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With the rapidly changing states of modern power systems, real-time state estimation based on phasor measurement units (PMUs) plays an increasingly important role in energy management systems. However, due to the complicated distribution of PMU measurement errors, conventional state estimation methods such as the weighted least squares estimator suffer from the estimation bias. Consequently, they do not represent the least variance unbiased estimators. To solve the estimation bias, a state estimation method combining the PMU linear measurement model and the linear Bayesian estimation theory is proposed. Specifically, considering the prior information on estimated parameters and the complicated probability distribution of PMU measurement errors, the linear Bayesian theory is applied to PMU-based state estimation to improve the performance of state estimation. To support this method, the correlation between real and imaginary errors is analyzed, and the prior information of estimated parameters is determined by the volatility of system states. When the real states of practical power systems are unavailable, performance indicators for state estimation are proposed based on the estimation residuals. The efficacies of the proposed estimation and evaluation methods are verified using IEEE 14 bus system and a large-scale power grid in China.

ABSTRACTPorcine epidemic diarrhea has become pandemic in the Asian pig-breeding industry, causing significant economic loss. In the present study, 11 complete genomes of porcine epidemic diarrhea virus (PEDV) field isolates from China were determined and analyzed. Frequently occurring mutations were observed, which suggested that full understanding of the genomic and epidemiological characteristics is critical in the fight against PEDV epidemics. Comparative analysis of 49 available genomes clustered the PEDV strains into pandemic (PX) and classical (CX) groups and identified four hypervariable regions (V1 to V4). Further study indicated key roles for the spike (S) gene and the V2 region in distinguishing between the PX and CX groups and for studying genetic evolution. Genotyping and phylogeny-based geographical dissection based on 219 S genes revealed the complexity and severity of PEDV epidemics in Asia. Many subgroups have formed, with a wide array of mutations in different countries, leading to the outbreak of PEDV in Asia. Spatiotemporal reconstruction based on the analysis suggested that the pandemic group strains originated from South Korea and then extended into Japan, Thailand, and China. However, the novel pandemic strains in South Korea that appeared after 2013 may have originated from a Chinese variant. Thus, the serious PED epidemics in China and South Korea in recent years were caused by the complex subgroups of PEDV. The data in this study have important implications for understanding the ongoing PEDV outbreaks in Asia and will guide future efforts to effectively prevent and control PEDV.

Decay-accelerating factor (DAF; CD55) is a membrane protein that regulates complement pathway activity at the level of C3. To test the hypothesis that DAF plays an essential role in limiting complement activation in the arterial wall and protecting from atherosclerosis, we crossed DAF gene targeted mice (daf-1−/−) with low-density lipoprotein-receptor deficient mice (Ldlr−/−). Daf-1−/−Ldlr−/−mice had more extensive en faceSudan IV staining of the thoracoabdominal aorta than Ldlr−/−mice, both following a 12-week period of low-fat diet or a high-fat diet. Aortic root lesions in daf-1−/−Ldlr−/−mice on a low-fat diet showed increased size and complexity. DAF deficiency increased deposition of C3d and C5b-9, indicating the importance of DAF for downstream complement regulation in the arterial wall. The acceleration of lesion development in the absence of DAF provides confirmation of the proinflammatory and proatherosclerotic potential of complement activation in the Ldlr−/−mouse model. Because upstream complement activation is potentially protective, this study underlines the importance of DAF in shielding the arterial wall from the atherogenic effects of complement.

Fierce competition in global economy has led to a change in service operation management. Researches argue that lean approach could be used to tackle issues such as how to lower operating cost and increase customer satisfaction. The key questions are what tools and processes can be used to implement the lean effectively and efficiently in service operations. This paper focuses on the study of effective lean toolbox available in service industries. It aims to improve the understanding of the lean tools and techniques and how these could be applied successfully in service operations to prevent the wastes in their operations.

ABSTRACTCancer immunotherapy relies upon the ability of T cells to infiltrate tumors. The endothelium constitutes a barrier between the tumor and effector T cells, and the ability to manipulate local vascular permeability could be translated into effective immunotherapy. Here, we show that in the context of adoptive T cell therapy, antitumor T cells, delivered at high enough doses, can overcome the endothelial barrier and infiltrate tumors, a process that requires local production of C3, complement activation on tumor endothelium and release of C5a. C5a, in turn, acts on endothelial cells promoting the upregulation of adhesion molecules and T-cell homing. Genetic deletion of C3 or the C5a receptor 1 (C5aR1), and pharmacological blockade of C5aR1, impaired the ability of T cells to overcome the endothelial barrier, infiltrate tumors, and control tumor progression in vivo, while genetic chimera mice demonstrated that C3 and C5aR1 expression by tumor stroma, and not leukocytes, governs T cell homing, acting on the local endothelium. In vitro, endothelial C3 and C5a expressions were required for endothelial activation by type 1 cytokines. Our data indicate that effective immunotherapy is a consequence of successful homing of T cells in response to local complement activation, which disrupts the tumor endothelial barrier.

No relevant conflicts of interest to declare.

Thrombotic thrombocytopenic purpura (TTP), a potential fatal syndrome, is often associated with severe deficiency of plasma ADAMTS13 activity, either resulting from ADAMTS13mutations or acquired anti-ADAMTS13 autoantibodies that inhibit plasma ADAMTS13 activity. Patients with severe ADAMTS13 do not always have TTP signs and symptoms, which often occur following infections or inflammatory responses. The mechanism of TTP flare is not fully understood. In the present study, complement activation markers (iC3b, C5b, Bb, and C4b) were determined by enzyme-linked absorbent assays (ELISA) in the initial plasmas (prior to plasma exchange) of 20 patients with acquired TTP with severe ADAMTS13 deficiency (less than 20% of normal) and plasmas from 20 healthy controls. Of 20 TTP patients, 19 exhibited positive inhibitor in the 50:50 mixing study. Plasma levels of iC3b (1,000 ± 1,062 ng/ml), sC5b-9 (1,342±867 ng/ml), and Bb (38.2±47.7 ng/ml), as well as C4b (74.3±49.5 ng/ml) in acquired TTP patients were significantly higher than those in healthy controls (pvalue less than 0.01) These results indicate that complement activation in both classic and alternative pathways is a common phenomenon in patients with acquired autoimmune TTP. To demonstrate the causative effect of complement activation in TTP, we turned to our Adamts13null mice. C57BL/6 (Adamts13-/-) mice are resistant to the development of spontaneous and Shigatoxin-induced TTP syndrome. When injected with a murine specific monoclonal antibody against complement factor H (CFH) (800 micro grams/mouse), which inhibits binding of circulating CFH to endothelial cells and C3b, Adamts13-/-mice (C57BL/6) developed more severe thrombocytopenia and anemia than wild type mice did within 6 days without additional challenge. However, renal insufficiency manifested by the increase of plasma BUN concentration was similar in both groups (Fig. 1). These results indicate that complement activation through an alternative pathway, following antibody-mediated inhibition of CFH or other complement regulatory components, may trigger the onset of TTP in light of severe ADAMTS13 deficiency.