Accurate parameter identification method for coupled sub/super-synchronous oscillations for high penetration wind power systems.

As the penetration of renewable energy increases to a large scale and power electronic devices become widespread, power systems are becoming prone to synchronous oscillations (SO). This event has a major impact on the stability of the power grid. The recent research has been mainly concentrated on identifying the parameters of sub-synchronous oscillation. Sub/Super synchronous oscillations (Sub/Sup-SO) simultaneously occur, increasing the difficulty in accurately identify the parameters of SO. This work presents a novel method for parameter identification that effectively handles the Sub/Sup-SO components by utilizing the Rife-Vincent window and discrete Fourier transform (DFT) simultaneously. To mitigate the impact of spectral leakage and the fence effect of DFT, we integrate the tri-spectral interpolation algorithm with the Rife-Vincent window. We use the instantaneous data of the phasor measurement unit (PMU) to identify Sub/Sup-SO-related parameters (Sub/Sup-SO damping ratio, frequency, amplitude and phase). First, the spectrum of the Sub/Sup-SO signals is analyzed after incorporating the Rife-Vincent window, and the characteristics of the Sub/Sup-SO signal are determined. Then, the signal spectrum is identified using a three-point interpolation algorithm, and the damping ratio, amplitude, frequency, and phase of the Sub/Sup-SO signals are obtained. In addition, we consider the identification accuracy of the algorithm under various complex conditions, such as the effect of Sub/Sup-SO parameter variations on parameter identification in the presence of a non-nominal frequency and noise. The proposed algorithm accurately identifies the parameters of multiple Sub/Sup-SO components and two Sub-SO components that are in close proximity. Testing with synthetic and real data demonstrates that the proposed algorithm outperforms existing methods in terms of identification accuracy, identification bandwidth, and adaptability.

Interleukin-3 plays a vital role in hyperoxic acute lung injury in mice via mediating inflammation.

BACKGROUND: Interleukin (IL)-3 amplifies inflammation. However, the effect of IL-3 in acute lung injury (ALI), an acute inflammatory disease, is unclear. The aim of this study was to test the hypothesis that IL-3 plays an important role in hyperoxia-induced ALI. METHODS: Hyperoxic ALI was induced in wild-type (WT) and IL-3 gene disrupted (IL-3-/-) mice by exposure to 100% O2 for 72 h. RESULTS: Hyperoxia increased IL-3 levels in plasma and lung tissues in WT mice. Pulmonary inflammation and edema were detected by histological assay in WT mice exposed to 100% O2 for 72 h. However, the hyperoxia-induced lung histological changes were improved in IL-3-/- mice. The hyperoxia-induced elevation of neutrophils in bronchoalveolar lavage fluids and circulation were reduced in IL-3-/- mice. Meanwhile, the levels of tumor necrosis factor-α and IL-6 were suppressed in IL-3-/- mice compared with WT mice. Moreover, the hyperoxia-induced the activation of IκBα kinase (IKK) ß, IκBα phosphorylation, and nuclear factor-κB translocation were inhibited in IL-3-/- mice compared with WT mice. CONCLUSIONS: Our results suggest IL-3 is a potential therapeutic target for hyperoxia-induced ALI.

High-level expression of periostin is significantly correlated with tumor angiogenesis in prostate cancer.

Periostin (PN), originally named osteoblast-specific factor-2 (OSF-2), is a multifunctional glycoprotein which can significantly promote EMT (epithelial-mesenchymal transition). Recently, many studies have shown that high-level expression of PN is correlated significantly with tumor angiogenesis and prognosis in many kinds of human cancer. In previous experiments, we screened PN from prostate cancer through iTRAQ technology and found that PN affects occurrence and development of prostate cancer (PCa). However, whether and how periostin expression influences tumor angiogenesis in prostate cancer remains unknown. Our study aimed to examine expression of PN in patients with PCa and explored the relationship of PN expression with clinicopathologic factors and tumor angiogenesis. Immunohistochemistry was performed to determine expression of PN in PCa and benign prostate hyperplasia (BPH). Vascular endothelial growth factor (VEGF) and CD31 (used to mark tumor angiogenesis) were also examined in tissues from the PCa patients and hyperplasia patients mentioned above. The results showed that PN expression was significantly (P<0.001) higher in PCa (58%) than in BPH (18.8%) and VEGF expression was significantly (P=0.003) higher in PCa (55%) than in BPH (24.5%). Increased PN protein expression was associated with Gleason score (P=0.005) but there was no correlation with age (P=0.548), PSA (P=0.343) or clinic tumor staging (P=0.049). The results also showed that high expression of PN correlated with VEGF expression (P<0.001) and that tumors with PN-positive expression had significantly higher microvessel density (38.7±14.4 vs. 29.7±10.5; P=0.026) compared to those with PN-negative. In conclusion, our findings suggest that PN may have an important role in tumor progression and may impact tumor angiogenesis in prostate cancer.

Coatomer subunit beta 2 (COPB2), identified by label-free quantitative proteomics, regulates cell proliferation and apoptosis in human prostate carcinoma cells.

Label-free quantitative proteomics has broad applications in the identification of differentially expressed proteins. Here, we applied this method to identify differentially expressed proteins (such as coatomer subunit beta 2 [COPB2]) and evaluated the functions and molecular mechanisms of these proteins in prostate cancer (PCA) cell proliferation. Proteins extracted from surgically resected PCA tissues and adjacent tissues of 3 patients were analyzed by label-free quantitative proteomics. The target protein was confirmed by bioinformatics and GEO dataset analyses. To investigate the role of the target protein in PCA, we used lentivirus-mediated small-interfering RNA (siRNA) to knockdown protein expression in the prostate carcinoma cell line, CWR22RV1 cells and assessed gene and protein expression by reverse transcription quantitative polymerase chain reaction and western blotting. CCK8 and colony formation assays were conducted to evaluate cell proliferation. Cell cycle distributions and apoptosis were assayed by flow cytometry. We selected the differentiation-related protein COPB2 as our target protein based on the results of label-free quantitative proteomics. High expression of COPB2 was found in PCA tissue and was related to poor overall survival based on a public dataset. Cell proliferation was significantly inhibited in COPB2-knockdown CWR22RV1 cells, as demonstrated by CCK8 and colony formation assays. Additionally, the apoptosis rate and percentage of cells in the G1 phase were increased in COPB2-knockdown cells compared with those in control cells. CDK2, CDK4, and cyclin D1 were downregulated, whereas p21 Waf1/Cip1 and p27 Kip1 were upregulated, affecting the cell cycle signaling pathway. COPB2 significantly promoted CWR22RV1 cell proliferation through the cell cycle signaling pathway. Thus, silencing of COPB2 may have therapeutic applications in PCA.