Analysis of double elastic steel wind driven magneto-electric vibration energy harvesting system

[[abstract]]This research proposes an energy harvesting system that collects the downward airflow from a helicopter or a multi-axis unmanned rotary-wing aircraft and uses this wind force to drive the magnet to rotate, generating repulsive force, which causes the double elastic steel system to slap each other and vibrate periodically in order to generate more electricity than the traditional energy harvesting system. The design concept of the vibration mechanism in this study is to allow the elastic steel carrying the magnet to slap another elastic steel carrying the piezoelectric patch to form a set of double elastic steel vibration energy harvesting (DES VEH) systems. The theoretical DES VEH mechanism of this research is composed of a pair of cantilever beams, with magnets attached to the free end of one beam, and PZT attached to the other beam. This study analyzes the single beam system first. The MOMS method is applied to analyze the frequency response of this nonlinear system theoretically, then combines the piezoelectric patch and the magneto-electric coupling device with this nonlinear elastic beam to analyze the benefits of the system’s converted electrical energy. In the theoretical study of the DES VEH system, the slapping force between the two elastic beams was considered as a concentrated load on each of the beams. Furthermore, both SES and DES VEH systems are studied and correlated. Finally, the experimental data and theoretical results are compared to verify the feasibility and correctness of the theory. It is proven that this DES VEH system can not only obtain the electric energy from the traditional SES VEH system but also obtain the extra electric energy of the steel vibration subjected to the slapping force, which generates optimal power to the greatest extent.[[notice]]補正完

Toward Optimal Resource Allocation of Virtualized Network Functions for Hierarchical Datacenters

Telecommunications service providers (TSPs) previously provided network functions to end users with dedicated hardware, but they are resorting to virtualized infrastructure for reducing costs and increasing flexibility in resource allocation. A representative case is the Central Office Re-architected as Datacenter (CORD) project from AT&T, which aims to deploy virtualized network functions (VNFs) to over 4000 central offices (COs) across the U.S. However, there is a wide spectrum of options for deploying VNFs over the COs, varying from highly distributed to highly centralized manners. The former benefits end users with short response time but has its inherent limitation on utilizing geographically dispersed resources, while the latter allows resources to be better utilized at a cost of longer response time. In this work, we model the TSP's virtualized infrastructure as hierarchical datacenters, namely hierarchical CORD, and provide a resource allocation solution to strike the optimal balance between the two extreme options. Our evaluations reveal that in general, the 3-tier architecture incurs the least cost in case of deploying VNFs under moderate or loose delay constraints. Furthermore, the margin of improvement on the resource allocation cost increases inversely with the overall system utilization rate. Our results also suggest that as heavy request load overwhelms the network infrastructure, the relevant VNFs shall be migrated to lower-tier edge datacenters or to some nearby datacenters with superior network capacity. The evaluations also demonstrate that the proposed model allows highly adaptive VNF deployment in the hierarchical architecture under various conditions.This work was supported in part by H2020 Collaborative Europe/Taiwan Research Project 5G-CORAL under Grant 761586, and in part by the Ministry of Science and Technology, Taiwan, under Grant MOST-106-2218-E-009-018 and Grant MOST-106-2221-E-194-021-MY3

Deletion of Forkhead Box M1 Transcription Factor from Respiratory Epithelial Cells Inhibits Pulmonary Tumorigenesis

The Forkhead Box m1 (Foxm1) protein is induced in a majority of human non-small cell lung cancers and its expression is associated with poor prognosis. However, specific requirements for the Foxm1 in each cell type of the cancer lesion remain unknown. The present study provides the first genetic evidence that the Foxm1 expression in respiratory epithelial cells is essential for lung tumorigenesis. Using transgenic mice, we demonstrated that conditional deletion of Foxm1 from lung epithelial cells (epFoxm1−/− mice) prior to tumor initiation caused a striking reduction in the number and size of lung tumors, induced by either urethane or 3-methylcholanthrene (MCA)/butylated hydroxytoluene (BHT). Decreased lung tumorigenesis in epFoxm1−/− mice was associated with diminished proliferation of tumor cells and reduced expression of Topoisomerase-2α (TOPO-2α), a critical regulator of tumor cell proliferation. Depletion of Foxm1 mRNA in cultured lung adenocarcinoma cells significantly decreased TOPO-2α mRNA and protein levels. Moreover, Foxm1 directly bound to and induced transcription of the mouse TOPO-2α promoter region, indicating that TOPO-2α is a direct target of Foxm1 in lung tumor cells. Finally, we demonstrated that a conditional deletion of Foxm1 in pre-existing lung tumors dramatically reduced tumor growth in the lung. Expression of Foxm1 in respiratory epithelial cells is critical for lung cancer formation and TOPO-2α expression in vivo, suggesting that Foxm1 is a promising target for anti-tumor therapy.</p

DICER1 regulated let-7 expression levels in p53-induced cancer repression requires cyclin D1.

Let-7 miRNAs act as tumour suppressors by directly binding to the 3\u27UTRs of downstream gene products. The regulatory role of let-7 in downstream gene expression has gained much interest in the cancer research community, as it controls multiple biological functions and determines cell fates. For example, one target of the let-7 family is cyclin D1, which promotes G0/S cell cycle progression and oncogenesis, was correlated with endoribonuclease DICER1, another target of let-7. Down-regulated let-7 has been identified in many types of tumours, suggesting a feedback loop may exist between let-7 and cyclin D1. A potential player in the proposed feedback relationship is Dicer, a central regulator of miRNA expression through sequence-specific silencing. We first identified that DICER1 is the key downstream gene for cyclin D1-induced let-7 expression. In addition, we found that let-7 miRNAs expression decreased because of the p53-induced cell death response, with deregulated cyclin D1. Our results also showed that cyclin D1 is required for Nutlin-3 and TAX-induced let-7 expression in cancer repression and the cell death response. For the first time, we provide evidence that let-7 and cyclin D1 form a feedback loop in regulating therapy response of cancer cells and cancer stem cells, and importantly, that alteration of let-7 expression, mainly caused by cyclin D1, is a sensitive indicator for better chemotherapies response

Introduction of a strong temperature-sensitive phenotype into enterovirus 71 by altering an amino acid of virus 3D polymerase

AbstractIn 1998, an enterovirus 71 (EV71) epidemic in Taiwan resulted in 78 deaths; however, the molecular basis of EV71 pathogenicity remains poorly understood. Comparison of the deduced amino acid sequences in 3D polymerases of EV71clinical isolates showed the T251V or T251I substitution from 1986 and 1998 outbreaks. An EV71 replicon system showed that introducing an I251T mutation did not affect luciferase activities at 35 °C when compared with wild type; however, lower luciferase activities were observed when they were incubated at 39.5 °C. In addition, the I251T mutation in the EV71 infectious clone not only reduced viral replication at 39.5 °C in vitro but also decreased the virulence of the mouse adaptive strain MP4 in neonatal mice in an i.p. infection model. Therefore, these results suggested that the threonine at position 251 results in a temperature sensitivity phenotype of EV71 which may contribute to the attenuation of circulating strains

Mean structure and variability of the cold dome northeast of Taiwan

Author Posting. © The Oceanography Society, 2011. This article is posted here by permission of The Oceanography Society for personal use, not for redistribution. The definitive version was published in Oceanography 24 no. 4 (2011): 100–109, doi:10.5670/oceanog.2011.98.The "cold dome" off northeastern Taiwan is one of the distinctive oceanic features in the seas surrounding Taiwan. The cold dome is important because persistent upwelling makes the region highly biologically productive. This article uses historical data, recent observations, and satellite-observed sea surface temperatures (SST) to describe the mean structure and variability of the cold dome. The long-term mean position of the cold dome, using the temperature at 50 m depth as a reference, is centered at 25.625°N, 122.125°E. The cold dome has a diameter of approximately 100 km, and is maintained by cold ( 34.5) waters upwelled along the continental slope. The ocean currents around the cold dome, although weak, flow counterclockwise. The monsoon-driven winter intrusion of the Kuroshio current onto the East China Sea shelf intensifies the upwelling and carries more subsurface water up to the cold dome than during the summer monsoon season. On a shorter timescale, the cold dome's properties can be significantly modified by the passage of typhoons, which creates favorable physical conditions for short-term Kuroshio intrusions in summer. The surface expression of the cold dome viewed from satellite SST images is often not domelike but instead is an irregular shape with numerous filaments, and thus may contribute substantially to shelf/slope exchange. As a result of persistent upwelling, typhoon passage, and monsoon forcing, higher chlorophyll a concentrations, and thus higher primary productivity, are frequently observed in the vicinity of the cold dome.The National Science Council (NSC) of Taiwan sponsored this study under grant NSC98-2611-M-002-019-MY3. NSC supported C.-C. Chen under grant NSC98-2611-M-003-001-MY3

Granulocyte Colony-Stimulating Factor Activating HIF-1α Acts Synergistically with Erythropoietin to Promote Tissue Plasticity

Stroke and peripheral limb ischemia are serious clinical problems with poor prognosis and limited treatment. The cytokines erythropoietin (EPO) and granulocyte-colony stimulating factor (G-CSF) have been used to induce endogenous cell repair and angiogenesis. Here, we demonstrated that the combination therapy of EPO and G-CSF exerted synergistic effects on cell survival and functional recovery from cerebral and peripheral limbs ischemia. We observed that even under normoxic conditions, G-CSF activates hypoxia-inducible factor-1α (HIF-1α), which then binds to the EPO promoter and enhances EPO expression. Serum EPO level was significantly increased by G-CSF injection, with the exception of Tg-HIF-1α+f/+f mice. The neuroplastic mechanisms exerted by EPO combined with G-CSF included enhanced expression of the antiapoptotic protein of Bcl-2, augmented neurotrophic factors synthesis, and promoted neovascularization. Further, the combination therapy significantly increased homing and differentiation of bone marrow stem cells (BMSCs) and intrinsic neural progenitor cells (INPCs) into the ischemic area. In summary, EPO in combination with G-CSF synergistically enhanced angiogenesis and tissue plasticity in ischemic animal models, leading to greater functional recovery than either agent alone