The results of modeling studies of an enhanced confinement in the drift wave turbulent plasma of the CSDX linear device are presented. The mechanism of enhanced confinement is investigated here using a reduced 1D, time-dependent model, which illustrates the exchange of enstrophy between two disparate scale structures: the mesoscale flow and profile, and the turbulence intensity fields. Mean density, mean vorticity, and turbulent potential enstrophy are the variables for this model. Total potential enstrophy is conserved in this model. Vorticity mixing occurs on a scale length related to an effective Rhines' scale of turbulence, and shrinks as both density and vorticity gradients steepen. Numerical results obtained from solution of the model agree well with the experimental data from CSDX showing: (i) a steepening of the mean density profile, indicating a radial transport barrier formation, (ii) the development of a radially sheared azimuthal flow velocity that coincides with the density steepening and initiates a turbulence quench, and (iii) negative Reynolds work values, indicating that fluctuations drive the shear flow. These observations as the magnitude of the magnetic field B increases are recovered using purely diffusive expressions for the vorticity and density fluxes. A new dimensionless turbulence parameter RDT-defined as the ratio of the integrated potential enstrophy transfer from turbulence to the flow, to the integrated potential enstrophy production due to relaxation of the density gradient is introduced as a turbulence collapse indicator that detects when the enhanced confinement state is triggered.

This paper describes the ecology of drift wave turbulence and mean flows in the coupled drift-ion acoustic wave plasma of a CSDX linear device. A 1D reduced model that studies the spatiotemporal evolution of plasma mean density n¯, and mean flows v¯y and v¯z, in addition to fluctuation intensity ε, is presented. Here, ε=〈ñ2+(∇⊥ϕ̃)2+ṽz2〉 is the conserved energy field. The model uses a mixing length lmix inversely proportional to both axial and azimuthal flow shear. This form of lmix closes the loop on total energy. The model self-consistently describes variations in plasma profiles, including mean flows and turbulent stresses. It investigates the energy exchange between the fluctuation intensity and mean profiles via particle flux 〈ñṽx〉 and Reynolds stresses 〈ṽxṽy〉 and 〈ṽxṽz〉. Acoustic coupling breaks parallel symmetry and generates a parallel residual stress Πxzres. The model uses a set of equations to explain the acceleration of v¯y and v¯z via Πxyres∝∇n¯ and Πxyres∝∇n¯. Flow dynamics in the parallel direction are related to those in the perpendicular direction through an empirical coupling constant σVT. This constant measures the degree of symmetry breaking in the 〈kmkz〉 correlator and determines the efficiency of ∇n¯ in driving v¯z. The model also establishes a relation between ∇v¯y and ∇v¯z, via the ratio of the stresses Πxyres and Πxzres. When parallel to perpendicular flow coupling is weak, axial Reynolds power PxzRe=−〈ṽxṽz〉∇v¯z is less than the azimuthal Reynolds power PxyRe=−〈ṽxṽy〉∇v¯y. The model is then reduced to a 2-field predator/prey model where v¯z is parasitic to the system and fluctuations evolve self-consistently. Finally, turbulent diffusion in CSDX follows the scaling: DCSDX=DBρ⋆0.6, where DB is the Bohm diffusion coefficient and ρ⋆ is the ion gyroradius normalized to the density gradient |∇n¯/n¯| −1.

This paper presents a theory for the collapse of the edge zonal shear layer, as observed at the density limit at low β. This paper investigates the scaling of the transport and mean profiles with the adiabaticity parameter α, with special emphasizes on fluxes relevant to zonal flow (ZF) generation. We show that the adiabaticity parameter characterizes the strength of production of zonal flows and so determines the state of turbulence. A 1D reduced model that self-consistently describes the spatiotemporal evolution of the mean density n¯, the azimuthal flow v¯y, and the turbulent potential enstrophy ε=⟨(ñ−∇2ϕ̃)2/2⟩—related to fluctuation intensity—is presented. Quasi-linear analysis determines how the particle flux Γn and vorticity flux Π=−χy∇2vy+Πres scale with α, in both hydrodynamic and adiabatic regimes. As the plasma response passes from adiabatic (α > 1) to hydrodynamic (α < 1), the particle flux Γn is enhanced and the turbulent viscosity χy increases. However, the residual flux Πres—which drives the flow—drops with α. As a result, the mean vorticity gradient ∇2v¯y=Πres/χy—representative of the strength of the shear—also drops. The shear layer then collapses and turbulence is enhanced. The collapse is due to a decrease in ZF production, not an increase in damping. A physical picture for the onset of collapse is presented. The findings of this paper are used to motivate an explanation of the phenomenology of low β density limit evolution. A change from adiabatic (α=kz2vth2/(|ω|νei)>1) to hydrodynamic (α < 1) electron dynamics is associated with the density limit.

Adeno-associated virus serotype 1 (AAV1) has many advantages as a gene therapy vector, but the presence of pre-existing neutralizing antibodies (NAbs) is an important limitation. This study was designed to determine: (1) characteristics of AAV NAbs in human subjects, (2) prevalence of AAV1 NAbs in heart failure patients and (3) utility of aggressive immunosuppressive therapy in reducing NAb seroconversion in an animal model. NAb titers were assessed in a cohort of heart failure patients and in patients screened for a clinical trial of gene therapy with AAV1 carrying the sarcoplasmic reticulum calcium ATPase gene (AAV1/SERCA2a). AAV1 NAbs were found in 59.5% of 1552 heart failure patients. NAb prevalence increased with age (P=0.001) and varied geographically. The pattern of NAb titers suggested that exposure is against AAV2, with AAV1 NAb seropositivity due to crossreactivity. The effects of immunosuppression on NAb formation were tested in mini-pigs treated with immunosuppressant therapy before, during and after a single AAV1/SERCA2a infusion. Aggressive immunosuppression did not prevent formation of AAV1 NAbs. We conclude that immunosuppression is unlikely to be a viable solution for repeat AAV1 dosing. Strategies to reduce NAbs in heart failure patients are needed to increase eligibility for gene transfer using AAV vectors.