Asymptotic Capacity of Large Relay Networks with Conferencing Links

In this correspondence, we consider a half-duplex large relay network, which consists of one source-destination pair and $N$ relay nodes, each of which is connected with a subset of the other relays via signal-to-noise ratio (SNR)-limited out-of-band conferencing links. The asymptotic achievable rates of two basic relaying schemes with the "$p$-portion" conferencing strategy are studied: For the decode-and-forward (DF) scheme, we prove that the DF rate scales as $\mathcal{O} (\log (N))$; for the amplify-and-forward (AF) scheme, we prove that it asymptotically achieves the capacity upper bound in some interesting scenarios as $N$ goes to infinity.Comment: submitted to IEEE Transactions on Communication

Apoe+/-ldlr+/- mice as a useful model to evaluate accelerated atherogenesis by Helicobacter pylori infection

Atherosclerosis is closely related to chronic infection. In the present study, we evaluated atherogenesis by gastric infection with Helicobacter pylori (H. pylori) in atherosclerosis-prone apoe+/-ldlr+/- mice. Six- week- old male apoe+/-ldlr+/- mice infected by H. pylori and apoe+/-ldlr+/- control mice were fed with a high cholesterol diet (1%). Eight weeks after the confirmation of infection, the extent of atherosclerosis, anti heat shock protein 60 of H. pylori (Hp-HSP60) serum titers, and the cellular immune responses against Hp-HSP60 were evaluated. Atherosclerosis was promoted by a Th1-mediated reaction against Hp-HSP60, accompanied by production of IFN-γ and IL-12, and mRNA expression of T-bet in the H. pylori -infected apoe+/-ldlr+/- mice. The over-expressed of HSP60 in stressed endothelial cells could be cross-recognized by T cells against Hp-HSP60 and contributed to the atherosclerosis. This mouse model would be useful for analyzing immunological mechanisms of atherogenesis

Asymptotic Capacity of Large Fading Relay Networks with Random Node Failures

To understand the network response to large-scale physical attacks, we investigate the asymptotic capacity of a half-duplex fading relay network with random node failures when the number of relays $N$ is infinitely large. In this paper, a simplified independent attack model is assumed where each relay node fails with a certain probability. The noncoherent relaying scheme is considered, which corresponds to the case of zero forward-link channel state information (CSI) at the relays. Accordingly, the whole relay network can be shown equivalent to a Rayleigh fading channel, where we derive the $\epsilon$-outage capacity upper bound according to the multiple access (MAC) cut-set, and the $\epsilon$-outage achievable rates for both the amplify-and-forward (AF) and decode-and-forward (DF) strategies. Furthermore, we show that the DF strategy is asymptotically optimal as the outage probability $\epsilon$ goes to zero, with the AF strategy strictly suboptimal over all signal to noise ratio (SNR) regimes. Regarding the rate loss due to random attacks, the AF strategy suffers a less portion of rate loss than the DF strategy in the high SNR regime, while the DF strategy demonstrates more robust performance in the low SNR regime.Comment: 24 pages, 5 figures, submitted to IEEE Transactions on Communication

Study of Gaussian Relay Channels with Correlated Noises

In this paper, we consider full-duplex and half-duplex Gaussian relay channels where the noises at the relay and destination are arbitrarily correlated. We first derive the capacity upper bound and the achievable rates with three existing schemes: Decode-and-Forward (DF), Compress-and-Forward (CF), and Amplify-and-Forward (AF). We present two capacity results under specific noise correlation coefficients, one being achieved by DF and the other being achieved by direct link transmission (or a special case of CF). The channel for the former capacity result is equivalent to the traditional Gaussian degraded relay channel and the latter corresponds to the Gaussian reversely-degraded relay channel. For CF and AF schemes, we show that their achievable rates are strictly decreasing functions over the negative correlation coefficient. Through numerical comparisons under different channel settings, we observe that although DF completely disregards the noise correlation while the other two can potentially exploit such extra information, none of the three relay schemes always outperforms the others over different correlation coefficients. Moreover, the exploitation of noise correlation by CF and AF accrues more benefit when the source-relay link is weak. This paper also considers the optimal power allocation problem under the correlated-noise channel setting. With individual power constraints at the relay and the source, it is shown that the relay should use all its available power to maximize the achievable rates under any correlation coefficient. With a total power constraint across the source and the relay, the achievable rates are proved to be concave functions over the power allocation factor for AF and CF under full-duplex mode, where the closed-form power allocation strategy is derived.Comment: 24 pages, 7 figures, submitted to IEEE Transactions on Communication

Loureirin B attenuates amiodarone-induced pulmonary fibrosis by suppression of TGFβ1/Smad2/3 pathway

Purpose: To investigate the therapeutic effect of loureirin B (LB) on amiodarone (AD)-induced pulmonary fibrosis (PF).Methods: Forty-eight male C57BL/6 mice, 8–10 weeks of age, were divided into four groups (n=12). Oral administration of amiodarone hydrochloride (AD) was performed for 4 weeks to induce pulmonary fibrosis. The degree of fibrosis was assessed by Masson staining, while collagen I and α-smooth muscle actin (α-SMA) levels were evaluated by Western blot analysis. ELISA was used to measure the levels of cytokines TNF-α, IL-1β, and IL-6 in bronchoalveolar lavage fluid (BALF) and lung tissue. Levels of p- Smad2, Smad2, p-Smad3 and Smad3 were determined by western blotting.Results: AD treatment increased the collagen levels and expression levels of collagen I and α-smooth muscle actin (α-SMA) in lung tissue and of inflammatory cytokines TNF-α, IL-1β, and IL-6, in both bronchoalveolar lavage fluid (BALF) and lung tissue in a dose-dependent manner (p < 0.01).Furthermore, AD increased the levels of p-Smad2/3. AD-induced increases in collagen I and α-SMA levels were reversed by loureirin B (LB). In addition, LB reduced AD-induced increased levels of the inflammatory cytokines TNF-α, IL-1β, and IL-6 in both bronchoalveolar lavage fluid (BALF) and lung tissue (p < 0.01).Conclusion: These results demonstrate that LB downregulates expression of fibrosis-related proteins and suppresses AD-induced PF. The  mechanism responsible for the protective effect of LB on ADinduced PF might involve inhibition of the Smad2/3 pathway. Thus, LB is a potential therapeutic agent for the management of PF. Keywords: Amiodarone, Loureirin B, Pulmonary fibrosis, Smad, Inflammatio