Hierarchical Segmentation Method for Generating Road Intersections from Crowdsourced Trajectory Data

Maintaining the data freshness and completeness of road intersection information is the key task of urban road map production and updating. Compared to professional surveying methods, crowdsourced trajectory data provide a low-cost, wide-coverage and real-time data resource for road map construction. However, there may exist the problems of spatio-temporal heterogeneity and uneven density distribution in crowdsourced trajectory data. Hence, in light of road hierarchies, the paper proposes a hierarchical segmentation method to generate road intersections from crowdsourced trajectories. The proposed method firstly implements an adaptive density homogenization processing on raw trajectory data in order to decrease the uneven density discrepancy. Then, a hierarchical segmentation strategy is developed to extract multi-level road intersection elements from coarse scale to fine scale. Finally, the structural models of road intersections are delineated by an iterative piecewise fitting method. Experimental results show that the proposed method can accurately and completely extract road intersections of different shapes and scales, with an accuracy of about 87–90%. Particularly, the precision and recall of road intersection detection are obviously increased by about 7% and 20% by adaptive density homogenization, indicating the advantages of dealing with uneven trajectory data

Comparing the prognostic impact of 131I or/and Artificial Liver Support System on liver function failure combined with hyperthyroidism

Objective: Hyperthyroidism, a prevalent endocrine disorder, can lead to complications such as liver failure due to the liver's essential role in thyroid hormone metabolism. The study aimed to elucidate the respective contributions of 131I or/and ALSS in managing hyperthyroidism alongside liver failure. Methods: A retrospective analysis was carried out on 74 patients diagnosed with severe liver dysfunction in the context of Graves' disease. Patients were categorized into three groups: Group A (n=34) received 131I treatment, group B (n=17) underwent 131I and ALSS treatment, and Group C (n=24) received ALSS treatment alone. Results: Throughout the treatment period, the liver function indexes in all groups exhibited a decline trend. The thyroid function of group A and B treated with 131I was significantly improved compared with that before treatment. There was no significant change in thyroid function in group C. After the correction of hyperthyroidism, significant improvements were observed in the liver function of individuals in group A and B, particularly with more noticeable amelioration compared to group C. After two months of treatment, the efficacy rates for the three groups were 79.41%, 82.35%, and 60.87% respectively. Mortality rates of the three groups were 5.88%,17.65% and 36%(p < 0.01). Group B, receiving both 131I and ALSS treatments, exhibited a lower mortality rate than group C. Conclusion: In cases of severe liver dysfunction accompanied by hyperthyroidism, prompt administration of 131I is recommended to alleviate the adverse effects of hyperthyroidism on liver function and facilitate a conducive environment for the recovery of liver functionality

Heat Stress-Induced Disruption of Endothelial Barrier Function Is via PAR1 Signaling and Suppressed by Xuebijing Injection

<div><p>Increased vascular permeability leading to acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) is central to the pathogenesis of heatstroke. Protease-activated receptor 1 (PAR1), the receptor for thrombin, plays a key role in disruption of endothelial barrier function in response to extracellular stimuli. However, the role of PAR1 in heat stress-induced endothelial hyper-permeability is unknown. In this study, we measured PAR1 protein expression in heat-stressed human umbilical venous endothelial cells (HUVECs), investigated the influences of PAR1 on endothelial permeability, F-actin rearrangement, and moesin phosphorylation by inhibiting PAR1 with its siRNA, neutralizing antibody (anti-PAR1), specific inhibitor(RWJ56110), and Xuebijing injection (XBJ), a traditional Chinese medicine used for sepsis treatment, and evaluated the role of PAR1 in heatstroke-related ALI/ARDS in mice by suppressing PAR1 with RWJ56110, anti-PAR1and XBJ. We found that heat stress induced PAR1 protein expression 2h after heat stress in endothelial cells, caused the release of endothelial matrix metalloprotease 1, an activator of PAR1, after 60 or 120 min of heat stimulation, as well as promoted endothelial hyper-permeability and F-actin rearrangement, which were inhibited by suppressing PAR1 with RWJ56110, anti-PAR1 and siRNA. PAR1 mediated moesin phosphorylation, which caused F-actin rearrangement and disruption of endothelial barrier function. To corroborate findings from in vitro experiments, we found that RWJ56110 and the anti-PAR1 significantly decreased lung edema, pulmonary microvascular permeability, protein exudation, and leukocytes infiltrations in heatstroke mice. Additionally, XBJ was found to suppress PAR1-moesin signal pathway and confer protective effects on maintaining endothelial barrier function both in vitro and in vivo heat-stressed model, similar to those observed above with the inhibition of PAR1. These results suggest that PAR1 is a potential therapeutic target in heatstroke.</p></div

Influences of heat stress on PAR1 protein expression and releases of endothelial MMP-1.

<p><b>(a)</b> Mono-layer HUVECs were cultured at 37°C or subjected to heat stress at 41°C for 2h, and time courses of PAR1 protein expression post heat stress were determined by western blot (n = 4, *P < 0.05, **P < 0.01, vs. 37°C). <b>(b)</b> Mono-layer HUVECs were subjected to heat stress at different temperatures for 2h, followed by recovery at 37°C for 4h, and PAR1 protein expressions were determined by western blot. Representative images of western blot and quantitative analysis of PAR1 protein normalized to β-actin were shown (n = 4, *vs. 37°C, ^#vs. 39°C, ^&vs. 41°C, P < 0.05). (c) Mono-layer HUVECs were subjected to heat stress (HS) at 41°C for 60 min or 120 min respectively, MMP-1 in medium were determined by western blot. Representative images of western blot and quantitative analysis of PAR1 protein normalized to β-actin were shown (n = 4, *vs. control, ^#vs. PBS in corresponding HS group, P < 0.05).</p

XBJ and suppression of PAR1 diminished ALI associated with heatstroke (HS).

<p>Mice were treated with XBJ (4ml/kg, intraperitoneally), RWJ56110 (RWJ; 25μg/kg, intraperitoneally), and PAR1 neutralizing antibody (anti-PAR1; 2mg/kg, subcutaneously) for 30min, followed by heat insult until Tc reached 42.7°C, and then recovered at room temperature for 2h. <b>(a)</b> Lung wet weight (LWW) to lung dry weight (LDW) ratio, <b>(b)</b> Envans blue leakage, <b>(c)</b> BAL proteins, and <b>(d)</b> BAL leukocytes numbers were determined (n = 6, *vs. sham, ^#vs. HS, P < 0.05). <b>(e)</b> Representative images of lung stained with H&E (scale bar: 10μm).</p

Heat stress increased phosphorylation levels for of moesin via PAR1 signal.

<p>Representative images of western blot and quantitative analysis of phosphorylation levels of moesin normalized to total moesin were shown (n = 4). <b>(a)</b> Mono-layer HUVECs were subjected to heat stress at 41°C for 2h, and time courses of moesin phosphorylation post heat stress were determined by western blot (*P < 0.05, **P < 0.01, vs. 37°C). <b>(b)</b> Mono-layer HUVECs were subjected to heat stress at different temperature for 2h, followed by recovery at 37°C for 2h, and phosphorylation levels of moesin was determined by western blot (*vs. 37°C, ^#vs. 39°C, ^&vs. 41°C, P < 0.05). <b>(c)</b> Mono-layer HUVECs were incubated with RWJ56110 (RWJ; 5μM), control IgG (IgG), anti-PAR1, PAR1 siRNA, or control siRNA, followed by heat stress at 39°C for 2h, and moesin phosphorylation was determined by western blot (*P < 0.05, vs. PBS at 37°C, ^#P < 0.01, vs. corresponding control at 41°C).</p

Influences of XBJ on PAR1 protein expression and phosphorylation levels of moesin.

<p>Mono-layer HUVECs were treated with PBS or XBJ at different concentrations for 30min, followed by heat stress for 2h at 41°C and recovery at 37°C for 2h. PAR1 protein <b>(a)</b> and phosphorylated moesin <b>(b)</b> were determined by western blot. Representative images of western blot and quantitative analysis of normalized protein levels were shown (n = 4, *P < 0.05, vs. 37°C, ^#P < 0.05, vs. PBS at 41°C).</p