Study on Actuator Line Modeling of Two NREL 5-MW Wind Turbine Wakes

The wind turbine wakes impact the efficiency and lifespan of the wind farm. Therefore, to improve the wind plant performance, research on wind plant control is essential. The actuator line model (ALM) is proposed to simulate the wind turbine efficiently. This research investigates the National Renewable Energy Laboratory 5 Million Watts (NREL 5-MW) wind turbine wakes with Open Field Operation and Manipulation (OpenFOAM) using ALM. Firstly, a single NREL 5-MW turbine is simulated. The comparison of the power and thrust with Fatigue, Aerodynamics, Structures, and Turbulence (FAST) shows a good agreement below the rated wind speed. The information relating to wind turbine wakes is given in detail. The top working status is proved at the wind speed of 8 m/s and the downstream distance of more than 5 rotor diameters (5D). Secondly, another case with two NREL 5-MW wind turbines aligned is also carried out, in which 7D is validated as the optimum distance between the two turbines. The result also shows that the upstream wind turbine has an obvious influence on the downstream one

On the nature of the lightest scalar resonances

We briefly review the recent progresses in the new unitarization approach being developed by us. Especially we discuss the large $N_c$ $\pi\pi$ scatterings by making use of the partial wave $S$ matrix parametrization form. We find that the $\sigma$ pole may move to the negative real axis on the second sheet of the complex $s$ plane, therefore it raises the interesting question that this `$\sigma$' pole may be related to the $\sigma$ in the linear $\sigma$ model.Comment: Talk presented by Zheng at ``Quark Confinement and Hadron Spectroscopy VI'', 21--25 Sept. 2004, Cagliari, Italy. 3 pages with 2 figure

Tick-borne encephalitis virus induces chemokine RANTES expression via activation of IRF-3 pathway.

BACKGROUND: Tick-borne encephalitis virus (TBEV) is one of the most important flaviviruses that targets the central nervous system (CNS) and causes encephalitides in humans. Although neuroinflammatory mechanisms may contribute to brain tissue destruction, the induction pathways and potential roles of specific chemokines in TBEV-mediated neurological disease are poorly understood. METHODS: BALB/c mice were intracerebrally injected with TBEV, followed by evaluation of chemokine and cytokine profiles using protein array analysis. The virus-infected mice were treated with the CC chemokine antagonist Met-RANTES or anti-RANTES mAb to determine the role of RANTES in affecting TBEV-induced neurological disease. The underlying signaling mechanisms were delineated using RANTES promoter luciferase reporter assay, siRNA-mediated knockdown, and pharmacological inhibitors in human brain-derived cell culture models. RESULTS: In a mouse model, pathological features including marked inflammatory cell infiltrates were observed in brain sections, which correlated with a robust up-regulation of RANTES within the brain but not in peripheral tissues and sera. Antagonizing RANTES within CNS extended the survival of mice and reduced accumulation of infiltrating cells in the brain after TBEV infection. Through in vitro studies, we show that virus infection up-regulated RANTES production at both mRNA and protein levels in human brain-derived cell lines and primary progenitor-derived astrocytes. Furthermore, IRF-3 pathway appeared to be essential for TBEV-induced RANTES production. Site mutation of an IRF-3-binding motif abrogated the RANTES promoter activity in virus-infected brain cells. Moreover, IRF-3 was activated upon TBEV infection as evidenced by phosphorylation of TBK1 and IRF-3, while blockade of IRF-3 activation drastically reduced virus-induced RANTES expression. CONCLUSIONS: Our findings together provide insights into the molecular mechanism underlying RANTES production induced by TBEV, highlighting its potential importance in the process of neuroinflammatory responses to TBEV infection

ZIKV infection activates the IRE1-XBP1 and ATF6 pathways of unfolded protein response in neural cells.

BACKGROUND: Many viruses depend on the extensive membranous network of the endoplasmic reticulum (ER) for their translation, replication, and packaging. Certain membrane modifications of the ER can be a trigger for ER stress, as well as the accumulation of viral protein in the ER by viral infection. Then, unfolded protein response (UPR) is activated to alleviate the stress. Zika virus (ZIKV) is a mosquito-borne flavivirus and its infection causes microcephaly in newborns and serious neurological complications in adults. Here, we investigated ER stress and the regulating model of UPR in ZIKV-infected neural cells in vitro and in vivo. METHODS: Mice deficient in type I and II IFN receptors were infected with ZIKV via intraperitoneal injection and the nervous tissues of the mice were assayed at 5 days post-infection. The expression of phospho-IRE1, XBP1, and ATF6 which were the key markers of ER stress were analyzed by immunohistochemistry assay in vivo. Additionally, the nuclear localization of XBP1s and ATF6n were analyzed by immunohistofluorescence. Furthermore, two representative neural cells, neuroblastoma cell line (SK-N-SH) and astrocytoma cell line (CCF-STTG1), were selected to verify the ER stress in vitro. The expression of BIP, phospho-elF2α, phospho-IRE1, and ATF6 were analyzed through western blot and the nuclear localization of XBP1s was performed by confocal immunofluorescence microscopy. RT-qPCR was also used to quantify the mRNA level of the UPR downstream genes in vitro and in vivo. RESULTS: ZIKV infection significantly upregulated the expression of ER stress markers in vitro and in vivo. Phospho-IRE1 and XBP1 expression significantly increased in the cerebellum and mesocephalon, while ATF6 expression significantly increased in the mesocephalon. ATF6n and XBP1s were translocated into the cell nucleus. The levels of BIP, ATF6, phospho-elf2α, and spliced xbp1 also significantly increased in vitro. Furthermore, the downstream genes of UPR were detected to investigate the regulating model of the UPR during ZIKV infection in vitro and in vivo. The transcriptional levels of atf4, gadd34, chop, and edem-1 in vivo and that of gadd34 and chop in vitro significantly increased. CONCLUSION: Findings in this study demonstrated that ZIKV infection activates ER stress in neural cells. The results offer clues to further study the mechanism of neuropathogenesis caused by ZIKV infection

Neutrino emission from a GRB afterglow shock during an inner supernova shock breakout

The observations of a nearby low-luminosity gamma-ray burst (GRB) 060218 associated with supernova SN 2006aj may imply an interesting astronomical picture where a supernova shock breakout locates behind a relativistic GRB jet. Based on this picture, we study neutrino emission for early afterglows of GRB 060218-like GRBs, where neutrinos are expected to be produced from photopion interactions in a GRB blast wave that propagates into a dense wind. Relativistic protons for the interactions are accelerated by an external shock, while target photons are basically provided by the incoming thermal emission from the shock breakout and its inverse-Compton scattered component. Because of a high estimated event rate of low-luminosity GRBs, we would have more opportunities to detect afterglow neutrinos from a single nearby GRB event of this type by IceCube. Such a possible detection could provide evidence for the picture described above.Comment: 6 pages, 2 figures, accepted for publication in MNRA