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Träfflista för sökning "WFRF:(Cui Jing) srt2:(2010-2014)"

Search: WFRF:(Cui Jing) > (2010-2014)

  • Result 1-9 of 9
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1.
  • Liu, Dedi, et al. (author)
  • Pressure-induced phase transitions of C70 nanotubes
  • 2011
  • In: The Journal of Physical Chemistry C. - : American Chemical Society. - 1932-7447 .- 1932-7455. ; 115:18, s. 8918-8922
  • Journal article (peer-reviewed)abstract
    • Single crystalline C70 nanotubes having a face-centered-cubic (fcc) structure with diameters on a nanometer scale were synthesized by a facile solution method. In situ high pressure Raman spectroscopy and X-ray diffraction have been employed to study the structural stability and phase transitions of the pristine sample. We show that the molecular orientation-related phase transition from the fcc structure to a rhombohedral structure occurs at about 1.5 GPa, which is 1 GPa higher than in bulk C70. Also, the C70 molecules themselves are more stable in the nanotubes than in bulk crystals, manifested by a partial amorphization at 20 GPa. The crystal structure of C70 nanotubes could partially return to the initial structure after a pressure cycle above 30.8 GPa, and the C70 molecules were intact up to 43 GPa. The bulk modulus of C70 nanotubes is measured to be 50 GPa, which is twice larger than that of bulk C70.
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2.
  • Ablikim, M., et al. (author)
  • Observation of the decay psi(3686) -> Lambda(Sigma)over-bar(+/-) pi(-/+) + c.c
  • 2013
  • In: Physical Review D. - 1550-7998 .- 1550-2368. ; 88:11, s. 112007-
  • Journal article (peer-reviewed)abstract
    • Using a sample of 1:06 X 10(8) psi(3686) events collected with the BESIII detector, we present the first observation of the decays of psi(3686) -> Lambda(Sigma) over bar (+) pi(-) + c.c. and psi(3686) -> Lambda(Sigma) over bar (-) pi(+) + c.c. The branching fractions are measured to be B(psi(3686) -> Lambda(Sigma) over bar (+) pi(-) + c.c.) = (1.40 +/- 0.03 +/- 0.13) X 10(-4) and B(psi(3686) -> Lambda (Sigma) over bar (-) pi(+) + c.c.) = (1.54 +/- 0.04 +/- 0.13) X 10(-4) where the first errors are statistical and the second ones systematic.
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3.
  • Ablikim, M., et al. (author)
  • Search for eta(c)(2S)h(c) -> p(p)over-bar decays and measurements of the chi(cJ) -> p(p)over-bar branching fractions
  • 2013
  • In: Physical Review D. - 1550-7998 .- 1550-2368. ; 88:11, s. 112001-
  • Journal article (peer-reviewed)abstract
    • Using a sample of 1.06 x 10(8)psi(3686) events collected with the BESIII detector at BEPCII, the decays eta(c)(2S) -> p (p) over bar and h(c) -> p (p) over bar are searched for, where eta(c)(2S) and h(c) are reconstructed in the decay chains psi(3686) -> gamma eta(c)(2S), eta(c)(2S) -> p (p) over bar and psi(3686) -> pi(0)h(c), h(c) -> p (p) over bar, respectively. No significant signals are observed. The upper limits of the product branching fractions are determined to be B(psi(3686) -> gamma eta(c)(2S)) x B(eta(c)(2S) -> p (p) over bar) < 1.4 x 10(-6) and B(psi(3686) -> pi(0)h(c)) x B(h(c) -> p<(p)over bar>) < 1.3 x 10(-7) at the 90% C.L.. The branching fractions for chi(cJ) -> p<(p)over bar> (J = 0, 1, 2) are also measured to be (24.5 +/- 0.8 +/- 1.3, 8.6 +/- 0.5 +/- 0.5, 8.4 +/- 0.5 +/- 0.5) x 10(-5), which are the world's most precise measurements.
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4.
  • Deng, Min, et al. (author)
  • Genome-wide association analyses in Han Chinese identify two new susceptibility loci for amyotrophic lateral sclerosis
  • 2013
  • In: Nature Genetics. - : Nature Publishing Group. - 1061-4036 .- 1546-1718. ; 45:6, s. 697-
  • Journal article (peer-reviewed)abstract
    • To identify susceptibility genes for amyotrophic lateral sclerosis (ALS), we conducted a genome-wide association study (GWAS) in 506 individuals with sporadic ALS and 1,859 controls of Han Chinese ancestry. Ninety top SNPs suggested by the current GWAS and 6 SNPs identified by previous GWAS were analyzed in an independent cohort of 706 individuals with ALS and 1,777 controls of Han Chinese ancestry. We discovered two new susceptibility loci for ALS at 1q32 (CAMK1G, rs6703183, P-combined = 2.92 x 10(-8), odds ratio (OR) = 1.31) and 22p11 (CABIN1 and SUSD2, rs8141797, P-combined = 2.35 x 10(-9), OR = 1.52). These two loci explain 12.48% of the overall variance in disease risk in the Han Chinese population. We found no association evidence for the previously reported loci in the Han Chinese population, suggesting genetic heterogeneity of disease susceptibility for ALS between ancestry groups. Our study identifies two new susceptibility loci and suggests new pathogenic mechanisms of ALS.
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5.
  • Jing, Cuiping, et al. (author)
  • ?2NC: Redundant and Random Network Codingfor Robust H.264/SVC Transmission
  • 2011
  • In: 14th IEEE International Conference on Network-Based Information Systems (NBiS), 2011. - : IEEE Computer Society. - 9781457707896 - 9780769544588 ; , s. 634-639
  • Conference paper (peer-reviewed)abstract
    • In this paper we are interested in improving the performance of constructive network coding schemes for video transmission over packet lossy networks. A novel unequal packet loss protection scheme R2NC based on low-triangular global coding matrix with ladder-shaped partition will be presented, which combines redundant and random network coding for robust H.264/SVC video transmission. Firstly, the error-correcting capabilities of redundant network coding make our scheme resilient to loss. Secondly, the implementation of random network coding at the intermediate nodes with multiple input links can reduce the cost of network bandwidth, thus reducing the end to end delay for video transmission. Thirdly, the low-triangular global coding matrix with ladder-shaped partition is maintained throughout R2NC process to provide unequal erasure protection for H.264/SVC priority layers. The redundant network coding avoids the retransmission of lost packets and improves error correcting capabilities of lost packets. Based only on the knowledge of the loss rates on the output links, the source node and intermediate nodes can make decisions for redundant network coding and random network coding (i.e., how much redundancy to add at this node). However, the redundancy caused by redundant network coding makes the network load increases, in order to improve network throughput, we perform random network coding at the intermediate nodes. Our approach is grounded on the overall distortion of reconstructed video minimization by optimizing the amount of redundancy assigned to each layer. Experimental results are shown to demonstrate the significant improvement of H.264/SVC video reconstruction quality with R2NC over packet lossy networks.
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6.
  • Okada, Yukinori, et al. (author)
  • Genetics of rheumatoid arthritis contributes to biology and drug discovery
  • 2014
  • In: Nature. - : Nature Publishing Group. - 0028-0836 .- 1476-4687. ; 506:7488, s. 376-381
  • Journal article (peer-reviewed)abstract
    • A major challenge in human genetics is to devise a systematic strategy to integrate disease-associated variants with diverse genomic and biological data sets to provide insight into disease pathogenesis and guide drug discovery for complex traits such as rheumatoid arthritis (RA)(1). Here we performed a genome-wide association study meta-analysis in a total of >100,000 subjects of European and Asian ancestries (29,880 RA cases and 73,758 controls), by evaluating similar to 10 million single-nucleotide polymorphisms. We discovered 42 novel RA risk loci at a genome-wide level of significance, bringing the total to 101 (refs 2-4). We devised an in silico pipeline using established bioinformatics methods based on functional annotation(5), cis-acting expression quantitative trait loci(6) and pathway analyses(7-9)-as well as novel methods based on genetic overlap with human primary immunodeficiency, haematological cancer somatic mutations and knockout mouse phenotypes-to identify 98 biological candidate genes at these 101 risk loci. We demonstrate that these genes are the targets of approved therapies for RA, and further suggest that drugs approved for other indications may be repurposed for the treatment of RA. Together, this comprehensive genetic study sheds light on fundamental genes, pathways and cell types that contribute to RA pathogenesis, and provides empirical evidence that the genetics of RA can provide important information for drug discovery.
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7.
  • Tan, Youwen, et al. (author)
  • The naturally occurring YMDD mutation among patients chronically infected HBV and untreated with lamivudine: A systematic review and meta-analysis
  • 2012
  • In: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 7
  • Review (other academic/artistic)abstract
    • Background: Several recent reports have demonstrated that tyrosine (Y)-methionine (M)-aspartic acid (D)-aspartic acid (D) (YMDD) motif mutations can naturally occur in chronic HBV patients without antiviral treatment such as lamivudine therapy. This paper aims to assess the overall spontaneous incidence and related risk factors of YMDD-motif mutations among lamivudine-naïve chronic HBV carriers, so as to provide some clue for clinical treatment of hepatitis B. Methodology/Principal Findings: Chinese and English literatures were searched for studies reporting natural YMDD mutations among untreated chronic HBV patients from 2001 to 2010. The incidence estimates were summarized and analyzed by meta-analyses. Forty-seven eligible articles from eight countries were selected in this review (13 in English and 34 in Chinese). The pooled incidence of YMDD-motif mutation among untreated chronic HBV patients from eight countries was 12.21% (95% CI: 9.69%-14.95%). China had an incidence of 13.38% (95% CI: 10.90%-16.07%) and seven other countries had an incidence of 9.90% (95% CI: 3.28%-19.55%), respectively. Lamivudine therapy would increase the risk of mutations 5.23 times higher than the untreated patients. A higher HBV DNA copy number was associated with increased incidence of natural YMDD mutation. No significant difference was found in YMDD mutation incidence between groups of different gender, age, HBeAg status, patients' ALT (alanine aminotransferase) level, and between the groups of HBV genotype B and C. Conclusions: The YMDD-motif mutations can occur spontaneously with a relatively high incidence in CHB patients untreated with lamivudine. These mutations might be the consequence of accumulated base mismatch due to the nature of viral polymerase. More fundamental and clinical studies are needed to clarify the influence of YMDD mutations in hepatitis B progression and antiviral treatment. © 2012 Tan et al.
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8.
  • Xu, Caihua, et al. (author)
  • WT1 promotes cell proliferation in non-small cell lung cancer cell lines through up-regulating cyclin D1 and p-pRb in vitro and in vivo
  • 2013
  • In: PLOS ONE. - San Francisco : PLoS, Public Library of Science. - 1932-6203. ; 8:8
  • Journal article (peer-reviewed)abstract
    • The Wilms' tumor suppressor gene (WT1) has been identified as an oncogene in many malignant diseases such as leukaemia, breast cancer, mesothelioma and lung cancer. However, the role of WT1 in non-small-cell lung cancer (NSCLC) carcinogenesis remains unclear. In this study, we compared WT1 mRNA levels in NSCLC tissues with paired corresponding adjacent tissues and identified significantly higher expression in NSCLC specimens. Cell proliferation of three NSCLC cell lines positively correlated with WT1 expression; moreover, these associations were identified in both cell lines and a xenograft mouse model. Furthermore, we demonstrated that up-regulation of Cyclin D1 and the phosphorylated retinoblastoma protein (p-pRb) was mechanistically related to WT1 accelerating cells to S-phase. In conclusion, our findings demonstrated that WT1 is an oncogene and promotes NSCLC cell proliferation by up-regulating Cyclin D1 and p-pRb expression.
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9.
  • Zhang, Xingjun, et al. (author)
  • Joint redundant and random network coding for robust video transmission over lossy networks
  • 2012
  • In: International Journal of Mobile Information Systems. - : IOS Press. - 1574-017X .- 1875-905X. ; 8:3, s. 213-230
  • Journal article (peer-reviewed)abstract
    • In this paper a novel unequal packet loss protection scheme R2NC based on low-triangular global coding matrix with ladder-shaped partition is presented, which combines redundant and random network coding for robust H.264/SVC video transmission. Firstly, the error-correcting capabilities of redundant network coding make our scheme resilient to loss. Secondly, the implementation of random network coding at the intermediate nodes with multiple input links can reduce the cost of network bandwidth, thus reducing the end-to-end delay for video transmission. Thirdly, the low-triangular global coding matrix with ladder-shaped partition is maintained throughout the R2NC processes to reduce the impact of global coding matrixs rank deficiency on video transmission and provide unequal erasure protection for H.264/SVC priority layers. The redundant network coding avoids the retransmission of lost packets and improves error-correcting capabilities of lost packets. Based only on the knowledge of the packet loss rates on the output links, the source node and intermediate nodes can make decisions for redundant network coding and random network coding (i.e., how much redundancy to add at this node). However, the redundancy caused by redundant network coding makes the network load increases. In order to improve network throughput, we performed random network coding at the intermediate nodes. Our approach is grounded on the overall distortion of reconstructed video minimization by optimizing the amount of redundancy assigned to each layer. The convex optimization model is constructed under the constraint of network coding and scalable video coding. Experimental results are shown to demonstrate the significant improvement of H.264/SVC video reconstruction quality with R2NC over packet lossy networks.
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  • Result 1-9 of 9

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