Lifting of the Vlasov-Maxwell Bracket by Lie-transform Method

The Vlasov-Maxwell equations possess a Hamiltonian structure expressed in terms of a Hamiltonian functional and a functional bracket. In the present paper, the transformation ("lift") of the Vlasov-Maxwell bracket induced by the dynamical reduction of single-particle dynamics is investigated when the reduction is carried out by Lie-transform perturbation methods. The ultimate goal of this work is to derive explicit Hamiltonian formulations for the guiding-center and gyrokinetic Vlasov-Maxwell equations that have important applications in our understanding of turbulent magnetized plasmas. Here, it is shown that the general form of the reduced Vlasov-Maxwell equations possesses a Hamiltonian structure defined in terms of a reduced Hamiltonian functional and a reduced bracket that automatically satisfies the standard bracket properties.Comment: 39 page

A gyro-gauge independent minimal guiding-center reduction by Lie-transforming the velocity vector field

International audienceWe introduce a gyro-gauge independent formulation of a simplified guiding-center reduction, which removes the fast time-scale from particle dynamics by Lie-transforming the velocity vector field. This is close to Krylov-Bogoliubov method of averaging the equations of motion, although more geometric. At leading order, the Lie-transform consists in the generator of Larmor gyration, which can be explicitly inverted, while working with gauge-independent coordinates and operators, by using the physical gyro-angle as a (constrained) coordinate. This brings both the change of coordinates and the reduced dynamics of the minimal guiding-center reduction order by order in a Larmor radius expansion. The procedure is algorithmic and the reduction is systematically derived up to full second order, in a more straightforward way than when Lie-transforming the phase-space Lagrangian or averaging the equations of motion. The results write up some structures in the guiding-center expansion. Extensions and limitations of the method are considered

Human fucosyltransferase 6 enables prostate cancer metastasis to bone

Background: The interaction between human prostate cancer (PCa) cells and bone marrow (BM) endothelium follows a rolling-and-adhesion cascade mediated by E-selectin ligand (ESL): E-selectin. This adhesion is enabled by elevated expression of α-1,3-fucosyltransferases (FTs), enzymes responsible for ESL-mediated bone metastasis in humans. In contrast, the incidence of bone metastasis in mice is rare. Methods: FT 3, 6 and 7 were overexpressed in mouse PCa cells. The rolling cell number, cell-rolling velocity and transendothelial migration were characterised in vitro. Fucosyltransferases-transduced mouse PCa cells expressing luciferase were inoculated into mice via left ventricle to compare the capability of bone metastasis. Mass spectrometry and immunoprecipitation were utilised for identification of ESLs. Results: Overexpression of FT3, FT6 or FT7 restored ESLs and enabled mouse PCa cells to roll and adhere in E-selectin-functionalised microtubes, similar to trafficking of circulating PCa cells in BM vessels. Following intracardiac inoculation, FT6-transduced cells induced robust bone metastasis in mice. Inhibition of FT6 by a fucose mimetic significantly reduced bone metastasis. Importantly, comparison of FT3, FT6 and FT7 gene expression in existing clinical samples showed significant upregulation of FT6 in PCa-distant metastases. Conclusion: FT6 is a key mediator of PCa cells trafficking to the BM. It may serve as a viable drug target in preclinical tests of therapeutics for reduction of PCa bone metastasis

Safety of deferring the reimplantation of pacing systems after their removal for infectious complications in selected patients: A 1-year follow-up study

Introduction: Recent expert consensus guidelines mention that one of the principles for infected device replacement following removal is to "reevaluate carefully if there is a continued need for a new cardiac device replacement." This is a Class I recommendation, which nevertheless suffers from a very low level of evidence (level of evidence C), since no study has revisited the systematic practice of reimplanting the same device based on a meticulous clinical reassessment. In the present paper, we examined the safety of withholding the implantation of pacing systems in selected patients. Methods and Results: Between January 2005 and December 2007, 188 consecutive patients underwent extractions of infected pacing systems at 2 medical centers. "Low-risk" patients were identified by (1) a spontaneous heart rate >45 bpm, (2) no symptomatic asystole during monitoring, (3) QRS duration <120 ms when history of AV block was noted, (4) no high-degree AV block during continuous monitoring. They remained device-free, unless an adverse clinical event occurred mandating the reimplantation. The primary study endpoint was rate of sudden death and syncope after a 12-month follow-up. Among the 74 (39.4%) "low-risk" patients, a single patient suffered a bradycardia-related syncopal event corresponding to a 1.3% (95% CI, 0.0-3.9) rate of primary endpoint. Pacing systems were also reimplanted in 24 patients (32.4%) for syncope (n = 1), nonsevere bradycardia-reated symptoms (n = 17), cardiac resynchronization (n = 2), and for reassurance in 4 asymptomatic patients. Conclusion: After removal of infected pacing systems, these preliminary data demonstrated that a strategy of nonsystematic device reimplantation associated with close surveillance was safe in "low-risk" patients, allowing the administration of antimicrobials in a device-free state. © 2009 Wiley Periodicals, Inc

NLRC4 GOF Mutations, a Challenging Diagnosis from Neonatal Age to Adulthood

International audienceThe NLRC4 inflammasome is part of the human immune innate system. Its activation leads to the cleavage of pro-inflammatory cytokines IL-1β and IL-18, promoting inflammation. NLRC4 gain-of-function (GOF) mutations have been associated with early-onset recurrent fever, recurrent macrophagic activation syndrome and enterocolitis. Herein, we describe two new patients with NLRC4 mutations. The first case presented with recurrent fever and vasoplegic syndrome, gut symptoms and urticarial rashes initially misdiagnosed as a severe protein-induced enterocolitis syndrome. The second case had recurrent macrophage activation syndrome (MAS) and shock, suggesting severe infection. We identified two NLRC4 mutations, on exon 4, within the nucleotide-binding protein domain (NBD). After a systematic review of NLRC4 GOF mutations, we highlight the wide spectrum of this disease with a limited genotype-phenotype correlation. Vasoplegic shock was only reported in patients with mutation in the NBD. Diagnosing this new entity combined with gastrointestinal symptoms and vasoplegic shocks is challenging. It mimics severe allergic reaction or sepsis. The plasma IL-18 level and genetic screening are instrumental to make a final diagnosis