Search

Accurate steady state speed prediction is one of the key indexes to improve vehicle safety. This paper presents a steady state speed prediction method for expressway vehicles under snow and ice conditions. Firstly, the torque balance equation of vehicle rollover time is established, and the critical state of vehicle stability is judged by the lateral acceleration of vehicle. Secondly, the steady-state speed prediction parameters, including friction coefficient, braking distance, driver reaction time and vehicle yaw Angle, were calculated according to the judgment results of stable critical state, and the steady-state speed prediction model was built according to the predicted parameters. Experimental results show that this method can accurately detect the critical state of vehicle stability, and the steady-state speed prediction results are basically consistent with the actual speed. [ABSTRACT FROM AUTHOR]

In order to effectively prevent and control the security risk to integrated transportation networks, it is necessary to identify the key nodes of integrated transportation networks. Under the consideration of the differences of various transportation modes, the evaluation method of the node importance of integrated transportation networks was studied based on the complex network theory. According to the statistical data on development of the transportation industry in 2017, the weights of transportation modes, expressways, ordinary railways, high-speed railways, water transportation and civil aviation were 1.0, 1.03, 19.75, 0.01, and 0.21, respectively. The integrated transportation network in jing-jin-ji region was taken as an example to verify the proposed method. The results showed that the determined weight values were reasonable; they fully reflected the differences among various transportation modes and identified importance nodes were consistent with the current situation. Therefore, the proposed method is effective and feasible. [ABSTRACT FROM AUTHOR]

A new polyoxovanadium supramolecular complex, [(N(CH2CH2NH3)3)2(V6O18)]·3H2O ( 1), was synthesized as a crystalline product from aqueous solution at room temperature. From single crystal X-ray structural analysis, the complex is monoclinic, space group P21/ n, with a = 15.878(2) Å, b = 11.3309(15) Å, c = 19.469(3) Å, β = 102.244(2)°, V = 3423.0(8) Å3, Z = 4, final R = 0.0469. The crystal structure comprises 1D spiral vanadate chain as the oxide moiety, doubly protonated cations of tris(2-aminoethyl)amine (tren) and three lattice molecules of water. There are numerous H bonds in the structure connecting the polyoxovanadium anion moiety, protonated tren cation and lattice water molecules; the average O...O and N...O distances are 2.753 Å for O-H...O and 2.879 Å for N-H...O, respectively. [ABSTRACT FROM AUTHOR]

A series of Cu(II) complexes Cu(2)[micro-pz](2)[HB(pz)(3)](2) (1), Cu[H(2)B(pz)(2)](2) (2), Cu[HB(pz)(3)](2) (3), Cu[HB(pz(Me2))(3)](2) (4), Cu[B(pz)(4)](2) (5) (pz=pyrazole), have been synthesized and characterized by elemental analysis, IR, UV-vis, X-ray diffraction, thermal analysis and theoretical analysis. The IR spectra give the Cu-N vibration modes at 322, 366, 344, 387, and 380 cm(-1) in complexes 1-5, respectively. The UV spectra show all the complexes have same UV absorption at 232 nm; there is another band at 332 nm for complexes 1, 2 and 4, while for complexes 3 and 5, the bands are at 272 and 308 nm, respectively. Complex 1 has a binuclear structure in which two pyrazole ligands bridge two Cu-Tp units. In 2-5, the Cu(II) centers are coordinated with dihydrobis(pyrazolyl)borate (Bp), hydrotris(pyrazolyl)borate (Tp), hydrotris(3,5-Me2pyrazolyl)borate (Tp'), tetrakis(pyrazolyl)borate (Tkp) respectively to form a mononuclear structure. The results of thermal analysis for complexes 1-5 are discussed too.

Puralpha, a single-stranded DNA binding protein, recognizes a PUR element (GGN repeat). We have reported that Puralpha binds to a single-stranded oligonucleotide probe containing the cAMP response element (CRE) of rat somatostatin gene using a gel mobility shift assay. Here, we showed that Puralpha binds to the probe only in the presence of a PUR element by a more detailed characterization. We also examined the effects of Puralpha on the enhancer activity of the somatostatin CRE in PC12 cells using the reporter gene assay. Transfected Puralpha suppressed the CRE enhancer activity stimulated by forskolin (which increases intracellular cAMP), but suppression was not observed when the PUR element was deleted. The neurite extension induced by forskolin was inhibited by the transfection of Puralpha, but that by NGF was not suppressed. The c-fos mRNA induced by forskolin, but not by NGF, was also suppressed by Puralpha transfection. These results indicate that Puralpha suppresses the biological activities induced by forskolin, but not by NGF, in PC12 cells and that Puralpha could interfere with a cAMP-CRE signal pathway.

Chronic administration of morphine is known to decrease the levels of neurofilaments (NFs) in the ventral tegmental area. We ligated a promoter region of the mouse 68-KDa neurofilament (NF-68) gene to the pGL3-enhancer vector containing a luciferase gene, transfected it into SK-N-SH cells and then analyzed transcriptional activity in the cells treated with agonists or antagonists of opiate receptors. The activity of the NF-68 promoter was suppressed by naloxone about 55% at 10(-5) M and 30% at 10(-7) M at 48 h, but suppressed not by morphine. Naltrexone at 10(-5) M suppressed the promoter activity about 20%, but levallorphan, DAMGO, DPDPE and U50488 did not. The inhibition by naloxone was dose-dependent and not reversed by morphine. The inhibitory effect of naloxone was not observed in N18TG-2 cells and PC12 cells. Experiments with various deletion mutants revealed that a region responsible for naloxone suppression spans from -328 to -101 in the gene. These results suggest that naloxone has the ability to suppress transcriptional activity in some neurons.

Pur alpha is a single stranded DNA-binding protein and binds to a consensus sequence (GGN)n. We have reported that the DNA-binding activity of a single stranded cyclic AMP response element-binding protein (ssCRE-BP) is suppressed in cerebellum treated chronically with morphine, ssCRE-BP is identical to Pur alpha and the DNA binding activity of Pur alpha is markedly enhanced by a heat stable activator in the nuclear extract. In this report, we purified this activator. The amino acid composition and partial amino acid sequence were determined to be identical to those of calmodulin (CaM), which enhanced the binding of GST-Pur alpha to various PUR elements in the 5' non-coding regions of the neuropeptide Y, myelin basic protein and nicotinic Ach receptor beta 4 subunit genes. The data suggest a novel gene expression pathway mediated by Ca/CaM-Pur alpha which may regulate a variety of genes in addition to those regulated through the CREB pathway., (Copyright 1999 Academic Press.)

ssCRE-BP/Pur alpha is a single stranded DNA-binding protein and may be involved in gene replication and transcription and in the development of morphine dependence. We found a ssCRE-BP/Pur alpha (45 kDa) in rat lung that was larger than those (40 kDa) identified in rat and mouse brains and mouse lung. Immunohistochemistry showed that ssCRE-BP/Pur alpha is primarily distributed in the lung epithelium. As allergic inflammation induces various gene expressions, we investigated the changes of Pur alpha during airway inflammation. Ovalbumin-sensitized rats were used for inducing allergic airway inflammation. The expression and DNA-binding activity of 45-kDa ssCRE-BP/Pur alpha were significantly increased in the sensitized rat lungs 24 hr after antigen challenge, but not in those of rats nonsensitized or sensitized with ovalbumin and challenged with saline. Immunohistochemistry and in situ hybridization demonstrated that the vascular endothelial cells and numerous infiltrated eosinophils around the airways were stained with anti-Pur alpha antibody. These data suggest that rat lung and the eosinophils contain a 45-kDa ssCRE-BP/Pur alpha that is increased when airway inflammation occurs.