Search

ABSTRACT In this paper, we study the performance limit of a wireless communication system over a fading channel. The system under study consists of 1) a finite-buffer discrete-time queueing system on the link layer; and 2) a rate-adaptive channel coding system on the physical layer. The objective of this paper is to analyze the relationship among data rate (R), packet error probability (E), and delay bound (D) under the interaction between the link layer and the physical layer. In our analysis, we consider three types of packet errors; that is, 1) packet drop due to full buffer; 2) packet drop due to delay bound violation; and 3) packet decoding error due to channel noise. We obtain an upper bound on the packet error probability. Furthermore, by minimizing the packet error probability over the transmission rate, we obtain an optimal rate control policy that guarantees the user-specified data rate and delay bound. In the case of constant arrival, the optimal rate control policy results in a rate-error-delay triplet; then, by varying data rate and delay bound, we obtain rate-error-delay Pareto-optimal surface, which serves as the performance limit of the system under study. Copyright © 2012 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

A recursive maximum likelihood carrier frequency offset (CFO) estimator is proposed in this work, where redundancy information contained in the cyclic prefix of multiple consecutive orthogonal frequency-division multiplexing (OFDM) symbols is exploited in an efficient recursive fashion. Because the estimator is based on multiple OFDM symbols, the time-varying CFO must be considered. We investigate the effect of time-varying CFO on the performance of the estimator and the trade-off between fast tracking ability and low estimation variance. We show that, without channel noise, the mean squared error (MSE) of estimation due to CFO estimation variation increases approximately quadratically with n, where n is the number of OFDM symbols used for CFO estimation (estimation window size), whereas the MSE due to channel noise decreases proportionally to 1/ n (approximately) if the CFO is constant. A closed-form expression of the optimal estimation window size (approximately) is derived by minimizing the MSE caused by both time-varying CFO and channel noise. For wireless systems with time-varying rate of change for CFO, the proposed estimator can be implemented adaptively. In addition, typical optimal estimation window sizes for WiMAX, DVB-SH and MediaFLO systems are evaluated as an example. Copyright © 2011 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

In this paper, we study efficient power control schemes for delay sensitive communication over fading channels. Our objective is to find a power control law that optimizes the link layer performance, specifically, minimizes the packet drop probability, subject to a long-term average power constraint. We assume the buffer at the transmitter is finite; hence packet drop happens when the buffer is full. The fading channel under our study has a continuous state, e.g., Rayleigh fading. Since the channel state space is continuous, dynamic programming is not applicable for power control. In this paper, we propose a sub-optimal power control law based on a parametric approach. The proposed power control scheme tries to minimize the packet drop probability by considering the queue length, i.e., reducing the probability of those queue-length states that will cause full buffer. Simulation results show that our proposed power control scheme reduces the packet drop probability by one or two orders of magnitude, compared to the time domain water filling (TDWF) and the truncated channel inversion (TCI) power control. Copyright © 2010 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

We consider the problem of optimal power control for quality-of-service-assured wireless communication. The quality of service (QoS) measures of our consideration are a triplet of data rate, delay, and delay bound violation probability (DBVP). Our target is to develop power control laws that can provide delay guarantees for real-time applications over wireless networks. The power control laws that aim at optimizing certain physical-layer performance measures, usually adapt the transmission power based on the channel gain; we call these 'channel-gain-based' (CGB) power control (PC). In this paper, we show that CGB-PC laws achieve poor link-layer delay performance. To improve the performance, we propose a novel scheme called hierarchical queue-length-aware (HQLA) power control. The key idea is to combine the best features of the two PC laws, i.e., a given CGB-PC law and the clear-queue (CQ) PC law; here, the CQ-PC is defined as a PC law that uses a transmission power just enough to empty the queue at the link layer. We analyze our proposed HQLA-PC scheme by the matrix-geometric method. The analysis agrees well with the simulation results. More importantly, our results show that the proposed HQLA power control scheme is superior to the corresponding CGB-PC in both average power consumption and effective capacity. Copyright © 2010 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

In this paper, we study the power allocation scheme for a single user, multi-channel system, e.g., orthogonal frequency-division multiplexing (OFDM) systems, under time-variant wireless fading channels. We assume the receiver feeds back perfectly estimated channel state information (CSI) to the transmitter after a processing delay. The objective of the power allocation is to maximize throughput subject to quality-of-service (QoS) constraint. The QoS measure of our consideration is a triplet of data rate, delay, and delay bound violation probability. A two-step sub-optimal power allocation scheme is proposed to address the impact of outdated CSI. In the first step, the total transmission power that can be used within one block is determined according to the summation of the channel gains of all the channels. In the second step, the total transmission power is allocated among all the channels. The proposed power control scheme is less sensitive to the feedback delay. Compared to the optimal power allocation scheme designed for the perfect CSI scenario, it has lower computational complexity while achieving comparable capacity. Copyright © 2010 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Sinomenine (SIN) is a bioactive component derived from a Chinese medicinal plant. Our previous studies demonstrated that SIN has cytotoxic effects on human lung cancer cells. However, the antitumor molecular mechanisms of SIN have yet to be elucidated in detail. In the present study, we further explored the effects of SIN on NCI-H460 human lung cancer cell viability and apoptosis and investigated the regulation and function of PI3K/Akt and ERK signaling pathways during SIN-induced apoptosis in various lung cancer cell lines. NCI-H460 cells were incubated with 200 µg/ml SIN for the indicated times (0, 24, 48 or 72 h). Cell viability was assessed by MTT assay. Akt, p-Akt, ERK1/2 and p-ERK1/2 protein levels were detected by western blotting, respectively. Two different selective inhibitors (LY294002 for the PI3K pathway; PD98059 for the MEK/ERK pathway) were used to characterize the relative roles of PI3K/Akt and ERK in SIN-induced apoptosis. Apoptosis was determined by flow cytometry. SIN inhibited the proliferation of NCI-H460 cells in a time-dependent manner, which was accompanied with significant activation of pAkt and pERK. LY294002 and PD98059 both significantly increased SIN-induced apoptosis in NCI-H460, NCI-H226 and NCI-H522 cells. Our findings suggest that the activation of the PI3K/Akt and ERK signaling pathways antagonize SIN-induced lung cancer cell apoptosis and molecules that inhibit these pathways should potentiate the effects of SIN. This study represents a significant step forward in our understanding of the signal transduction pathways associated with the apoptosis elicited by SIN.

Adriamycin (ADM) is a drug used in the treatment of various types of cancer and exerts an antineoplastic effect mainly through the induction of apoptosis. Phosphoinositide 3 kinase (PI3K)/Akt and MAPK are fundamental survival pathways activated by exposure to most chemotherapeutical agents. However, the role of these pathways in the ADM-induced apoptosis of leukemia cells remains unclear. In the present study, ADM triggered dose-dependent cytotoxicity and resulted in a significant loss of cell viability in HL-60 cells. Moreover, treatment with ADM significantly reduced mitochondrial membrane potential (ΔΨm) in the cells. Akt and ERK activation was also detected, and the inhibition of these two pathways resulted in the enhancement of ADM-induced apoptosis. These results indicate that the PI3K/Akt and ERK survival pathways antagonize the chemotherapeutic effect of ADM. Thus, inhibiting these pathways may serve to enhance the effect of ADM.