A digital-controlled SiC-based solid state circuit breaker with soft switch-off method for DC power system

Due to the lower on-state resistance, direct current (DC) solid state circuit breakers (SSCBs) based on silicon-carbide (SiC) metal-oxide-semiconductor field-effect transistors (MOSFETs) can reduce on-state losses and the investment of the cooling system when compared to breakers based on silicon (Si) MOSFETs. However, SiC MOSFETs, with smaller die area and higher current density, lead to weaker short-circuit ability, shorter short-circuit withstand time and higher protection requirements. To improve the reliability and short-circuit capability of SiC-based DC solid state circuit breakers, the short-circuit fault mechanisms of Si MOSFETs and SiC MOSFETs are revealed. Combined with the desaturation detection (DESAT), a “soft turn-off” short-circuit protection method based on source parasitic inductor is proposed. When the DESAT protection is activated, the “soft turn-off” method can protect the MOSFET against short-circuit and overcurrent. The proposed SSCB, combined with the flexibility of the DSP, has the μs-scale ultrafast response time to overcurrent detection. Finally, the effectiveness of the proposed method is validated by the experimental platform. The method can reduce the voltage stress of the power device, and it can also suppress the short-circuit current

Model of a multiverse providing the dark energy of our universe

It is shown that the dark energy presently observed in our universe can be regarded as the energy of a scalar field driving an inflation-like expansion of a multiverse with ours being a subuniverse among other parallel universes. A simple model of this multiverse is elaborated: Assuming closed space geometry, the origin of the multiverse can be explained by quantum tunneling from nothing; subuniverses are supposed to emerge from local fluctuations of separate inflation fields. The standard concept of tunneling from nothing is extended to the effect that in addition to an inflationary scalar field, matter is also generated, and that the tunneling leads to an (unstable) equilibrium state. The cosmological principle is assumed to pertain from the origin of the multiverse until the first subuniverses emerge. With increasing age of the multiverse, its spatial curvature decays exponentially so fast that, due to sharing the same space, the flatness problem of our universe resolves by itself. The dark energy density imprinted by the multiverse on our universe is time-dependent, but such that the ratio $w{=}\varrho/(c^2p)$ of its mass density and pressure (times $c^2$) is time-independent and assumes a value $-1{+}\epsilon$ with arbitrary $\epsilon{>}0$. $\epsilon$ can be chosen so small, that the dark energy model of this paper can be fitted to the current observational data as well as the cosmological constant model.Comment: 32 pages, 4 figure

OPCML Is a Broad Tumor Suppressor for Multiple Carcinomas and Lymphomas with Frequently Epigenetic Inactivation

Background: Identification of tumor suppressor genes (TSGs) silenced by CpG methylation uncovers the molecular mechanism of tumorigenesis and potential tumor biomarkers. Loss of heterozygosity at 11q25 is common multiple tumors including nasopharyngeal carcinoma (NPC). OPCML, located at 11q25, is one of the downregulated genes we identified through digital expression subtraction. Methodology/Principal Findings: Semi-quantitative RT-PCR showed frequent OPCML silencing in NPC and other common tumors, with no homozygous deletion detected by multiplex differential DNA-PCR. Instead, promoter methylation of OPCML was frequently detected in multiple carcinoma cell lines (nasopharyngeal, esophageal, lung, gastric, colon, liver, breast, cervix, prostate), lymphoma cell lines (non-Hodgkin and Hodgkin lymphoma, nasal NK/T-cell lymphoma) and primary tumors, but not in any non-tumor cell line and seldom weakly methylated in normal epithelial tissues. Pharmacological and genetic demethylation restored OPCML expression, indicating a direct epigenetic silencing. We further found that OPCML is stress-responsive, but this response is epigenetically impaired when its promoter becomes methylated. Ecotopic expression of OPCML led to significant inhibition of both anchorage-dependent and -indendent growth of carcinoma cells with endogenous silencing. Conlusions/Significance: Thus, through functional epigenetics, we identified OPCML as a broad tumor suppressor, which is frequently inactivated by methylation in multiple malignancies. © 2008 Cui et al.published_or_final_versio

Genome-Wide Screening for Genetic Alterations in Esophageal Cancer by aCGH Identifies 11q13 Amplification Oncogenes Associated with Nodal Metastasis

Esophageal squamous cell carcinoma (ESCC) is highly prevalent in China and other Asian countries, as a major cause of cancer-related mortality. ESCC displays complex chromosomal abnormalities, including multiple structural and numerical aberrations. Chromosomal abnormalities, such as recurrent amplifications and homozygous deletions, directly contribute to tumorigenesis through altering the expression of key oncogenes and tumor suppressor genes.To understand the role of genetic alterations in ESCC pathogenesis and identify critical amplification/deletion targets, we performed genome-wide 1-Mb array comparative genomic hybridization (aCGH) analysis for 10 commonly used ESCC cell lines. Recurrent chromosomal gains were frequently detected on 3q26-27, 5p15-14, 8p12, 8p22-24, 11q13, 13q21-31, 18p11 and 20q11-13, with frequent losses also found on 8p23-22, 11q22, 14q32 and 18q11-23. Gain of 11q13.3-13.4 was the most frequent alteration in ESCC. Within this region, CCND1 oncogene was identified with high level of amplification and overexpression in ESCC, while FGF19 and SHANK2 was also remarkably over-expressed. Moreover, a high concordance (91.5%) of gene amplification and protein overexpression of CCND1 was observed in primary ESCC tumors. CCND1 amplification/overexpression was also significantly correlated with the lymph node metastasis of ESCC.These findings suggest that genomic gain of 11q13 is the major mechanism contributing to the amplification. Novel oncogenes identified within the 11q13 amplicon including FGF19 and SHANK2 may play important roles in ESCC tumorigenesis

Structural analysis on mutation residues and interfacial water molecules for human TIM disease understanding

10.1186/1471-2105-14-S16-S11BMC Bioinformatics14SUPPL16-BBMI

Measurements of the Mass and Full-Width of the ηc\eta_c Meson

In a sample of 58 million $J/\psi$ events collected with the BES II detector, the process J/$\psi\to\gamma\eta_c$ is observed in five different decay channels: $\gamma K^+K^-\pi^+\pi^-$, $\gamma\pi^+\pi^-\pi^+\pi^-$, $\gamma K^\pm K^0_S \pi^\mp$ (with $K^0_S\to\pi^+\pi^-$), $\gamma \phi\phi$ (with $\phi\to K^+K^-$) and $\gamma p\bar{p}$. From a combined fit of all five channels, we determine the mass and full-width of $\eta_c$ to be $m_{\eta_c}=2977.5\pm1.0 ({stat.})\pm1.2 ({syst.})$ MeV/$c^2$ and $\Gamma_{\eta_c} = 17.0\pm3.7 ({stat.})\pm7.4 ({syst.})$ MeV/$c^2$.Comment: 9 pages, 2 figures and 4 table. Submitted to Phys. Lett.