Traffic-Aware Transmission Mode Selection in D2D-enabled Cellular Networks with Token System

We consider a D2D-enabled cellular network where user equipments (UEs) owned by rational users are incentivized to form D2D pairs using tokens. They exchange tokens electronically to "buy" and "sell" D2D services. Meanwhile the devices have the ability to choose the transmission mode, i.e. receiving data via cellular links or D2D links. Thus taking the different benefits brought by diverse traffic types as a prior, the UEs can utilize their tokens more efficiently via transmission mode selection. In this paper, the optimal transmission mode selection strategy as well as token collection policy are investigated to maximize the long-term utility in the dynamic network environment. The optimal policy is proved to be a threshold strategy, and the thresholds have a monotonicity property. Numerical simulations verify our observations and the gain from transmission mode selection is observed.Comment: 7 pages, 6 figures. A shorter version is submitted to EUSIPC

Loss of ATF3 exacerbates liver damage through the activation of mTOR/p70S6K/ HIF-1α signaling pathway in liver inflammatory injury.

Activating transcription factor 3 (ATF3) is a stress-induced transcription factor that plays important roles in regulating immune and metabolic homeostasis. Activation of the mechanistic target of rapamycin (mTOR) and hypoxia-inducible factor (HIF) transcription factors are crucial for the regulation of immune cell function. Here, we investigated the mechanism by which the ATF3/mTOR/HIF-1 axis regulates immune responses in a liver ischemia/reperfusion injury (IRI) model. Deletion of ATF3 exacerbated liver damage, as evidenced by increased levels of serum ALT, intrahepatic macrophage/neutrophil trafficking, hepatocellular apoptosis, and the upregulation of pro-inflammatory mediators. ATF3 deficiency promoted mTOR and p70S6K phosphorylation, activated high mobility group box 1 (HMGB1) and TLR4, inhibited prolyl-hydroxylase 1 (PHD1), and increased HIF-1α activity, leading to Foxp3 downregulation and RORγt and IL-17A upregulation in IRI livers. Blocking mTOR or p70S6K in ATF3 knockout (KO) mice or bone marrow-derived macrophages (BMMs) downregulated HMGB1, TLR4, and HIF-1α and upregulated PHD1, increasing Foxp3 and decreasing IL-17A levels in vitro. Silencing of HIF-1α in ATF3 KO mice ameliorated IRI-induced liver damage in parallel with the downregulation of IL-17A in ATF3-deficient mice. These findings demonstrated that ATF3 deficiency activated mTOR/p70S6K/HIF-1α signaling, which was crucial for the modulation of TLR4-driven inflammatory responses and T cell development. The present study provides potential therapeutic targets for the treatment of liver IRI followed by liver transplantation

Ethnobiological notes and volatile profiles of two rare Chinese desert truffles

The production of a distinct profile of volatile organic compounds plays a crucial role in the ecology of hypogeous Ascomycetes, and is also key to their gastronomic relevance. In this study, we explored the aroma components of two rarely investigated Chinese desert truffles, namely Mattirolomyces terfezioides and Choiromyces cerebriformis, using headspace solid-phase microextraction (HS-SPME) coupled with gas chromatography-mass spectrometry (GC-MS). Our investigation revealed the significant presence of sulphur-containing volatiles in the aroma of M. terfezioides but not in C. cerebriformis. We discussed available information on the distribution of these interesting truffles in China and their use as choice food by local people

Original Article Correlations of IFN-γ-inducible protein-10 with the risk of chronic hepatitis B and the efficacy of interferon therapy in Asians

Abstract: Purpose: The aim of this study was to identify the correlations of IFN-γ-inducible protein-10 (IP-10) with the risk of chronic hepatitis B (CHB) and the efficacy of interferon therapy in Asians. Method: Serum IP-10 levels were assayed using enzyme linked immunosorbent assay (ELISA) in both CHB and control group. CHB group received interferon-α2b treatment to compare the pre-treatment and post-treatment serum IP-10 levels. Relevant studies met predefined inclusion and exclusion criteria were enrolled into further meta-analysis. Stata 12.0 software was applied for data analysis. Result: Our case-control study demonstrated that CHB group had evaluated serum IP-10 levels compared with control group (285.7 ± 41.6 pg/mL vs. 79.1 ± 33.8 pg/mL, t = 21.85, P < 0.001. After treatment for 12 weeks, CHB group had remarkably decreased post-treatment serum IP-10 levels than pre-treatment (78.5 ± 20.4 pg/mL vs. 285.7 ± 41.6 pg/mL, t = 33.76, P < 0.001). No significance was observed on post-treatment serum IP-10 levels between CHB and control group (78.5 ± 20.4 pg/mL vs. 78.1 ± 33.8 pg/mL, t = 0.07, P = 0.947). Meta-analysis results demonstrated that serum IP-10 levels in CHB group were obviously higher than healthy controls (SMD = 2.21, 95% CI = 1.55~2.87, P < 0.001). A subgroup based on the HBeAg states revealed that serum IP-10 levels in both HBeAg-positive and HBeAg-negative CHB patients were notably higher than healthy controls (HBeAg-positive: SMD = 2.00, 95% CI = 1.13-2.87, P < 0.001; HBeAg-negative: SMD = 1.34, 95% CI = 0.97-1.72, P < 0.001). Conclusion: Serum IP-10 may be correlated with the risk of CHB and the efficiency of interferon therapy, thus IP-10 may be a good biomarker for the diagnosis and treatment of CHB