Despite growing importance of long non-coding RNAs (lncRNAs) in normal physiological and disease conditions, our knowledge of RA-related lncRNAs remains limited. Therefore, we aimed to identify lncRNA signatures that have prognostic values in RA. There was a notably high expression level of Hotair in blood mononuclear cells and serum exosome of rheumatoid arthritis (RA) patients, leading the migration of active macrophage. In contrast, markedly lower level of Hotair was detected in differentiated osteoclasts and rheumatoid synoviocytes and enforced expression of Hotair led to significantly decreased levels of MMP-2 and MMP-13. This exploratory study provides novel empirical evidence that Hotair could be one of potential biomarkers for diagnosing RA.

Recently, underwater wireless sensor networks (UWSNs) have attracted much research attention from both academia and industry, in order to explore the vast underwater environment. UWSNs have peculiar characteristics; that is, they have large propagation delay, high error rate, low bandwidth, and limited energy. Therefore, designing network/routing protocols for UWSNs is very challenging. Also, in UWSNs, improving the energy efficiency is one of the most important issues since the replacement of the batteries of underwater sensor nodes is very expensive due to the unpleasant underwater environment. In this paper, we therefore propose an energy efficient routing protocol, named (energy-efficient depth-based routing protocol) EEDBR for UWSNs. EEDBR utilizes the depth of sensor nodes for forwarding data packets. Furthermore, the residual energy of sensor nodes is also taken into account in order to improve the network lifetime. Based on the comprehensive simulation using NS2, we observe that EEDBR contributes to the performance improvements in terms of the network lifetime, energy consumption, and end-to-end delay. A previous version of this paper was accepted in AST-2011 conference.

Abstract. Recently, Underwater Wireless Sensor Networks (UWSNs) have attracted much research attention from both academia and industry, in order to explore the vast underwater environment. However, designing network protocols is challenging in UWSNs since UWSNs have peculiar characteristics of large propagation delay, high error rate, low bandwidth and limited energy. In UWSNs, improving the energy efficiency is one of the most important issues since the replacement of the batteries of such nodes is very expensive due to harsh underwater environment. Hence, in this paper, we propose an energy efficient routing protocol, named EEDBR (Energy-Efficient Depth Based Routing protocol) for UWSNs. Our proposed protocol utilizes the depth of the sensor nodes for forwarding the data packets. Furthermore, the residual energy of the sensor nodes is also taken into account in order to improve the network life-time. Based on the comprehensive simulation using NS2, we observe that our proposed routing protocol contributes to the performance improvements in terms of the network lifetime, energy consumption and end-to-end delay.

SUMMARYRecently, underwater wireless sensor networks (UWSNs) have attracted much research attention to support various applications for pollution monitoring, tsunami warnings, offshore exploration, tactical surveillance, etc. However, because of the peculiar characteristics of UWSNs, designing communication protocols for UWSNs is a challenging task. Particularly, designing a routing protocol is of the most importance for successful data transmissions between sensors and the sink. In this paper, we propose a reliable and energy‐efficient routing protocol, named R‐ERP2R (Reliable Energy‐efficient Routing Protocol based on physical distance and residual energy). The main idea behind R‐ERP2R is to utilize physical distance as a routing metric and to balance energy consumption among sensors. Furthermore, during the selection of forwarding nodes, link quality towards the forwarding nodes is also considered to provide reliability and the residual energy of the forwarding nodes to prolong network lifetime. Using the NS‐2 simulator, R‐ERP2R is compared against a well‐known routing protocol (i.e. depth‐based routing) in terms of network lifetime, energy consumption, end‐to‐end delay and delivery ratio. The simulation results proved that R‐ERP2R performs better in UWSNs.Copyright © 2012 John Wiley & Sons, Ltd.

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Dysregulated Foxp3 Treg functions result in uncontrolled immune activation and autoimmunity. Therefore, identifying cellular factors modulating Treg functions is an area of great importance. Here, using Treg-specific mice, we report that IL-27 signaling in Foxp3 Tregs is essential for Tregs to control autoimmune inflammation in the central nervous system (CNS). Following experimental autoimmune encephalomyelitis (EAE) induction, Treg-specific mice develop more severe EAE. Consistent with the severe disease, the numbers of IFNγ- and IL-17-producing CD4 T cells infiltrating the CNS tissues are greater in these mice. Treg accumulation in the inflamed CNS tissues is not affected by the lack of IL-27 signaling in Tregs, suggesting a functional defect of Tregs. IL-10 production by conventional CD4 T cells and their CNS accumulation are rather elevated in Treg-specific mice. Analysis with Treg fate-mapping reporter mice further demonstrates that IL-27 signaling in Tregs may control stability of Foxp3 expression. Finally, systemic administration of recombinant IL-27 in Treg-specific mice fails to ameliorate the disease even in the presence of IL-27-responsive conventional CD4 T cells. These findings uncover a previously unknown role of IL-27 in regulating Treg function to control autoimmune inflammation.

BackgroundEven though osteoarthritis (OA) is the most common musculoskeletal dysfunction, there are no effective pharmacological treatments to treat OA due to lack of understanding in OA pathology. To better understand the mechanism in OA pathogenesis and investigate its effective target, we analyzed miRNA profiles during OA pathogenesis and verify the role and its functional targets of miR-488.ResultsHuman articular chondrocytes were obtained from cartilage of OA patients undergoing knee replacement surgery and biopsy samples of normal cartilage and the expression profile of miRNA was analyzed. From expression profile, most potent miR was selected and its target and functional role in OA pathogenesis were investigated using target validation system and OA animal model system. Among miRNAs tested, miR-488 was significantly decreased in OA chondrocytes Furthermore, we found that exposure of IL-1β was also suppressed whereas exposure of TGF-β3 induced the induction of miR-488 in human articular chondrocytes isolated from biopsy samples of normal cartilages. Target validation study showed that miR-488 targets ZIP8 and suppression of ZIP8 in OA animal model showed the reduced cartilage degradation. Target validation study showed that miR-488 targets ZIP8 and suppression of ZIP8 in OA animal model showed the reduced cartilage degradation.ConclusionsmiR-488 acts as a positive role for chondrocyte differentiation/cartilage development by inhibiting MMP-13 activity through targeting ZIP-8.

BackgroundEven though increasing evidences on miRNA involvement in human pathological responses, the distinct roles and related mechanisms of miRNAs in the pathology of osteoarthritis (OA) are not yet fully understood.MethodRNA levels or protein levels of Apoptotic genes, HDACs, MMP-13, and miRNAs in human chondrocytes isolated from normal biopsy sample and OA cartilages were analyzed by real-time PCR or western blotting. Exogenous modulation of miR-222 level was performed using delivery of its specific precursor or specific inhibitor and target validation assay was applied to identify its potent target. In vivo study using DMM mice model was performed and assessed the degree of cartilage degradation.ResultsAccording to miRNA profiling, miR-222 was significantly down-regulated in OA chondrocytes. Over-expression of miR-222 significantly suppressed apoptotic death by down-regulating HDAC-4 and MMP-13 level. Moreover, 3′-UTR reporter assays showed that HDAC-4 is a direct target of miR-222. The treatment of chondrocytes with the HDAC inhibitor, trichostatin A (TSA), suppressed MMP-13 protein level and apoptosis, whereas the over-expression of HDAC-4 displayed opposite effects. The introduction of miR-222 into the cartilage of medial meniscus destabilized mice significantly reduced cartilage destruction and MMP-13 level.ConclusionTaken together, our data suggest that miR-222 may be involved in cartilage destruction by targeting HDAC-4 and regulating MMP-13 level.