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A Hook Turn (HT) traffic control scheme has been successfully implemented in urban Melbourne (Australia) ever since 1950s, for the regulation of right-turning vehicles at the intersections (in traffic system where driving is on the left). This paper addresses the optimal signal-timing of the HT scheme, which is still an open question in the literature. Under the HT scheme, right-turning vehicles should enter the intersection and stop at a waiting area. Hence, it is common to have a spillback from these vehicles if the right-turning volume is high. This paper provides an in-depth analysis of the spillback phenomenon on the traffic movements and the average delays, and proposes the models for the calculation of average delay in different cases. With the aim of minimizing the average delay of all the vehicles, a nonlinear integer-programming model is proposed for the optimal signal-timing problem of HT scheme. A Genetic Algorithm (GA) is used to solve this model, considering the complexity of its objective function. A realistic example developed based on one intersection with HT in urban Melbourne is adopted to assess the proposed methodology. Based on real survey data in morning peak and nonpeak hours, we compare the existing signal plan and optimal plan. The numerical test shows that compared with the existing plan, the optimal plan can reduce the average delay for 12.05% in peak hour and 19.96% in nonpeak hour. Sensitive analysis is also conducted to investigate the variation of right-turning ratio on the intersection operational performance.

Autophagy and lysosomal function are important for protein homeostasis and their dysfunction have been associated with Alzheimer's disease (AD). Increased immunoreactivities of an important lysosomal protease, cathepsin D (Cat D), are evident in amyloid plaques and neurons in patients with AD. This study tests the hypothesis that deleting one allele of the cathepsin D gene (Ctsd) impacts cerebral β-amyloidosis in amyloid-β precursor protein (APP)sw/PS1dE9 (APP/PS1) double transgenic mice. Despite a significant 38% decrease in Cat D level in APP/PS1/Ctsd+/- compared with APP/PS1/Ctsd+/+ mice, no changes in steady state levels and deposition of Aβ were found in the brain. There were also no differences in APP processing, the levels of two other Aβ-degrading proteases, the levels of autophagy related protein, such as LAMP2, P62, LC3-I, LC3-II, and Beclin-1, or the markers of neuroinflammation, observed between the APP/PS1/Ctsd+/+ and APP/PS1/Ctsd+/- mice. Our findings demonstrate that in wild-type mice, Cat D protein levels are either in excess or redundant with other factors in the brain, and at least one allele of Ctsd is dispensable for cerebral β-amyloidosis and autophagy in APP/PS1 transgenic mice.

Neonatal hypoxic-ischemic brain damage (HIBD) survivors present with long-term neurological disorders affecting their quality of life, and there remains a lack of effective treatment. Toll-like receptor 4 (TLR4) is widely distributed in nerve cells and its inhibition has a neuroprotective effect against brain injury. The present study aimed to evaluate the long-term neuroprotective effects of early inhibition of TLR4 during HIBD. Seven-day-old rat pups were subjected to left carotid artery ligation followed by 2 h of hypoxia (8.0% O2). A single dose of TAK-242 (0.5 mg/kg), a TLR4-specific antagonist, was intraperitoneally injected half an hour prior to hypoxic ischemia (HI). The long-term effects of TAK-242 inhibition on the induced hippocampal injury were investigated by assessing behaviour at P28, and then using a variety of methods to exploring the mechanism, including immunofluorescence, Golgi silver staining, Western blotting and real-time polymerase chain reaction (RT-PCR). TAK-242 treatment significantly reduced the expression levels of TLR4 and its downstream signalling molecules in the ipsilateral lesion of the hippocampus 24 h after HIBD. The Morris water maze (MWM) test demonstrated that TAK-242 treatment reduced the loss of HI-induced learning and memory functions. Immunofluorescence experiments showed that TAK-242 administration attenuated HI-induced loss of neurons, prevented the activation of microglia and astrocytes, and increased the expression of the glutamate receptor subtype, N-methyl d -aspartate 2A (NR2A) in the ipsilateral hippocampus region. Golgi silver staining revealed that TAK-242 prevented an HI-induced decline in spine density in the ipsilateral hippocampus. Western blot and RT-PCR results indicated that the expression of NR2A protein and mRNA in the ipsilateral hippocampi of adolescent rats decreased after neonatal HIBD; early TAK-242 administration may reverse these effects. In conclusion, our findings indicate that early inhibition of TLR4 signalling may improve the long-term prognosis of neonatal HIBD. The mechanisms contributing to this improvement involve reductions in neuronal loss, a decrease in glial cell activation, and an improvement in synaptic plasticity.

Isoprenoids and prenylated proteins have been implicated in the pathophysiology of Alzheimer disease (AD), including amyloid-β precursor protein metabolism, Tau phosphorylation, synaptic plasticity, and neuroinflammation. However, little is known about the relative importance of the two protein prenyltransferases, farnesyltransferase (FT) and geranylgeranyltransferase-1 (GGT), in the pathogenesis of AD. In this study, we defined the impact of deleting one copy of FT or GGT on the development of amyloid-β (Aβ)-associated neuropathology and learning/memory impairments in APPPS1 double transgenic mice, a well established model of AD. Heterozygous deletion of FT reduced Aβ deposition and neuroinflammation and rescued spatial learning and memory function in APPPS1 mice. Heterozygous deletion of GGT reduced the levels of Aβ and neuroinflammation but had no impact on learning and memory. These results document that farnesylation and geranylgeranylation play differential roles in AD pathogenesis and suggest that specific inhibition of protein farnesylation could be a potential strategy for effectively treating AD.

Bus fare equity has attracted significant attention in China in the past few years. Compared with developed countries, China’s intelligent transportation systems are in their infancy, with immature bus fare policies being used in many public transit systems. The methods used for evaluating public transit fare equity in developed countries compare different fare policies based on rich data and cannot be directly applied in developing countries like China. In this paper, we present a method that uses IC card data, bus-mounted GPS data, and relevant statistical yearbook data to evaluate the equity of flat bus fare. The method ranks the factors that influence the impacts of bus fare on social equity for different passenger groups and indicates that trip distance and passenger boarding time are the two primary factors for bus fare equity from a resource allocation perspective. Finally, we present a case study that evaluates the flat fare policy for route 204 in Suzhou using the proposed method. The results show that the proposed method is feasible.

Why certain diseases primarily affect one specific neuronal subtype rather than another is a puzzle whose solution underlies the development of specific therapies. Selective basal forebrain cholinergic (BFC) neurodegeneration participates in cognitive impairment in Alzheimer’s disease (AD), yet the underlying mechanism remains elusive. Here, we report the first recapitulation of the selective BFC neuronal loss that is typical of human AD in a mouse model termed GAP. We created GAP mice by crossing Tg2576 mice that over-express the Swedish mutant human β-amyloid precursor protein gene with G protein-coupled receptor kinase-5 (GRK5) knockout mice. This doubly defective mouse displayed significant BFC neuronal loss at 18 months of age, which was not observed in either of the singly defective parent strains or in the wild type. Along with other supporting evidence, we propose that GRK5 deficiency selectively renders BFC neurons more vulnerable to degeneration.

This paper proposes a novel concept, stop-line setback (SLSB), aimed at enhancing the capacity of signalized roundabouts and solving the problem of unbalanced flow patterns. This method is believed to avoid wasting acceptable time gaps and therefore increase the capacity of the approach with SLSB. However, to the best of the authors’ knowledge, no analytical work and little empirical work has yet explored the impact of SLSB. To bridge this gap, the phasing scheme and an adaptive control algorithm are developed for the roundabout with SLSB. Case studies are conducted under different traffic demands to evaluate the method. The findings show that (1) in peak hours the SLSB method is useful to improve the operational performance of the signalized roundabout and solve the problem of unbalanced flow patterns; (2) the right-turning vehicle volume is the critical factor that influences the benefits of the SLSB method; and (3) the phasing scheme and adaptive signal control algorithm developed in this paper...

Two major isoprenoids, farnesyl pyrophosphate and geranylgeranyl pyrophosphate, serve as lipid donors for the posttranslational modification (known as prenylation) of proteins that possess a characteristic C-terminal motif. The prenylation reaction is catalyzed by prenyltransferases. The lipid prenyl group facilitates to anchor the proteins in cell membranes and mediates protein-protein interactions. A variety of important intracellular proteins undergo prenylation, including almost all members of small GTPase superfamilies as well as heterotrimeric G protein subunits and nuclear lamins. These prenylated proteins are involved in regulating a wide range of cellular processes and functions, such as cell growth, differentiation, cytoskeletal organization, and vesicle trafficking. Prenylated proteins are also implicated in the pathogenesis of different types of diseases. Consequently, isoprenoids and/or prenyltransferases have emerged as attractive therapeutic targets for combating various disorders. This review attempts to summarize the pharmacological agents currently available or under development that control isoprenoid availability and/or the process of prenylation, mainly focusing on statins, bisphosphonates, and prenyltransferase inhibitors. Whereas statins and bisphosphonates deplete the production of isoprenoids by inhibiting the activity of upstream enzymes, prenyltransferase inhibitors directly block the prenylation of proteins. As the importance of isoprenoids and prenylated proteins in health and disease continues to emerge, the therapeutic potential of these pharmacological agents has expanded across multiple disciplines. This review mainly discusses their potential application in Alzheimer's disease.

Membrane G protein-coupled receptor kinase 5 (GRK5) deficiency is linked to Alzheimer disease, yet its precise roles in the disease pathogenesis remain to be delineated. We have previously demonstrated that GRK5 deficiency selectively impairs desensitization of presynaptic M2 autoreceptors, which causes presynaptic M2 hyperactivity and inhibits acetylcholine release. Here we report that inactivation of one copy of Grk5 gene in transgenic mice overexpressing β-amyloid precursor protein (APP) carrying Swedish mutations (Tg2576 or APPsw) resulted in significantly increased β-amyloid (Aβ) accumulation, including increased Aβ(+) plaque burdens and soluble Aβ in brain lysates and interstitial fluid (ISF). In addition, secreted β-APP fragment (sAPPβ) also increased, whereas full-length APP level did not change, suggesting an alteration in favor of β-amyloidogenic APP processing in these animals. Reversely, perfusion of methoctramine, a selective M2 antagonist, fully corrected the difference between the control and GRK5-deficient APPsw mice for ISF Aβ. In contrast, a cholinesterase inhibitor, eserine, although significantly decreasing the ISF Aβ in both control and GRK5-deficient APPsw mice, failed to correct the difference between them. However, combining eserine with methoctramine additively reduced the ISF Aβ further in both animals. Altogether, these findings indicate that GRK5 deficiency accelerates β-amyloidogenic APP processing and Aβ accumulation in APPsw mice via impaired cholinergic activity and that presynaptic M2 hyperactivity is the specific target for eliminating the pathologic impact of GRK5 deficiency. Moreover, a combination of an M2 antagonist and a cholinesterase inhibitor may reach the maximal disease-modifying effect for both amyloid pathology and cholinergic dysfunction.

A few studies have proposed the notion of deploying automated speed photo enforcement at signalized intersections to deter drivers from intentionally running yellow lights. An appropriate speed limit is the critical determinant for automated speed photo enforcement, but this has rarely been explored. Hence, this study attempts to investigate the speeds of vehicles entering the intersection after yellow onset. Data used for the analysis were collected via field observation from eleven high-speed signalized intersections in Harbin, China. Statistical hypothesis testing was performed. The results show that entry speeds are lower than the posted speed limit and follow normal distribution with a unimodal curve. The posted speed limit, through lane number, land position and width, vehicle type, peak period, and free flow condition significantly impact entry speed. These findings imply that setting up a speed limit for preventing deliberately violating yellow light should consider the entry speed and its influential factors.

Assessing equity of public transit fare policy is meaningful to both passengers and bus companies. In this paper, fare equity is defined as reasonable difference in the distribution of unit cost among different groups. Unit fare, unit cost and fare box recovery ratio are taken as evaluating indexes of fare equity. Then, the theory of Lorenz curve and Gini coefficient are applied into the equity evaluation of unit fares distribution among the passengers and the “subsidy threshold” is used to analyze the cross-subsidy. Finally, as an example, the evaluating indexes and methods are applied into the equity evaluation of flat fare. Results show that using the established indexes and methods to evaluate fare equity is feasible and flat fare is unfair.

Based on price mechanisms, a Stackelberg non-cooperation game model between airport and airline was proposed to deal with the aircraft pushback slot allocation problem. The optimization objectivess of this model are to reduce the loss of airport caused by both ground-holding after pushback and the price mechanism and balance the pushback cost between airlines. In the process of gambling, the airport first determines the price of pushback slot, the airline then "play games" between price and other competitors’ strategies and return the gambling result to the airport. The artificial fish swarm algorithm is put forward for solving the integrated model. Through the case studies, the rationality and validity of the model has been proved. The research result shows that the model can generate optimal equilibrium solution to both the individual users as well as the whole system, finally reaching collective rationality and game equilibrium.

The far field beam profile is of significant importance to the analysis of the atmospheric propagation effect and evaluation of the beam control capability, tracking and aiming precision of laser system. In the paper, technology of laser beam measurement such as mid-infrared laser detection at wide temperature range, power density attenuation, photoelectric and calorimetric compound method for laser measurement, synchronous detecting of multi-channel pulsed signal are introduced. A series of instrumented target with detector array are developed for laser beam power density distribution measurement at far field. The power in the bucket, strehl ratio, centroid and jitter of beam can be calculated from the measured results.

Triptolide, a major bioactive ingredient of a widely used herbal medicine, has been shown to possess multiple pharmacological functions, including potential neuroprotective effects pertinent to Alzheimer's disease (AD) in vitro. However, the therapeutic potential of triptolide for AD in vivo has not been thoroughly evaluated. In the present study, we investigated the impact of peripherally administered triptolide on AD-related behavior and neuropathology in APPswe/PS1ΔE9 (APP/PS1) mice, an established model of AD. Our results showed that two-month treatment with triptolide rescued cognitive function in APP/PS1 mice. Immunohistochemical analyses indicated that triptolide treatment led to a significant decrease in amyloid-β (Aβ) deposition and neuroinflammation in treated mice. In contrast to previous findings in vitro, biochemical analyses showed that triptolide treatment did not significantly affect the production pathway of Aβ in vivo. Intriguingly, further analyses revealed that triptolide treatment upregulated the level of insulin-degrading enzyme, a major Aβ-degrading enzyme in the brain, indicating that triptolide treatment reduced Aβ pathology by enhancing the proteolytic degradation of Aβ. Our findings demonstrate that triptolide treatment ameliorates key behavioral and neuropathological changes found in AD, suggesting that triptolide may serve as a potential therapeutic agent for AD.

In order to provide a scientific basis for the resource allocation in the stage of checked baggage, improve the service efficiency of airport passenger terminal. According to the flight data of an international airport passenger terminal in 2012 May, this paper establish the BP artificial neural network and multiple regression prediction models respectively, in which the influencing factors are decided by grey relationship weight analysis. A set of comparative predictions were done by analyzing three types of data, namely all flight data, single flight data and data of flights with the same destination respectively. The results show that the prediction effect is better when using the last type of data as the sample data and the result of multiple regression model is superior to the BP neural network. It will have great practical significance in the actual source allocation in the stage of checked baggage.

In order to solve the problem of terminal resources waste and improve the resource utilization efficiency of airport terminals, this paper proposes a prediction method based on the RBF neural network to predict future terminal departure passenger traffic at the next period. Data from Harbin Taiping International Airport are used to confirm the accuracy and applicability of this method in the field of terminal departure passenger traffic prediction.

From analysis of the flight departure process in an airport, this paper studied the behavioral characteristics of the departure process and built its model. Combined with the theory of fuzzy control, an algorithm of aircraft pushback control was given and the internal rules of fuzzy control were discussed. Using the Matlab/Simulink software, a simulation process was built to do a simulation experiment. Finally, the paper demonstrated the effectiveness of the fuzzy control algorithm and the scheme by comparing the simulation data with the actual data.

The airport terminal departure passenger traffic forecast is the key premise for the airport passenger traffic management system to control and guide passenger traffic flow. However, because the flow is affected by many factors, it is strongly random and nonlinear; so, it can be difficult to forecast traffic accurately. The fuzzy decision tree approach is developed based on the decision tree method combined with the fuzzy mathematics theory. This approach is mainly used in the field of decision making. This paper applies the thinking of decision to forecast and applies the improved fuzzy decision tree method to terminal departure passenger traffic forecast. The case analysis indicates that a more concise and accurate forecast can be achieved using the fuzzy decision tree approach.

Dynamic allocation and intelligent scheduling of terminal passenger service resources (TPSR) is a focus in the field of the international civil aviation. To address the issue of data integration for dynamic allocation and intelligent scheduling of airport terminal resources, a geodatabase-based spatial data model of airport terminal Layout and a multidimensional data model of on-line analytical processing(OLAP) of airport terminal operation are presented. The models can efficiently organize data from airport terminal layout design, manual survey for passenger service processes(PSP), passenger flow detector, departure control system, management information system for airport security and global distribution system, and assure logical rationality and efficiency of data query for dynamic allocation and intelligent scheduling of airport terminal resources, and then, support passenger flow prediction and simulation and optimizing for passenger service process. The proposed models have reference value to data integration for dynamic allocation and intelligent scheduling of airport terminal resources.

The ramifications of statins on plasma cholesterol and coronary heart disease have been well documented. However, there is increasing evidence that inhibition of the mevalonate pathway may provide independent neuroprotective and procognitive pleiotropic effects, most likely via inhibition of isoprenoids, mainly farnesyl pyrophosphate (FPP) and geranylgeranyl pyrophosphate (GGPP). FPP and GGPP are the major donors of prenyl groups for protein prenylation. Modulation of isoprenoid availability impacts a slew of cellular processes including synaptic plasticity in the hippocampus. Our previous work has demonstrated that simvastatin (SV) administration improves hippocampus-dependent spatial memory, rescuing memory deficits in a mouse model of Alzheimer’s disease. Treatment of hippocampal slices with SV enhances long-term potentiation (LTP), and this effect is dependent on the activation of Akt (protein kinase B). Further studies showed that SV-induced enhancement of hippocampal LTP is driven by depletion of FPP and inhibition of farnesylation. In the present study, we report the functional consequences of exposure to SV at cellular/synaptic and molecular levels. While application of SV has no effect on intrinsic membrane properties of CA1 pyramidal neurons, including hyperpolarization-activated cyclic-nucleotide channel-mediated sag potentials, the afterhyperpolarization (AHP), and excitability, SV application potentiates the N-methyl D-aspartate receptor (NMDAR)-mediated contribution to synaptic transmission. In mouse hippocampal slices and human neuronal cells, SV treatment increases the surface distribution of the GluN2B subunit of the NMDAR without affecting cellular cholesterol content. We conclude that SV-induced enhancement of synaptic plasticity in the hippocampus is likely mediated by augmentation of synaptic NMDAR components that are largely responsible for driving synaptic plasticity in the CA1 region.

Summary Background Aging is a highly complex process that affects various tissues and systems in the body. Senescent changes are relatively more prevalent and severe in the postmitotic cells. Mitochondria play an important role in the aging process. Recently, cell cultures have been widely used as an in vitro model to study aging. The present study was designed to investigate mitochondrial dysfunction associated with aging in a long-term cell culture system. Material/Methods Rat hippocampal neurons were maintained in culture in serum-free medium for 30 days in vitro (DIV). The morphology and development of hippocampal neurons was observed by phase contrast microscope. The levels of cellular senescence were evaluated by cytochemical staining of senescence-associated β-galactosidase (SA-β-Gal) at DIV 5, 10, 15, 20, 25 and 30. In addition, we investigated the changes in mitochondrial membrane potential (Δψm) and intracellular reactive oxygen species (ROS) generation of hippocampal neurons by flow cytometry at different ages. Results The proportion of the senescent cells steadily increased with age in neuron cultures. Δψm decreased gradually with age in long-term culture, while ROS generation increased. Conclusions This study indicates an age-related decrease in mitochondrial function in long-term hippocampal neuronal culture and suggests that DIV 25 neurons could possibly serve as a platform for the future study of anti-aging from the perspective of mitochondrial function.

Bus arrival times are influenced by stochastic variations in number of factors, (e.g., intersection delays, traffic congestion, and weather conditions) resulting in buses to deviate from the predetermined schedule and lengthening of passenger waiting times for buses. Providing passengers with accurate bus arrival times through advanced traveler information systems can help passengers' decision making and reduce average waiting time for buses. In this paper, a set of models, predicting bus arrival times at stops along a route, are developed through mining historical data collected by automated passenger counters (APC). The data applied for developing the models were collected by APC installed on buses operated by the public transit agency in Harbin, a city of northeast region of China. The results obtained are promising, and indicate that the developed models can be used to estimate bus arrival times.

beta-Amyloid (Abeta) is strongly involved in the pathogenesis of Alzheimer's disease (AD), and mitochondria play an important role in neurodegenerative disorders. To determine whether any different effect of melatonin on cultured neurons treated with Abeta in vitro and which may be produced through its different action on mitochondria at different stages of culture, we investigated the damage of cultured rat hippocampal neurons mitochondrial function induced by Abeta in young neurons [days in vitro 10 (DIV 10)] and senescent neurons (DIV 25) and the protective effect of melatonin. Rat hippocampal neurons were incubated with amyloid-beta peptide 25-35 (Abeta25-35) alone or pretreatment with melatonin. Cell viability, mitochondrial membrane potential (Deltapsim), ATP and the activity of the respiratory chain complexes were measured. Data showed that Abeta25-35 caused a reduction in Deltapsim, inhibited the activity of the respiratory chain complexes and led to ATP depletion, melatonin attenuated Abeta25-35-induced mitochondrial impairment in young neurons, whereas melatonin had no effect on Abeta25-35-induced mitochondrial damage in senescent neurons. These results demonstrate that melatonin has differential effect on Abeta25-35-induced mitochondrial dysfunction at different stages of culture and suggest that melatonin is useful for the prevention of AD, rather than treatment.

To deliver emergency materials and evacuees to the destination within a limited amount of time, various traffic management and control measures must be employed to manage numerous traffic flows. A Freeway Emergency Traffic Organization Scenario (FETOS) is one of various combinations of traffic management and control measures. A framework of simulation system for the FETOS is presented in this paper. It consists of function modules of the simulation system, core models of the simulation system, and key technologies of implementing the simulation system. The simulation models include a freeway infrastructure model, a data model of the FETOS, a dynamic traffic flow model under the FETOS, FETOS simulation indexes, and their respective statistical models. Function modules include modules of modeling freeway networks, modules of modeling the FETOS, modules of system parameters configuration, module of simulation execution and control, module of visualizing simulation running process, module of generating and printing simulation reports, modules of open data interface, and modules of data backup and recovery. The key technologies of system implementation are also discussed. INTRODUCTION Emergency management can be divided into four periods (McLoughlin. D.1985): mitigation, response, relief and recovery. During the response period, a large number of people and materials need to be transported from one place to another (Henry X.Liu, Jeff X.Ban, Wenteng Ma, Pitu B. Mirchandani, 2006). In some cases, people and materials transportation must traverse multiple cities or provinces and freeway transportation is one of the main means of transportation (Henry X.Liu, Jeff X.Ban, Wenteng Ma, Pitu B. Mirchandani.2006). To ensure that the operation of emergency traffic flow on a freeway is efficient and orderly, effective traffic management and control measures must be taken. A FETOS can be ICCTP 2009: Critical Issues in Transportation Systems Planning, Development, and Management ©2009 ASCE 1479

The study was to evaluate the therapeutic benefit of transplanted bone mesenchymal stem cells (BMSCs) transfected never growth factor (NGF) gene and GFP gene (as a reporter gene), in treating the rat with fimbria-fornix lesion. After transduction of NGF gene via recombinant retroviral vectors into the rat BMSCs, BMSCs were therefore transformed into the GFP-NGF positive BMSCs, nearly 100% of BMSCs expressed NGF, and then transplanted into basal forebrain of rat with fimbria-fornix lesion. After 2 weeks post-transplantation, the GFP-NGF positive BMSCs survive and fuse in vivo with astroglia or NGFR p75 positive neurons in the basal forebrain, no evidence of transdifferentiation was observed in this study. The number of NGFR p75 positive neurons in basal forebrain of NGF group was significantly higher than those of the void plasmid group (p0.05) or the PBS group (p0.01). These results indicate that the GFP-NGF positive BMSCs provide, by way of paracrine, NGF that effectively perform the functions of neuroprotection, which cell fusion may be also contribute to.

Carbon monoxide (CO) and nitric oxide (NO) are two endogenously produced gases that can function as second messenger molecules in the nervous system. The enzyme systems responsible for CO and NO biosynthesis are heme oxygenase (HO) and nitric oxide synthase (NOS), respectively. The present study was undertaken to examine the distribution of HO-2 and NOS of the trigeminal primary afferent neurons of the rat, located in the trigeminal ganglion (TG) and mesencephalic trigeminal nucleus (MTN), using histochemistry and immunohistochemistry. NADPH-d staining was found in most neurons in TG. The intensely NADPH-d-stained neurons were small- or medium-sized, while the large-sized neurons were less intensely stained. Immunocytochemistry for HO-2 revealed that almost all neurons in TG expressed HO-2, but they did not appear cell size-specific pattern. NADPH-d and HO-2 positive neurons appeared the same pattern, which was NADPH-d activity and HO-2 expression progressively declined from the caudal to rostral part of the MTN. A double staining revealed that the colocalization of NADPH-d/HO-2 neurons was 97.3% in TG and 97.6% in MTN. The remarkable parallels between NADPH-d and HO-2 suggest that NO and CO are likely neurotransmitters and mediate the orofacial nociception and sensory feedback of the masticatory reflex arc together.

A purpose of this study is to compare the differential effects of melatonin on hippocampal neurodegeneration in accelerated senescence prone mouse-8 (SAMP8) which is initiated treatment at different age.The 4-months old SAMP8 mice were injected subcutaneously with melatonin (1 mg/kg/day) for 4 months. Similar treatments were performed in the 7-months old mice. When the animals were complete 11-months old, a series of tests were performed. Y maze test and Eight-arm radial maze task were used to assess cognitive performance. Hippocampal pyramidal cells were estimated by Nissl's staining. By using Gomori's methenamine silver methods, the methenamine silver staining granules (MSSG) were observed in area CA1 of hippocampus. A computer-assisted morphometric study was carried out on the ultrastructure of perikaryal CA1 pyramidal cell mitochondria. The volume density (Vv), surface density (Sv), numerical density (Nv) and mean volume (V) of the mitochondria were calculated.Melatonin treatment obviously reduced the deposition of MSSG and elevated hippocampal pyramidal cell number while improving the learning and memory deficits of SAMP8. The mice initiated treatment from 4-months old exhibited a greater response to melatonin supplementation than 7-months old mice. It also decreased mean volume (V) and significantly elevated the Sv and Nv of the mitochondria in hippocampal CA1 region. However, 7-months old mice showed little effects on it.Our results indicate that the protective effects of melatonin on hippocampal neurodegeneration of SAMP8 are age dependent.

It is well known that intersections are the most hazardous locations; however, only little is known about driver injury severity in intersection crashes. Hence, the main goal of this study was to further examine the different factors contributing to driver injury severity involved in fatal crashes at intersections. Data used for the present analysis was from the US DOT-Fatality Analysis Reporting System (FARS) crash database from the year 2011. An ordered probit model was employed to fit the fatal crash data and analyze the factors impacting each injury severity level. The analysis results displayed that driver injury severity is significantly affected by many factors. They include driver age and gender, driver ethnicity, vehicle type and age (years of use), crash type, driving drunk, speeding, violating stop sign, cognitively distracted driving, and seat belt usage. These findings from the current study are beneficial to form a solid basis for adopting corresponding measures to effectively drop injury severity suffering from intersection crash. More insights into the effects of risk factors on driver injury severity could be acquired using more advanced statistical models.

Map-matching (MM) algorithms integrate positioning data with spatial road network data to identify the correct link on which a vehicle is travelling and determine the location of a vehicle on a link. There are four classes of MM algorithms, including geometric, topological, probabilistic and advanced. The topological map-matching (tMM) algorithms are relatively simple, easy and quick. Due to considering information of heading, proximity, link connectivity and turn-restriction weights, weight- based tMM algorithms are most robust and widely used tMM algorithms. As is known to all, a metropolis usually has intricate road network. And the urban road density has various performances in different parts of a metropolis’ urban area, which makes the weight scores used in tMM algorithm different. As a result, it can affect the accuracy of matched results. In this paper, the authors develop an enhanced weight-based tMM algorithm considering the urban road density. This algorithm was verified using actual taxi global positioning system (GPS) data collected in the urban area of Harbin, China, about 600 positioning points and a 1:80,000 scale digital map of Harbin. The results show that this enhanced weight-based tMM algorithm outperforms the base algorithm and has potential to support many applications of Intelligent Transport System (ITS) service.