Apply blockchain technology to electric vehicle battery refueling

Battery swapping is a solution of electric vehicle (EV) battery refueling. For EV owners, the battery information and transaction’s correctness, openness, traceability and immutability is difficult to get guarantee in traditional centralized system. The trust lacking between EV owners and swapping station is caused, and becomes a big challenge to EV’s rapid development. An objective mechanism based on decentralized blockchain system is proposed to manage battery swapping and solve the trust lacking issue. With this solution, both battery’s life-cycle information and all operations histories are permanently saved in blockchain network. All key logics are driven by smart contracts, the battery price calculation and the digital currency exchange between EV owners and station are realized by smart contracts automatically and accurately. A primary prototype based on Ethereum is analyzed and implemented to illustrate the feasibility of managing battery swapping and refueling based on blockchain system to solve the trust lacking issue

Rayleigh-Schroedinger-Goldstone variational perturbation theory for many fermion systems

We present a Rayleigh-Schroedinger-Goldstone perturbation formalism for many fermion systems. Based on this formalism, variational perturbation scheme which goes beyond the Gaussian approximation is developed. In order to go beyond the Gaussian approximation, we identify a parent Hamiltonian which has an effective Gaussian vacuum as a variational solution and carry out further perturbation with respect to the renormalized interaction using Goldstone's expansion. Perturbation rules for the ground state wavefunctional and energy are found. Useful commuting relations between operators and the Gaussian wavefunctional are also found, which could reduce the calculational efforts substantially. As examples, we calculate the first order correction to the Gaussian wavefunctional and the second order correction to the ground state of an electron gas system with the Yukawa-type interaction.Comment: 11pages, 1figur

Sphingosine kinase 1–mediated inhibition of Fas death signaling in rheumatoid arthritis B lymphoblastoid cells

Objective It is becoming increasingly apparent that B cells play an important role in the pathogenesis of rheumatoid arthritis (RA). Due to the scarcity of B cells in RA, it has been technically difficult to functionally characterize B cell apoptosis in this disease. As a necessary first step to identify candidate aberrations, we investigated Fas-mediated signaling events in immortalized peripheral blood B lymphoblastoid cell lines (LCLs) from patients with RA and controls. Methods Cell death was determined by the MTS assay, and apoptosis was detected by the TUNEL assay and DNA laddering. Proteolytic activation of caspase 3 was determined by immunoblotting, and its enzymatic activity was determined by a fluorometric technique. Messenger RNA (mRNA) expression was quantified by real-time polymerase chain reaction (PCR) analysis. The functional role of sphingosine kinase (SPHK) was determined by measuring its enzymatic activity, by quantifying the levels of its product, sphingosine 1-phosphate (S1P), and by investigating the ability of the SPHK inhibitor N , N -dimethylsphingosine and isozyme-specific small interfering RNA (siRNA) oligonucleotides to reverse signaling aberrations. Results LCLs from patients with RA displayed disease-specific Fas-mediated signal transduction impairment with consequent resistance to cell death. RA LCLs displayed high constitutive SPHK activity and increased levels of S1P. Real-time PCR analysis showed higher SPHK-1 mRNA expression levels in RA patients compared with paired controls. Increased SPHK-1 (but not SPHK-2) mRNA levels were observed in synovial tissue from RA patients. Competitive inhibitors of SPHK reversed the resistance of RA LCLs to Fas-induced apoptosis. Additionally, resistance to Fas-mediated signaling was reversed by siRNA oligonucleotides specific for SPHK-1 but not by oligonucleotides specific for SPHK-2. Conclusion These findings demonstrate disease-specific resistance to Fas-mediated death signaling in patients with RA and implicate increased SPHK-1 activity as the cause of this aberration.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/49513/1/21635_ftp.pd