We apply the nonequilibrium Green's function formalism to the problem of a multiterminal nanojunction subject to an arbitrary time-dependent bias. In particular, we show that taking a generic one-particle system Hamiltonian within the wide-band-limit approximation, it is possible to obtain a closed analytical expression for the current in each lead. Our formula reduces to the well-known result of Jauho et al. [Phys. Rev. B 50, 5528 (1994)] in the limit where the switch-on time is taken to the remote past, and to the result of Tuovinen et al. [Phys. Rev. B 89, 085131 (2014)] when the bias is maintained at a constant value after the switch-on. As we use a partition-free approach, our formula contains both the long-time current and transient effects due to the sudden switch-on of the bias. Numerical calculations performed for the simple case of a single-level quantum dot coupled to two leads are performed for a sinusoidally varying bias. At certain frequencies of the driving bias, we observe "ringing" oscillations of the current, whose dependence on the dot level, level width, oscillation amplitude, and temperature is also investigated.

Objective Genetic associations imply a role for CD8+ T cells and the interleukin‐23 (IL‐23)/IL‐17 axis in psoriatic arthritis (PsA) and other spondyloarthritides (SpA). IL‐17A+CD8+ (Tc17) T cells are enriched in the synovial fluid (SF) of patients with PsA, and IL‐17A blockade is clinically efficacious in PsA/SpA. This study was undertaken to determine the immunophenotype, molecular profile, and function of synovial Tc17 cells in order to elucidate their role in PsA/SpA pathogenesis. Methods Peripheral blood (PB) and SF mononuclear cells were isolated from patients with PsA or other types of SpA. Cells were phenotypically, transcriptionally, and functionally analyzed by flow cytometry (n = 6–18), T cell receptor β (TCRβ) sequencing (n = 3), RNA‐Seq (n = 3), quantitative reverse transcriptase–polymerase chain reaction (n = 4), and Luminex or enzyme‐linked immunosorbent assay (n = 4–16). Results IL‐17A+CD8+ T cells were predominantly TCRαβ+ and their frequencies were increased in the SF versus the PB of patients with established PsA (P < 0.0001) or other SpA (P = 0.0009). TCRβ sequencing showed that these cells were polyclonal in PsA (median clonality 0.08), while RNA‐Seq and deep immunophenotyping revealed that PsA synovial Tc17 cells had hallmarks of Th17 cells (RORC/IL23R/CCR6/CD161) and Tc1 cells (granzyme A/B). Synovial Tc17 cells showed a strong tissue‐resident memory T (Trm) cell signature and secreted a range of proinflammatory cytokines. We identified CXCR6 as a marker for synovial Tc17 cells, and increased levels of CXCR6 ligand CXCL16 in PsA SF (P = 0.0005), which may contribute to their retention in the joint. Conclusion Our results identify synovial Tc17 cells as a polyclonal subset of Trm cells characterized by polyfunctional, proinflammatory mediator production and CXCR6 expression. The molecular signature and functional profiling of these cells may help explain how Tc17 cells can contribute to synovial inflammation and disease persistence in PsA and possibly other types of SpA.

Dual-specificity phosphatase (DUSP) 1 dephosphorylates and inactivates members of the MAPK superfamily, in particular, JNKs, p38α, and p38β MAPKs. It functions as an essential negative regulator of innate immune responses, hence disruption of the Dusp1 gene renders mice extremely sensitive to a wide variety of experimental inflammatory challenges. The principal mechanisms behind the overexpression of inflammatory mediators by Dusp1−/− cells are not known. In this study, we use a genetic approach to identify an important mechanism of action of DUSP1, involving the modulation of the activity of the mRNA-destabilizing protein tristetraprolin. This mechanism is key to the control of essential early mediators of inflammation, TNF, CXCL1, and CXCL2, as well as the anti-inflammatory cytokine IL-10. The same mechanism also contributes to the regulation of a large number of transcripts induced by treatment of macrophages with LPS. These findings demonstrate that modulation of the phosphorylation status of tristetraprolin is an important physiological mechanism by which innate immune responses can be controlled.

The time dependent full counting statistics of charge transport through an interacting quantum junction is evaluated from its generating function, controllably computed with the inchworm Monte Carlo method. Exact noninteracting results are reproduced; then, we continue to explore the effect of electron-electron interactions on the time-dependent charge cumulants, first-passage time distributions and n-electron transfer distributions. We observe a crossover in the noise from Coulomb blockade-to Kondo-dominated physics as the temperature is decreased. In addition, we uncover long-tailed spin distributions in the Kondo regime and analyze queuing behavior caused by correlations between single electron transfer events. arXiv:1801.05010v1 [cond-mat.mes-hall]