Canonical circuit quantization with linear nonreciprocal devices

Nonreciprocal devices effectively mimic the breaking of time-reversal symmetry for the subspace of dynamical variables that they couple, and can be used to create chiral information processing networks. We study the systematic inclusion of ideal gyrators and circulators into Lagrangian and Hamiltonian descriptions of lumped-element electrical networks. The proposed theory is of wide applicability in general nonreciprocal networks on the quantum regime. We apply it to pedagogical and pathological examples of circuits containing Josephson junctions and ideal nonreciprocal elements described by admittance matrices, and compare it with the more involved treatment of circuits based on nonreciprocal devices characterized by impedance or scattering matrices. Finally, we discuss the dual quantization of circuits containing phase-slip junctions and nonreciprocal devices.Comment: 12 pages, 4 figures; changes made to match the accepted version in PR

Gene deficiency in activating Fcγ receptors influences the macrophage phenotypic balance and reduces atherosclerosis in mice

Immunity contributes to arterial inflammation during atherosclerosis. Oxidized low-density lipoproteins induce an autoimmune response characterized by specific antibodies and immune complexes in atherosclerotic patients. We hypothesize that specific Fcγ receptors for IgG constant region participate in atherogenesis by regulating the inflammatory state of lesional macrophages. In vivo we examined the role of activating Fcγ receptors in atherosclerosis progression using bone marrow transplantation from mice deficient in γ-chain (the common signaling subunit of activating Fcγ receptors) to hyperlipidemic mice. Hematopoietic deficiency of Fcγ receptors significantly reduced atherosclerotic lesion size, which was associated with decreased number of macrophages and T lymphocytes, and increased T regulatory cell function. Lesions of Fcγ receptor deficient mice exhibited increased plaque stability, as evidenced by higher collagen and smooth muscle cell content and decreased apoptosis. These effects were independent of changes in serum lipids and antibody response to oxidized low-density lipoproteins. Activating Fcγ receptor deficiency reduced pro-inflammatory gene expression, nuclear factor-κB activity, and M1 macrophages at the lesion site, while increasing anti-inflammatory genes and M2 macrophages. The decreased inflammation in the lesions was mirrored by a reduced number of classical inflammatory monocytes in blood. In vitro, lack of activating Fcγ receptors attenuated foam cell formation, oxidative stress and pro-inflammatory gene expression, and increased M2-associated genes in murine macrophages. Our study demonstrates that activating Fcγ receptors influence the macrophage phenotypic balance in the artery wall of atherosclerotic mice and suggests that modulation of Fcγ receptor-mediated inflammatory responses could effectively suppress atherosclerosis

Reduction of a metapopulation genetic model to an effective one island model

We explore a model of metapopulation genetics which is based on a more ecologically motivated approach than is frequently used in population genetics. The size of the population is regulated by competition between individuals, rather than by artificially imposing a fixed population size. The increased complexity of the model is managed by employing techniques often used in the physical sciences, namely exploiting time-scale separation to eliminate fast variables and then constructing an effective model from the slow modes. Remarkably, an initial model with 2$\mathcal{D}$ variables, where $\mathcal{D}$ is the number of islands in the metapopulation, can be reduced to a model with a single variable. We analyze this effective model and show that the predictions for the probability of fixation of the alleles and the mean time to fixation agree well with those found from numerical simulations of the original model.Comment: 16 pages, 4 figures. Supplementary material: 22 pages, 3 figure

Considering Fluctuation Energy as a Measure of Gyrokinetic Turbulence

In gyrokinetic theory there are two quadratic measures of fluctuation energy, left invariant under nonlinear interactions, that constrain the turbulence. The recent work of Plunk and Tatsuno [Phys. Rev. Lett. 106, 165003 (2011)] reported on the novel consequences that this constraint has on the direction and locality of spectral energy transfer. This paper builds on that work. We provide detailed analysis in support of the results of Plunk and Tatsuno but also significantly broaden the scope and use additional methods to address the problem of energy transfer. The perspective taken here is that the fluctuation energies are not merely formal invariants of an idealized model (two-dimensional gyrokinetics) but are general measures of gyrokinetic turbulence, i.e. quantities that can be used to predict the behavior of the turbulence. Though many open questions remain, this paper collects evidence in favor of this perspective by demonstrating in several contexts that constrained spectral energy transfer governs the dynamics.Comment: Final version as published. Some cosmetic changes and update of reference

Brillouin light scattering study of Co2_{2}Cr0.6_{0.6}Fe0.4_{0.4}Al and Co2_{2}FeAl Heusler compounds

The thermal magnonic spectra of Co$_{2}$Cr$_{0.6}$Fe$_{0.4}$Al (CCFA) and Co$_2$FeAl were investigated using Brillouin light scattering spectroscopy (BLS). For CCFA, the exchange constant A (exchange stiffness D) is found to be 0.48 $\mu$erg/cm (203 meV A$^2$), while for Co$_2$FeAl the corresponding values of 1.55 $\mu$erg/cm (370 meV A$^2$) were found. The observed asymmetry in the BLS spectra between the Stokes and anti-Stokes frequencies was assigned to an interplay between the asymmetrical profiles of hybridized Damon-Esbach and perpendicular standing spin-wave modes, combined with the optical sensitivity of the BLS signal to the upper side of the CCFA or Co$_2$FeAl film

MTHFD1 controls DNA methylation in Arabidopsis.

DNA methylation is an epigenetic mechanism that has important functions in transcriptional silencing and is associated with repressive histone methylation (H3K9me). To further investigate silencing mechanisms, we screened a mutagenized Arabidopsis thaliana population for expression of SDCpro-GFP, redundantly controlled by DNA methyltransferases DRM2 and CMT3. Here, we identify the hypomorphic mutant mthfd1-1, carrying a mutation (R175Q) in the cytoplasmic bifunctional methylenetetrahydrofolate dehydrogenase/methenyltetrahydrofolate cyclohydrolase (MTHFD1). Decreased levels of oxidized tetrahydrofolates in mthfd1-1 and lethality of loss-of-function demonstrate the essential enzymatic role of MTHFD1 in Arabidopsis. Accumulation of homocysteine and S-adenosylhomocysteine, genome-wide DNA hypomethylation, loss of H3K9me and transposon derepression indicate that S-adenosylmethionine-dependent transmethylation is inhibited in mthfd1-1. Comparative analysis of DNA methylation revealed that the CMT3 and CMT2 pathways involving positive feedback with H3K9me are mostly affected. Our work highlights the sensitivity of epigenetic networks to one-carbon metabolism due to their common S-adenosylmethionine-dependent transmethylation and has implications for human MTHFD1-associated diseases

Serum levels and removal by haemodialysis and haemodiafiltration of tryptophan-derived uremic toxins in ESKD patients

Tryptophan is an essential dietary amino acid that originates uremic toxins that contribute to end-stage kidney disease (ESKD) patient outcomes. We evaluated serum levels and removal during haemodialysis and haemodiafiltration of tryptophan and tryptophan-derived uremic toxins, indoxyl sulfate (IS) and indole acetic acid (IAA), in ESKD patients in different dialysis treatment settings. This prospective multicentre study in four European dialysis centres enrolled 78 patients with ESKD. Blood and spent dialysate samples obtained during dialysis were analysed with high-performance liquid chromatography to assess uremic solutes, their reduction ratio (RR) and total removed solute (TRS). Mean free serum tryptophan and IS concentrations increased, and concentration of IAA decreased over pre-dialysis levels (67%, 49%, -0.8%, respectively) during the first hour of dialysis. While mean serum total urea, IS and IAA concentrations decreased during dialysis (-72%, -39%, -43%, respectively), serum tryptophan levels increased, resulting in negative RR (-8%) towards the end of the dialysis session (p < 0.001), despite remarkable Trp losses in dialysate. RR and TRS values based on serum (total, free) and dialysate solute concentrations were lower for conventional low-flux dialysis (p < 0.001). High-efficiency haemodiafiltration resulted in 80% higher Trp losses than conventional low-flux dialysis, despite similar neutral Trp RR values. In conclusion, serum Trp concentrations and RR behave differently from uremic solutes IS, IAA and urea and Trp RR did not reflect dialysis Trp losses. Conventional low-flux dialysis may not adequately clear Trp-related uremic toxins while high efficiency haemodiafiltration increased Trp losses