Economic Proof of Work

Blockchain is the distributed system allowing multiple parties to host a service. Nakamoto Consensus, also named Proof of Work (PoW), is widely used in Bitcoin and other blockchain systems. PoW is an important consensus algorithm. It solves the Byzantine Generals problem in an open network. It also protects the blockchain security from longest chain attack. World widely virtual currency mining was commonly regarded as over energy consuming. How to make use of the computation capacity provided by mining, is one of the most important problems to solve in blockchain. We extend Proof of Work to be useful and economic. And discover a simple method to generate the proof of storing useful data with PoW. In a blockchain based distributed file storage system, any storage resource owner could freely join as a service provider. It requires the service provider to show the proof of honestly keeping the data content, because the malicious provers may use other\u27s content to generate the proof in order to reduce their resource cost. This is out-sourcing attack. Furtherly, we proposed a novel technique to combine data replica process with Proof of Work\u27s contributing to blockchain security

Gn blending multiple surfaces in polar coordinates

International audienceThis paper proposes a method of Gn blending multiple parametric surfaces in polar coordinates. It models the geometric continuity conditions of parametric surfaces in polar coordinates and presents a mechanism of converting a Cartesian parametric surface into its polar coordinate form. The basic idea is first to reparameterize the parametric blendees into the form of polar coordinates. Then they are blended simultaneously by a basis function in the complex domain. To extend its compatibility, we also propose a method of converting polar coordinate blending surface into N NURBS patches. One application of this technique is to fill N-sided holes. Examples are presented to show its feasibility and practicability

Silencing of c-Ski augments TGF-b1-induced epithelial-mesenchymal transition in cardiomyocyte H9C2 cells

Background: The shRNA lentiviral vector was constructed to silence c-Ski expression in cardiac mus-  cle cells, with the aim of exploring the role of c-Ski in transforming growth factor b1 (TGF-b1)-induced epithelial-mesenchymal transitions (EMT) in H9C2 cells. Methods: Real-time polymerase chain reaction (RT-PCR) and western blot were used to detect c-Ski ex- pression at protein and messenger ribonucleic acid (mRNA) levels in 5 different cell lines. Then, lentiviral vector was constructed to silence or overexpress c-Ski in H9C2 cells. MTT and/or soft agar assay and tran- swell assay were used to detect cell proliferation and migration, respectively. The expression levels of c-Ski under different concentrations of TGF-b1 stimulation were detected by RT-qPCR and immunocytochemi- cal analysis. In the presence or absence of TGF-b1 stimulation, the proteins’ expression levels of a-SMA, FN and E-cadherin, which are closely correlated with the process of EMT, were measured by western blot after c-Ski silencing or overexpression. Meanwhile, the effect of c-Ski on Samd3 phosphorylation with TGF-b1 stimulation was investigated.  Results: There is a high expression of c-Ski at protein and mRNA levels in H9C2 cell line, which first demonstrated the presence of c-Ski expression in H9C2 cells. Overexpression of c-Ski significantly increased H9C2 cell proliferation. The ability of c-Ski gene silencing to suppress cell proliferation was gradually enhanced, and inhibition efficiency was the highest after 6 to 7 d of transfection. Moreover, H9C2 cells with c-Ski knockdown gained significantly aggressive invasive potential when compared with the control group. TGF-b1 stimulation could dose-independently reduce c-Ski expression in H9C2 cells and lead to obvious down-regulated expression of E-cadherin. Interestingly, c-Ski could restore E-cadherin expression while suppressing a-SMA and/or FN expression stimulated by TGF-b1. How- ever, shRNA-induced c-Ski knockdown aggravated only the TGF-b1-induced EMT. Moreover, c-Ski- -shRNA also promoted the phosphorylation of Samd3 induced by TGF-b1.  Conclusions: c-Ski expression in cardiac muscle cells could be down-regulated by TGF-b1. Silencing of c-Ski gene was accompanied by down-regulation of E-cadherin, up-regulation of a-SMA and/or FN and Smad3 phosphorylation induced by TGF-b1, promoting EMT process. Therefore, c-Ski may be closely associated with TGF-b1-induced EMT and play an important role in cardiac fibrosis develop- ment and progression.