Speed, speed variation and crash relationships for urban arterials

Speed and speed variation are closely associated with traffic safety. There is, however, a dearth of research on this subject for the case of urban arterials in general, and in the context of developing nations. In downtown Shanghai, the traffic conditions in each direction are very different by time of day, and speed characteristics during peak hours are also greatly different from those during off-peak hours. Considering that traffic demand changes with time and in different directions, arterials in this study were divided into one-way segments by the direction of flow, and time of day was differentiated and controlled for. In terms of data collection, traditional fixed-based methods have been widely used in previous studies, but they fail to capture the spatio-temporal distributions of speed along a road. A new approach is introduced to estimate speed variation by integrating spatio-temporal speed fluctuation of a single vehicle with speed differences between vehicles using taxi-based high frequency GPS data. With this approach, this paper aims to comprehensively establish a relationship between mean speed, speed variation and traffic crashes for the purpose of formulating effective speed management measures, specifically using an urban dataset. From a total of 234 one-way road segments from eight arterials in Shanghai, mean speed, speed variation, geometric design features, traffic volume, and crash data were collected. Because the safety effects of mean speed and speed variation may vary at different segment lengths, arterials with similar signal spacing density were grouped together. To account for potential correlations among these segments, a hierarchical Poisson log-normal model with random effects was developed. Results show that a 1% increase in mean speed on urban arterials was associated with a 0.7% increase in total crashes, and larger speed variation was also associated with increased crash frequency

The improvement of Mo/4H-SiC Schottky diodes via a P2O5 surface passivation treatment

Molybdenum (Mo)/4H-silicon carbide (SiC) Schottky barrier diodes have been fabricated with a phosphorus pentoxide (P2O5) surface passivation treatment performed on the SiC surface prior to metallization. Compared to the untreated diodes, the P2O5-treated diodes were found to have a lower Schottky barrier height by 0.11 eV and a lower leakage current by two to three orders of magnitude. Physical characterization of the P2O5-treated Mo/SiC interfaces revealed that there are two primary causes for the improvement in electrical performance. First, transmission electron microscopy imaging showed that nanopits filled with silicon dioxide had formed at the surface after the P2O5 treatment that terminates potential leakage paths. Second, secondary ion mass spectroscopy revealed a high concentration of phosphorus atoms near the interface. While only a fraction of these are active, a small increase in doping at the interface is responsible for the reduction in barrier height. Comparisons were made between the P2O5 pretreatment and oxygen (O2) and nitrous oxide (N2O) pretreatments that do not form the same nanopits and do not reduce leakage current. X-ray photoelectron spectroscopy shows that SiC beneath the deposited P2O5 oxide retains a Si-rich interface unlike the N2O and O2 treatments that consume SiC and trap carbon at the interface. Finally, after annealing, the Mo/SiC interface forms almost no silicide, leaving the enhancement to the subsurface in place, explaining why the P2O5 treatment has had no effect on nickel- or titanium-SiC contacts

Myelin Activates FAK/Akt/NF-κB Pathways and Provokes CR3-Dependent Inflammatory Response in Murine System

Inflammatory response following central nervous system (CNS) injury contributes to progressive neuropathology and reduction in functional recovery. Axons are sensitive to mechanical injury and toxic inflammatory mediators, which may lead to demyelination. Although it is well documented that degenerated myelin triggers undesirable inflammatory responses in autoimmune diseases such as multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), there has been very little study of the direct inflammatory consequences of damaged myelin in spinal cord injury (SCI), i.e., there is no direct evidence to show that myelin debris from injured spinal cord can trigger undesirable inflammation in vitro and in vivo. Our data showed that myelin can initiate inflammatory responses in vivo, which is complement receptor 3 (CR3)-dependent via stimulating macrophages to express pro-inflammatory molecules and down-regulates expression of anti-inflammatory cytokines. Mechanism study revealed that myelin-increased cytokine expression is through activation of FAK/PI3K/Akt/NF-κB signaling pathways and CR3 contributes to myelin-induced PI3K/Akt/NF-κB activation and cytokine production. The myelin induced inflammatory response is myelin specific as sphingomyelin (the major lipid of myelin) and myelin basic protein (MBP, one of the major proteins of myelin) are not able to activate NF-κB signaling pathway. In conclusion, our results demonstrate a crucial role of myelin as an endogenous inflammatory stimulus that induces pro-inflammatory responses and suggest that blocking myelin-CR3 interaction and enhancing myelin debris clearance may be effective interventions for treating SCI

Functional oxide as an extreme high-k dielectric towards 4H-SiC MOSFET incorporation

MOS Capacitors are demonstrated on 4H-SiC using an octahedral ABO3 ferroic thin-film as a dielectric prepared on several buffer layers. Five samples were prepared: ABO3 on SiC, ABO3 on SiC with a SiO2 buffer (10 nm and 40 nm) and ABO3 on SiC with an Al2O3 buffer (10nm and 40 nm). Depending on the buffer material the oxide forms in either the pyrochlore or perovskite phase. A better lattice match with the Al2O3 buffer yields a perovskite phase with internal switchable dipoles. Hysteresis polarization-voltage loops show an oxide capacitance of ~ 0.2 μF/cm2 in the accumulation region indicating a dielectric constant of ~120

Cell Division Control Protein 42 Interacts With Hepatitis E Virus Capsid Protein and Participates in Hepatitis E Virus Infection

Hepatitis E Virus (HEV) causes viral hepatitis in humans worldwide, while a subset of HEV species, avian HEV, causes hepatitis-splenomegaly syndrome in chickens. To date, there are few reports on the host proteins interacting with HEV and being involved in viral infection. Previous pull-down assay combining mass spectrometry indicated that cell division control protein 42 (CDC42), a member belonging to the Rho GTPase family, was pulled down by avian HEV capsid protein. We confirmed the direct interaction between CDC42 and avian and mammalian HEV capsid proteins. The interaction can increase the amount of active guanosine triphosphate binding CDC42 state (GTP-CDC42). Subsequently, we determined that the expression and activity of CDC42 were positively correlated with HEV infection in the host cells. Using the different inhibitors of CDC42 downstream signaling pathways, we found that CDC42-MRCK (a CDC42-binding kinase)-non-myosin IIA (NMIIA) pathway is involved in naked avian and mammalian HEV infection, CDC42-associated p21-activated kinase 1 (PAK1)-NMIIA/Cofilin pathway is involved in quasi-enveloped mammalian HEV infection and CDC42-neural Wiskott-Aldrich syndrome protein-actin-polymerizing protein Arp2/3 pathway (CDC42-(N-)WASP-Arp2/3) pathway participates in naked and quasi-enveloped mammalian HEV infection. Collectively, these results demonstrated for the first time that HEV capsid protein can directly bind to CDC42, and non- and quasi-enveloped HEV use different CDC42 downstream signaling pathways to participate in viral infection. The study provided some new insights to understand the life cycle of HEV in host cells and a new target of drug design for combating HEV infection

Optimization of 1700-V 4H-SiC superjunction Schottky rectifiers with implanted p-pillars for practical realization

A class of vertical 1700-V 4H-SiC superjunction (SJ) Schottky diodes have been simulated and optimized, producing results that are below the unipolar limit, while also ensuring practical and cost-effective realization. A conventional vertical SJ is obtained in T-CAD software, using an n-type drift region of 9-μm and etching trenches through this region to the substrate to leave isolated mesa structures. P-columns are then created through implantation into the trench sidewalls. The charge-balanced SJ diode maximizes the breakdown voltage (VBD) and minimizes the specific on-resistance (Ron,SP). However, a narrow implantation window would make the vertical structure hard to fabricate. Therefore, by introducing an angled trench sidewall (α ), 10° off vertical, a graded charge profile is introduced reducing VBD by 2.5% and increasing Ron,SP by 9%. However, the implantation window is widened by 20% compared with the vertical device, making the successful production of the devices more likely. To rebalance the 10° structure, a 1-μm region of increased n-type doping is introduced at the top of the n-pillar. This partially recovers the lost VBD and Ron,SP while maintaining an implantation window wider than the vertical SJ. The balance between Ron,SP and implantation window can be tuned depending on the doping of the 1-μm top region. The 10° structure can also be rebalanced by introducing a second 4-μm region of intermediate n-type doping, underneath the 1-μm surface region. This recovers Ron,SP, while maintaining an implantation window that is 7% wider

Insight-HXMT observations of Swift J0243.6+6124 during its 2017-2018 outburst

The recently discovered neutron star transient Swift J0243.6+6124 has been monitored by {\it the Hard X-ray Modulation Telescope} ({\it Insight-\rm HXMT). Based on the obtained data, we investigate the broadband spectrum of the source throughout the outburst. We estimate the broadband flux of the source and search for possible cyclotron line in the broadband spectrum. No evidence of line-like features is, however, found up to $\rm 150~keV$. In the absence of any cyclotron line in its energy spectrum, we estimate the magnetic field of the source based on the observed spin evolution of the neutron star by applying two accretion torque models. In both cases, we get consistent results with $B\rm \sim 10^{13}~G$, $D\rm \sim 6~kpc$ and peak luminosity of $\rm >10^{39}~erg~s^{-1}$ which makes the source the first Galactic ultraluminous X-ray source hosting a neutron star.Comment: publishe