Publications by authors named "Arita C"

We consider the exclusion process on a ring with time-dependent defective bonds at which the hopping rate periodically switches between zero and one. This system models main roads in city traffics, intersecting with perpendicular streets. We explore basic properties of the system, in particular dependence of the vehicular flow on the parameters of signalization as well as the system size and the car density.

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A diffusive lattice gas is characterized by the diffusion coefficient depending only on the density. The Green-Kubo formula for diffusivity can be represented as a variational formula, but even when the equilibrium properties of a lattice gas are analytically known, the diffusion coefficient can be computed only in the exceptional situation when the lattice gas is gradient. In the general case, minimization over an infinite-dimensional space is required.

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We reply to the Comment of Becker, Nelissen, Cleuren, Partoens, and Van den Broeck [Phys. Rev. E 93, 046101 (2016)1539-375510.

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A class of generalized exclusion processes with symmetric nearest-neighbor hopping which are parametrized by the maximal occupancy, k≥1, is investigated. For these processes on hypercubic lattices we compute the diffusion coefficient in all spatial dimensions. In the extreme cases of k=1 (symmetric simple exclusion process) and k=∞ (noninteracting symmetric random walks) the diffusion coefficient is constant, while for 2≤k<∞ it depends on the density and k.

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We study a one-dimensional totally asymmetric simple exclusion process with one special site from which particles fly to any empty site (not just to the neighboring site). The system attains a nontrivial stationary state with a density profile varying over the spatial extent of the system. The density profile undergoes a nonequilibrium phase transition when the average density passes through the critical value 1-[4(1-ln2)](-1)=0.

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The exclusive queueing process (EQP) has recently been introduced as a model for the dynamics of queues that takes into account the spatial structure of the queue. It can be interpreted as a totally asymmetric exclusion process of varying length. Here we investigate the case of deterministic bulk hopping p=1 that turns out to be one of the rare cases where exact nontrivial results for the dynamical properties can be obtained.

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Recently, the stationary state of a parallel-update totally asymmetric simple exclusion process with varying system length, which can be regarded as a queueing process with excluded-volume effect (exclusive queueing process), was obtained [C Arita and D Yanagisawa, J. Stat. Phys.

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Queueing process with excluded-volume effect.

Phys Rev E Stat Nonlin Soft Matter Phys

November 2009

We introduce an extension of the M/M/1 queueing process with a spatial structure and excluded-volume effect. The rule of particle hopping is the same as for the totally asymmetric simple exclusion process (TASEP). A stationary-state solution is constructed in a slightly arranged matrix product form of the open TASEP.

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Background: The combination of corticosteroids and azathioprine is the standard therapy for autoimmune hepatitis. The aim of this study was to describe our experience on long-term corticosteroid doses reducing and withdrawal in a large cohort of children with autoimmune hepatitis (AIH).

Methods: All children presenting with AIH in our institution, from 1990 to 2006, were retrospectively included.

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New Mo and W tetraphosphine-dihalide complexes [MX2(kappa4-P4)] (2, MX=MoCl, MoBr, WBr; P4=meso-o-C6H4(PPhCH2CH2PPh2)2) with uncommon trigonal-prismatic geometries have been prepared. Treatment of ethyl diazoacetate with 2 (MX=MoCl) resulted in catalytic carbenoid-group coupling to give diethyl maleate and fumarate, whereas reactions of 2 with trimethylsilyldiazoalkane formed the diazoalkane complexes trans-[MX(NN=CHSiMe3)-(kappa4-P4)]+ (3+) and cis,mer-[MoCl2(NN=CHSiMe3)(kappa3-P4)]. The molecular structures of 2 (MX=MoCl) and 3[PF6] (MX=WBr) were crystallographically determined.

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In vitro data support the view that T cells in adjuvant-induced arthritis (AIA) respond to the proteoglycan (PG) component of articular cartilage; however, an in vivo role for PG in AIA has yet to be shown. To do so, we examined the effects of pretreatment with bovine cartilage high density PG (HDPG) on AIA induced by heat-killed Mycobacterium butyricum in Lewis rats. Purified bovine cartilage HDPG emulsified in Freund's incomplete adjuvant (FIA) was injected intradermally into rats 7 days before challenge with Myco.

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12 anemic and 10 non-anemic patients with rheumatoid arthritis were treated with recombinant human erythropoietin (rHuEPO) before arthroplasty. The patients received 400-800 units/kg of rHuEPO subcutaneously once a week. Autologous blood was collected after the hemoglobin concentration was increased by 5 percent or more.

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Type II collagen-induced arthritis (CIA) is a pathologic process mediated, in part, by humoral immune mechanisms. Because many antibody-mediated reactions are neutrophil-dependent, the role of this cell population was examined in passive CIA transferred with anti-type II collagen (CII) antibody. In cyclophosphamide (CY)-induced leukocytopenic rats, swelling and inflammation associated with the arthritic response were significantly reduced.

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We investigated the effect of a novel immunosuppressive agent, FK506, in comparison with cyclosporin A (CsA) on the development of passive arthritis induced by anti-type II collagen (CII) antisera in rats. FK506 pretreatment shortly before serum transfer markedly suppressed the incidence and the severity of passive arthritis, while CsA pretreatment had no observable effects on this disease when used in doses sufficient to suppress the development of active arthritis induced by CII immunization. In an additional study, we examined whether these agents affect antibody-mediated tolerance induction.

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We investigated the superior potency of the immunosuppressive agent FK506 on collagen-induced arthritis in rats. In our initial studies, we demonstrated that only one shot administration of FK506 at a dose of 10 mg/kg on the same day as type II collagen immunization suppressed the incidence of arthritis completely as well as humoral and delayed-type hypersensitivity (DTH) skin test responses to type II collagen. Yet no major side effects were observed in the rats treated with such a high dose of FK506.

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We have tested the effects of FK506 (FK), a new immunosuppressive agent, on a rat limb allograft model. Histoincompatible BN limb allografts were rejected in untreated F344 hosts within 11 +/- 1 days (mean +/- SD) after operation. A single injection of 2 mg/kg, 10 mg/kg, or 50 mg/kg of FK on the day of limb transplantation (day 0) significantly prolonged graft survival in a dose-dependent manner--i.

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We performed limb allografts in three inbred rat strains immunosuppressed with cyclosporine. As controls, 10 autografts and 10 isografts exhibited an excellent result. In minor-mismatched allografts (Lewis to Fischer, n = 45), with the use of cyclosporine, the grafted limbs survived and the articular cartilage retained normal architecture and cell viability 52 weeks after grafting, but without cyclosporine treatment severe degeneration and destruction of articular cartilage were shown by 16 weeks after operation.

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The effect of the new immunosuppressive agent FK-506 on rat limb allograft was investigated across the BN-to-F344 histocompatibility barrier. A 14-day course of FK-treatment at doses of 1 mg/kg per day or more, begun on the day of operation, significantly increased the period of graft survival. Additional studies demonstrated that single treatment with FK only on the day of operation prolonged the graft survival in a dose-dependent manner.

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Arthritis could be passively transferred with a serum concentrate from collagen arthritic rats to nude rats and cyclosporin-treated, type II collagen-tolerant rats. These findings suggest that collagen arthritis could be inducible by humoral immunity alone in the absence of cellular immunity to type II collagen or functional T cells. In addition, passive arthritis induced by anticollagen antibody is a mild, transient disease from which the animals normally recover and the rats that have recovered from passive arthritis are resistant to develop a second phase of arthritis following a second administration of anticollagen antibody or the subsequent challenge with type II collagen.

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The effects of cyclophosphamide (CY) and its structurally related analogs, ifosfamide (Ifo), sufosfamide (Sufo), and mafosfamide (Mafo), on collagen arthritis in Sprague-Dawley rats were examined. Prophylactic treatment with 7.5-10 mg/kg/day of CY.

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Treatment of rats with intravenous injection of 1 mg of soluble native type II collagen induced resistance against the subsequent induction of active arthritis by type II collagen immunization. This resistant state was accompanied by suppressed antibody response and delayed-type hypersensitivity (DTH) skin reaction to type II collagen. However, pretreatment of rats with 20 mg/kg of cyclophosphamide (CY), an agent reputed to damage suppressor T-cell function, 2 days before intravenous injection of soluble type II collagen abrogated the antigen-induced resistance against the subsequent induction of active arthritis.

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Affinity-purified rat anti-type II collagen antibodies were used to prepare anti-idiotypic antibodies in rabbits. It has been demonstrated that such anti-idiotypic antibodies are capable of binding to anti-type II collagen antibodies in vitro. Intravenous administration of heterologous anti-idiotypic antisera at the time of immunization with type II collagen resulted in a significant suppression of anti-type II collagen antibody formation and the development of arthritis, although delayed-type hypersensitivity skin test response to type II collagen was not affected.

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The effect of tilorone, which is known to suppress adjuvant arthritis, on the induction of collagen arthritis in rats was investigated. Combined data of the present experiments show that all of the tilorone-treated rats except one in the lowest dosage group developed arthritis but that the incidence of arthritis in the tilorone-treated groups was not significantly different from that of the control group. The results also show that the two higher dosages (12.

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