CCACK: Efficient Network Coding Based Opportunistic Routing Through Cumulative Coded Acknowledgments

The use of random linear network coding (NC) has significantly simplified the design of opportunistic routing (OR) protocols by removing the need of coordination among forwarding nodes for avoiding duplicate transmissions. However, NC-based OR protocols face a new challenge: How many coded packets should each forwarder transmit? To avoid the overhead of feedback exchange, most practical existing NC-based OR protocols compute offline the expected number of transmissions for each forwarder using heuristics based on periodic measurements of the average link loss rates and the ETX metric. Although attractive due to their minimal coordination overhead, these approaches may suffer significant performance degradation in dynamic wireless environments with continuously changing levels of channel gains, interference, and background traffic. In this paper, we propose CCACK, a new efficient NC-based OR protocol. CCACK exploits a novel Cumulative Coded ACKnowledgment scheme that allows nodes to acknowledge network coded traffic to their upstream nodes in a simple way, oblivious to loss rates, and with practically zero overhead. In addition, the cumulative coded acknowledgment scheme in CCACK enables an efficient credit-based, rate control algorithm. Our experiments on a 22-node 802.11 WMN testbed show that compared to MORE, a state-of-the-art NC based OR protocol, CCACK improves both throughput and fairness, by up to 3.2x and 83%, respectively, with average improvements of 11- 36% and 5.7-8.3%, respectively, for different numbers of concurrent flows. Our extensive simulations show that the gains are actually much higher in large networks, with longer routing paths between sources and destinations

Janus monolayers of transition metal dichalcogenides.

Structural symmetry-breaking plays a crucial role in determining the electronic band structures of two-dimensional materials. Tremendous efforts have been devoted to breaking the in-plane symmetry of graphene with electric fields on AB-stacked bilayers or stacked van der Waals heterostructures. In contrast, transition metal dichalcogenide monolayers are semiconductors with intrinsic in-plane asymmetry, leading to direct electronic bandgaps, distinctive optical properties and great potential in optoelectronics. Apart from their in-plane inversion asymmetry, an additional degree of freedom allowing spin manipulation can be induced by breaking the out-of-plane mirror symmetry with external electric fields or, as theoretically proposed, with an asymmetric out-of-plane structural configuration. Here, we report a synthetic strategy to grow Janus monolayers of transition metal dichalcogenides breaking the out-of-plane structural symmetry. In particular, based on a MoS2 monolayer, we fully replace the top-layer S with Se atoms. We confirm the Janus structure of MoSSe directly by means of scanning transmission electron microscopy and energy-dependent X-ray photoelectron spectroscopy, and prove the existence of vertical dipoles by second harmonic generation and piezoresponse force microscopy measurements

Shear stress regulation of miR-93 and miR-484 maturation through nucleolin.

Pulsatile shear (PS) and oscillatory shear (OS) elicit distinct mechanotransduction signals that maintain endothelial homeostasis or induce endothelial dysfunction, respectively. A subset of microRNAs (miRs) in vascular endothelial cells (ECs) are differentially regulated by PS and OS, but the regulation of the miR processing and its implications in EC biology by shear stress are poorly understood. From a systematic in silico analysis for RNA binding proteins that regulate miR processing, we found that nucleolin (NCL) is a major regulator of miR processing in response to OS and essential for the maturation of miR-93 and miR-484 that target mRNAs encoding Krüppel-like factor 2 (KLF2) and endothelial nitric oxide synthase (eNOS). Additionally, anti-miR-93 and anti-miR-484 restore KLF2 and eNOS expression and NO bioavailability in ECs under OS. Analysis of posttranslational modifications of NCL identified that serine 328 (S328) phosphorylation by AMP-activated protein kinase (AMPK) was a major PS-activated event. AMPK phosphorylation of NCL sequesters it in the nucleus, thereby inhibiting miR-93 and miR-484 processing and their subsequent targeting of KLF2 and eNOS mRNA. Elevated levels of miR-93 and miR-484 were found in sera collected from individuals afflicted with coronary artery disease in two cohorts. These findings provide translational relevance of the AMPK-NCL-miR-93/miR-484 axis in miRNA processing in EC health and coronary artery disease

Non-Fermi-liquid to Fermi-liquid transports in iron-pnictide Ba(Fe₁₋ₓCoₓ)₂As₂ and the electronic correlation strength in superconductors newly probed by the normal-state Hall angle

Electrical transports in iron-pnictide Ba(Fe1−x Co x )2As2 (BFCA) single crystals are heavily debated in terms of the hidden Fermi-liquid (HFL) and holographic theories. Both HFL and holographic theories provide consistent physic pictures and propose a universal expression of resistivity to describe the crossover of transports from the non-Fermi-liquid (FL) to FL behavior in these so-called \u27strange metal\u27 systems. The deduced spin exchange energy J and model-dependent energy scale W in BFCA are almost the same, or are of the same order of several hundred Kelvin for over-doped BFCA, which is in agreement with the HFL theory. Moreover, a drawn line of W/3.5 for BFCA in the higher-doping region up to the right demonstrates the crossover from non-FL-like behavior to FL-like behavior at high doping, and shows a new phase diagram of BFCA. The electronic correlation strength in superconductors has been newly probed by the normal-state Hall angle, which found that, for the first time, correlation strength can be characterized by the ratios of T c to the Fermi temperature T F, J/T F, and the transverse mass to longitudinal mass

MicroRNA-483 amelioration of experimental pulmonary hypertension.

Endothelial dysfunction is critically involved in the pathogenesis of pulmonary arterial hypertension (PAH) and that exogenously administered microRNA may be of therapeutic benefit. Lower levels of miR-483 were found in serum from patients with idiopathic pulmonary arterial hypertension (IPAH), particularly those with more severe disease. RNA-seq and bioinformatics analyses showed that miR-483 targets several PAH-related genes, including transforming growth factor-β (TGF-β), TGF-β receptor 2 (TGFBR2), β-catenin, connective tissue growth factor (CTGF), interleukin-1β (IL-1β), and endothelin-1 (ET-1). Overexpression of miR-483 in ECs inhibited inflammatory and fibrogenic responses, revealed by the decreased expression of TGF-β, TGFBR2, β-catenin, CTGF, IL-1β, and ET-1. In contrast, inhibition of miR-483 increased these genes in ECs. Rats with EC-specific miR-483 overexpression exhibited ameliorated pulmonary hypertension (PH) and reduced right ventricular hypertrophy on challenge with monocrotaline (MCT) or Sugen + hypoxia. A reversal effect was observed in rats that received MCT with inhaled lentivirus overexpressing miR-483. These results indicate that PAH is associated with a reduced level of miR-483 and that miR-483 might reduce experimental PH by inhibition of multiple adverse responses

Hedgehog pathway dysregulation contributes to the pathogenesis of human gastrointestinal stromal tumors via GLI-mediated activation of KIT expression.

Gastrointestinal stromal tumors (GIST) arise within the interstitial cell of Cajal (ICC) lineage due to activating KIT/PDGFRA mutations. Both ICC and GIST possess primary cilia (PC), which coordinate PDGFRA and Hedgehog signaling, regulators of gastrointestinal mesenchymal development. Therefore, we hypothesized that Hedgehog signaling may be altered in human GIST and controls KIT expression. Quantitative RT-PCR, microarrays, and next generation sequencing were used to describe Hedgehog/PC-related genes in purified human ICC and GIST. Genetic and pharmacologic approaches were employed to investigate the effects of GLI manipulation on KIT expression and GIST cell viability. We report that Hedgehog pathway and PC components are expressed in ICC and GIST and subject to dysregulation during GIST oncogenesis, irrespective of KIT/PDGFRA mutation status. Using genomic profiling, 10.2% of 186 GIST studied had potentially deleterious genomic alterations in 5 Hedgehog-related genes analyzed, including in the PTCH1 tumor suppressor (1.6%). Expression of the predominantly repressive GLI isoform, GLI3, was inversely correlated with KIT mRNA levels in GIST cells and non-KIT/non-PDGFRA mutant GIST. Overexpression of the 83-kDa repressive form of GLI3 or small interfering RNA-mediated knockdown of the activating isoforms GLI1/2 reduced KIT mRNA. Treatment with GLI1/2 inhibitors, including arsenic trioxide, significantly increased GLI3 binding to the KIT promoter, decreased KIT expression, and reduced viability in imatinib-sensitive and imatinib-resistant GIST cells. These data offer new evidence that genes necessary for Hedgehog signaling and PC function in ICC are dysregulated in GIST. Hedgehog signaling activates KIT expression irrespective of mutation status, offering a novel approach to treat imatinib-resistant GIST