Optimized operator-splitting methods in numerical integration of Maxwell's equations

Optimized operator splitting methods for numerical integration of the time domain Maxwell's equations in computational electromagnetics (CEM) are proposed for the first time. The methods are based on splitting the time domain evolution operator of Maxwell's equations into suboperators, and corresponding time coefficients are obtained by reducing the norm of truncation terms to a minimum. The general high-order staggered finite difference is introduced for discretizing the three-dimensional curl operator in the spatial domain. The detail of the schemes and explicit iterated formulas are also included. Furthermore, new high-order Padé approximations are adopted to improve the efficiency of the proposed methods. Theoretical proof of the stability is also included. Numerical results are presented to demonstrate the effectiveness and efficiency of the schemes. It is found that the optimized schemes with coarse discretized grid and large Courant-Friedrichs-Lewy (CFL) number can obtain satisfactory numerical results, which in turn proves to be a promising method, with advantages of high accuracy, low computational resources and facility of large domain and long-time simulation. In addition, due to the generality, our optimized schemes can be extended to other science and engineering areas directly. © 2012 Z. X. Huang et al.published_or_final_versio

Fast computation of radar cross-section by fast multipole method in conjunction with lifting wavelet-like transform

The fast multipole method (FMM) in conjunction with the lifting wavelet-like transform scheme is proposed for the scattering analysis of differently shaped three-dimensional perfectly electrical conducting objects. As a flexible and efficient matrix compression technique, the proposed method can sparsify the aggregation matrix and disaggregation matrix in real time with compression ratio about 30%. The computational complexity and choice of proper wavelet are also discussed. Numerical simulation and complexity analysis have shown that the proposed method can speed up the aggregation and disaggregation steps of the FMM with lower memory requirements. © 2010 The Institution of Engineering and Technology.postprin

Adaptive frequency sweep analysis for electromagnetic problems using the Thiele interpolating continued fractions

A direct rational approximation method based on Thiele interpolating continued fractions theory is proposed for fast frequency sweep analysis of electromagnetic problems. And an adaptive algorithm is also formed. Compared with the conventional rational approximation method, the proposed method can get a rational approximation directly without a great number of matrix inverse computations and doesn't need to allocate much memory for high derivatives of the dense impedance matrix. Meanwhile, the computation of surface currents by continued fractions can be sped up as compared with the traditional rational approximation. Numerical simulations for broad band scattering analysis of different shaped objects are discussed to shown the effectiveness of the present method. © 2010 IEEE.published_or_final_versionThe 2nd International Conference on Education Technology and Computer (ICETC 2010), Shanghai, China, 22-24 June 2010. In Proceedings of 2nd ICETC, 2010, v. 5, p. 126-12

Neuropilin 1 sequestration by neuropathogenic mutant glycyl-tRNA synthetase is permissive to vascular homeostasis

The mechanism by which dominantly inherited mutations in the housekeeping gene GARS, which encodes glycyl-tRNA synthetase (GlyRS), mediate selective peripheral nerve toxicity resulting in Charcot-Marie-Tooth disease type 2D (CMT2D) is still largely unresolved. The transmembrane receptor protein neuropilin 1 (Nrp1) was recently identifed as an aberrant extracellular binding partner of mutant GlyRS. Formation of the Nrp1/mutant GlyRS complex antagonises Nrp1 interaction with one of its main natural ligands, vascular endothelial growth factor-A (VEGF-A), contributing to neurodegeneration. However, reduced extracellular binding of VEGF-A to Nrp1 is known to disrupt post-natal blood vessel development and growth. We therefore analysed the vascular system at early and late symptomatic time points in CMT2D mouse muscles, retina, and sciatic nerve, as well as in embryonic hindbrain. Mutant tissues show no diference in blood vessel diameter, density/growth, and branching from embryonic development to three months, spanning the duration over which numerous sensory and neuromuscular phenotypes manifest. Our fndings indicate that mutant GlyRS-mediated disruption of Nrp1/VEGF-A signalling is permissive to maturation and maintenance of the vasculature in CMT2D mice

Anti-Tumor Effect of Cactus Polysaccharides on Lung Squamous Carcinoma Cells (SK-MES-1)

Background: Cactus polysaccharides are the active components of Opuntia dillenii which have been used extensively in folk medicine. In thisstudy, we investigate the anti-tumor effect of cactus polysaccharides on lung squamous carcinoma cells SK-MES-1.Materials and Methods: The inhibitory effect of Cactus polysaccharides on lung squamous carcinoma cells were detected by MTT assay. Cellcycle was determined by flow cytometry and cell apoptosis was determined by AnnexinV assay. Western-blotting was applied to detect P53 andPTEN protein expression in the cells treated with cactus polysaccharides.Results: Results showed that different concentrations of wild cactus polysaccharides prevent SK-MES-1 cells growth and induces S phase arrest.The data also revealed that cactus polysaccharides cause apoptosis in SK-MES-1 cells determined by Annexin-V assay. Furthermore, cactuspolysaccharides induced growth arrest and apoptosis may be due to the increase of P53 and phosphatase and tension homolog deleted onchromosome ten (PTEN) protein.Conclusion: Cactus polysaccharides have anti-tumor activity on lung squamous carcinoma cells.Key words: Cactus polysaccharides, Lung squamous carcinoma, Anti-tumor effect, P53, PTEN Abbreviations: PTEN :phosphatase and tension homolog deleted on chromosome ten; NSCLC: Non-small-cell lung cancer; FBS :Phosphate buffered saline; MTT:3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide; PBS: Phosphate buffered saline; DMSO:Dimethyl sulfoxide; PI: Propidium iodide

ERα inhibits epithelial-mesenchymal transition by suppressing Bmi1 in breast cancer

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ERα inhibits epithelial-mesenchymal transition by suppressing Bmi1 in breast cancer

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Dramatic escalation in metabolic syndrome and cardiovascular risk in a Chinese population experiencing rapid economic development

Background Metabolic syndrome (MetSyn) increases the incidence of cardiovascular disease. Information on changes in prevalence of MetSyn in developing countries is limited. This study aims to compare MetSyn prevalence and its associated vascular risk over the period between 2002 and 2010 in a population which has had the world’s fastest economic development over the past three decades. Methods Two health surveys were conducted by using the multistage cluster random sampling method in a Chinese population of 85 million in southern China. The participants received a full medical check-up, including measurement of blood pressure (BP), obesity indices, fasting lipids and glucose levels. Data describing socio-economic status and lifestyle factors were also collected through interview. Metabolic syndrome was defined in accordance with the International Diabetes Federation criteria. Results A total of 3,561 participants from Survey 2010 were included in the data analysis. Women had a significantly higher prevalence of MetSyn than men. Comparison between the two surveys shows that age-standardized prevalence of MetSyn increased fourfold (from 5.4% in 2002 to 21.3% in 2010) in those ≧ 20 years. Among the MetSyn components, prevalence of hyperglycaemia has increased most (from 9.1% to 53.1%). The age-standardized prevalence of central obesity, hypertension, hypertriglyceridaemia and low HDL-cholesterol increased from 13.5% to 25.4%, from 23.6% to 40.8%, from 12.1% to 17.4% and from 32.1% to 71.1%, respectively. Differences between rural and urban residents in the prevalence in MetSyn and its components narrowed in 2010. Conclusions Cardiovascular risk escalated dramatically in this population between 2002 and 2010. The escalation may relate to the rapid economic development, which led to accelerating changes in nutrition, lifestyle, and socio-economic status. Our findings suggest that health transition in rapidly developing second- and third-world countries may be much faster than what has been observed in Western countries.published_or_final_versio

Trk receptor signaling and sensory neuron fate are perturbed in human neuropathy caused by Gars mutations

Charcot-Marie-Tooth disease type 2D (CMT2D) is a peripheral nerve disorder caused by dominant, toxic, gain-of-function mutations in the widely expressed, housekeeping gene, GARS. The mechanisms underlying selective nerve pathology in CMT2D remain unresolved, as does the cause of the mild-to-moderate sensory involvement that distinguishes CMT2D from the allelic disorder distal spinal muscular atrophy type V. To elucidate the mechanism responsible for the underlying afferent nerve pathology, we examined the sensory nervous system of CMT2D mice. We show that the equilibrium between functional subtypes of sensory neuron in dorsal root ganglia is distorted by Gars mutations, leading to sensory defects in peripheral tissues and correlating with overall disease severity. CMT2D mice display changes in sensory behaviour concordant with the afferent imbalance, which is present at birth and non-progressive, indicating that sensory neuron identity is pre-natally perturbed and that a critical developmental insult is key to the afferent pathology. Through in vitro experiments, mutant, but not wild-type, GlyRS was shown to aberrantly interact with the Trk receptors and cause mis-activation of Trk signalling, which is essential for sensory neuron differentiation and development. Together, this work suggests that both neurodevelopmental and neurodegenerative mechanisms contribute to CMT2D pathogenesis, and thus has profound implications for the timing of future therapeutic treatments