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A reliable and accurate monitoring of traffic load is of significance for the operational management and safety assessment of bridges. Traditional weight-in-motion techniques are capable of identifying moving vehicles with satisfactory accuracy and stability, whereas the cost and construction induced issues are inevitable. A recently proposed traffic sensing methodology, combining computer vision techniques and traditional strain based instrumentation, achieves obvious overall improvement for simple traffic scenarios with less passing vehicles, but are enfaced with obstacles in complicated traffic scenarios. Therefore, a traffic monitoring methodology is proposed in this paper with extra focus on complicated traffic scenarios. Rather than a single sensor, a network of strain sensors of a pre-installed bridge structural health monitoring system is used to collect redundant information and hence improve accuracy of identification results. Field tests were performed on a concrete box-girder bridge to investigate the reliability and accuracy of the method in practice. Key parameters such as vehicle weight, velocity, quantity, type and trajectory are effectively identified according to the test results, in spite of the presence of one-by-one and side-by-side vehicles. The proposed methodology is infrastructure safety oriented and preferable for traffic load monitoring of short and medium span bridges with respect to accuracy and cost-effectiveness.

The aim of this study was to investigate the therapeutic efficacy and neuroprotective mechanisms of UCF-101, a novel Omi/HtrA2 inhibitor, following ischemia/reperfusion brain injury. Male Wistar rats were subjected to 2 hr of middle cerebral artery occlusion followed by reperfusion. Animals were divided into 3 groups: sham, vehicle-treated ischemia/reperfusion, and UCF-101 treatment. In the UCF-101 treatment group, rats were intraperitoneally administered UCF-101 (1.5 lmol/kg) 10 min prior to reperfusion. The rats were evaluated for neurological deficits, and brain infarct volume was assessed by 2,3,5-triphenyl tetrazolium chloride. TUNEL staining was utilized to evaluate the amount of apoptosis. In addition, expressions of protein caspase-8, caspase-3, FasL, and FLIP were examined by Western blot analysis. Results demonstrated that UCF-101 treatment significantly decreased cerebral infarct size by about 16.27% (P < 0.05) and also improved neurological behavior. TUNEL staining revealed that UCF-101 treatment significantly reduced TUNELpositive cells in the cerebral cortex. Furthermore, the upregulation in the expression of FasL and the cleavage products of active caspase-8 and caspase-3 induced by ischemia was attenuated in mice treated with UCF-101, whereas upregulation of FLIP levels was increased. The present results demonstrated that UCF-101 protects against cerebral ischemia/ reperfusion injury in mice. UCF-101 provided neuroprotection in vivo, and this was correlated with regulation of Fas-mediated apoptotic proteins. Taken together, the use of UCF-101 is a potent, neuroprotective factor for the treatment of focal cerebral ischemia. Anat Rec, 292:854-861, 2009. V V C 2009 Wiley-Liss, Inc.