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Nonlinear analysis of complex traffic flow systems can provide a deep understanding of the causes of various traffic phenomena and reduce traffic congestion, and bifurcation analysis is a powerful method for it. In this paper, based on the improved Aw-Rascle model, a new macroscopic traffic flow model is proposed, which takes into account the road factors and driver psychological factor in the curve environment which can effectively simulate many realistic traffic phenomena on curves. The macroscopic traffic flow model on curved road is analyzed by bifurcation, firstly, it is transformed into a nonlinear dynamical system, then its stability conditions and the existence conditions of bifurcations are derived, and the changes of trajectories near the equilibrium points are described by phase plane. From an equilibrium point, various bifurcation structures describing the nonlinear traffic flow are obtained. In this paper, the influence of different bifurcations on traffic flow is analyzed, and the causes of special traffic phenomena such as stop-and-go and traffic clustering are described using Hopf bifurcation as the starting point of density temporal evolution. The derivation and simulation show that both road factors and driver psychological factor affect the stability of traffic flow on curves, and the study of bifurcation in the curved traffic flow model provides decision support for traffic management.

Interferon-γ (IFN-γ) regulates a number of cellular genes using a variety of cellular signaling pathways. Previously, we identified a novel IFN-regulated element, IFN-γ-activated transcriptional element (GATE), in the promoter of the murine IFN regulatory factor-9 (IRF-9) gene. This element binds to novel factors. We have recently characterized a novel regulatory factor, GATE binding factor 1 (GBF1), which promoted IFN-γ-induced transcription. Although GBF1 was a potent inducer of transcription, it did not bind to DNA well in vitro. To understand its role in IFN-γ-induced actions, we raised monoclonal antibodies (mAb) against GBF1. These antibodies are highly useful in Western, immunoprecipitation, and immunocytochemical analyses. Employing these antibodies, we show that GBF1 is recruited to the endogenous IRF-9 promoter. We also show GBF1 interacts with CAAAT/enhancer binding protein-β (C/EBP-β), the other GATE binding factor. Furthermore, other cytokines, such as interleukin-1 (IL-1) and IL-6, induced the expression of GBF1. These antibodies may be useful tools for investigating the role of GBF1 in cytokine-induced responses.

A combination of interferon-β (IFN-β) and all-trans retinoic acid (IFN/RA) induces tumor cell apoptosis via some unknown mechanisms. Apoptosis is a gene-directed process that limits the proliferation of undesired cells. Several genes are required to regulate cell death in the higher-order animals. Earlier, we employed a gene expression knockout technique to isolate cell death-related genes. A novel gene, the gene associated with retinoid-interferon-induced mortality-19 (GRIM-19), was found to be essential for tumor cell death induced by IFN/RA. Here, we describe the development and characterization of three monoclonal antibodies (mAbs) against GRIM-19. GRIM-19 is present in the nucleus and cytoplasm. Its expression is induced by the IFN/RA combination. We also show that GRIM-19 inhibits the cell-transforming property of viral oncogenic protein viral IFN regulatory factor-1 (vIRF-1) via a physical interaction. mAbs developed in this study should be useful for studying the other physiologic roles of GRIM-19 and serve as a potent tool for studying tumor responses to IFN/RA therapy.

We have previously identified a novel interferon (IFN)-stimulated cis-acting enhancer element, γ-IFN-activated transcriptional element (GATE). GATE differs from the known IFN-stimulated elements in its primary sequence. Preliminary analysis has indicated that the GATE-dependent transcriptional response requires the binding of novel transacting factors. A cDNA expression library derived from an IFN-γ-stimulated murine macrophage cell line was screened with a32P-labeled GATE probe to identify the potential GATE-binding factors. A cDNA coding for a novel transcription-activating factor was identified. Based on its discovery, we named it as GATE-binding factor-1 (GBF-1). GBF-1 homologs are present in mouse, human, monkey, and Drosophila. It activates transcription from reporter genes carrying GATE. It possesses a strong transactivating activity but has a weak DNA binding property. GBF-1 is expressed in most tissues with relatively higher steady-state levels in heart, liver, kidney, and brain. Its expression is induced by IFN-γ treatment. GBF-1 is present in both cytosolic and nuclear compartments. These studies thus identify a novel transactivating factor in IFN signaling pathways.