Outage Probability of Dual-Hop Multiple Antenna AF Relaying Systems with Interference

This paper presents an analytical investigation on the outage performance of dual-hop multiple antenna amplify-and-forward relaying systems in the presence of interference. For both the fixed-gain and variable-gain relaying schemes, exact analytical expressions for the outage probability of the systems are derived. Moreover, simple outage probability approximations at the high signal to noise ratio regime are provided, and the diversity order achieved by the systems are characterized. Our results suggest that variable-gain relaying systems always outperform the corresponding fixed-gain relaying systems. In addition, the fixed-gain relaying schemes only achieve diversity order of one, while the achievable diversity order of the variable-gain relaying scheme depends on the location of the multiple antennas.Comment: Accepted to appear in IEEE Transactions on Communication

Flutter analysis for bridge decks using Lattice Boltzmann Method

Aiming at using the Lattice Boltzmann Method for flutter analysis of the bridge decks, a fluid- structure interaction algorithm is developed  within the framework of multiple –relaxation- time Lattice Boltzmann  Method. In the present algorithm, the unsteady fluid dynamics  is computed by the extended two-dimensional Lattice Boltzmann Method by incorporating the dynamic Smagorinsky subgrid scale  model, while the structure is modelled by an elastically suspended rigid body and its dynamic analysis is performed by using a Runge–Kutta method. A staggered coupling strategy is adopted to couple the fluid solver and the structure solver. To demonstrate the applicability of the presented algorithm, flutter analyses of the Second Forth Road Bridge and the Guamá River Bridge are employed. The numerical results are compared with wind tunnel measurements. It is shown that the  presented algorithm has a good prediction for the flutter onset  velocities of the Forth Road Bridge and the Guamá River Bridge and thus indicates, to a certain extent, the applicability of the presented algorithm

Modeling and Performance Evaluation of Multistage Serial Manufacturing Systems with Rework Loops and Product Polymorphism

This paper studies multistage serial manufacturing systems with the integrated consideration of machine failures, process defects, multiple rework loops, etc. In particular, multiple rework loops and product polymorphism lead to a more complex conversion of internal material flows, and therefore it's difficult to model and analyse such manufacturing systems. A modular modeling method based on Generalized Stochastic Petri Nets (GSPN) is presented to characterize the material flows, it is capable of representing the processing differences resulting from product polymorphism comparing with traditional Markov model or Queuing network model. By analysing the model, the processing ratio of each workstation is inferred. Using 2M1B (two-machine and one-buffer) Markov cell model as the building blocks, which is obtained based on the GSPN models for their isomorphism, an overlapping decomposition method is then developed for evaluating the performance of the multistage serial systems with rework loops. Numerical experiments and a case study of a powertrain assembly line illustrate the efficiency of the proposed method

Human cytomegalovirus inhibits apoptosis by proteasome-mediated degradation of bax at endoplasmic reticulum-mitochondrion contacts

Human cytomegalovirus (HCMV) encodes the UL37 exon 1 protein (pUL37x1), which is the potent viral mitochondrion-localized inhibitor of apoptosis (vMIA), to increase survival of infected cells. HCMV vMIA traffics from the endoplasmic reticulum (ER) to ER subdomains, which are physically linked to mitochondria known as mitochondrion-associated membranes (MAM), and to mitochondria. The antiapoptotic function of vMIA is thought to primarily result from its ability to inhibit Bax-mediated permeabilization of the outer mitochondrial membrane (OMM). Here, we establish that vMIA retargets Bax to the MAM as well as to the OMM from immediate early through late times of infection. However, MAM localization of Bax results in its increased ubiquitination and proteasome-mediated degradation. Surprisingly, HCMV infection does not increase OMM-associated degradation (OMMAD) of Bax, even though the ER and mitochondria are physically connected at the MAM. It was recently found that lipid rafts at the plasma membrane can connect extrinsic and intrinsic apoptotic pathways and can serve as sites of apoptosome assembly. In transfected permissive human fibroblasts, vMIA mediates, through its cholesterol affinity, association of Bax and apoptosome components with MAM lipid rafts. While Bax association with MAM lipid rafts was detected in HCMV-infected cells, association of apoptosome components was not. These results establish that Bax recruitment to the MAM and its MAM-associated degradation (MAMAD) are a newly described antiapoptotic mechanism used by HCMV infection to increase cell survival for its growth