A Survey on Problems in Smart Grid with Large Capacity Wind Farm Interconnected

AbstractThe basic concepts and development of smart grid is described. The influence of large capacity wind farm interconnected on the smart grid is analyzed particularly, following contents are emphatically presented: model of wind farm, basic operation performance, output forecasting of wind farm, power flow in smart grid including wind farm, balance of voltage and raeactive power, small disturbance stability, transient stability, faults and reliability, etc., in the hope of offering references for the fast development of smart grids absorbing more capacity of wind power

Preparation and characterization of ZnO microcantilever for nanoactuation

Zinc oxide [ZnO] thin films are deposited using a radiofrequency magnetron sputtering method under room temperature. Its crystalline quality, surface morphology, and composition purity are characterized by X-ray diffraction [XRD], atomic force microscopy [AFM], field-emission scanning electron microscopy [FE-SEM], and energy-dispersive X-ray spectroscopy [EDS]. XRD pattern of the ZnO thin film shows that it has a high c-axis-preferring orientation, which is confirmed by a FE-SEM cross-sectional image of the film. The EDS analysis indicates that only Zn and O elements are contained in the ZnO film. The AFM image shows that the film's surface is very smooth and dense, and the surface roughness is 5.899 nm. The microcantilever (Au/Ti/ZnO/Au/Ti/SiO2/Si) based on the ZnO thin film is fabricated by micromachining techniques. The dynamic characterizations of the cantilever using a laser Doppler vibrometer show that the amplitude of the cantilever tip is linear with the driving voltage, and the amplitude of this microcantilever's tip increased from 2.1 to 13.6 nm when the driving voltage increased from 0.05 to 0.3 Vrms. The calculated transverse piezoelectric constant d31 of the ZnO thin film is -3.27 pC/N. This d31 is high compared with other published results. This ZnO thin film will be used in smart slider in hard disk drives to do nanoactuation in the future

Systematic analysis and prediction for disease burden of ovarian cancer attributable to hyperglycemia: a comparative study between China and the world from 1990 to 2019

BackgroundOvarian cancer is one of the most common female malignancies worldwide, and metabolic factors, such as hyperglycemia, are becoming potential risk factors. This study aimed to analyze the disease burden and its changing trend of ovarian cancer attributable to hyperglycemia in the Chinese population from 1990 to 2019.MethodsUsing the data released by the Global Burden of Disease study 2019 (GBD 2019), we analyze the disease burden of ovarian cancer attributable to hyperglycemia in Chinese from 1990 to 2019 via morbidity, death, disability-adjusted life years (DALY); compare it with the global population; and predict the incidence and death trend in Chinese women for the next 10 years (2020–2029).ResultsThe incidence, death cases, and DALY numbers of ovarian cancer attributable to hyperglycemia in Chinese in 2019 were 2,751, 1,758, and 44,615 person-years, respectively, with an increase of 352.5%, 356.6%, and 329.0% compared with 1990, and the growth rate was higher than the global level. The age-standardized incidence rate (ASIR), age-standardized mortality rate (ASMR), and age-standardized DALY rate (ASDR) in 2019 were 0.270/100,000, 0.164/100,000, and 4.103/100,000, respectively. Moreover, the average annual percent changes (AAPCs) were 2.3%, 2.0%, and 2.0%, respectively, all higher than the global average. The disease burden of ovarian cancer attributable to hyperglycemia increased with age, reaching a peak in the 45–75 age group. The prediction of the neural network model showed that the incidence and death of the disease would remain high and rise in the next 10 years.ConclusionThe disease burden caused by ovarian cancer attributable to hyperglycemia in Chinese accounts for a large proportion globally, and the ASIR, ASMR, and ASDR are increasing year by year. We should continue to pay attention to the role of metabolic factors, such as hyperglycemia, in the occurrence and development of ovarian cancer, perform a good job in tertiary prevention, and strive to reduce health losses

Inactivation of Fam20C in Cells Expressing Type I Collagen Causes Periodontal Disease in Mice

FAM20C is a kinase that phosphorylates secretory proteins. Previous studies have shown that FAM20C plays an essential role in the formation and mineralization of bone, dentin and enamel. The present study analyzed the loss-of-function effects of FAM20C on the health of mouse periodontal tissues.By crossbreeding 2.3 kb Col 1a1-Cre mice with Fam20Cfl/fl mice, we created 2.3 kb Col 1a1-Cre;Fam20Cfl/fl (cKO) mice, in which Fam20C was inactivated in the cells that express Type I collagen. We analyzed the periodontal tissues in the cKO mice using X-ray radiography, histology, scanning electron microscopy and immunohistochemistry approaches.The cKO mice underwent a remarkable loss of alveolar bone and cementum, along with inflammation of the periodontal ligament and formation of periodontal pockets. The osteocytes and lacuno-canalicular networks in the alveolar bone of the cKO mice showed dramatic abnormalities. The levels of bone sialoprotein, osteopontin, dentin matrix protein 1 and dentin sialoprotein were reduced in the Fam20C-deficient alveolar bone and/or cementum, while periostin and fibrillin-1 were decreased in the periodontal ligament of the cKO mice.Loss of Fam20C function leads to periodontal disease in mice. The reduced levels of bone sialoprotein, osteopontin, dentin matrix protein 1, dentin sialoprotein, periostin and fibrillin-1 may contribute to the periodontal defects in the Fam20C-deficient mice

Vascular niche IL-6 induces alternative macrophage activation in glioblastoma through HIF-2α.

Spatiotemporal regulation of tumor immunity remains largely unexplored. Here we identify a vascular niche that controls alternative macrophage activation in glioblastoma (GBM). We show that tumor-promoting macrophages are spatially proximate to GBM-associated endothelial cells (ECs), permissive for angiocrine-induced macrophage polarization. We identify ECs as one of the major sources for interleukin-6 (IL-6) expression in GBM microenvironment. Furthermore, we reveal that colony-stimulating factor-1 and angiocrine IL-6 induce robust arginase-1 expression and macrophage alternative activation, mediated through peroxisome proliferator-activated receptor-γ-dependent transcriptional activation of hypoxia-inducible factor-2α. Finally, utilizing a genetic murine GBM model, we show that EC-specific knockout of IL-6 inhibits macrophage alternative activation and improves survival in the GBM-bearing mice. These findings illustrate a vascular niche-dependent mechanism for alternative macrophage activation and cancer progression, and suggest that targeting endothelial IL-6 may offer a selective and efficient therapeutic strategy for GBM, and possibly other solid malignant tumors

Specific ablation of mouse Fam20C in cells expressing type I collagen leads to skeletal defects and hypophosphatemia

AbstractFAM20C mutations in humans cause Raine syndrome and our previous studies showed that global inactivation of mouse Fam20C led to bone and dental defects. By crossbreeding 2.3  kb Col 1a1-Cre mice with Fam20C flox/flox mice, we created 2.3  kb Col 1a1-Cre;Fam20C foxl/flox (cKO) mice, in which Fam20C was inactivated in cells expressing Type I collagen. This study showed that the long bones of cKO mice were shorter and had a lower level of mineralization compared to the normal mice. The collagen fibrils in Fam20C-deficient bone were disorganized and thicker while the growth plate cartilage in cKO mice was disorganized and wider compared to the normal mice. The Fam20C-deficient bone had a lower level of dentin matrix protein 1, and higher levels of osteopontin and bone sialoprotein than the normal. The blood of cKO mice had an elevated level of fibroblast growth factor 23 and reduced level of phosphorus. These findings indicate that inactivation of Fam20C in cells expressing type I collagen led to skeletal defects and hypophosphatemia. The altered levels of dentin matrix protein 1 and osteopontin in Fam20C-deficient bone may be significant contributors to the mineralized tissue defects in human patients and animals suffering from the functional loss of FAM20C.</jats:p

Innate Immune Response of Human Plasmacytoid Dendritic Cells to Poxvirus Infection Is Subverted by Vaccinia E3 via Its Z-DNA/RNA Binding Domain

Plasmacytoid dendritic cells (pDCs) play important roles in antiviral innate immunity by producing type I interferon (IFN). In this study, we assess the immune responses of primary human pDCs to two poxviruses, vaccinia and myxoma virus. Vaccinia, an orthopoxvirus, was used for immunization against smallpox, a contagious human disease with high mortality. Myxoma virus, a Leporipoxvirus, causes lethal disease in rabbits, but is non-pathogenic in humans. We report that myxoma virus infection of human pDCs induces IFN-α and TNF production, whereas vaccinia infection does not. Co-infection of pDCs with myxoma virus plus vaccinia blocks myxoma induction effects. We find that heat-inactivated vaccinia (Heat-VAC; by incubating the virus at 55°C for 1 h) gains the ability to induce IFN-α and TNF in primary human pDCs. Induction of IFN-α in pDCs by myxoma virus or Heat-VAC is blocked by chloroquine, which inhibits endosomal acidification required for TLR7/9 signaling, and by inhibitors of cellular kinases PI3K and Akt. Using purified pDCs from genetic knockout mice, we demonstrate that Heat-VAC-induced type I IFN production in pDCs requires the endosomal RNA sensor TLR7 and its adaptor MyD88, transcription factor IRF7 and the type I IFN feedback loop mediated by IFNAR1. These results indicate that (i) vaccinia virus, but not myxoma virus, expresses inhibitor(s) of the poxvirus sensing pathway(s) in pDCs; and (ii) Heat-VAC infection fails to produce inhibitor(s) but rather produces novel activator(s), likely viral RNA transcripts that are sensed by the TLR7/MyD88 pathway. Using vaccinia gene deletion mutants, we show that the Z-DNA/RNA binding domain at the N-terminus of the vaccinia immunomodulatory E3 protein is an antagonist of the innate immune response of human pDCs to poxvirus infection and TLR agonists. The myxoma virus ortholog of vaccinia E3 (M029) lacks the N-terminal Z-DNA/RNA binding domain, which might contribute to the immunostimulating properties of myxoma virus