The Grad-Shafranov Reconstruction of Toroidal Magnetic Flux Ropes: Method Development and Benchmark Studies

We develop an approach of Grad-Shafranov (GS) reconstruction for toroidal structures in space plasmas, based on in-situ spacecraft measurements. The underlying theory is the GS equation that describes two-dimensional magnetohydrostatic equilibrium as widely applied in fusion plasmas. The geometry is such that the arbitrary cross section of the torus has rotational symmetry about the rotation axis $Z$, with a major radius $r_0$. The magnetic field configuration is thus determined by a scalar flux function $\Psi$ and a functional $F$ that is a single-variable function of $\Psi$. The algorithm is implemented through a two-step approach: i) a trial-and-error process by minimizing the residue of the functional $F(\Psi)$ to determine an optimal $Z$ axis orientation, and ii) for the chosen $Z$, a $\chi^2$ minimization process resulting in the range of $r_0$. Benchmark studies of known analytic solutions to the toroidal GS equation with noise additions are presented to illustrate the two-step procedures and to demonstrate the performance of the numerical GS solver, separately. For the cases presented, the errors in $Z$ and $r_0$ are 9$^\circ$ and 22\%, respectively, and the relative percent error in the numerical GS solutions is less than 10\%. We also make public the computer codes for these implementations and benchmark studies.Comment: submitted to Sol. Phys. late Dec 2016; under review; code will be made public once review is ove

Catastrophic eruption of magnetic flux rope in the corona and solar wind with and without magnetic reconnection

It is generally believed that the magnetic free energy accumulated in the corona serves as a main energy source for solar explosions such as coronal mass ejections (CMEs). In the framework of the flux rope catastrophe model for CMEs, the energy may be abruptly released either by an ideal magnetohydrodynamic (MHD) catastrophe, which belongs to a global magnetic topological instability of the system, or by a fast magnetic reconnection across preexisting or rapidly-developing electric current sheets. Both ways of magnetic energy release are thought to be important to CME dynamics. To disentangle their contributions, we construct a flux rope catastrophe model in the corona and solar wind and compare different cases in which we either prohibit or allow magnetic reconnection to take place across rapidly-growing current sheets during the eruption. It is demonstrated that CMEs, even fast ones, can be produced taking the ideal MHD catastrophe as the only process of magnetic energy release. Nevertheless, the eruptive speed can be significantly enhanced after magnetic reconnection sets in. In addition, a smooth transition from slow to fast eruptions is observed when increasing the strength of the background magnetic field, simply because in a stronger field there is more free magnetic energy at the catastrophic point available to be released during an eruption. This suggests that fast and slow CMEs may have an identical driving mechanism.Comment: 7 pages, 4 figures, ApJ, in press (vol. 666, Sept. 2007

Brueckner-Hartree-Fock and its renormalized calculations for finite nuclei

We have performed self-consistent Brueckner-Hartree-Fock (BHF) and its renormalized theory to the structure calculations of finite nuclei. The $G$-matrix is calculated within the BHF basis, and the exact Pauli exclusion operator is determined by the BHF spectrum. Self-consistent occupation probabilities are included in the renormalized Brueckner-Hartree-Fock (RBHF). Various systematics and convergences are studies. Good results are obtained for the ground-state energy and radius. RBHF can give a more reasonable single-particle spectrum and radius. We present a first benchmark calculation with other {\it ab initio} methods using the same effective Hamiltonian. We find that the BHF and RBHF results are in good agreement with other $\it{ab}$ $\it{initio}$ methods

Geometric entanglement from matrix product state representations

An efficient scheme to compute the geometric entanglement per lattice site for quantum many-body systems on a periodic finite-size chain is proposed in the context of a tensor network algorithm based on the matrix product state representations. It is systematically tested for three prototypical critical quantum spin chains, which belong to the same Ising universality class. The simulation results lend strong support to the previous claim [Q.-Q. Shi, R. Or\'{u}s, J. O. Fj{\ae}restad, and H.-Q. Zhou, New J. Phys \textbf{12}, 025008 (2010); J.-M. St\'{e}phan, G. Misguich, and F. Alet, Phys. Rev. B \textbf{82}, 180406R (2010)] that the leading finite-size correction to the geometric entanglement per lattice site is universal, with its remarkable connection to the celebrated Affleck-Ludwig boundary entropy corresponding to a conformally invariant boundary condition.Comment: 4+ pages, 3 figure

Supersymmetric Modified Korteweg-de Vries Equation: Bilinear Approach

A proper bilinear form is proposed for the N=1 supersymmetric modified Korteweg-de Vries equation. The bilinear B\"{a}cklund transformation of this system is constructed. As applications, some solutions are presented for it.Comment: 8 pages, LaTeX using packages amsmath and amssymb, some corrections mad

HSV-2 Infection of Human Genital Epithelial Cells Upregulates TLR9 Expression Through the SP1/JNK Signaling Pathway

It is known that herpes simplex virus type 2 (HSV-2) triggers the activation of Toll-like receptor (TLR) 9 signaling pathway and the consequent production of antiviral cytokines in dendritic cells. However, the impact of HSV-2 infection on TLR9 expression and signaling in genital epithelial cells, the primary HSV-2 targets, has yet to be determined. In the current study, by using both human genital epithelial cell lines and primary genital epithelial cells as models, we found that HSV-2 infection enhances TLR9 expression at both mRNA and protein levels. Such enhancement is virus replication-dependent and CpG-independent, while the HSV-2-mediated upregulation of TLR9 does not activate TLR9 signaling pathway. Mechanistically, a SP1 binding site on TLR9 promoter appears to be essential for HSV-2-induced TLR9 transactivation. Upon HSV-2 infection, SP1 translocates from the cytoplasm to the nucleus, and consequently binds to TLR9 promoter. By using specific inhibitors, the JNK signaling pathway is shown to be involved in the HSV-2-induced TLR9 transactivation, while HSV-2 infection increases the phosphorylation but not the total level of JNK. In agreement, antagonism of JNK signaling pathway inhibits the HSV-2-induced SP1 nuclear translocation. Taken together, our study demonstrates that HSV-2 infection of human genital epithelial cells promotes TLR9 expression through SP1/JNK signaling pathway. Findings in this study provide insights into HSV-2-host interactions and potential targets for immune intervention