Ping Xu

Shanghai Jiao Tong University, Shanghai, Shanghai Shi, China

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Publications (77)126.4 Total impact

  • Ping Xu · Xiao-Li Lou · Cheng Chen
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    ABSTRACT: Objective: The objective of this study was to determine the mechanism by which activation of peroxisome proliferator-activated receptor-γ promotes apoptosis of acinar cells in pancreatitis. Methods: AR42j cells pretreated with the peroxisome proliferator-activated receptor-γ agonist pioglitazone were activated by cerulein as an in vitro model of acute pancreatitis. Inflammatory cytokines and amylase were detected by enzyme-linked immunosorbent assay. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Cell apoptosis was measured by flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining. Activity of caspases was determined. Bax and Bcl-2 levels were assayed by Western blot. Results: Cytokines, amylase, and cellular proliferation decreased in pioglitazone-pretreated cells. Pioglitazone increased the activity of caspases 3, 8, and 9 in cerulein-activated AR42j cells as well as in the pancreas of rats 3 hours after induction of severe acute pancreatitis. Acinar cell apoptosis was induced by reducing the mitochondrial membrane potential in the pioglitazone group. Pioglitazone increased expression of proapoptotic Bax proteins and decreased antiapoptotic Bcl-2 in cerulein-induced AR42j cells and decreased Bcl-2 levels in pancreatic tissue of severe acute pancreatitis rats 1 and 3 hours after induction. Conclusion: Pioglitazone may promote apoptosis of acinar cells through both intrinsic and extrinsic apoptotic pathways in acute pancreatitis.This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially.
    No preview · Article · Oct 2015 · Pancreas
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    ABSTRACT: Severe acute pancreatitis (SAP) is an acute abdominal disease with the strong systemic inflammatory response, and rapidly progresses from a local pancreatic damage into multiple organ dysfunction. For many decades, the contributions of neutrophils to the pathology of SAP were traditionally thought to be the chemokine and cytokine cascades that accompany inflammation. In this review, we focus mainly on those recently recognized aspects of neutrophils in SAP processes. First, emerging evidence suggests that therapeutic interventions targeting neutrophils significantly lower tissue damage and protect against the occurrence of pancreatitis. Second, trypsin activation promotes the initial neutrophils recruitment into local pancreas, and subsequently neutrophils infiltration in turn triggers trypsin production. Finally, neutrophils have the unique ability to release neutrophil extracellular traps even in the absence of pathogens. © 2015 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
    Preview · Article · Aug 2015 · Journal of Cellular and Molecular Medicine
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    ABSTRACT: Gastric cancer is the second most common cause of cancer-related death partially because of its aggressive metastasis and the fact that it is often diagnosed at an advanced stage. Recent studies have shown that long noncoding RNAs (lncRNAs) play critical roles in multiple biological processes including oncogenesis. In the present study, we found for the first time that the lncRNA ZMAT1 transcript variant 2 is downregulated in gastric cancer tissues compared with adjacent normal tissues (P < 0.001). The expression of ZMAT1 transcript variant 2 was inversely correlated with lymph node metastasis (P < 0.05), depth of tumor invasion and tumor node metastasis stage (P < 0.05). Univariate and multivariate analyses showed that ZMAT1 transcript variant 2 expression was an independent predictor for overall survival (P < 0.05). Our study suggests that ZMAT1 transcript variant 2 is a potential diagnostic factor in patients with gastric cancer.
    No preview · Article · Jul 2015 · International journal of clinical and experimental pathology
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    ABSTRACT: To investigate the changes in the amount and ultrastructure of interstitial cells of Cajal (ICC) in rats with severe acute pancreatitis (SAP) and their importance. A modified Aho method was employed to establish a SAP rat model. Laser scanning confocal immunofluorescence microscopy was employed to detect the amount of ICC, and transmission electron microscopy was employed for observation of ultrastructure of ICC and nerve-ICC-smooth muscle network. The amount of ICC reduced, the intercellular space of ICC was enlarged, cell processes reduced or were absent, cell morphology was irregular, and ICC had unclear borderline, reduced organelles, impaired organelles, nuclear shrinkage and deformation. The junctions between ICC and between ICC and smooth muscle cell/nerve reduced, and the network-like structure was disrupted. In SAP, ICC reduces, with disrupted ultrastructure, and the integrity of network among intestinal nerve, ICC and smooth muscle is impaired, both of which may affect the intestinal functions.
    No preview · Article · Jul 2015 · International Journal of Clinical and Experimental Medicine
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    ABSTRACT: The receptor for advanced glycation end-products (RAGE) gene expresses two major alternative splicing isoforms, full-length membrane-bound RAGE (mRAGE) and secretory RAGE (esRAGE). Both isoforms play important roles in Alzheimer's disease (AD) pathogenesis, either via interaction of mRAGE with β-amyloid peptide (Aβ) or inhibition of the mRAGE-activated signaling pathway. In the present study, we showed that heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) and Transformer2β- 1 (Tra2β-1) were involved in the alternative splicing of mRAGE and esRAGE. Functionally, two factors had an antagonistic effect on the regulation. Glucose deprivation induced an increased ratio of mRAGE/esRAGE via up-regulation of hnRNP A1 and down-regulation of Tra2β-1. Moreover, the ratios of mRAGE/esRAGE and hnRNP A1/Tra2β-1 were increased in peripheral blood mononuclear cells (PBMCs) from AD patients. The results provide a molecular basis for altered splicing of mRAGE and esRAGE in AD pathogenesis. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    No preview · Article · Feb 2015 · Journal of Neurochemistry
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    ABSTRACT: This study focuses on the function of NSSR1, a splicing factor, in neuronal injury in the ischemic mouse brain using the transient global cerebral ischemic mouse model and the cultured cells treated with oxygen-glucose deprivation (OGD). The results showed that the cerebral ischemia triggers the expression of NSSR1 in hippocampal astrocytes, predominantly the dephosphorylated NSSR1 proteins, and the Exon3 inclusive NCAM-L1 variant and the Exon4 inclusive CREB variant. While in the hippocampus of astrocyte-specific NSSR1 conditional knockdown (cKD) mice, where cerebral ischemia no longer triggers NSSR1 expression in astrocytes, the expression of Exon3 inclusive NCAM-L1 variant and Exon4 inclusive CREB variant were no longer triggered as well. In addition, the injury of hippocampal neurons was more severe in astrocyte-specific NSSR1 cKD mice compared with in wild-type mice after brain ischemia. Of note, the culture media harvested from the astrocytes with overexpression of NSSR1 or the Exon3 inclusive NCAM-L1 variant, or Exon4 inclusive CREB variant were all able to reduce the neuronal injury induced by OGD. The results provide the evidence demonstrating that: (1) Splicing factor NSSR1 is a new factor involved in reducing ischemic injury. (2) Ischemia induces NSSR1 expression in astrocytes, not in neurons. (3) NSSR1-mediated pathway in astrocytes is required for reducing ischemic neuronal injury. (4) NCAM-L1 and CREB are probably mediators in NSSR1-mediated pathway. In conclusion, our results suggest for the first time that NSSR1 may provide a novel mechanism for reducing neuronal injury after ischemia, probably through regulation on alternative splicing of NCAM-L1 and CREB in astrocytes. GLIA 2015
    No preview · Article · Jan 2015 · Glia
  • Min Liu · Meiwan Chen · Ping Xu · Zhiwen Yang
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    ABSTRACT: Cubosomes are formed by amphiphilic molecules, with the bicontinuous contortions of inter-connecting hydrophilic and hydrophobic domains. The inner cubic-phase structure of cubosomes makes it an attractive drug-delivery system in pharmaceutical applications. This review mainly describes the potential applications of cubosomes as a drug delivery system for oral administration, highlights the mechanisms involved in the transcellular transport and digestive process, challenges involved in formulation development and evaluations of the in vivo and in vitro study. As pointed out throughout this review, a number of critical points on cubosome products need to be solved in order to attain practical applications.
    No preview · Article · Jan 2015 · Current Pharmaceutical Biotechnology
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    ABSTRACT: The oral administration of amphotericin B (AmB) has a major drawback of poor bioavailability. The aim of this study was to investigate the potential of glyceryl monoolein (GMO) cubosomes as lipid nanocarriers to improve the oral efficacy of AmB. Antifungal efficacy was determined in vivo in rats after oral administration, to investigate its therapeutic use. The human colon adenocarcinoma cell line (Caco-2) was used in vitro to evaluate transport across a model of the intestinal barrier. In vivo antifungal results showed that AmB, loaded in GMO cubosomes, could significantly enhance oral efficacy, compared against Fungizone®, and that during a 2 day course of dosage 10 mg/kg the drug reached effective therapeutic concentrations in renal tissue for treating fungal infections. In the Caco-2 transport studies, GMO cubosomes resulted in a significantly larger amount of AmB being transported into Caco-2 cells, via both clathrin- and caveolae-mediated endocytosis, but not macropinocytosis. These results suggest that GMO cubosomes, as lipid nanovectors, could facilitate the oral delivery of AmB.
    Preview · Article · Jan 2014 · International Journal of Nanomedicine
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    ABSTRACT: The phosphatidylinositol 3-kinase(PI3K)/protein kinase B (Akt) pathway plays a key role in inflammation. However, the regulatory roles of PI3K/Akt in severe acute pancreatitis (SAP) have not been elucidated. The aim of this study was to investigate the impact of wortmannin, a PI3K/Akt inhibitor, on SAP rats through exposure to sodium taurocholate (STC) after 3 h and 6 h. The SAP group was found to have a significant increase in pancreas Akt expression, along with the activation of serum amylase, TNF-α, IL-1β, and IL-6, and pancreas histological aggravation. The administration of wortmannin in SAP rats reduced Akt expression, attenuated the level of serum amylase and inflammation factor, and alleviated the damage of pancreatic tissue. Furthermore, the administration of wortmannin led to an obvious reduction in NF-κB and p38MAPK expression in SAP rats. These findings showed that the PI3K/Akt inhibitor wortmannin decreases inflammatory cytokines in SAP rats and suggests its regulatory mechanisms may occur through the suppression on NF-κB and p38MAPK activity.
    Preview · Article · Nov 2013 · PLoS ONE

  • No preview · Article · Nov 2013 · Academic Journal of Second Military Medical University
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    ABSTRACT: To investigate the effects and mechanisms of peroxisome proliferator-activated receptor-γ (PPAR-γ) activation on the induction of apoptosis in rats with acute pancreatitis. Severe acute pancreatitis (SAP) and mild acute pancreatitis (MAP) were induced and pre-treated with pioglitazone, which is a ligand of PPAR-γ. The expression of inflammatory factors (TNF-α and IL6) of the pancreas was detected by ELISA. The apoptosis in pancreas were detected by TUNEL assay and the activity of caspase 3 was determined. Phosphorylation of p65 in pancreas of SAP or MAP was determined by western-blot. Expression levels of PPAR-γ proteins were elevated in the pancreases of SAP or MAP rats pre-injected with pioglitazone intraperitoneally. Downregulation of the expression TNF-α and IL6 and relief of pathological changes in the pancreas suggested that pioglitazone had protective effects on acute panceatitis. In pioglitazone pre-treated groups, a TUNEL assay indicated a high level of apoptosis in SAP but little apoptosis in MAP, showing pioglitazone could promote taurocholate-induced apoptosis but inhibit ceruleininduced apoptosis in pancraeatic aniniar cells. Furthermore, caspase 3 activity was high in SAP but low in MAP, implying that the apoptotic mechanism in pancreatic acinar cells of AP rats was correlated with caspase 3 activity. Phosphorylation of p65 was reduced in SAP or MAP group pretreated with pioglitazone, indicating that pioglitazone reduced the inflammation reaction by inhibiting the activation of the NF-κB. These results indicated that activation of PPAR-γ induced apoptosis in pancreatic acinar cells of SAP rats but inhibited apoptosis in pancraeatic acinar cells of MAP rats, which demonstrated that PPAR-γ may be an efficiently therapeutic target in pancreatic inflammation.
    No preview · Article · Nov 2013 · Digestive Diseases and Sciences
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    ABSTRACT: Regulator of G protein signaling 4 (RGS4) is a critical modulator of G protein-coupled receptor (GPCR)-mediated signaling and plays important roles in many neural process and diseases. Particularly, drug-induced alteration in RGS4 protein levels is associated with acute and chronic effects of drugs of abuse. However, the precise mechanism underlying the regulation of RGS4 expression is largely unknown. Here, we demonstrated that the expression of RGS4 gene was subject to regulation by alternative splicing of the exon 6. Transformer-2β (Tra2β), an important splicing factor, bound to RGS4 mRNA and increased the relative level of RGS4-1 mRNA isoform by enhancing the inclusion of exon 6. Meanwhile, Tra2β increased the expression of full-length RGS4 protein. In rat brain, Tra2β was co-localized with RGS4 in multiple opioid action-related brain regions. In addition, the acute and chronic morphine treatment induced alteration in the expression level of Tra2β in rat locus coerulus (LC) in parallel to that of RGS4 proteins. It suggests that induction of this splicing factor may contribute to the change of RGS4 level elicited by morphine. Taken together, the results provide the evidence demonstrating the function of Tra2β as a new mediator in opioid-induced signaling pathway via regulating RGS4 expression.
    Preview · Article · Aug 2013 · PLoS ONE
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    ABSTRACT: Hepatitis B virus (HBV) infection is a global public health problem, because patients with chronic hepatitis B (CHB) may progress to liver cirrhosis and eventually evolve into hepatocellular carcinoma. Decoy receptor 3 (DcR3) is a soluble receptor of the tumor necrosis factor receptor superfamily, and has been implicated in anti-apoptotic and anti-inflammatory pathways. In this study, we explored the clinical value of serum DcR3 in predicting the active status of CHB in hepatitis B e antigen-negative patients (active HBeAg (-) CHB), which was determined with ELISA. The serum level of DcR3 in active HBeAg (-) CHB patients (1.92 ± 0.68 ng/ml) was higher than that in healthy controls (0.80 ± 0.25 ng/ml, p < 0.0001) and that in inactive status of HBeAg (-) CHB (inactive hepatitis B surface antigen carrier, HBsAg-IaC) patients (0.95 ± 0.26 ng/ml, p < 0.0001). DcR3 level was correlated with HBV DNA level (r = 0.819, p < 0.0001) and alanine transaminase level (ALT, r = 0.704, p < 0.0001) in active HBeAg (-) CHB patients. The area under the Receiver Operating Characteristics curve of DcR3 for detecting the active status of HBeAg (-) CHB patients was 0.914 (95% confidence interval, 0.851-0.977). The optimal cut-off value for DcR3 to predict active HBeAg (-) CHB was 1.22 ng/ml, which had a sensitivity of 87.5% and a specificity of 84.4%. These results suggest that serum DcR3 level may be useful for detecting HBeAg (-) CHB in the active stage, which requires medical treatment.
    No preview · Article · Aug 2013 · The Tohoku Journal of Experimental Medicine
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    ABSTRACT: We investigated whether pancreatitis-associated ascitic fluid (PAAF) could induce the expression of tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6) in THP-1 cells and the mechanism(s) involved. THP-1 cells were divided into control and PAAF groups. The PAAF group was incubated with different final concentrations of PAAF, whereas the control group was incubated with culture medium. Effects and mechanisms were determined by measuring the levels of TNF-α and IL-6 mRNA expression; phospho-p38-MAPK, nuclear factor κB, peroxisome proliferator-activated receptor γ activation; and the effect on the inhibitory activity of SB203580 and BAY-117082. In response to PAAF, overexpression of TNF-α and IL-6 mRNA was found in THP-1 cells compared with those of the corresponding control (P < 0.05), and in a dose-dependent manner. The levels of phospho-p38 and nuclear factor κB p65 were also increased in different PAAF groups, whereas low expression of peroxisome proliferator-activated receptor γ was found compared with the control group (P < 0.05). Furthermore, we presented that the inflammatory response could be partly alleviated by inhibitors SB203580 or BAY-117082, whereas it was markedly inhibited by the simultaneous treatment of 2 inhibitors. Pancreatitis-associated ascitic fluid up-regulated proinflammatory cytokines by interfering with proinflammatory and anti-inflammatory signaling pathways, thus exacerbating activation in acute pancreatitis.
    No preview · Article · Jul 2013 · Pancreas
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    ABSTRACT: The serine/arginine-rich (SR) proteins are one type of major actors in regulation of pre-mRNA splicing. Their functions are closely related to the intracellular spatial organization. The RS domain and phosphorylation status of SR proteins are two critical factors in determining the subcellular distribution. Mammalian Transformer-2β(Tra2β) protein, a member of SR proteins, is known to play multiple important roles in development and diseases. In the present study, we characterized the subcellular and subnuclear localization of Tra2β protein and its related mechanisms. The results demonstrated that in the brain the nuclear and cytoplasmic localization of Tra2β were correlated with its phosphorylation status. Using deletional mutation analysis, we showed that the nuclear localization of Tra2β was determined by multiple nuclear localization signals (NLSs) in the RS domains. The point-mutation analysis disclosed that phosphorylation of serine residues in the NLSs inhibited the function of NLS in directing the Tra2β to the nucleus. In addition, we identified at least two nuclear speckle localization signals within the RS1 domain, but not in the RS2 domain. The nuclear speckle localization signals determined the localization of RS1 domain-contained proteins to the nuclear speckle. The function of the signals did not depend on the presence of serine residues. The results provide new insight into the mechanisms by which the subcellular and subnuclear localization of Tra2β proteins are regulated.
    No preview · Article · Feb 2013 · Journal of Biological Chemistry
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    ABSTRACT: Recombinant adeno-associated viral vector serotype 2 (rAAV2) has been used with success to deliver retina-targeted gene therapeutics in retinal degeneration. However, one of the major limitations of this approach is the vector's low transduction efficiency. This study is designed to increase AAV2 transduction efficiency in vitro and in vivo. Green fluorescence protein (GFP) or luciferase reporter gene-carried rAAV2 vectors were applied to cultured human RPE cells (ARPE-19) or animal eyes with or without chemotherapeutic agents. GFP transduction efficiency was evaluated by image, flow cytometry analysis, and Western blot. The ciliary neurotrophic factor (rAAV2-CNTF)-carried AAV2 vector was coinjected to subretinal space with or without chemotherapeutic agent. The therapeutic efficacy was evaluated by counting numbers of remaining photoreceptors in retina sections of treated or untreated eyes. Coadministration of 0.1 μg/mL doxorubicin (DXR), 0.14 μg/mL cytarabine (Ara-C), 1 μg/mL etoposide (VP-16), or 20 μg/mL cisplatin (DDP) significantly increased rAAV2-mediated GFP and/or luciferase expression in cultured hRPE cells without any detectable toxicity. Pretreatment with DXR for 24 h prior to infection was most effective in enhancing rAAV2 transgene expression in hRPE cells. In addition, subretinal coinjection of rAAV2-CMV-ciliary neurotrophic factor (rAAV2-CNTF) and DXR into the eyes of rats with inherited retinal degeneration resulted in an approximately 2-fold increase in photoreceptor layer thickness and cellular density of the outer nuclear layer (ONL) compared to rAAV2-CNTF alone, reflecting a pronounced protection effect mediated by the enhanced expression of CNTF. The method described here to improve rAAV2-based gene delivery is simple and feasible without any detectable toxicity. This strategy might be therapeutically exploited in the gene therapy of degenerative retinal diseases.
    No preview · Article · Mar 2012 · Investigative ophthalmology & visual science
  • Qian Wang · Ping Xu · Kui Ren · Xiang-Yang Li
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    ABSTRACT: Anti-jamming communication without pre-shared secrets has gained increasing research interest recently and is commonly tackled by utilizing the technique of uncoordinated frequency hopping (UFH). Existing researches, however, are almost all based on ad hoc designs of frequency hopping strategies, mainly due to lack of theoretical foundations for scheme performance evaluation. To fill this gap, in this paper we introduce the online optimization theory into our solution and, for the first time, make the thorough quantitative performance characterization possible for UFH-based anti-jamming communications. Specifically, we formulate the UFH-based anti-jamming communication as a non-stochastic multi-armed bandit (MAB) problem and propose an online learning-based UFH algorithm achieving asymptotic optimum. To reduce the time and space complexity, we further develop an enhanced algorithm exploiting the internal structure of strategy selection process. We analytically prove the optimality of the proposed algorithms under various message coding scenarios. An extensive simulation study is conducted to validate our theoretical analysis and show that the learning-based UFH algorithms are resilient against both oblivious and adaptive jamming attacks.
    No preview · Article · Jan 2012 · IEEE Journal on Selected Areas in Communications
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    Ping Xu · Xiang-Yang Li · Shaojie Tang
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    ABSTRACT: In this paper, we study the spectrum assignment problem for wireless access networks. We assume that each secondary user will bid a certain value for exclusive usage of some spectrum channels for a certain time period or for a certain time duration. A secondary user may also require the exclusive usage of a subset of channels, or require the exclusive usage of a certain number of channels. Thus, several versions of problems are formulated under various different assumptions. For the majority of problems, we design PTAS or efficient constant-approximation algorithms such that overall profit is maximized. Here, the profit is defined as the total bids of all satisfied secondary users. As a side product of our algorithms, we are able to show that a previously studied Scheduling Split Interval Problem (SSIP), in which each job is composed of t intervals, cannot be approximated within O(t<sup>1-∈</sup>) for any small ∈ >; 0 unless NP = ZPP. Opportunistic spectrum usage, although a promising technology, could suffer from the selfish behavior of secondary users. In order to improve opportunistic spectrum usage, we then propose to combine the game theory with wireless modeling. We show how to design a truthful mechanism based on all of these algorithms such that the best strategy of each secondary user to maximize its own profit is to truthfully report its actual bid.
    Preview · Article · May 2011 · IEEE Transactions on Computers
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    Ping Xu · Xiang-Yang Li
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    ABSTRACT: In wireless networks, we need to allocate spectrum efficiently. One challenge is that the spectrum usage requests often come in an online fashion. The second challenge is that the secondary users in a cognitive radio network are often selfish and prefer to maximize their own benefits. In this paper, we address these two challenges by proposing TOFU, a semi-truthful online frequency allocation method for wireless networks when primary users can sublease the spectrums to secondary users. In our protocol, secondary users are required to submit the spectrum bid α time slots before its usage. Upon receiving an online spectrum request, our protocol will decide whether to grant its exclusive usage or not, within at least γ time slots of requests' arrival. We assume that existing spectrum usage can be preempted with some compensation. For various possible known information, we analytically prove that the competitive ratios of our methods are within small constant factors of the optimum online method. Furthermore, in our mechanisms, no selfish users will gain benefits by bidding lower than their willing payment. Our extensive simulation results show that they perform almost optimum: Our methods get a total profit that is more than 95% of the offline optimum when γ is about the duration of spectrum usage Δ.
    Preview · Article · May 2011 · IEEE/ACM Transactions on Networking
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    ABSTRACT: Studies suggest that peroxisome proliferator-activated receptor γ(PPARγ) ligands may represent a therapeutic option in acute pancreatitis, yet most of them have been prophylactic administrated. To evaluate the therapeutic effect of pioglitazone in rats with severe acute pancreatitis induced by sodium taurocholate. Severe acute pancreatitis (SAP) was induced in male Sprague-Dawley rats by the retrograde injection of 5% sodium taurocholate into the pancreatic duct. After SAP was induced, pioglitazone was injected intraperitoneally and its role on the severity of inflammatory response and pancreatic injury was investigated. Amylase activity, inflammatory cytokines production, pathological changes of pancreas, PPARγ mRNA expression, and the survival rate were examined. Treatment with pioglitazone decreased the level of amylase activity, proinflammatory factors IL-6 and TNF-α, ameliorated pancreatic histological score, and upregulated the expression of PPARγ mRNA. The survival rate in the early stage of severe acute pancreatitis was also improved. Pioglitazone can be used as a therapeutic drug and relieve the damages caused by SAP, which suggests PPARγ ligand-pioglitazone offers a potent approach for the treatment of severe acute pancreatitis.
    No preview · Article · Apr 2011 · Digestive Diseases and Sciences

Publication Stats

591 Citations
126.40 Total Impact Points

Institutions

  • 2005-2015
    • Shanghai Jiao Tong University
      • • School of Pharmacy
      • • School of Medicine
      Shanghai, Shanghai Shi, China
    • First People's Hospital Chenzhou
      Chenchow, Hunan, China
  • 2003-2015
    • Fudan University
      • • Department of Neurology
      • • State Key Laboratory of Medical Neurobiology
      Shanghai, Shanghai Shi, China
  • 2004-2013
    • Shanghai University
      • Department of Gastroenterology
      Shanghai, Shanghai Shi, China
  • 2012
    • IIT Research Institute (IITRI)
      Chicago, Illinois, United States
  • 2008-2011
    • Illinois Institute of Technology
      • Department of Computer Science
      Chicago, Illinois, United States
    • University of Utah
      • Department of Internal Medicine
      Salt Lake City, Utah, United States
  • 2010
    • University of California, Davis
      • Department of Computer Science
      Davis, California, United States
  • 2007
    • Nanchang University
      Nan-ch’ang-shih, Jiangxi Sheng, China
  • 2004-2005
    • Hangzhou First People's Hospital
      Hang-hsien, Zhejiang Sheng, China