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Articles by Y Zhu
Total Records ( 14 ) for Y Zhu
  H Jiang , Y Zhu , H Xu , Y Sun and Q. Li
 

Accumulating data suggested that hypoxia inducible factor (HIF)-1 plays an important role in the evolution and propagation of the inflammatory process. To characterize the activation of HIF-1 in rats with chronic obstructive pulmonary disease (COPD) and examine the possible role of nuclear factor (NF)-B in this process, rats were challenged by introtracheal instillation of lipopolysaccharide (LPS) and exposure to cigarette smoke. Pyrrolidine dithiocarbamate (PDTC) was administered via the oral route 1 h before LPS or cigarettes administration. Four weeks later, pulmonary function and histology were tested; bronchoalveolar lavage fluid (BALF) and arterial blood gases were assayed. Activation of pulmonary NF-B was assessed by quantitative PCR, immunoblot analysis, and electrophoretic mobility shift assay, respectively. Results showed that LPS and smog induced the characteristics of COPD seen in human. PDTC alleviated the development of COPD and the levels of cytokines in BALF of PDTC+COPD group were significantly decreased compared with that of COPD group. The activation of pulmonary NF-B was inhibited by PDTC and the accumulation of HIF-1 gene expression in the COPD group was attenuated by PDTC pretreatment. Furthermore, the mRNA levels of HIF-1 target genes heme oxygenase-1 (HO-1) and vascular endothelial growth factor (VEGF) were parallel to the attenuation of HIF-1 by PDTC. These findings indicated that the activation of HIF-1 pathway via NF-B contributes to the development of COPD, and administration of NF-B inhibitor may attenuate the development of COPD.

  C. M Canuso , B Dirks , J Carothers , C Kosik Gonzalez , C. A Bossie , Y Zhu , C. V Damaraju , A. H Kalali and R. Mahmoud
 

OBJECTIVE: The authors compared paliperidone extended-release and quetiapine in patients with recently exacerbated schizophrenia requiring hospitalization. METHOD: In a 6-week double-blind study, inpatients with a recent exacerbation of schizophrenia were randomly assigned to treatment with paliperidone extended-release, quetiapine, or placebo. A 2-week monotherapy phase was followed by a 4-week additive-therapy phase. Target doses were at the upper end of recommended ranges: paliperidone extended-release, 9 or 12 mg/day, and quetiapine, 600 or 800 mg/day. The primary endpoint was the difference in mean total change score on the Positive and Negative Syndrome Scale (PANSS) between paliperidone extended-release and quetiapine at the 2-week monotherapy phase endpoint. RESULTS: Six-week completion rates were 77.5% (124/160) with paliperidone extended-release, 66.7% (106/159) quetiapine, and 63.8% (51/80) placebo. Improvement in mean PANSS total change score was greater with paliperidone extended-release than with quetiapine from day 5 (–11.4 versus –8.2) through the monotherapy phase endpoint (–23.4 versus –17.1). Only paliperidone extended-release showed significantly greater PANSS improvement compared with placebo at 2 weeks. At the 6-week study endpoint, there was a significantly greater improvement with paliperidone extended-release compared with quetiapine despite similar use of additive therapy (predominantly other antipsychotics). Common adverse events with paliperidone extended-release, quetiapine, and placebo, respectively, were tremor (13.9%, 5.0%, 7.5%), somnolence (8.9%, 11.9%, 1.3%), insomnia (10.1%, 9.4%, 11.3%), and headache (12.0%, 7.5%, 13.8%). Six-week adverse event-related discontinuation rates were 6.3%, 10.1%, and 6.3%, respectively, in the paliperidone extended-release, quetiapine, and placebo groups. CONCLUSIONS: Compared with quetiapine, paliperidone extended-release improved symptoms earlier and to a greater degree in patients with recently exacerbated schizophrenia requiring hospitalization, with no unexpected tolerability findings.

  S Yao , S Wang , Y Zhu , L Luo , G Zhu , S Flies , H Xu , W Ruff , M Broadwater , I. H Choi , K Tamada and L. Chen
 

Programmed death one (PD-1) is an inducible molecule belonging to the immunoglobulin superfamily. It is expressed on activated T and B lymphocytes and plays pivotal roles in the negative regulation of adaptive immune responses. We report here an unexpected finding: that PD-1 could also be induced on splenic dendritic cells (DCs) by various inflammatory stimuli. Adoptive transfer of PD-1–deficient DCs demonstrates their superior capacity to wild-type DCs in innate protection of mice against lethal infection by Listeria monocytogenes. Furthermore, PD-1–deficient mice are also more resistant to the infection than wild-type controls, even in the absence of T and B cells, accompanied by elevated production of DC-derived interleukin-12 and tumor necrosis factor-. Our results reveal a novel role of PD-1 in the negative regulation of DC function during innate immune response.

  S. L Zheng , V. L Stevens , F Wiklund , S. D Isaacs , J Sun , S Smith , K Pruett , K. E Wiley , S. T Kim , Y Zhu , Z Zhang , F. C Hsu , A. R Turner , J. E Johansson , W Liu , J. W Kim , B. L Chang , D Duggan , J Carpten , C Rodriguez , W Isaacs , H Gronberg and J. Xu
 

Single nucleotide polymorphisms (SNP) at 11q13 were recently implicated in prostate cancer risk by two genome-wide association studies and were consistently replicated in multiple study populations. To explore prostate cancer association in the regions flanking these SNPs, we genotyped 31 tagging SNPs in a ~110 kb region at 11q13 in a Swedish case-control study (Cancer of the Prostate in Sweden), including 2,899 cases and 1,722 controls. We found evidence of prostate cancer association for the previously implicated SNPs including rs10896449, which we termed locus 1. In addition, multiple SNPs on the centromeric side of the region, including rs12418451, were also significantly associated with prostate cancer risk (termed locus 2). The two groups of SNPs were separated by a recombination hotspot. We then evaluated these two representative SNPs in an additional ~4,000 cases and ~3,000 controls from three study populations and confirmed both loci at 11q13. In the combined allelic test of all four populations, P = 4.0 x 10–11 for rs10896449 at locus 1 and P = 1.2 x 10–6 for rs12418451 at locus 2, and both remained significant after adjusting for the other locus and study population. The prostate cancer association at these two 11q13 loci was unlikely confounded by prostate-specific antigen (PSA) detection bias because neither SNP was associated with PSA levels in controls. Unlike locus 1, in which no known gene is located, several putative mRNAs are in close proximity to locus 2. Additional confirmation studies at locus 2 and functional studies for both loci are needed to advance our knowledge on the etiology of prostate cancer. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1815–20)

  J Zhou , Y Zhu , M Cheng , D Dinesh , T Thorne , K. K Poh , D Liu , C Botros , Y. L Tang , N Reisdorph , R Kishore , D. W Losordo and G. Qin
 

Background— Recent studies have identified a polymorphism in the endothelin-converting enzyme (ECE)–1b promoter (–338C/A) that is strongly associated with hypertension in women. The polymorphism is located in a consensus binding sequence for the E2F family of transcription factors. E2F proteins are crucially involved in cell-cycle regulation, but their roles in cardiovascular function are poorly understood. Here, we investigated the potential role of E2F2 in blood pressure regulation.

Methods and Results— Tail-cuff measurements of systolic and diastolic blood pressures were significantly higher in E2F2-null (E2F2–/–) mice than in their wild-type littermates, and in ex vivo ring assays, aortas from the E2F2–/– mice exhibited significantly greater contractility in response to big endothelin-1. Big endothelin-1 is activated by ECE-1, and mRNA levels of ECE-1b, the repressive ECE-1 isoform, were significantly lower in E2F2–/– mice than in wild-type mice. In endothelial cells, chromatin immunoprecipitation assays confirmed that E2F2 binds the ECE-1b promoter, and promoter-reporter assays indicated that E2F2 activates ECE-1b transcription. Furthermore, loss or downregulation of E2F2 led to a decline in ECE-1b levels, to higher levels of the membranous ECE-1 isoforms (ie, ECE-1a, -1c, and -1d), and to deregulated ECE-1 activity. Finally, Sam68 coimmunoprecipitated with E2F2, occupied the ECE-1b promoter (chromatin immunoprecipitation), and repressed E2F2-mediated ECE-1b promoter activity (promoter-reporter assays).

Conclusion— Our results identify a cell-cycle–independent mechanism by which E2F2 regulates endothelial function, arterial contractility, and blood pressure.

  C Hidalgo , B Hudson , J Bogomolovas , Y Zhu , B Anderson , M Greaser , S Labeit and H. Granzier
 

Rationale: Protein kinase C (PKC) regulates contractility of cardiac muscle cells by phosphorylating thin- and thick- filament-based proteins. Myocardial sarcomeres also contain a third myofilament, titin, and it is unknown whether titin can be phosphorylated by PKC and whether it affects passive tension.

Objective: The purpose of this study was to examine the effect of PKC on titin phosphorylation and titin-based passive tension.

Methods and Results: Phosphorylation assays with PKC revealed that titin is phosphorylated in skinned myocardial tissues; this effect is exacerbated by pretreating with protein phosphatase 1. In vitro phosphorylation of recombinant protein representing titin’s spring elements showed that PKC targets the proline – glutamate – valine – lysine (PEVK) spring element. Furthermore, mass spectrometry in combination with site-directed mutagenesis identified 2 highly conserved sites in the PEVK region that are phosphorylated by PKC (S11878 and S12022); when these 2 sites are mutated to alanine, phosphorylation is effectively abolished. Mechanical experiments with skinned left ventricular myocardium revealed that PKC significantly increases titin-based passive tension, an effect that is reversed by protein phosphatase 1. Single molecule force-extension curves show that PKC decreases the PEVK persistence length (from 1.20 nm to 0.55 nm), without altering the contour length, and using a serially-linked wormlike chain model we show that this increases titin-based passive force with a sarcomere length dependence that is similar to that measured in skinned myocardium after PKC phosphorylation.

Conclusions: PKC phosphorylation of titin is a novel and conserved pathway that links myocardial signaling and myocardial stiffness.

  L Wang , J Zheng , Y Du , Y Huang , J Li , B Liu , C. j Liu , Y Zhu , Y Gao , Q Xu , W Kong and X. Wang
 

Rational: Vascular smooth muscle cells (VSMCs) switching from a contractile/differentiated to a synthetic/dedifferentiated phenotype has an essential role in atherosclerosis, postangioplastic restenosis and hypertension. However, how normal VSMCs maintain the differentiated state is less understood.

Objective: We aimed to indentify the effect of cartilage oligomeric matrix protein (COMP), a normal vascular extracellular matrix, on modulation of VSMCs phenotype.

Methods and Results: We demonstrated that COMP was associated positively with the expression of VSMC differentiation marker genes during phenotype transition. Knockdown of COMP by small interfering (si)RNA favored dedifferentiation. Conversely, adenoviral overexpression of COMP markedly suppressed platelet-derived growth factor-BB-elicited VSMC dedifferentiation, characterized by altered VSMC morphology, actin fiber organization, focal adhesion assembly, and the expression of phenotype-dependent markers. Whereas 7 integrin coimmunoprecipitated with COMP in normal rat VSMCs and vessels, neutralizing antibody or siRNA against 7 integrin inhibited VSMC adhesion to COMP, which indicated that 7β1 integrin is a potential receptor for COMP. As well, blocking or interference by siRNA of 7 integrin completely abolished the effect of COMP on conserving the contractile phenotype. In accordance, ectopic adenoviral overexpression of COMP greatly retarded VSMC phenotype switching, rescued contractility of carotid artery ring, and inhibited neointima formation in balloon-injured rats.

Conclusions: Our data suggest that COMP is essential for maintaining a VSMC contractile phenotype and the protective effects of COMP are mainly mediated through interaction with 7β1 integrin. Investigations to identify the factors affecting the expression and integrity of COMP may provide a novel therapeutic target for vascular disorders.

  L Xia , Y Zhu , J Yang , J Ye and Z. Gu
 

As power dissipation causes thermal issues in cooling costs, lifetime and reliability, thermal management has become an important issue in today's OS and processor design. Early OS-level thermal management schemes were proposed and evaluated mainly with simulators or analytical models. In this paper, we implement a thermal-aware round-robin scheduling algorithm in the Linux kernel, and compare its performance with the ‘Heat-and-Run’ algorithm and the default Linux baseline scheduler on an Intel Core 2 Duo processor using representative benchmarks from SPEC2000, MiBench and NetBench. Our results indicate that the current Linux scheduler can easily be enhanced with thermal-awareness to show improved performance in terms of both the on-chip temperature condition and application throughput.

  O Wurtzel , R Sapra , F Chen , Y Zhu , B. A Simmons and R. Sorek
 

Organisms of the third domain of life, the Archaea, share molecular characteristics both with Bacteria and Eukarya. These organisms attract scientific attention as research models for regulation and evolution of processes such as transcription, translation, and RNA processing. We have reconstructed the primary transcriptome of Sulfolobus solfataricus P2, one of the most widely studied model archaeal organisms. Analysis of 625 million bases of sequenced cDNAs yielded a single-base-pair resolution map of transcription start sites and operon structures for more than 1000 transcriptional units. The analysis led to the discovery of 310 expressed noncoding RNAs, with an extensive expression of overlapping cis-antisense transcripts to a level unprecedented in any bacteria or archaea but resembling that of eukaryotes. As opposed to bacterial transcripts, most Sulfolobus transcripts completely lack 5'-UTR sequences, suggesting that mRNA/ncRNA interactions differ between Bacteria and Archaea. The data also reveal internal hotspots for transcript cleavage linked to RNA degradation and predict sequence motifs that promote RNA destabilization. This study highlights transcriptome sequencing as a key tool for understanding the mechanisms and extent of RNA-based regulation in Bacteria and Archaea.

  J Karman , J. L Tedstone , N. K Gumlaw , Y Zhu , N Yew , C Siegel , S Guo , A Siwkowski , M Ruzek , C Jiang and S. H. Cheng
 

Lipid rafts reportedly play an important role in modulating the activation of mast cells and granulocytes, the primary effector cells of airway hyperresponsiveness and asthma. Activation is mediated through resident signaling molecules whose activity, in part, may be modulated by the composition of glycosphingolipids (GSLs) in membrane rafts. In this study, we evaluated the impact of inhibiting GSL biosynthesis in mast cells and in the ovalbumin (OVA)-induced mouse model of asthma using either a small molecule inhibitor or anti-sense oligonucleotides (ASOs) directed against specific enzymes in the GSL pathway. Lowering GSL levels in mast cells through inhibition of glucosylceramide synthase (GCS) reduced phosphorylation of Syk tyrosine kinase and phospholipase C gamma 2 (PLC-2) as well as cytoplasmic Ca2+ levels. Modulating these intracellular signaling events also resulted in a significant decrease in mast cell degranulation. Primary mast cells isolated from a GM3 synthase (GM3S) knockout mouse exhibited suppressed activation-induced degranulation activity further supporting a role of GSLs in this process. In previously OVA-sensitized mice, intra-nasal administration of ASOs to GCS, GM3S or lactosylceramide synthase (LCS) significantly suppressed metacholine-induced airway hyperresponsiveness and pulmonary inflammation to a subsequent local challenge with OVA. However, administration of the ASOs into mice that had been sensitized and locally challenged with the allergen did not abate the consequent pulmonary inflammatory sequelae. These results suggest that GSLs contribute to the initiation phase of the pathogenesis of airway hyperreactivity and asthma and lowering GSL levels may offer a novel strategy to modulate these manifestations.

  Y Zhu and K. Jarausch
  No Description
  M Okuda , M Takeguchi , O O Ruairc , M Tagaya , Y Zhu , A Hashimoto , N Hanagata , W Schmitt and T. Ikoma
 

Magnetic nanoparticle (MNP) composites with a magnetite (Fe3O4) core and a hydroxyapatite (HAp, Ca10(PO4)6(OH)2) coating were prepared using a precipitation method and a subsequent hydrothermal treatment. The hydrothermal treatment diminished the lepidocrocite layer on the magnetite, enhanced the crystal growth of HAp and dissolved the MNPs. The divalent iron ions dissolved into solvent were not substituted for the HAp lattice. The three-dimensional (3D) nanostructure, the crystal morphology of HAp covered with the MNPs and the interfacial nanostructure of magnetite/HAp were analyzed using an energy-filter transmission electron microscopy (EF-TEM) and visualized by computer tomography in transmission electron microscopy (TEM). EF-TEM and 3D reconstruction images using a tilted series of high-angle annular dark-field images showed that the needlelike HAp nanocrystals covered with a magnetite core and the crystal growth of HAp attached to the magnetite surface was inhibited as a result of the lower density of the nucleation site of the lepidocrocite layer. The dissolution of iron ion from MNPs and the interfacial interaction of HAp and magnetite could cause the needlelike morphology of HAp nanocrystals.

  C Jiang , H Zhang , W Zhang , W Kong , Y Zhu , Q Xu , Y Li and X. Wang
 

Adipokines may represent a mechanism linking insulin resistance to cardiovascular disease. We showed previously that homocysteine (Hcy), an independent risk factor for cardiovascular disease, can induce the expression and secretion of resistin, a novel adipokine, in vivo and in vitro. Since vascular smooth muscle cell (VSMC) migration is a key event in vascular disease, we hypothesized that adipocyte-derived resistin is involved in Hcy-induced VSMC migration. To confirm our hypothesis, Sprague-Dawley rat aortic SMCs were cocultured with Hcy-stimulated primary rat epididymal adipocytes or treated directly with increasing concentrations of resistin for up to 24 h. Migration of VSMCs was investigated. Cytoskeletal structure and cytoskeleton-related proteins were also detected. The results showed that Hcy (300–500 µM) increased migration significantly in VSMCs cocultured with adipocytes but not in VSMC cultured alone. Resistin alone also significantly increased VSMC migration in a time- and concentration-dependent manner. Resistin small interfering RNA (siRNA) significantly attenuated VSMC migration in the coculture system, which indicated that adipocyte-derived resistin mediates Hcy-induced VSMC migration. On cell spreading assay, resistin induced the formation of focal adhesions near the plasma membrane, which suggests cytoskeletal rearrangement via an 5β1-integrin-focal adhesion kinase/paxillin-Ras-related C3 botulinum toxin substrate 1 (Rac1) pathway. Our data demonstrate that Hcy promotes VSMC migration through a paracrine or endocrine effect of adipocyte-derived resistin, which provides further evidence of the adipose-vascular interaction in metabolic disorders. The migratory action exerted by resistin on VSMCs may account in part for the increased incidence of restenosis in diabetic patients.

 
 
 
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