAC-0982 also inhibited the expression and secretion of IL-4 and TNF-α in mast cells. Furthermore, CAC-0982 suppressed the mast cell-mediated allergic responses in mice in a dose-dependent manner (ED{sub 50} 27.9 mg/kg). As for the mechanism, CAC-0982 largely suppressed the phosphorylation of Syk and its downstream signaling molecules, including LAT, Akt, Erk1/2, p38, and JNK. Notably, the tyrosine kinase assay of antigen-stimulated mast cells showed that CAC-0982 inhibited Fyn kinase, one of the upstream tyrosine kinases for Syk activation in mast cells. Taken together, these results suggest that CAC-0982 may be used as a new treatment for regulating IgE-mediated allergic diseases through the inhibition of the Fyn/Syk pathway in mast cells. - Highlights: • The anti-allergic effect of 5-bromo-4-chloro-3-indolyl 1,3-diacetate, CAC-0982, was measured. • CAC-0982 reversibly suppressed the activation of mast cells by IgE and antigen. • CAC-0982 inhibited passive cutaneous anaphylaxis in mice. • CAC-0982 suppresses mast cells through inhibition of Fyn activation in mast cells.

60 APPLIED LIFE SCIENCES↗

Th17 cell-mediated immune responses promote mast cell proliferation by triggering stem cell factor in keratinocytes

Although mast cells are traditionally thought to function as effector cells in allergic responses, they have increasingly been recognized as important regulators of various immune responses. Mast cells mature locally; thus, tissue-specific influences are important for promoting mast cell accumulation and survival in the skin and the gastrointestinal tract. In this study, we determined the effects of keratinocytes on mast cell accumulation during Th17-mediated skin inflammation. We observed increases in dermal mast cells in imiquimod-induced psoriatic dermatitis in mice accompanied by the expression of epidermal stem cell factor (SCF), a critical mast cell growth factor. Similar to mouse epidermal keratinocytes, SCF was highly expressed in the human HaCaT keratinocyte cell line following stimulation with IL−17. Further, keratinocytes promoted mast cell proliferation following stimulation with IL−17 in vitro. However, the effects of keratinocytes on mast cells were significantly diminished in the presence of anti−CD117 (stem cell factor receptor) blocking antibodies. Taken together, our results revealed that the Th17-mediated inflammatory environment promotes mast cell accumulation through keratinocyte-derived SCF. - Highlights: • Psoriasis-like skin inflammation increase dermal mast cells. • Keratinocyte produce stem cell factor in psoriasis-like skin inflammation. • Keratinocyte promote mast cell proliferation by stem cell factor dependent manner.

60 APPLIED LIFE SCIENCES↗

Error field correction strategies in preparation to MAST-U operation

In magnetic fusion devices, unwanted non-axisymmetric magnetic field perturbations, known as error fields (EF), can have detrimental effects on plasma stability and confinement. Such EFs may originate from several sources, such as axi-symmetric coil misalignments, coil feeds, 3D structures in the wall surrounding the plasma, presence of ferromagnetic materials near the plasma surface, blanket materials in future devices. To minimize their impact on plasma performance and on the available operational space, it is important to identify the EF sources and develop EF control strategies. MAST Upgrade (MAST-U) is a spherical tokamak which will operate in the near future after a series of enhancements from the previous MAST experiment. To deliver a machine with EF amplitude low enough to allow a high quality experimental programme, systematic analysis of the intrinsic EF sources has been carried out for poloidal eld (P) and divertor (D) coils. To deliver a machine with EF amplitude low enough to allow a high quality experimental programme, systematic analysis of the intrinsic EF sources has been carried out for poloidal field (P) and divertor (D) coils, whose magnetic eld measurements were available when writing this paper. Such measurements reveal that P and D coils are 3D deformed and thus are responsible for intrinsic EFs, with mainly n=1 and n=2 toroidal mode numbers. In preparation to MAST-U operation, both passive and active EF control strategies have been adopted for n=1 and n=2 EFs compensation. Passive EF control consisted of installing finely each D and P coil within MAST-U device so as to minimize the intrinsic n=1 EF amplitude. The optimal coil alignment has been determined based on magnetic eld measurements and the corresponding 3D electro-magnetic modelling, and envisaged coil shift and tilt of 3.2 mm and 0.7 mrad, respectively, in the case of P coil named P4. Conversely, active control will be use during MAST-U operation to reduce the n=2 EF which is associated mainly with P4 and P5, as well. Since these coils have been re-used from the MAST device, studies attempting n=2 EF control, based on MAST plasmas, have been modelled utilizing the MARS-F code to interpret experimental results in MAST and to give hints for future n=2 EF control studies in MAST-U. Here, a model-based control set for n=2 EF control has been identified which would allow for the minimization of rotation braking, of the resonant magnetic field at the q=2 and of the plasma displacement in MAST-U, simultaneously.

70 PLASMA PHYSICS AND FUSION TECHNOLOGY↗

Inhibitory effect of putranjivain A on allergic inflammation through suppression of mast cell activation

A great number of people are suffering from allergic inflammatory disease such as asthma, atopic dermatitis, and sinusitis. Therefore discovery of drugs for the treatment of these diseases is an important subject in human health. Putranjivain A (PJA), member of ellagitannin, is known to possess beneficial effects including anti-cancer and anti-viral activities. The aim of the present study was to elucidate whether PJA modulates the allergic inflammatory reaction and to study its possible mechanisms of action using mast cell-based in vitro and in vivo models. The study was performed in anaphylaxis mouse model and cultured mast cells. PJA inhibited the expression of pro-inflammatory cytokines in immunoglobulin E-stimulated mast cells. PJA reduced this expression by inhibiting nuclear factor (NF)-κB and nuclear factor of activated T cell. The oral administration of PJA reduced systemic and cutaneous anaphylaxis, the release of serum histamine, and the expression of the histamine H{sub 1} receptor. In addition, PJA attenuated the activation of mast cells. PJA inhibited the release of histamine from various types of mast cells by the suppression of intracellular calcium. The inhibitory activity of PJA on the allergic reaction was similar to that of disodium cromoglycate, a known anti-allergic drug. These results suggest that PJA can facilitate the prevention or treatment of allergic inflammatory diseases mediated by mast cells. - Highlights: • PJA reduced the degranulation of mast cells. • PJA inhibited the production of inflammatory cytokines. • The effect of PJA on allergic reaction was comparable to the DSCG. • PJA might be a candidate for the treatment of allergic inflammatory diseases.

60 APPLIED LIFE SCIENCES↗

Nonclinical evaluation of the potential for mast cell activation by an erythropoietin analog

The erythropoietin analog peginesatide was withdrawn from marketing due to unexpected severe anaphylactic reactions associated with administration of the multi-use formulation. The adverse events occurred rapidly following the first ever administration of the drug with most affected patients becoming symptomatic in less than 30 min. This is most consistent with an anaphylactoid reaction due to direct activation of mast cells. Laboratory evaluation was undertaken using rat peritoneal mast cells as the model system. Initial studies showed that high concentrations of the formulated drug as well as formulated vehicle alone could cause mast cell degranulation as measured by histamine release. The purified active drug was not able to cause histamine release whereas the vehicle filtrate and lab created drug vehicle were equally potent at causing histamine release. Individual formulations of vehicle leaving one component out showed that histamine release was due to phenol. Dose response studies with phenol showed a very sharp dose response curve that was similar in three buffer systems. Cellular analysis by flow cytometry showed that the histamine release was not due to cell death, and that changes in light scatter parameters consistent with degranulation were rapidly observed. Limited testing with primary human mast cells showed a similar dose response of histamine release with exposure to phenol. To provide in vivo confirmation, rats were injected with vehicle formulated with various concentrations of phenol via a jugular vein cannula. Significant release of histamine was detected in blood samples taken 2 min after dosing at the highest concentrations tested. - Highlights: • Peginesatide caused severe anaphylactoid reactions in 0.2% of patients. • Both formulated drug and vehicle cause degranulation of rat mast cells. • Phenol was identified as the vehicle component causing degranulation. • Human mast cells show similar dose response to phenol as rat mast cells. • Histamine release could be caused in vivo in rats by rapid phenol injection.

60 APPLIED LIFE SCIENCES↗

Suppression of IgE-mediated mast cell activation and mouse anaphylaxis via inhibition of Syk activation by 8-formyl-7-hydroxy-4-methylcoumarin, 4μ8C

Mast cells trigger IgE-mediated allergic reactions by releasing various allergic mediators. 8-Formyl-7-hydroxy-4-methylcoumarin, also called 4μ8C, was originally known as an inositol-requiring enzyme 1 (IRE1) suppressant, but no study has examined its relationship with mast cells and allergic diseases. Therefore, the purpose of this study was to determine whether 4μ8C is effective in suppressing allergic reactions in mast cells and in IgE-mediated allergic animal model. 4μ8C suppressed the degranulation of IgE-mediated mast cells (IC{sub 50} = 3.2 μM) and the production of cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-4 (IL-4) in a dose-dependent manner. 4μ8C also suppressed passive cutaneous anaphylaxis (PCA) in mice (ED{sub 50} = 25.1 mg/kg). In an experiment on mast cell signaling pathways stimulated by antigen, the phosphorylation and activation of Syk was decreased by 4μ8C, and phosphorylation of downstream signaling molecules, such as linker for activated T cells (LAT), Akt, and the three MAP kinases, ERK, p38, and JNK, were suppressed. Mechanistic studies showed that 4μ8C inhibited the activity of Lyn and Fyn in vitro. Based on the results of those experiments, the suppressor mechanism of allergic reaction by 4μ8C involved reduced activity of Lyn and Fyn, which is pivotal in an IgE-mediated signaling pathway. In summary, for the first time, this study shows that 4μ8C inhibits Lyn and Fyn, thus suppressing allergic reaction by reducing the degranulation and the production of inflammatory cytokines. This suggests that 4μ8C can be used as a new medicinal candidate to control allergic diseases such as seasonal allergies and atopic dermatitis. - Highlights: • Anti-allergic effect of 8-formyl-7-hydroxy-4-methylcoumarin, 4μ8C, was investigated in vitro and in vivo. • 4μ8C reversibly inhibited the degranulation of mast cells by antigen. • 4μ8C suppressed passive cutaneous anaphylaxis (PCA) in mice. • The anti-allergic effect of 4μ8C was mediated by inhibition of Lyn and Fyn in mast cells.

60 APPLIED LIFE SCIENCES↗

Observation of a new pedestal stability regime in MAST Upgrade H-mode plasmas

Abstract The first pedestal stability and structure analysis on the new MAST Upgrade (MAST-U) spherical tokamak H-mode plasmas is presented. Our results indicate that MAST-U pedestals are close to the low toroidal mode number ( n ) peeling branch of the peeling-ballooning instability, in contrast with MAST H-mode pedestals which were deeply in the high- n ballooning branch. This offers the possibility of reaching the ELM-free quiescent H-mode (Burrell et al 2005 Plasma Phys. Control. Fusion 47 B37–B52) or high-performance super H-mode (Snyder et al 2015 Nucl. Fusion 55 083026; Snyder et al 2019 Nucl. Fusion 59 086017) regimes. In addition, the coupling between the peeling and ballooning branches is weak in MAST-U, suggesting that a path to very high pedestal pressure gradient at high density may exist with sufficient heating power. A possible explanation for the differences between MAST and MAST-U pedestal stability is given in terms of plasma shaping parameters, in particular squareness and elongation, as well as the pedestal top temperature and collisionality.

70 PLASMA PHYSICS AND FUSION TECHNOLOGY↗

GPR30 decreases cardiac chymase/angiotensin II by inhibiting local mast cell number

Chronic activation of the novel estrogen receptor GPR30 by its agonist G1 mitigates the adverse effects of estrogen (E2) loss on cardiac structure and function. Using the ovariectomized (OVX) mRen2.Lewis rat, an E2-sensitive model of diastolic dysfunction, we found that E2 status is inversely correlated with local cardiac angiotensin II (Ang II) levels, likely via Ang I/chymase-mediated production. Since chymase is released from cardiac mast cells during stress (e.g., volume/pressure overload, inflammation), we hypothesized that GPR30-related cardioprotection after E2 loss might occur through its opposing actions on cardiac mast cell proliferation and chymase production. Using real-time quantitative PCR, immunohistochemistry, and immunoblot analysis, we found mast cell number, chymase expression, and cardiac Ang II levels were significantly increased in the hearts of OVX-compared to ovary-intact mRen2.Lewis rats and the GPR30 agonist G1 (50 mg/kg/day, s.c.) administered for 2 weeks limited the adverse effects of estrogen loss. In vitro studies revealed that GPR30 receptors are expressed in the RBL-2H3 mast cell line and G1 inhibits serum-induced cell proliferation in a dose-dependent manner, as determined by cell counting, BrdU incorporation assay, and Ki-67 staining. Using specific antagonists to estrogen receptors, blockage of GPR30, but not ERα or ERβ, attenuated the inhibitory effects of estrogen on BrdU incorporation in RBL-2H3 cells. Further study of the mechanism underlying the effect on cell proliferation showed that G1 inhibits cyclin-dependent kinase 1 (CDK1) mRNA and protein expression in RBL-2H3 cells in a dose-dependent manner. - Highlights: • GPR30 activation limits mast cell number in hearts from OVX mRen2.Lewis rats. • GPR30 activation decreases cardiac chymase/angiotensin II after estrogen loss. • GPR30 activation inhibits RBL-2H3 mast cell proliferation and CDK1 expression.

60 APPLIED LIFE SCIENCES↗

Cornuside inhibits mast cell-mediated allergic response by down-regulating MAPK and NF-κB signaling pathways

Aims: The present study is to investigate the effect of cornuside on mast cell-mediated allergic response, as well as its possible mechanisms of action. Methods: To test the anti-allergic effects of cornuside in vivo, local extravasation was induced by local injection of anti-dinitrophenyl immunoglobulin E (IgE) followed by intravenous antigenic challenge in passive cutaneous anaphylaxis model rats. Mast cell viability was determined using MTT assay. Histamine content from rat peritoneal mast cells was measured by the radioenzymatic method. To investigate the mechanisms by which cornuside affects the reduction of histamine release, the levels of calcium uptake were measured. To examine whether cornuside affects the expression of pro-inflammatory cytokines, Western blotting and ELISA were carried out. Results: Oral administration of cornuside inhibited passive cutaneous anaphylaxis in rats. Presence of cornuside attenuated IgE-induced histamine release from rat peritoneal mast cells. The inhibitory effect of cornuside on histamine release was mediated by the modulation of intracellular calcium. In addition, cornuside decreased phorbol 12-myristate 13-acetate (PMA) and calcium ionophore A23187-stimulated production and secretion of pro-inflammatory cytokines such as TNF-α and IL-6 in human mast cells. The inhibitory effect of cornuside on pro-inflammatory cytokines was dependent on nuclear factor-κB and p38 mitogen-activated protein kinase. Conclusions: The present study provides evidence that cornuside inhibits mast cell-derived inflammatory allergic reactions by blocking histamine release and pro-inflammatory cytokine expression. Furthermore, in vivo and in vitro anti-allergic effects of cornuside suggest a possible therapeutic application of this agent in inflammatory allergic diseases.

60 APPLIED LIFE SCIENCES↗

Projected global stability of high beta MAST-U spherical tokamak plasmas

Assessment of the limits of stability of tokamak plasmas is essential to operation in high fusion performance ranges without disruption of the plasma current. Projected equilibria have been generated for the MAST-U spherical tokamak experiment, an upgrade of the previous MAST device, in order to prepare for operation. These equilibria are scanned in pressure and current profiles, and assessed with the DCON and MARS-F stability codes to find the so-called 'no-wall' beta limit, above which resistive wall mode instabilities can be expected in the absence of other stabilising effects. The no-wall limit was generally found to increase as plasma internal inductance increased. The equilibria are also assessed for the 'with-wall' limit, theoretically the highest achievable performance point, again with the DCON and MARS-F codes, including different approximate axisymmetric walls, and with the VALEN code which includes a 3D model of the surrounding conducting structure. Similar limits were found, despite the difference between the 2D and 3D codes in the treatment of the wall. Conducting passive stabilisation plates, which were newly installed in MAST-U, are in a region of significant mode perturbation when the plasma β N is sufficiently high and eddy currents are driven in these structures. Due to the increased stabilising effect of the wall in MAST-U vs. MAST, a significant gap exists between the approximate no-wall limits of β N / l i = 6.71 and 7.13, found from DCON and MARS-F respectively, and the with-wall limits of β N / l i = 8.23 and 8.53 for the equilibrium profiles analysed in this study. This opens a region of high beta operating space in MAST-U for potentially stable operation if non-ideal effects or active control can stabilise the resistive wall mode.

70 PLASMA PHYSICS AND FUSION TECHNOLOGY↗

Operational space and performance limiting events in the first physics campaign of MAST-U

Abstract The MAST-U fusion plasma research device, an upgrade to the Mega Amp Spherical Tokamak, has recently completed its first campaign of physics operation. MAST-U operated with Ohmic, or one or two neutral beams for heating, at 400–800 kA plasma current, in conventional or ‘SuperX’ divertor configurations. Equilibrium reconstructions provide key plasma physics parameters vs. time for each discharge, and diagrams are produced which show where the prevalence of operation occurs as well as the limits in various operational spaces. When compared to stability limits, the operation of MAST-U so far has generally stayed out of the low q , low density instability region, and below the high density Greenwald limit, high beta global stability limit, and high elongation vertical stability limit. MAST-U still has the potential to reach higher elongation, which could benefit the plasma performance. Despite the majority of operations happening below established stability limits, disruptions do occur in the flat-top phase of MAST-U plasmas. The reasons for these disruptions are highlighted, and possible strategies to avoid them and to extend the operational space of MAST-U in future campaigns are discussed.

70 PLASMA PHYSICS AND FUSION TECHNOLOGY↗

Framework for assessment of magnetic equilibrium controller performance on the MAST upgrade spherical tokamak

Here, in this work we present the assessment framework for magnetic equilibrium controllers on MAST Upgrade spherical tokamak (MAST-U) spherical tokamak. Such controllers are essential for the MAST-U since exhaust physics and core-edge integration studies require advanced divertor plasma configurations. The developed framework is based on the TokSys suite of plasma control codes, which was adapted and upgraded for MAST-U. However, extra capabilities were added on top of TokSys to support the development of new control algorithms, deployment of controllers to the plasma control system (PCS) and evaluation of their performance. The controller assessment was realized via closed-loop integrated control simulations with the actual MAST-U PCS and different physics-based plasma models. Since all components of the assessment chain were experimentally validated, these simulations provide qualified controllers applicable for direct use in the experiment. This resulted in the successful experimental demonstration of advanced plasma shape control on MAST-U with minimal on-machine development time. A similar methodology would be beneficial to other tokamaks, both existing and future.

70 PLASMA PHYSICS AND FUSION TECHNOLOGY↗