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Chen T.,National University of Defense Technology | Chen T.,Beijing Institute of Radiation Medicine | Chen T.,State Key Laboratory of Proteomics | Chen T.,Beijing Proteome Research Center | And 2 more authors.
Ruan Jian Xue Bao/Journal of Software | Year: 2013

Object-Based storage is a good choice for large scale storage systems. Load balancing of metadata is important to improve the performance of I/O. The existing load balancing schemas cannot evenly distribute the accesses of metadata in a dynamic way. Moreover, the adaptability and fault-tolerance ability need to be improved. This paper presents an adaptable distributed load balancing of metadata (ADMLB) which is composed of basic load balancing algorithm (BBLA) and distributed incremental load balancing algorithm (IBLA). Specially, ADMLB first uses BBLA to distribute metadata loads according to the performances of the metadata servers and then uses IBLA to incrementally reorganize loads on each metadata server. ADMLB can evenly distribute loads between metadata servers and adapts well to the changes of loads. It also has good fault-tolerance ability, and locates metadata servers very quickly. ©2013 ISCAS.

Liu M.,Fudan University | Zhang Y.,Fudan University | Chen Y.,Fudan University | Yan G.,Fudan University | And 10 more authors.
Journal of Proteome Research | Year: 2014

Study of site-specific N-glycosylation in complex sample remains a huge analytical challenge because protein glycosylation is structurally diverse in post-translational modifications, resulting in an intricacy of N-glycopeptides. Here we have developed a novel approach for high-throughput N-glycopeptide profiling based on a network-centric algorithm for deciphering glycan fragmentation in mass spectrometry. We performed an extensive validation and a high-throughput N-glycosylation study on serum and identified thousands of N-glycopeptide spectra with high confidence. The results revealed a similar level of glycan microheterogeneity to that of conventional glycomics approach on individual proteins and provided the unique in-depth site-specific information that could only be studied through glycopeptide profiling. © 2014 American Chemical Society.

Tong Y.-G.,State Key Laboratory of Pathogen and Biosecurity | Shi W.-F.,Institute of Pathogen Biology | Liu D.,CAS Institute of Microbiology | Qian J.,Key Laboratory of Jilin Province for Zoonosis Prevention and Control | And 53 more authors.
Nature | Year: 2015

A novel Ebola virus (EBOV) first identified in March 2014 has infected more than 25,000 people in West Africa, resulting in more than 10,000 deaths. Preliminary analyses of genome sequences of 81 EBOV collected from March to June 2014 from Guinea and Sierra Leone suggest that the 2014 EBOV originated from an independent transmission event from its natural reservoir followed by sustained human-to-human infections. It has been reported that the EBOV genome variation might have an effect on the efficacy of sequence-based virus detection and candidate therapeutics. However, only limited viral information has been available since July 2014, when the outbreak entered a rapid growth phase. Here we describe 175 full-length EBOV genome sequences from five severely stricken districts in Sierra Leone from 28 September to 11 November 2014. We found that the 2014 EBOV has become more phylogenetically and genetically diverse from July to November 2014, characterized by the emergence of multiple novel lineages. The substitution rate for the 2014 EBOV was estimated to be 1.23 × 10 â '3 substitutions per site per year (95% highest posterior density interval, 1.04 × 10 â '3 to 1.41 × 10 â '3 substitutions per site per year), approximating to that observed between previous EBOV outbreaks. The sharp increase in genetic diversity of the 2014 EBOV warrants extensive EBOV surveillance in Sierra Leone, Guinea and Liberia to better understand the viral evolution and transmission dynamics of the ongoing outbreak. These data will facilitate the international efforts to develop vaccines and therapeutics. © 2015 Macmillan Publishers Limited. All rights reserved.

Zheng W.-W.,Beijing Institute of Radiation Medicine | Yang Y.,Purdue University | Zhang M.-J.,Tianjin University | Dong X.-M.,Beijing University of Technology | And 10 more authors.
Progress in Biochemistry and Biophysics | Year: 2013

Nucleophosmin (NPM1 or B23.1) is a ubiquitously expressed nuclear phosphoprotein that plays key role in several cellular processes, including ribosome biogenesis, centrosome duplication, cell cycle progression, cell growth, and transformation. NPM1 is one of the most frequently mutated genes in AML. EDAG is a hematopoietic tissue-specific transcription regulator that plays a key role in maintaining the homeostasis of hematopoietic lineage commitment. In AML patients, the high expression level of EDAG is associated with poor prognosis. Our previous study suggest that EDAG is a physiological binding partner of NPM1 and regulates NPM1 protein stability, however, whether EDAG regulates NPM1 in AML patients and whether EDAG regulates NPM1 mutations remain unknown. In the present study, we found that in bone marrow CD34+ cells from AML patients, silencing of EDAG led to decreased protein stability of NPM1 protein and increased cell sensitivity to daunorubicin. Although EDAG failed to interact with NPMc+ and regulate its protein stability in normal culture condition, with leptomycin B treatment, EDAG overexpression enhanced the protein stability of NPMc+. In AML patients with NPMc+, the CD34 cells were more responsive to daunorubicin treatment than the cells from AML with wild type NPM1, and silencing of EDAG weakly increased the sensitivity to daunorubicin. These results suggested a potential role of EDAG in chemotherapy of AML and the "escape" of NPMc + protein from EDAG stabilization might contribute to the favorable prognosis of AML with NPMc+.

Li C.-Y.,Beijing Institute of Radiation Medicine | Cao C.-Z.,Beijing Institute of Radiation Medicine | Xu W.-X.,State Key Laboratory of Proteomics | Cao M.-M.,Tianjin University | And 12 more authors.
Gut | Year: 2010

Background: Human hepassocin (HPS) was originally detected by subtractive and differential cDNA cloning as a liver-specific gene that was markedly upregulated during liver regeneration. Previous studies suggested that HPS showed mitogenic activity on isolated hepatocytes in vitro. However, its in vivo functions remained largely unknown. Therefore, the function of recombinant human HPS during liver regeneration and chemically induced liver injury was investigated. Methods: The proliferation of primary hepatocytes was examined by [3H]thymidine incorporation and immunohistological staining of proliferating cell nuclear antigen (PCNA). RNA interference was performed to knock down the endogenous expression of HPS. The proliferation of L02 cells was examined by MTS assay. The phosphorylation of ERK1/2 (extracellular signal-regulated kinase 1/2) was investigated by western blotting analysis. Assessment of liver injury (histology, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels) and of apoptosis, by TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling) assay, was performed. Results: Purified recombinant human HPS showed specific mitogenic activity on primary hepatocytes and normal liver cell lines in a mitogen-activated protein kinase (MAPK)-dependent manner and stimulated the proliferation of hepatocytes in rats with 70% partial hepatectomy. Administration of HPS to rats after D-galactose and carbon tetrachloride (CCl4) treatment protected against liver injury (minimal liver necrosis, depressed ALT and AST levels, and decreased lethality), reduced apoptosis and enhanced proliferation. Knock-down of endogenous HPS in vivo enhanced the liver injury induced by D-galactose by increasing the apoptosis and elevating ALT and AST levels. Conclusions: HPS is a hepatic growth factor which can accelerate hepatocyte proliferation in vivo and protect against liver injury. These data point to the potential interest of HPS in the treatment of fulminant hepatic failure.

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