Abstract-We propose a quality-of-service (QoS) driven power and rate adaptation scheme over wireless links in mobile wireless networks. Specifically, our proposed scheme aims at maximizing the system throughput subject to a given delay QoS constraint. First, we derive an optimal adaptation policy by integrating information theory with the concept of effective capacity for a block fading channel model. Our analyses reveal an important fact that there exists a fundamental tradeoff between throughput and QoS provisioning. In particular, when the QoS constraint becomes loose, the optimal power-control policy converges to the well-known water-filling scheme, where Shannon (ergodic) capacity can be achieved. On the other hand, when the QoS constraint gets stringent, the optimal policy converges to the total channel inversion scheme under which the system operates at a constant rate. Inspired by the above observations, we then consider a more practical scenario where variable-power adaptive modulation is employed over both block fading and Markov correlated fading channels. In both cases, we derive the associated power and rate adaptation policies. The obtained results suggest that the channel correlation has a significant impact on QoS-driven power and rate adaptations. The higher the correlation is, the faster the power-control policy converges to the total channel inversion when the QoS constraint becomes more stringent. Finally, we conduct simulations to verify that the adaptation policy proposed for Markov channel models can also be applied to the more general channel models.Index Terms-Mobile wireless networks, quality-of-service (QoS), effective capacity, power control, adaptive modulation, information theory, cross-layer design and optimization.

Abstract-We propose a quality-of-service (QoS) driven power and rate adaptation scheme over wireless links in mobile wireless networks. Specifically, our proposed scheme aims at maximizing the system throughput subject to a given delay QoS constraint. First, we derive an optimal adaptation policy by integrating information theory with the concept of effective capacity for a block fading channel model. Our analyses reveal an important fact that there exists a fundamental tradeoff between throughput and QoS provisioning. In particular, when the QoS constraint becomes loose, the optimal power-control policy converges to the well-known water-filling scheme, where Shannon (ergodic) capacity can be achieved. On the other hand, when the QoS constraint gets stringent, the optimal policy converges to the total channel inversion scheme under which the system operates at a constant rate. Inspired by the above observations, we then consider a more practical scenario where variable-power adaptive modulation is employed over both block fading and Markov correlated fading channels. In both cases, we derive the associated power and rate adaptation policies. The obtained results suggest that the channel correlation has a significant impact on QoS-driven power and rate adaptations. The higher the correlation is, the faster the power-control policy converges to the total channel inversion when the QoS constraint becomes more stringent. Finally, we conduct simulations to verify that the adaptation policy proposed for Markov channel models can also be applied to the more general channel models.Index Terms-Mobile wireless networks, quality-of-service (QoS), effective capacity, power control, adaptive modulation, information theory, cross-layer design and optimization.

Abstract-We propose a cross-layer approach to investigate the impact of physical-layer infrastructure on data-link-layer quality-of-service (QoS) performance over wireless links in mobile networks. At the physical layer, we take multiple-inputmultiple-output (MIMO) diversity schemes as well as adaptivemodulation-and-coding (AMC) techniques into account. At the data-link layer, our focus is on how this physical-layer infrastructure influences the real-time multimedia delay-bound QoS performance. To achieve this goal, we first model the physical-layer service process as a finite-state Markov chain (FSMC). Based on this FSMC model, we then characterize the QoS performance at data-link-layer using the effective capacity approach, which turns out to be critically important for the statistical QoS guarantees over wireless links in mobile networks. We also investigate the impact of physical-layer power control and channel-state information (CSI) feedback delay on the QoS performance. The numerical results obtained demonstrate that our proposed cross-layer model can efficiently characterize the interactions between the physical-layer infrastructure and datalink-layer QoS performance.Index Terms-Cross-layer design and optimization, mobile wireless networks, quality-of-service (QoS), effective capacity, adaptive-modulation-and-coding (AMC), multiple-inputmultiple-output (MIMO), real-time multimedia delay-bound.

Abstract-We propose a cross-layer-model based adaptive resource-allocation scheme for the diverse quality-of-service (QoS) guarantees over downlink mobile wireless networks. Our proposed scheme dynamically assigns power-levels and timeslots for heterogeneous real-time mobile users to satisfy the variation of statistical delay-bound QoS requirements. To achieve this goal, we apply Wu and Negi's effective capacity approach to derive the admission-control and power/time-slot allocation algorithms, guaranteeing the statistical delay-bound for heterogeneous mobile users. When designing such an algorithm, we study the impact of physical-layer issues such as adaptive power-control and channel-state information (CSI) feedback delay on the QoS provisioning performance. Through numerical and simulation results, we observe that the adaptive power adaptation has a significant impact on statistical QoS-guarantees. In addition, the analyses indicate that our proposed resourceallocation algorithms are shown to be able to efficiently support the diverse QoS requirements for various real-time mobile users over different wireless channels. Also, in an in-door mobile environment, e.g., the widely used wireless local-area networks (WLAN), our proposed algorithm is shown to be robust to the CSI feedback delay.

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Glycine is a simple nonessential amino acid known to have neuroprotective properties. Treatment with glycine results in reduced infarct volume of the brain, neurologic function scores, and neuronal and microglial death in ischemic stroke injury. Neuroinflammation has been considered a major contributor to cerebral ischemia–induced brain damage. However, the role of glycine in neuroinflammation following ischemic stroke is unclear. The present study aimed to determine whether neuroinflammation is involved in the neuroprotective effects of glycine in cerebral ischemia injury. Ischemic stroke promotes M1 microglial polarization. Interestingly, we found that the injection of glycine in rats after injury can inhibit ischemia-induced inflammation and promote M2 microglial polarization in vivo (Sprague–Dawley rats) and in vitro (cortical microglia and BV-2 cells). We show that glycine suppresses Hif-1α by inhibiting the upregulation of NF-κB p65 after ischemia-reperfusion injury, resulting in the inhibition of proinflammatory activity. The activation of AKT mediates the inhibition of NF-κB p65/Hif-1α signaling by glycine. Moreover, we confirm that glycine-regulated AKT activation is mediated by the inhibition of PTEN in a PTEN depletion cell line, U251 cells. Glycine modulates microglial polarization after ischemic stroke, which indirectly inhibits ischemia-induced neuronal death and functional recovery. Taken together, our findings provide a new understanding of glycine in neuroprotection by inhibiting M1 microglial polarization and promoting anti-inflammation by suppressing NF-κB p65/Hif-1α signaling.

Bisperoxovanadium (pyridine-2-carboxyl) [bpV(pic)] is a commercially available PTEN inhibitor. Previous studies from us and others have shown that bpV(pic) confers neuroprotection in cerebral ischemia injury. We set up to determine whether ERK 1/2 activation plays a role in bpV(pic)-induced neuroprotective effect in cerebral ischemia injury. We found that the phosphorylation levels of Akt (p-AKT) and ERK1/2 (p-ERK 1/2) were down-regulated after cerebral ischemia–reperfusion injury. The injection of bpV(pic) after injury not only increased the level of p-AKT but also the level of p-ERK 1/2. While the inhibition of PTEN mediated the up-regulatation of p-AKT and p-ERK 1/2 by bpV(pic). Interestingly, the ERK 1/2 activation induced by bpV(pic) was also independent of the inhibition of PTEN. Our results indicate that bpV(pic) protects against OGD-induced neuronal death and promotes the functional recovery of stroke animals through PTEN inhibition and ERK 1/2 activation, respectively. This study suggests that the effect of bpV(pic) on ERK 1/2 signaling should be considered while using bpV(pic) as a PTEN inhibitor.Electronic supplementary materialThe online version of this article (10.1007/s11064-018-2558-z) contains supplementary material, which is available to authorized users.