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Identifying the root cause of congestion and taking appropriate strategies to improve traffic network performance are important goals of Advanced Traffic Management Systems (ATMS). On many occasions, the causes of congestion are not necessarily attributable to road infrastructures themselves. Instead, signal control strategies at intersections are very often the major contributors of congestion. In lieu of this, in this paper, a root cause identification method is developed with consideration of the impact from both road infrastructure and traffic signal control. Firstly, we differentiate congestion effects between road segments and intersections to attribute the causes of congestion to road infrastructure and signal control respectively. Then, we construct causal congestion trees to model congestion propagation and quantify congestion costs for each road segment and intersection in the whole road network. A Markov model is utilized to capture congestion spatio-temporal correlation among multiple road segments and intersections simultaneously, with which the most critical root cause can be located. Furthermore, a gradient boosting decision tree based method is presented to predict the root cause of congestion according to traffic flows, signal control strategies and road topology in traffic networks. Finally, simulations based on Simulation of Urban Mobility (SUMO) validate the effectiveness of our proposed method in identifying and predicting the congestion root cause. Experiments are further conducted using inductive loop detector data to identify the root cause for the road network of Taipei. [ABSTRACT FROM AUTHOR]

Random access systems are potential for Internet of Things in the future wireless communication network for its operational simplicity. Irregular repetition slotted ALOHA (IRSA) system is one of the high-efficiency random access systems. In this paper, performance analysis of the irregular repetition slotted ALOHA systems with short-packet, i.e. finite-blocklength, transmission for the quasi-static Rayleigh fading channel is given. A cumulative distribution function of signal-to-interference power ratio (SIR) is derived and thus a closed-form expression of an average packet error probability (PEP) at the SIR with short packets for the Rayleigh fading channel is given. The closed-form expression makes it possible to optimize the degree distributions at a specific blocklength in the sense that the systems give the maximum system load. [ABSTRACT FROM AUTHOR]

Traffic incidents are recognized as a key contributor to non-recurrent congestion, which causes many negative effects in economy, environment, health and lifestyle. In this article, we investigate an incident management policy considering both signal control and route choice, which presents a real-time systematic effort to provide a rapid recovery from an incident and mitigate incident-related congestion according to different incident effects. Firstly, we introduce a route choice method on a multiple-route urban road network with consideration of bottleneck delays. Then, we analyze the route travel costs under incident effects and give the equilibrium existence condition after the occurrence of an incident. Furthermore, combining with the route choice method, a novel traffic signal control policy is proposed and the condition for equilibrium existence is given with the consideration of dynamic signal control and route choice simultaneously. Sufficient conditions for the dynamic road system to be stable are also derived and validated by using Lyapunov stability theorem. The analytical results indicate that opposite signal control policies should be applied in road networks under different incident circumstances and the proposed control policy can achieve the improved recovery rate and system stability than existing control policies in terms of dynamic incident effects in road networks. Finally, numerical results have been conducted to demonstrate the effectiveness of our proposed incident control policy and confirm the conditions for road system stability when different incident circumstances had been identified. [ABSTRACT FROM AUTHOR]

Due to the rapid development of vehicular transportation and urbanization, traffic congestion has been increasing and becomes a serious problem in almost all major cities worldwide. Many instances of traffic congestion can be traced to their root causes, the so-called traffic bottlenecks, where relief of traffic congestion at bottlenecks can bring network-wide improvement. Therefore, it is important to identify the locations of bottlenecks and very often the most effective way to improve traffic flow and relieve traffic congestion is to improve traffic situations at bottlenecks. In this article, we first propose a novel definition of traffic bottleneck taking into account both the congestion level cost of a road segment itself and the contagion cost that the congestion may propagate to other road segments. Then, an algorithm is presented to identify congested road segments and construct congestion propagation graphs to model congestion propagation in urban road networks. Using the graphs, maximal spanning trees are constructed that allow an easy identification of the causal relationship between congestion at different road segments. Moreover, using Markov analysis to determine the probabilities of congestion propagation from one road segment to another road segment, we can calculate the aforementioned congestion cost and identify bottlenecks in the road network. Finally, simulation studies using SUMO confirm that traffic relief at the bottlenecks identified using the proposed technique can bring more effective network-wide improvement. Furthermore, when considering the impact of congestion propagation, the most congested road segments are not necessarily bottlenecks in the road network. The proposed approach can better capture the features of urban bottlenecks and lead to a more effective way to identify bottlenecks for traffic improvement. Experiments are further conducted using data collected from inductive loop detectors in Taipei road network and some road segments are identified as bottlenecks using the proposed method. [ABSTRACT FROM AUTHOR]

In this paper, we investigate a hybrid dynamical system which incorporates flow swap process, green-time proportion swap process, and flow divergence for a general network with multiple Origin-Destination (OD) pairs and multiple routes, where flow swap process is specified in which traffic swaps from more costly to less costly input links, green-time proportion swap process is specified in which green time at each intersection swaps from less pressurized stages to more pressurized stages, flow may diverge at each intersection from one OD pair to other OD pairs. Unlike the dynamical system model, where bottleneck delays need to be intentionally constructed to yield the equilibrium flow vector and green-time proportion vector, we propose a novel control policy to fill the gap by only adjusting the green-time proportion vector. We derive a sufficient condition for the existence of equilibrium of the dynamical system under the mild constraints that 1) the travel cost function and stage pressure function should be continuous functions and 2) the flow and green-time proportion swap processes project all flow and green-time proportion vectors on the boundary of the feasible region onto itself. We derive the condition of unique equilibrium for fixed green-time proportion vector and show that with varying green-time proportion vector, the set of equilibria is a compact, non-convex set, and with the same partial derivative of travel cost function with respect to the flow and green-time proportion vectors. Finally, we prove the stability of the proposed dynamical system by using Lyapunov stability analysis. [ABSTRACT FROM AUTHOR]

Platelets play an important role in atherothrombosis. As the most common site plaque occurs, left anterior descending artery (LAD) infarct location always associate with poor prognosis. We sought to assess whether mean platelet volume (MPV) could predict LAD infarct location and short-term clinical outcome. In this study, 190 consecutive patients with non-ST-elevation myocardial infarction (NSTEMI) were enrolled. Clinical, electrocardiography and laboratory characteristics were measured. All patients underwent coronary angiography examination and had definite culprit vessel during hospitalization. The results showed that MPV was smaller in patients with a LAD infarct location than that of left circumflex artery or right coronary artery (9.0 ± 1.5 versus 9.8 ± 1.6, p < 0.001). Multivariate analysis also showed that MPV was the only independent factor to predict LAD infarct location [Odds ratio (OR) = 0.65, 95% confidence interval (CI) 0.53-0.80, p < 0.0001] in patients with NSTEMI. B-type natriuretic peptide and electrocardiography were unreliable predictive factors to locate culprit vessel. Receiver operating characteristic curve analysis showed MPV (area under the curve: 0.65, 95% CI 0.56-0.74, p < 0.01) could reliably discriminate those patients with NSTEMI who had a major in-hospital event. Multivariate regression analyses also showed that MPV (OR = 1.46, 95% CI 1.15-1.86, p < 0.01) were predictors of major in-hospital events. In conclusion, MPV was the only factor independently associated with LAD infarct location in patients with non-ST-elevation myocardial infarction. [ABSTRACT FROM AUTHOR]

Heart failure is one of the most serious diseases worldwide, and can be caused by many factors, among them hyperhomocysteinemia can increase the risk for development of heart failure. In this study, we treated rats with high methionine diet (HMD), which can be conversed to homocysteine in human body, to induce a novel model of heart failure. We proved the successful establishment of this model by echocardiography and pathological evaluation at the termination of treatment. Ejection fraction and fractional shortening were significantly deceased after HMD treatment, while left ventricular volume in systole was increased. HMD treatment caused hypertrophy of cardiomyocytes, disarrangement of myofibers, and infiltration of inflammatory cells, as well as abundant apoptotic cells appeared after HMD treatment. Plasmatic homocysteine level was elevated after HMD treatment. Furthermore, through electrophoretic mobility shift assay and chromatin immunoprecipitation, the activity of NF-κB in nuclear extract was also significantly elevated, showing evidence of positive relationship between hyperhomocysteinemia and activation of NF-κB in HMD-induced heart failure. The successful development and validation of this model have made it a new tool for translational medical research of metabolic disorders-related cardiovascular disease.