Fast Magnetic Reconnection: "Ideal" Tearing and the Hall Effect

One of the main questions in magnetic reconnection is the origin of triggering behavior with on/off properties that accounts, once it is activated, for the fast magnetic energy conversion to kinetic and thermal energies at the heart of explosive events in astrophysical and laboratory plasmas. Over the past decade progress has been made on the initiation of fast reconnection via the plasmoid instability and what has been called "ideal" tearing, which sets in once current sheets thin to a critical inverse aspect ratio $(a/L)_c$: as shown by Pucci and Velli (2014), at $(a/L)_c \sim S^{-1/3}$ the time scale for the instability to develop becomes of the order of the Alfv\'en time and independent of the Lundquist number (here defined in terms of current sheet length $L$). However, given the large values of $S$ in natural plasmas, this transition might occur for thicknesses of the inner resistive singular layer which are comparable to the ion inertial length $d_i$. When this occurs, Hall currents produce a three-dimensional quadrupole structure of magnetic field, and the dispersive waves introduced by the Hall effect accelerate the instability. Here we present a linear study showing how the "ideal" tearing mode critical aspect ratio is modified when Hall effects are taken into account, including more general scaling laws of the growth rates in terms of sheet inverse aspect ratio: the critical inverse aspect ratio is amended to $a/L \simeq (di/L)^ {0.29} (1/S)^{0.19}$, at which point the instability growth rate becomes Alfv\'enic and does not depend on either of the (small) parameters $d_i/L, 1/S$. We discuss the implications of this generalized triggering aspect ratio for recently developed phase diagrams of magnetic reconnection

"Ideal" tearing and the transition to fast reconnection in the weakly collisional MHD and EMHD regimes

This paper discusses the transition to fast growth of the tearing instability in thin current sheets in the collisionless limit where electron inertia drives the reconnection process. It has been previously suggested that in resistive MHD there is a natural maximum aspect ratio (ratio of sheet length and breadth to thickness) which may be reached for current sheets with a macroscopic length L, the limit being provided by the fact that the tearing mode growth time becomes of the same order as the Alfv\`en time calculated on the macroscopic scale (Pucci and Velli (2014)). For current sheets with a smaller aspect ratio than critical the normalized growth rate tends to zero with increasing Lundquist number S, while for current sheets with an aspect ratio greater than critical the growth rate diverges with S. Here we carry out a similar analysis but with electron inertia as the term violating magnetic flux conservation: previously found scalings of critical current sheet aspect ratios with the Lundquist number are generalized to include the dependence on the ratio $(d_e/L)^2$ where de is the electron skin depth, and it is shown that there are limiting scalings which, as in the resistive case, result in reconnecting modes growing on ideal time scales. Finite Larmor Radius effects are then included and the rescaling argument at the basis of "ideal" reconnection is proposed to explain secondary fast reconnection regimes naturally appearing in numerical simulations of current sheet evolution.Comment: 15 pages, 3 Figures, 1 Tabl

Dynamic evolution of current sheets, ideal tearing, plasmoid formation and generalized fractal reconnection scaling relations

Magnetic reconnection may be the fundamental process allowing energy stored in magnetic fields to be released abruptly, solar flares and coronal mass ejection (CME) being archetypal natural plasma examples. Magnetic reconnection is much too slow a process to be efficient on the large scales, but accelerates once small enough scales are formed in the system. For this reason, the fractal reconnection scenario was introduced (Shibata and Tanuma 2001) to explain explosive events in the solar atmosphere: it was based on the recursive triggering and collapse via tearing instability of a current sheet originally thinned during the rise of a filament in the solar corona. Here we compare the different fractal reconnection scenarios that have been proposed, and derive generalized scaling relations for the recursive triggering of fast, `ideal' - i.e. Lundquist number independent - tearing in collapsing current sheet configurations with arbitrary current profile shapes. An important result is that the Sweet-Parker scaling with Lundquist number, if interpreted as the aspect ratio of the singular layer in an ideally unstable sheet, is universal and does not depend on the details of the current profile in the sheet. Such a scaling however must not be interpreted in terms of stationary reconnection, rather it defines a step in the accelerating sequence of events of the ideal tearing mediated fractal cascade. We calculate scalings for the expected number of plasmoids for such generic profiles and realistic Lundquist numbers.Comment: 11 pages, 2 figure

Tubulin nitration in human gliomas

Immunohistochem. and biochem. investigations showed that significant protein nitration occurs in human gliomas, esp. in grade IV glioblastomas at the level of astrocytes and oligodendrocytes and neurons. Enhanced alpha-tubulin immunoreactivity was co-present in the same elements in the glioblastomas. Proteomic methodologies were employed to identify a nitrated protein band at 55 kDa as alpha-tubulin. Peptide mass fingerprinting procedures demonstrated that tubulin is nitrated at Tyr224 in grade IV tumor samples but is unmodified in grade I samples and in non-cancerous brain tissue. These results provide the first characterization of endogenously nitrated tubulin from human tumor samples

Expression level of CCR5 chemokine receptor on blood CD4+ and CD8+ T-cells plays an important role in the Ascending Aortic Aneurysm pathophysiology.

Background and aim: The CC chemokine receptor 5 (CCR5) is involved in the migration of circulating NK and Th1 cells towards inflammatory sites. CCR5 expression has also been demonstrated on endothelial cells, aortic smooth muscle cells and implicated in the development of abdominal aortic aneurysm. Thoracic aortic aneurysm (TAA) is a lethal disease burdened by complications such as aortic dissection/rupture. The risk of these acute events has been related to the severity of aortic enlargement. The aim of our study is to investigate a possible role of CCR5 expression on peripheral blood CD4+ and CD8+ T-lymphocytes in the pathogenesis of TAA. Methods: We have studied 14 patients (8 female, 6 male) with mean age of 67.35?7.70, undergoing isolated aortic valve replacement (AVR) and/or TAA surgery. Preoperatively, venous blood samples were obtained. A three colors flow cytometric analysis was performed by appropriate combinations of monoclonal antibodies directed against the following surface molecules: CD3, CD4, CD8, CCR5. Data are expressed in terms of percentage of positivity. Maximal aortic diameter (MAD) was determined by transesophageal echocardiography. For each patient we calculated the aortic size index (ASI), defined as MAD/BSA (mm/m2). Results: Aortic index was 21.52?3.14 mm/m2. Nine patients underwent isolated AVR (group 1) and five patients underwent TAA surgery (group 2). The percentage of CCR5+ on CD4+ was significantly higher in group 2 (17.03?3.08 vs 13.03?2.72, p=0.0269). A trend towards a higher percentage of CCR5+ on CD8+ was observed in group 2 (22.74?8,39 vs 16.26?3.75, p=0.0653). A significant correlation between aortic index and the percentage of CD4+ and CD8+ T-cells expressing CCR5 was observed (p=0.048, R2=0.287 and p=0.0067, R2=0.471 respectively). Conclusions: The correlation between the percentage of CD4+ and CD8+ T-cells expressing CCR5 and aortic index suggests the role of a T-cell immune-mediated cytotoxic mechanism in the progression of TAA disease

Natalizumab affects T-cell phenotype in multiple sclerosis: implications for JCV reactivation

The anti-CD49d monoclonal antibody natalizumab is currently an effective therapy against the relapsing-remitting form of multiple sclerosis (RRMS). Natalizumab therapeutic efficacy is limited by the reactivation of the John Cunningham polyomavirus (JCV) and development of progressive multifocal leukoencephalopathy (PML). To correlate natalizumab-induced phenotypic modifications of peripheral blood T-lymphocytes with JCV reactivation, JCV-specific antibodies (serum), JCV-DNA (blood and urine), CD49d expression and relative abundance of peripheral blood T-lymphocyte subsets were longitudinally assessed in 26 natalizumab-treated RRMS patients. Statistical analyses were performed using GraphPad Prism and R. Natalizumab treatment reduced CD49d expression on memory and effector subsets of peripheral blood T-lymphocytes. Moreover, accumulation of peripheral blood CD8+ memory and effector cells was observed after 12 and 24 months of treatment. CD4+ and CD8+ T-lymphocyte immune-activation was increased after 24 months of treatment. Higher percentages of CD8+ effectors were observed in subjects with detectable JCV-DNA. Natalizumab reduces CD49d expression on CD8+ T-lymphocyte memory and effector subsets, limiting their migration to the central nervous system and determining their accumulation in peripheral blood. Impairment of central nervous system immune surveillance and reactivation of latent JCV, can explain the increased risk of PML development in natalizumab-treated RRMS subjects