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Final Technical Report Transport Task Force
The Transport Task Force has functioned as the primary scientific organization in the area of magnetic-fusion confinement and transport since its inception in 1988. It has defined and set research directions, coordinated broad research efforts, advocated new funding initiatives, and created a highly successful and widely admired interactive culture between experiment, theory and modeling. The Transport Task Force carries out its activities under the direction of its chair and the Executive Committee. The Executive Committee is comprised of the leaders and deputy leaders of the scientific working groups. The working groups are structured and organized according to research needs and priorities and have been organized around the areas of Core Transport, H Mode and Pedestal, Fast Particle Transport, Transient Transport Phenomena, and Modeling and Simulation. A steering committee provides advise on TTF activities. Further information on the working groups and the structure and management of the TTF can be found at http://psfcwww2.psfc.mit.edu/ttf/index.html. The TTF holds an annual workshop. A summary of the workshops held during the period of this report is given in Appendix I. During the period of this report the Transport Task Force was involved in several significant activities. Foremost of these was a sweeping review of the status of transport science, the key research tasks for progress during the next 5-10 years, and a proposal for a funding initiative to ensure application of adequate resources to these problems. The conclusions of this study were incorporated into a white paper, which is copied below in Appendix II. Other significant activities have included the introduction of an extended, ongoing discussion on verification and validation as a requisite for defining and codifying the path toward predictive capability, the orchestration of a gradual shift of focus from ion thermal confinement to electron thermal confinement, and a joining of efforts on edge physics by coordinating and uniting efforts of the Transport Task Force and Edge Coordinating Committee. During the next biennium the TTF is chaired by Keith Burrell
Saturation Physics of Threshold Heat-Flux Reduction
The saturation physics of ion-temperature-gradient-driven turbulence is examined in relation to the temperature-gradient variation of the heat flux, which can exhibit an upshift of the critical gradient for significant flux relative to the linear instability threshold. Gyrokinetic measurements of saturation properties and spectral energy transfer, which will be defined in Sec. II, are presented, indicating that the physics of saturation is fundamentally unchanged on either side of the upshifted gradient. To analyze heat transport below and above the upshifted critical gradient, a fluid model for toroidal ion-temperature-gradient turbulence is modified to include the kinetic instability threshold. The model and the heat flux are rendered in the eigenmode decomposition to track the dominant mode-coupling channel of zonal-flow-catalyzed transfer to a conjugate stable mode. Given linear and nonlinear symmetries, the stable mode level and the cross-correlation of the unstable and stable mode amplitudes are related to the unstable mode level via linear physics. The heat flux can then be written in terms of the unstable-mode level, which through a nonlinear balance depends on the eigenmode-dependent coupling coefficients and the triplet correlation time of the dominant coupled modes. Resonance in these quantities leads to suppressed heat flux above the linear threshold, with a nonlinear upshift of the critical gradient set by the resonance broadening of a finite perpendicular wavenumber and collisionality.</p
Threshold Heat-Flux Reduction by Near-Resonant Energy Transfer
Near-resonant energy transfer to large-scale stable modes is shown to reduce transport above the linear critical gradient, contributing to the onset of transport at higher gradients. This is demonstrated for a threshold fluid theory of ion temperature gradient turbulence based on zonal-flow-catalyzed transfer. The heat flux is suppressed above the critical gradient by resonance in the triplet correlation time, a condition enforced by the wave numbers of the interaction of the unstable mode, zonal flow, and stable mode.</p
Effect of Triangularity on Ion-Temperature-Gradient-Driven Turbulence
The linear and nonlinear properties of ion-temperature-gradient-driven (ITG) turbulence with adiabatic electrons are modeled for axisymmetric configurations for a broad range of triangularities δ, both negative and positive. Peak linear growth rates decrease with negative δ but increase and shift toward a finite radial wavenumber kx with positive δ. The growth-rate spectrum broadens as a function of kx with negative δ and significantly narrows with positive δ. The effect of triangularity on linear instability properties can be explained through its impact on magnetic polarization and curvature. Nonlinear heat flux is weakly dependent on triangularity for |δ| ≤ 0.5, decreasing significantly with extreme δ, regardless of sign. Zonal modes play an important role in nonlinear saturation in the configurations studied, and artificially suppressing zonal modes increased nonlinear heat flux by a factor of about four for negative δ, increasing with positive δ by almost a factor of 20. Proxies for zonal-flow damping and drive suggest that zonal flows are enhanced with increasing positive δ.</p
Kinetic Turbulence
The weak collisionality typical of turbulence in many diffuse astrophysical
plasmas invalidates an MHD description of the turbulent dynamics, motivating
the development of a more comprehensive theory of kinetic turbulence. In
particular, a kinetic approach is essential for the investigation of the
physical mechanisms responsible for the dissipation of astrophysical turbulence
and the resulting heating of the plasma. This chapter reviews the limitations
of MHD turbulence theory and explains how kinetic considerations may be
incorporated to obtain a kinetic theory for astrophysical plasma turbulence.
Key questions about the nature of kinetic turbulence that drive current
research efforts are identified. A comprehensive model of the kinetic turbulent
cascade is presented, with a detailed discussion of each component of the model
and a review of supporting and conflicting theoretical, numerical, and
observational evidence.Comment: 31 pages, 3 figures, 99 references, Chapter 6 in A. Lazarian et al.
(eds.), Magnetic Fields in Diffuse Media, Astrophysics and Space Science
Library 407, Springer-Verlag Berlin Heidelberg (2015
Soluble forms of tau are toxic in Alzheimer's disease
Accumulation of neurofibrillary tangles (NFT), intracellular inclusions of fibrillar forms of tau, is a hallmark of Alzheimer Disease. NFT have been considered causative of neuronal death, however, recent evidence challenges this idea. Other species of tau, such as soluble misfolded, hyperphosphorylated, and mislocalized forms, are now being implicated as toxic. Here we review the data supporting soluble tau as toxic to neurons and synapses in the brain and the implications of these data for development of therapeutic strategies for Alzheimer’s disease and other tauopathies
SARS-CoV-2-specific nasal IgA wanes 9 months after hospitalisation with COVID-19 and is not induced by subsequent vaccination
BACKGROUND: Most studies of immunity to SARS-CoV-2 focus on circulating antibody, giving limited insights into mucosal defences that prevent viral replication and onward transmission. We studied nasal and plasma antibody responses one year after hospitalisation for COVID-19, including a period when SARS-CoV-2 vaccination was introduced. METHODS: In this follow up study, plasma and nasosorption samples were prospectively collected from 446 adults hospitalised for COVID-19 between February 2020 and March 2021 via the ISARIC4C and PHOSP-COVID consortia. IgA and IgG responses to NP and S of ancestral SARS-CoV-2, Delta and Omicron (BA.1) variants were measured by electrochemiluminescence and compared with plasma neutralisation data. FINDINGS: Strong and consistent nasal anti-NP and anti-S IgA responses were demonstrated, which remained elevated for nine months (p < 0.0001). Nasal and plasma anti-S IgG remained elevated for at least 12 months (p < 0.0001) with plasma neutralising titres that were raised against all variants compared to controls (p < 0.0001). Of 323 with complete data, 307 were vaccinated between 6 and 12 months; coinciding with rises in nasal and plasma IgA and IgG anti-S titres for all SARS-CoV-2 variants, although the change in nasal IgA was minimal (1.46-fold change after 10 months, p = 0.011) and the median remained below the positive threshold determined by pre-pandemic controls. Samples 12 months after admission showed no association between nasal IgA and plasma IgG anti-S responses (R = 0.05, p = 0.18), indicating that nasal IgA responses are distinct from those in plasma and minimally boosted by vaccination. INTERPRETATION: The decline in nasal IgA responses 9 months after infection and minimal impact of subsequent vaccination may explain the lack of long-lasting nasal defence against reinfection and the limited effects of vaccination on transmission. These findings highlight the need to develop vaccines that enhance nasal immunity. FUNDING: This study has been supported by ISARIC4C and PHOSP-COVID consortia. ISARIC4C is supported by grants from the National Institute for Health and Care Research and the Medical Research Council. Liverpool Experimental Cancer Medicine Centre provided infrastructure support for this research. The PHOSP-COVD study is jointly funded by UK Research and Innovation and National Institute of Health and Care Research. The funders were not involved in the study design, interpretation of data or the writing of this manuscript
Large-scale phenotyping of patients with long COVID post-hospitalization reveals mechanistic subtypes of disease
One in ten severe acute respiratory syndrome coronavirus 2 infections result in prolonged symptoms termed long coronavirus disease (COVID), yet disease phenotypes and mechanisms are poorly understood1. Here we profiled 368 plasma proteins in 657 participants ≥3 months following hospitalization. Of these, 426 had at least one long COVID symptom and 233 had fully recovered. Elevated markers of myeloid inflammation and complement activation were associated with long COVID. IL-1R2, MATN2 and COLEC12 were associated with cardiorespiratory symptoms, fatigue and anxiety/depression; MATN2, CSF3 and C1QA were elevated in gastrointestinal symptoms and C1QA was elevated in cognitive impairment. Additional markers of alterations in nerve tissue repair (SPON-1 and NFASC) were elevated in those with cognitive impairment and SCG3, suggestive of brain–gut axis disturbance, was elevated in gastrointestinal symptoms. Severe acute respiratory syndrome coronavirus 2-specific immunoglobulin G (IgG) was persistently elevated in some individuals with long COVID, but virus was not detected in sputum. Analysis of inflammatory markers in nasal fluids showed no association with symptoms. Our study aimed to understand inflammatory processes that underlie long COVID and was not designed for biomarker discovery. Our findings suggest that specific inflammatory pathways related to tissue damage are implicated in subtypes of long COVID, which might be targeted in future therapeutic trials
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