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Articles by X Zhu
Total Records ( 9 ) for X Zhu
  Q Li , Y Guo , Q Ou , C Cui , W. J Wu , W Tan , X Zhu , L. B Lanceta , S. K Sanganalmath , B Dawn , K Shinmura , G. D Rokosh , S Wang and R. Bolli

Background— Although inducible nitric oxide synthase (iNOS) is known to impart powerful protection against myocardial infarction, the mechanism for this salubrious action remains unclear.

Methods and Results— Adenovirus-mediated iNOS gene transfer in mice resulted 48 to 72 hours later in increased expression not only of iNOS protein but also of heme oxygenase (HO)-1 mRNA and protein; HO-2 protein expression did not change. iNOS gene transfer markedly reduced infarct size in wild-type mice, but this effect was completely abrogated in HO-1–/– mice. At 48 hours after iNOS gene transfer, nuclear factor-B was markedly activated. In transgenic mice with cardiomyocyte-restricted expression of a dominant negative mutant of IB (IBS32A,S36A), both basal HO-1 levels and upregulation of HO-1 by iNOS gene transfer were suppressed. Chromatin immunoprecipitation analysis of mouse hearts provided direct evidence that nuclear factor-B subunits p50 and p65 were recruited to the HO-1 gene promoter (–468 to –459 bp) 48 hours after iNOS gene transfer.

Conclusions— This study demonstrates for the first time the existence of a close functional coupling between cardiac iNOS and cardiac HO-1: iNOS upregulates HO-1 by augmenting nuclear factor-B binding to the region of the HO-1 gene promoter from –468 to –459 bp, and HO-1 then mediates the cardioprotective effects of iNOS. These results also reveal an important role of nuclear factor-B in both basal and iNOS-induced expression of cardiac HO-1. Collectively, the present findings significantly expand our understanding of the regulation of cardiac HO-1 and of the mechanism whereby iNOS exerts its cardioprotective actions.

  X Zhu , Q Song and Z. Jia

A new associative classification algorithm based on weighted voting (ACWV) is presented. ACWV takes advantage of two methods: the optimal rule method preferring high-quality rules and the voting method considering the majority of the rules. Moreover, the method takes into account both the length and convictions of rules to calculate their weights. First, ACWV builds a class-count FP-tree (called CCFP-tree) from the given historical data. After that, the weighted voting result for a new instance can be obtained from the CCFP-tree directly without storing, retrieving and sorting rules explicitly. The label of the class with maximal sum of weighted votes is then that of the new instance. Results of the experiments with 36 data sets selected from the UCI machine learning repository show that the proposed method has its advantages in comparison with previous methods in terms of classification accuracy.

  J Liao , Q Qi , X Zhu , Y Cao and T. Li

IP multimedia subsystem (IMS) is over IP network architecture, but mobile IP cannot directly support session mobility controlled by session initiation protocol-based signaling. The long signaling delay for session reestablishment in application layer always results in session interruptions during the handoff. Therefore, handoff poses a challenge for quality of service (QoS) maintenance in IMS that targets to offer real-time multimedia applications over wireless mobile networks. The existing approaches to solve this problem depend on the advance resource reservation and the optimization of handoff control. Unfortunately, big cost of the advance resource reservation in neighboring domains is a major problem that leads to a serious signaling load and a waste of wireless bandwidth. To solve this issue, we present an enhanced IMS handoff mechanism (EHM) based on user mobility prediction to save network resources by avoiding multiple useless advance reservations. In addition, to support the heterogeneous access networks in IMS domain, EHM evolves a network selective scheme to utilize the network resources more efficiently. The architecture of EHM and the advance QoS negotiation signaling are also presented. We model the cost, the handoff delay and the session blocking probability for EHM and the previous work. Analytical and simulation results show that EHM can enhance the handoff performance, such as reducing resource reservation cost greatly, decreasing session reestablishment delay and making good use of multiple access network resources.

  N Chalhoub , G Zhu , X Zhu and S. J. Baker

Loss of PTEN causes unregulated activation of downstream components of phosphatidylinositol 3-kinase (PI3K) signaling, including PDK1, and disrupts normal nervous system development and homeostasis. We tested the contribution of Pdk1 to the abnormalities induced by Pten deletion in the brain. Conditional deletion of Pdk1 caused microcephaly. Combined deletion of Pdk1 and Pten rescued hypertrophy, but not migration defects of Pten-deficient neurons. Pdk1 inactivation induced strikingly different effects on the regulation of phosphorylated Akt in glia versus neurons. Our results show Pdk1-dependent and Pdk1-independent abnormalities in Pten-deficient brains, and demonstrate cell type specific differences in feedback regulation of the ubiquitous PI3K pathway.

  X Du , Z Chen , W Li , Y Tan , J Lu , X Zhu , T Zhao , G Dong and L. Zeng

The objectives of this study are to establish microsatellite loci for the Mongolian gerbil based on mouse microsatellite DNA sequences and to investigate genetic variation in the laboratory gerbil (Capital Medical University, CMU) and 2 wild gerbil populations (from Yin Chuan city [YIN] and the Hohehot Municipality [HOH]). In total, 536 mouse microsatellite markers were chosen to identify polymorphic dinucleotide repeat loci in the gerbil by cross-amplification. Of these markers, 313 (58.39%) have been discretely amplified from the CMU laboratory gerbil and been sequenced. Of the 313 sequenced markers, 130 were confirmed as simple sequence repeat (SSR) loci in the gerbil. In total, 6 of those newly identified loci plus 6 identified in previous reports were used to estimate the genetic polymorphism for 30 laboratory gerbils and 54 wild gerbils (27 each of the HOH and YIN groups). A total of 29 alleles were observed in the 3 populations, and 11 of 12 loci (91.67%) are polymorphic markers. Nei's standard genetic distances of 0.0592 (CMU vs. HOH) and 0.1033 (CMU vs. YIN) were observed. The averages of observed versus expected heterozygosity are 0.5231/0.4008, 0.5051/0.3882, and 0.4825/0.3665 for the YIN, HOH, and CMU populations, respectively. These results show that cross-amplification using mouse microsatellite primers is an efficient way to identify gerbil SSR loci. By using these 12 selected markers, we have demonstrated that genetic variation level within the CMU population is higher than that has been reported previously and are comparable with the levels found in 2 wild populations.

  X Zhu , S. L Asa and S. Ezzat

Recent genome-wide association studies have identified fibroblast growth factor receptor (FGFR)2 as one of a few candidate genes linked with breast cancer susceptibility. In particular, the disease-predisposing allele of FGFR2 is inherited as a 7.5-kb region within intron 2 that harbors eight single nucleotide polymorphisms. The relationship between these single nucleotide polymorphisms and FGFR2 gene expression remains unclear. Here we show the common occurrence of polymorphisms within the intron 2 region in a panel of 10 breast cancer cell lines. High FGFR2-expressing cell lines such as MCF-7 cells displayed polymorphic sequences with constitutive histone acetylation at multiple intron 2 sequences harboring putative transcription binding sites. Knockdown of Runx2 or CCAAT enhancer binding protein β in these cells resulted in diminished endogenous FGFR2 gene expression. In contrast FGFR2-negative MDA-231 cells were wild type and showed evidence of histone 3/4 deacetylation at the rs2981578, rs10736303, and rs7895676 disease-associated alleles that harbor binding sites for Runx2, estrogen receptor, and CCAAT enhancer binding protein β, respectively. Histone deacetylation inhibition with trichostatin A resulted in enhanced acetylation at these intron 2 sites, an effect associated with robust FGFR2 reexpression. Isoform analysis proved reexpression of the FGFR2-IIIc variant the splicing of which was positively influenced by trichostatin A-mediated recruitment of the Fas-activated serine/threonine phosphoprotein survival protein. Our findings highlight the potential role of histone acetylation in modulating access to selected polymorphic sites within intron 2 as well as downstream splicing sites in generating variable FGFR2 levels and isoforms in breast cancer.

  C Guo , J Li , L Myatt , X Zhu and K. Sun

Cytosolic phospholipase A (cPLA2) catalyzes the formation of arachidonic acid in prostaglandin synthesis. In contrast to the well-described down-regulation of cPLA2, up-regulation of cPLA2 by glucocorticoids has been reported in human amnion fibroblasts, which may play a key role in parturition. The mechanisms underlying this paradoxical induction of cPLA2 by glucocorticoids remain largely unknown. Using cultured human amnion fibroblasts, we found that the induction of cPLA2 by cortisol required ongoing transcription and synthesis of at least one other protein. The induction of cPLA2 by cortisol was abolished by mutagenesis of a glucocorticoid response element (GRE) in the promoter. The same GRE was found mediating the classical inhibition of cPLA2 expression by cortisol in human fetal lung fibroblasts (HFL-1). Cortisol increased Gs expression in amnion fibroblasts but not in HFL-1 cells. Inhibition of Gs with NF449 attenuated the phosphorylation of cAMP response element-binding protein-1 (CREB-1) and the induction of cPLA2 by cortisol in amnion fibroblasts. Both glucocorticoid receptor (GR) and CREB-1 were found bound to the GRE upon cortisol stimulation of amnion fibroblasts. The induction of cPLA2 by cortisol was blocked by GR antagonist RU486 or protein kinase A inhibitor H89 or dominant-negative CREB-1. In conclusion, cortisol activates the cAMP/protein kinase A/CREB-1 pathway via Gs induction, and the phosphorylated CREB-1 interacts with GR at the GRE to promote cPLA2 expression in amnion fibroblasts.

  X Zhu , S Pattathil , K Mazumder , A Brehm , M. G Hahn , S. P Dinesh Kumar and C. P. Joshi

Virus-induced gene silencing (VIGS) is a powerful genetic tool for rapid assessment of plant gene functions in the post-genomic era. Here, we successfully implemented a Tobacco Rattle Virus (TRV)-based VIGS system to study functions of genes involved in either primary or secondary cell wall formation in Nicotiana benthamiana plants. A 3-week post-VIGS time frame is sufficient to observe phenotypic alterations in the anatomical structure of stems and chemical composition of the primary and secondary cell walls. We used cell wall glycan-directed monoclonal antibodies to demonstrate that alteration of cell wall polymer synthesis during the secondary growth phase of VIGS plants has profound effects on the extractability of components from woody stem cell walls. Therefore, TRV-based VIGS together with cell wall component profiling methods provide a high-throughput gene discovery platform for studying plant cell wall formation from a bioenergy perspective.

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