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In this paper, we focus on the problem with the objective to maximize the system performance, while guaranteeing multiple QoS (quality of service) constraints for wireless data networks accommodating multiclass services with different quality requirements. First, we formulate and solve the opportunistic scheduling problem with multiple general long-term QoS constraints. Then, we generalize this problem to include short-term QoS constraints for real-time multimedia users and long-term QoS constraints for non-real-time data users simultaneously in multiclass services networks. Simulation results illustrate that the proposed scheduling schemes guarantee the different QoS constraints, and achieve high system performance.

In this paper, we focus on the problem with the objective to maximize the system performance, while guaranteeing specified QoS constraints for multiple user classes in wireless data networks. First, we propose two opportunistic scheduling algorithms that exploit time-varying channel conditions for the special two-constraint case, and then propose an opportunistic scheduling algorithm for the general case. Simulation results illustrate that the proposed scheduling algorithms guarantee the different constraints, and achieve high system performance that is close to the true optimal value using a known general-purpose optimization package, lingo

In this paper, we study the fundamental problem of allocating the available resources with efficiency and fairness in a wireless CDMA network. In particular, we first introduce an ideal fair scheduling (IFS) scheme. The allocation of resources in IFS is strictly fair. Then we introduce the proportional compensation based fair scheduling (PCFS) algorithm. PCFS distinguishes the services in different application levels. In PCFS, a channel-adaptive resource allocation policy is introduced to improve the system throughput and a compensation model is introduced to achieve fair services. Based on the assignment of PCFS, we propose the traffic aided PCFS (T-PCFS) algorithm that incorporates traffic information into compensation model to achieve better fairness. Extensive simulation results show that our scheme can operate well in wireless CDMA networks.

Objective: Hyperhomocysteinemia (HHcy) is a risk factor for cardiovascular disease and has been reported to inhibit endothelial cell (EC) growth. Notwithstanding, precisely how HHcy regulates EC growth in vivo remains unknown. In this study, we established a mouse model of endothelial injury and reendothelialization and examined the role and mechanism of HHcy in endothelial repair. Methods and results: A mouse model of carotid artery air-dry endothelium denudation and reendothelialization was established and used to evaluate post-injury endothelial repair in mice with the gene deletion of cystathionine-h-synthase (CBS). Moderate and severe HHcy were induced in CBS +/+ and CBS /+ mice through a high-methionine diet. Post-injury reendothelialization, which correlated with increased postinjury neointima formation, was impaired in severe HHcy mice. To elucidate the underlying mechanism, we examined circulating endothelial progenitor cells (EPC) in HHcy mice and studied the effect of homocysteine (Hcy) on proliferation, migration, and adhesion of human umbilical vein endothelial cells (HUVEC). The peripheral EPC population was not significantly altered in HHcy mice. Hcy had a profound inhibitory effect on EC proliferation and migration at physiologically relevant concentrations and inhibited EC adhesion at concentrations of 200 AM and higher. Conclusion: We have established a convenient and accurate mouse model of carotid injury in which the reendothelialization process can be precisely quantified. In addition, we have observed impaired reendothelialization and increased neointimal formation in severe HHcy mice. The capacity of Hcy to inhibit proliferation and migration of EC may be responsible for impaired reendothelialization and contribute to arteriosclerosis in HHcy.

Fair queuing has long been a popular paradigm for providing bounded delay channel access and separation between users in wired networks. However, adapting fair queuing to the wireless domain is not a trivial task because of the unique problems in wireless channels such as location dependent and bursty channel error. In this paper, we incorporate traffic information into wireless fair scheduling using compensation scheme. In particular, we first establish general properties for fair scheduling using proportional compensation scheme in CDMA cellular networks. It distinguishes the services in different application levels. A compensation model and a reallocation method in the scheme were introduced to achieve wireless fair services. Then, we develop a new traffic aided fair scheduling scheme based on compensation model by making use of file size information. Extensive simulation results show that our scheme can operate well in CDMA cellular networks.

We first discuss the need for computational electromagnetics (CEM) in high-frequency IC design. We then review recent advances in CEM, present chip design challenges to CEM analysis, and analyze the shortcomings of current CEM methodology. We then emphasize the importance of chip-design-driven CEM development, and finally present some promising full-wave electromagnetic-based solutions that can achieve full-chip analysis and design.

To investigate the effect of Tauroursodeoxycholic acid (TUDCA) on Taurodeoxycholic acid (TDCA)-induced HepG2 cell apoptosis and to clarify the molecular mechanism of its anti-apoptosis effect of TUDCA.Morphologic evaluation of apoptotic cells was performed by Hoechst 33258 staining and electron microscope. DNA fragment was detected by electrophoresis on 1.5% agarose gels. Apoptosis rate was measured by flow cytometry using PI dye. Following incubation of HepG2 cells either with TDCA alone, or coincubation with TUDCA and TDCA, the releasing level of cytochrome c from mitochondria into cytosol was determined by western blot, also the activity of caspase-3, 8, 9.Incubating the cells with 400 micromol/L TDCA for 12 h induced the cells apoptosis significantly. The apoptotic rate decreased from 50.35% +/- 2.20% to 13.78% +/- 0.84% after coincubation with TUDCA, and this anti-apoptotic effect of TUDCA was confirmed by morphological and DNA ladder detection. TUDCA significantly inhibited the release of cytochrome C from mitochondria into cytosol, and the activity of caspase-9, 3 (tor = 13.00, P0.01), especially at 12 h, caspase-3 activity decreased by 54.9% (t = 16.88, P0.01) and 52.5%, however it had no obvious effect on the activity of caspase-8 (t = 1.94, P0.05).TUDCA prevents HepG2 cells apoptosis induced by TDCA through modulating mitochondrial membrane stability, inhibiting the release of cytochrome c and the activation of procaspase-9 and 3. Anti-apoptotic mechanism of TUDCA may be considered to be one of the most important reasons that TUDCA exerts significant efficacy in the treatment of cholestatic liver diseases.

AIM:To study the effect of hepatocyte apoptosis and necrosis induced by TNF-alpha on the pathogenesis of acute severe hepatitis (ASH).METHODS:The model of ASH was prepared in D-galactosamine (GalN) sensitized BALB/c mice by injection of either endotoxin (ET) or tumor necrosis factor-alpha(TNF-alpha. Morphological changes of apoptotic hepatocytes were studied by both light and electron microscope and in site end labeling method (ISEL). Molecular biological changes of DNA ladder were observed by electrophoresis of extract from liver tissues. Biochemical changes were measured by alanine aminotransferase (ALT), aspartic aminotransferase (AST) and TNF-alpha. The relation between apoptosis and necrosis was evaluated simultaneously.RESULTS:The sequence of hepatocyte apoptosis, necrosis, and final death from ASH was observed both in GalN/ET and GalN/TNF-alpha group. Apoptosis was prominent at 3.5h and 6h after injection of inducer, while necrosis became dominant at 9h after challenge. The appearance of apoptosis was earlier in GalN/TNF-alpha group than that in GalN/ET group. Pretreatment of mice with antiTNF IgG1 may completely prevent the liver injury induced by GalN/ET.CONCLUSION:TNF-alpha can cause liver amage by inducing hepatic apoptosis and necrosis in mice with endotoxemia.

The Combitube ® is a relatively new device used for blind insertion emergency intubation. We report a case of successful Combitube ® treatment of an acute respiratory arrest secondary to an acute asthma exacerbation. An advanced EMT-II (National Park Service Parkmedic) utilized this device. Our review of the literature revealed no reported cases of an advanced EMT-II, nor any other cases, using the Combitube ® in asthma-related respiratory failure.

We have developed a photolytic method to determine the concentration of reactive hemes in a solution in the presence of a trace amount of CO. By measurement of the bimolecular rate of CO binding, and by calibration of the rate constant under equivalent conditions, the concentration of the reactive hemes can be determined. In a solution of sickle hemoglobin, the molecules in the gel contribute negligibly to the recombination rate, allowing the concentration of the molecules in the solution phase to be determined. To optimize signal to noise, modulated excitation methods were employed, although the method could also be used with pulse techniques and suitable signal averaging. Because the optical method employs a microspectrophotometer, only a few microliters of concentrated Hb solution is required to reproduce the entire temperature dependence of the solubility previously determined by centrifugation using milliliter quantities of solutions of the same concentration. This should be especially useful for studies of site-directed mutants, and we present results obtained on one such HbS in which Leu 88 beta has been replaced by Ala. The free energy difference in the polymerization of the Leu 88 beta double mutant is consistent with known differences in the amino acid hydrophobicities. The calibration required for these experiments also provides an excellent determination of the activation energy for binding the first CO to deoxy Hb.

IMU rotation of an inertial navigation system (INS) can bound the free propagation of the INS error introduced by the drifts of inertial sensors. The rotation scheme of the IMU will directly affect the accuracy, structure and costs of the system. A reasonable rotation scheme should remove most of the system errors arising from the drifts of the inertial sensors, and at the same time, should not introduce other additional errors. First, this paper discusses the design and analysis approach of the rotation scheme based on the error propagation equations of the INS. Then, a conventional 8-position rotation scheme is analyzed for the applications of the optical gyro INS, and its drawbacks are discussed in detail. Following these, an improved 8-position rotation scheme and a novel 16-position rotation scheme are proposed for the optical gyro INS, and their merits are also discussed. Simulation results have shown that the 16-position rotation scheme, which can compensate not only the drifts but also the scale factor errors and the misalignment errors of the inertial sensors, is the best rotation scheme and can be used as a practical solution to compensate the drifts of the inertial sensors in the rotational INS.

Increasing energy demand for building has made it imperative that energy conservation is an emergency in China. In this paper, calculation methodology on energy performance of residential building envelopes is studied by the Evaluation of Envelope Thermal Performance (EETP) index, the parameters related to EETP indexes are calculated from the eQUEST software. The formulae about energy performance of residential building envelopes in cooling season, heating season and the whole year in Changsha of China with EETPc, EETPh, and EETPy have been built; this calculation methodology are much simpler than the eQUEST on comparing the relative energy efficiency of different building envelope designs.

Hepatocellular transplantation (HCT) could provide a therapeutic alternative to orthotopic liver transplantation (OLT) in the treatment of hepatic metabolic defects and experimental hepatic failure[1-4]. Under appropriate conditions, the engrafted liver cells can continue to express liver-specific functions for an indefinite period of time. The major limitation of many animal studies in HCT is that, since the donor hepatocytes are often indistinguishable from those of the host, it has often been difficult to demonstrate a clear correlation between engraftment and the therapeutic effect. In order to verify engraftment dependent on the therapeutic response, a recombinant retroviral vector carrying marker genes is used to label the donor hepatocytes[5,6]. The vector is capable of transducing hepatocytes, integrating gene stably into the genome and directing expression. Efficient retroviral-mediated gene transfer has introduced the possibility of targeting genetic markers to hepatic cells and somatic gene therapy for liver diseases[7-11]. Stable integration and expression of retroviral genes is dependent upon active division of the infected cell[9-13]. Although hepatocytes maintain growth potential in vivo and are capable of substantial regeneration following partial hepatectomy, their ability to grow in culture is quite limited. In the present study, we explored the optimal culture system for hepatocyte proliferation and the potential for retroviral-mediated gene transfer into primary hepatocytes. We successfully demostrated the efficient and stable transduction of primary culture of adult rat hepatocyte by replication of defective retrovirus carrying β-gal gene and NeoR gene.

Cloud computing has become a cost-effective paradigm for deploying online service applications in large data centers in recent years. Virtualization technology enables flexible and efficient management of physical resources in cloud data centers and improves the resource utilization. A request for resources to a data center can be abstracted as a virtual data center (VDC) request. Due to the use of a large number of resources and at various locations, reliability is an important issue that should be addressed in large and multiple data centers. However, most research focuses on the problem of reliable VDC embedding in a single data center. In this paper, we study the problem of reliable VDC embedding across multiple data centers, such that the total bandwidth consumption in the inter-data center backbone network is minimized, while satisfying the reliability requirement of each VDC request. We model the problem by using mixed integer linear programming (MILP) and propose a heuristic algorithm to address this NP-hard problem efficiently. Simulation results show that the proposed algorithm performs better in terms of lowering physical resource consumption and VDC request blocking ratio compared with existing solution.

Background Mitogen- and Stress-Activated Kinase 1 (MSK1) is a nuclear kinase that serves as active link between extracellular signals and the primary response of gene expression. However, the involvement of MSK1 in malignant transformation and cancer development is not well understood. In this study, we aimed to explore the role of MSK1 in Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1)-promoted carcinogenesis of nasopharyngeal carcinoma (NPC). Methods The level of MSK1 phosphorylation at Thr581 was detected by the immunohistochemical analysis in NPC tissues and normal nasopharynx tissues, and its correlation with LMP1 was analyzed in NPC tissues and cell lines. Using MSK1 inhibitor H89 or small interfering RNA (siRNA)-MSK1, the effects of MSK1 on LMP1-promoted CNE1 cell proliferation and transformation were evaluated by CCK-8 assay, flow cytometry and focus-forming assay respectively. Furthermore, the regulatory role of MSK1-mediated histone H3 phosphorylation at Ser10 on the promoter activity and expression of Fra-1 or c-Jun was determined by reporter gene assay and western blotting analysis. Results Immunohistochemical analysis revealed that the level of MSK1 phosphorylation at Thr581 was significantly higher in the poorly differentiated NPC tissues than that in normal nasopharynx tissues (P