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 Articles by G Xie Total Records ( 4 ) for G Xie
 Phospho-sulindac (OXT-922) inhibits the growth of human colon cancer cell lines: a redox/polyamine-dependent effect L Huang , C Zhu , Y Sun , G Xie , G. G Mackenzie , G Qiao , D Komninou and B. Rigas Non-steroidal anti-inflammatory drugs such as sulindac are promising chemoprevention agents against colon cancer, but their weak potency and side effects limit their use for both chemoprevention and chemotherapy. Here, we evaluated the effect of a new sulindac derivative, phospho-sulindac or OXT-922, on the growth of human cancer cell lines and its mechanism of action. OXT-922 inhibited the growth of human cancer cell lines originating from colon, pancreas and breast ~11- to 30-fold more potently than sulindac. This effect was mediated by a strong cytokinetic effect. Compared with control, OXT-922 inhibited cell proliferation by up to 67%, induced apoptosis 4.1-fold over control and blocked the G1 to S cell cycle phase transition. OXT-922 suppressed the levels of cell cycle regulating proteins, including cyclins D1 and D3 and Cyclin-dependent kinases (CDK) 4 and 6. The levels of intracellular reactive oxygen species (ROS), especially those of mitochondrial $${\hbox{ O }}_{\hbox{ 2 }}^{\bullet -}$$, were markedly elevated (5.5-fold) in response to OXT-922. ROS collapsed the mitochondrial membrane potential and triggered apoptosis, which was largely abrogated by antioxidants. OXT-922 suppressed nuclear factor-kappaB activation and downregulated thioredoxin-1 expression. It also suppressed the production of prostaglandin E2 and decreased cyclooxygenase-1 expression. Similar to sulindac, OXT-922 enhanced spermidine/spermine N1-acetyltransferase activity, reduced the cellular polyamine content and synergized with difluoromethylornithine to inhibit cancer cell proliferation and induce apoptosis. Our results suggest that OXT-922 possesses promising anticancer properties and deserves further evaluation.
 Complete genome of the cellulolytic thermophile Acidothermus cellulolyticus 11B provides insights into its ecophysiological and evolutionary adaptations R. D Barabote , G Xie , D. H Leu , P Normand , A Necsulea , V Daubin , C Medigue , W. S Adney , X. C Xu , A Lapidus , R. E Parales , C Detter , P Pujic , D Bruce , C Lavire , J. F Challacombe , T. S Brettin and A. M. Berry We present here the complete 2.4-Mb genome of the cellulolytic actinobacterial thermophile Acidothermus cellulolyticus 11B. New secreted glycoside hydrolases and carbohydrate esterases were identified in the genome, revealing a diverse biomass-degrading enzyme repertoire far greater than previously characterized and elevating the industrial value of this organism. A sizable fraction of these hydrolytic enzymes break down plant cell walls, and the remaining either degrade components in fungal cell walls or metabolize storage carbohydrates such as glycogen and trehalose, implicating the relative importance of these different carbon sources. Several of the A. cellulolyticus secreted cellulolytic and xylanolytic enzymes are fused to multiple tandemly arranged carbohydrate binding modules (CBM), from families 2 and 3. For the most part, thermophilic patterns in the genome and proteome of A. cellulolyticus were weak, which may be reflective of the recent evolutionary history of A. cellulolyticus since its divergence from its closest phylogenetic neighbor Frankia, a mesophilic plant endosymbiont and soil dweller. However, ribosomal proteins and noncoding RNAs (rRNA and tRNAs) in A. cellulolyticus showed thermophilic traits suggesting the importance of adaptation of cellular translational machinery to environmental temperature. Elevated occurrence of IVYWREL amino acids in A. cellulolyticus orthologs compared to mesophiles and inverse preferences for G and A at the first and third codon positions also point to its ongoing thermoadaptation. Additional interesting features in the genome of this cellulolytic, hot-springs-dwelling prokaryote include a low occurrence of pseudogenes or mobile genetic elements, an unexpected complement of flagellar genes, and the presence of three laterally acquired genomic islands of likely ecophysiological value.
 Smoothness equivalence properties of interpolatory Lie group subdivision schemes G Xie and T. P. Y. Yu We prove that any interpolatory Lie group subdivision scheme based on combining a linear interpolatory subdivision scheme with the log– exp adaption to Lie-group-valued data in Ur Rahman et al. (2005, Multiscale Model. Simul., 4, 1201–1232) produces parameterized curves on the Lie group that are as smooth as the smoothness of —no matter how smooth is. We present both an extrinsic proof and an intrinsic proof. We discuss two variations of our main result. (i) We illustrate how smoothness equivalence can break down in a variant of the original log– exp scheme. (ii) We show that the main result of this paper can be easily extended to a multivariate setting.
 Performance of Pediatric Risk of Mortality, Pediatric Index of Mortality and PIM2 in term Chinese neonates C Wang , G Xie , B Cheng , L Du , L Shi , L Tan , Q Shu and X. Fang Pediatric Risk of Mortality (PRISM), Pediatric Index of Mortality (PIM) and PIM2 could be applicable to the subset of term neonates has not been well investigated. The purpose of this study is to access and compare the performance of these scoring systems in predicting mortality probability in term Chinese neonates with critical illness. PRISM, PIM and PIM2 scores were calculated prospectively during a 1-year period on 243 neonates admitted to the neonatal intensive care unit (NICU) in the Children’s Hospital of Zhejiang University in China. Of these, 36 neonates (14.81%) died in the NICU, while the mortality rates estimated by PRISM, PIM and PIM2 were 16.19, 14.58 and 11.12%, respectively. The area under the receiver-operating characteristic (ROC) curve [95% confidence intervals (CIs)] were 0.834 (0.767–0.902), 0.851 (0.786–0.916) and 0.854 (0.790–0.918) for PRISM, PIM and PIM2, respectively. The Hosmer–Lemeshow test gave a chi-square of 1.35 (p = 0.930) for PRISM, 1.03 (p = 0.960) for PIM and 4.58 (p = 0.469) for PIM2. The standardized mortality rates (SMRs) (95% CI) using PRISM, PIM and PIM2 were 0.92 (0.79–1.08), 1.02 (0.88–1.20) and 1.33 (1.13–1.62), respectively. Although PRISM, PIM and PIM2 have displayed good discrimination and calibration in the present setting, PIM is considered as the most accurate and appropriate tool for predicting mortality in the studied NICU.