RESUMEN
Large-scale telematics data enable a high-resolution inference of road network's safety conditions and driver behavior. Although many researchers have investigated how to define meaningful safety surrogates and crash predictors from telematics, no comprehensive study analyzes the driver behavior derived from large-scale telematics data and relates them to crash data and the road networks in metropolitan cities. This study extracts driver behavior indices (e.g., speed, speed variation, hard braking rate, and hard acceleration rate) from large-scale telematics data, collected from 4000 vehicles in New York City five boroughs. These indices are compared to collision frequencies and collision rates at the street level. Moderate correlations were found between the safety surrogate measures and collision rates, summarized as follows: (i) When normalizing crash frequencies with traffic volume, using a traffic AADT model, safety-critical regions almost remain the same. (ii) The correlation magnitude of hard braking and hard acceleration varies by road types: hard braking clusters are more indicative of higher collision rates on highways, whereas hard acceleration is a stronger hazard indicator on non-highway urban roads. (iii) Locations with higher travel times coincide with locations of high crash incidence on non-highway roads. (iv) However, speeding on highways is indicative of collision risks. After establishing the spatial correlation between the driver behavior indices and crash data, two prototype safety metrics are proposed: speed corridor maps and hard braking and hard acceleration hot-spots. Overall, this paper shows that data-driven network screening enabled by telematics has great potential to advance our understanding of road safety assessment.
Asunto(s)
Accidentes de Tránsito , Viaje , Humanos , Accidentes de Tránsito/prevención & control , Ciudades , Ciudad de Nueva YorkRESUMEN
Previously we have shown that expression of the deubiquitinating enzyme USP17 is required for cell proliferation and motility. More recently we reported that USP17 deubiquitinates RCE1 isoform 2 and thus regulates the processing of 'CaaX' motif proteins. Here we now show that USP17 expression is induced by epidermal growth factor and that USP17 expression is required for clathrin mediated endocytosis of epidermal growth factor receptor. In addition, we show that USP17 is required for the endocytosis of transferrin, an archetypal substrate for clathrin mediated endocytosis, and that USP17 depletion impedes plasma membrane recruitment of the machinery required for clathrin mediated endocytosis. Thus, our data reveal that USP17 is necessary for epidermal growth factor receptor and transferrin endocytosis via clathrin coated pits, indicate this is mediated via the regulation of the recruitment of the components of the endocytosis machinery and suggest USP17 may play a general role in receptor endocytosis.