T1 and T2 relaxation times are relatively sensitive to early degenerative changes in the patellar cartilage, whereas the MTR may have some limitations with regard to early detection of OA. In addition, The T1 and T2 relaxation times negatively correlate with each other, which is a novel finding.

Because of the non-uniformity of the electric power CPS network and the dynamic nature of the risk propagation process, it is difficult to quantify the critical point of a cyber risk explosion. From the perspective of the dependency network, this paper proposes a method for quantitative evaluation of the risk propagation threshold of power CPS networks based on the percolation theory. First, the power CPS network is abstracted as a dual-layered network-directed unweighted graph according to topology correlation and coupling logic, and the asymmetrical balls-into-bins allocation method is used to establish a "one-to-many" and "partially coupled" non-uniform power CPS characterization model. Then, considering the directionality between the cyber layer and the physical layer link, the probability of percolation flow is introduced to establish the propagation dynamic equations for the internal coupling relationship of each layer. Finally, the risk propagation threshold is numerically quantified by defining the survival function of power CPS network nodes, and the validity of the proposed method is verified by the IEEE 30-bus system and 150-node Barabsi-Albert model. 2169-3536 (c) INDEX TERMS Electric power CPS, interdependent network, Percolation probability, Propagation dynamics

Aim: Inflammation plays an important role in coronary microembolization (CME)-induced myocardial injury. The present study was designed to investigate the role of extracellular signal-regulated kinases 1/2 (ERK1/2) signaling pathway in regulating myocardial inflammation and cardiac function in a rat model of CME. Methods: Sprague-Dawley rats were randomly divided into three groups: sham-operated group (sham group), CME group and PD98059 group (15 animals per group). CME was produced by injection of 42-µm microspheres into the left ventricle with occlusion of the ascending aorta. Rats in the PD98059 group were injected with PD98059, a specific ERK1/2 inhibitor, 30 min before the CME operation. Western blotting and immunohistochemistry analysis were used to determine the activation of ERK1/2. Echocardiography was employed to evaluate cardiac function. Hematoxylin-eosin staining was performed to assay myocardial inflammation. Expression of TNF-α mRNA was determined by RT-PCR analysis, and activity of NF-ĸB was assessed by electrophoretic mobility shift assay. Results: CME dramatically induced cardiac dysfunction (left ventricular ejection fraction, LVEF, was 72.97 ± 3.20% in the CME vs. 82.69 ± 3.50% in the sham group, p < 0.05) and local myocardial inflammatory response, both of which were ameliorated significantly by PD98059 (LVEF was 76.46 ± 4.46 and p < 0.05 vs. CME group). When compared to the CME group, PD98059 markedly attenuated the increased phosphorylation of ERK1/2 (0.48 ± 0.11 vs. 0.92 ± 0.10, p < 0.05), expression of TNF-α mRNA (0.42 ± 0.06 vs. 0.94 ± 0.04, p < 0.05) and activity of NF-ĸB (104.83 ± 13.65 vs. 540.79 ± 24.95, p < 0.05) in CME rat myocardium. Conclusions: The present study demonstrates a novel role of the ERK1/2 signaling pathway in promoting myocardium inflammation and dysfunction in CME, and suggests that ERK1/2 is a novel potential therapeutic target for CME.

Background:About 50% of the cerebral ischemia events are induced by intracranial and extracranial atherosclerosis. This study aimed to evaluate the feasibility and accuracy for displaying atherosclerotic plaques in carotid arteries and analyzing their ingredients by using high-resolution new magnetic resonance imaging (MRI) techniques.Methods:Totally, 49 patients suspected of extracranial carotid artery stenosis were subjected to cranial MRI scan and magnetic resonance angiography (MRA) examination on carotid arteries, and high-resolution bright-blood and black-blood MRI analysis was carried out within 1 week. Digital subtraction angiography (DSA) examination was carried out for 16 patients within 1 month.Results:Totally, 103 plaques were detected in the 49 patients, which were characterized by localized or diffusive thickening of the vessel wall, with the intrusion of crescent-shaped abnormal signal into lumens. Fibrous cap was displayed as isointensity in T1-weighted image (T1WI) and hyperintensities in proton density weighted image (PDWI) and T2-weighted image (T2WI), lipid core was displayed as isointensity or slight hyperintensities in T1WI, isointensity, hyperintensities or hypointensity in PDWI, and hypointensity in T2WI. Calcification in plaques was detected in 11 patients. Eight patients were detected with irregular plaque surface or ulcerative plaques, which were characterized by irregular intravascular space surface in the black-blood sequences, black hypointensity band was not detected in three-dimensional time-of-flight, or the hypointensity band was not continuous, and intrusion of hyperintensities into plaques can be detected. Bright-blood and black-blood techniques were highly correlated with the diagnosis of contrast-enhanced MRA in angiostenosis degree, Rs = 0.97, P < 0.001. In comparison to DSA, the sensitivity, specificity, and accuracy of MRI diagnosis of stenosis for ≥50% were 88.9%, 100%, and 97.9%, respectively.Conclusions:High-resolution bright-blood and black-blood sequential MRI analysis can accurately analyze ingredients in atherosclerotic plaques. Determined by DSA, MRI diagnosis of stenosis can correctly evaluate the serious degree of arteriostenosis.

PurposeTo investigate the biomarkers change in serum and the correlation with quantitative MRI markers by histopathologic evaluation of the cartilage in surgically-induced osteoarthritis(OA) rabbit model.Materials and MethodsThirty-six mature New Zealand rabbits were used. Eighteen rabbits were divided into six groups randomly and equally and subjected to surgery using the improved Hulth method. The other eighteen rabbits were also allocated into six groups randomly and equally which served as the control. At multiple time points after surgery, the BMP-2, CTX-II and COMP levels in the serum were analyzed by ELISA, and quantitative MRI was performed. Histopathology was examined with HE, and Mankin scores were assessed. The changes in the biochemical biomarkers and imaging markers in the OA groups were compared with those in the control groups using paired-samples T tests. The correlation of quantitative MRI markers with biomarkers and Mankin scores were analyzed. The analysis of Mankin scores was conducted with non-parametric wilcoxon signed rank tests.ResultsThe BMP-2 levels were increased at various times after surgery, and significant differences were observed between the OA and control groups(all the P values <0.001). CTX-II levels were significantly elevated at several intervals after surgery, including W2, W8, W12, W16 and W20(P=0.019, 0.004, 0.007, <0.001 and 0.016 respectively), but not at W4(P=0.764). Significant differences in the COMP levels from W2 to W20 were observed between the OA and the control groups(P<0.001, <0.001, <0.001, <0.001,=0.002 and =0.004 respectively). The T2 values increased at W8 post-surgery and were significantly different between the OA and control groups(P=0.001, <0.001, <0.001 and <0.001 respectively). T2* values increased from W2 to W20 and were significantly different between the control and OA groups(P=0.002, =0.001, <0.001, <0.001, =0.001 and <0.001 respectively). T2 values had significant correlation with BMP-2 and CTX-II(P<0.001 and =0.014), except COMP(P=0.305)., while the correlation of T2* values with BMP-2, CTX-II and COMP was significant(P=0.043, 0.005 and 0.025 respectively). In addition, a positive correlation of T2 values and Mankin scores was observed(P<0.001).ConclusionWith the relevance of the multiple time point analysis of the serum biomarkers and imaging markers compared with histological findings, BMP-2, CTX-II and COMP combined with T2 and T2* can be used to reflect and monitor OA progression potentially.

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The scale of the electric cyber physical system (ECPS) is continuously extending, and the existing cascade failure models ignore both the information flow and power flow transferring characteristics and also lack effective survivability analysis. In this paper, the quantitative evaluation method for cascading failure of ECPS survivability considering optimal load allocation is proposed. Firstly, according to the system topological structure and correlation, the degree-betweenness weighted correlation matrix of ECPS is established by defining the degree function as well as the electric betweenness, and the formal representation of coupled ECPS network model is realized. Secondly, based on the structural connectivity change and risk propagation range of ECPS cascade failure, the survivability evaluation model is designed by taking into account the constraints such as node load capacity limitation, information flow optimal allocation strategy, power flow optimization equation, and system safety operation. Finally, the firefly algorithm with chaotic Lévy flight is proposed to solve the evaluation model efficiently. The case study vividly shows that the evaluation method can effectively quantify the survivability of ECPS and thus enhance the evaluation efficiency of large-scale coupled systems.

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