Leveraging Intelligent Computation Offloading with Fog/Edge Computing for Tactile Internet: Advantages and Limitations

[EN] With the recent advancement in wireless communication and networks, we are at the doorstep of the Tactile Internet. The Tactile Internet aims to enable the skill delivery and thereafter democratize the specialized skills for many emerging applications (e.g., remote medical, industrial machinery, remote robotics, autonomous driving). In this article, we start with the motivation of applying intelligent edge computing for computation offloading in the Tactile Internet. Afterward, we outline the main research challenges to leverage edge intelligence at the master, network, and controlled domain of the Tactile Internet. The key research challenges in the Tactile Internet lie in its stringent requirements such as ultra-low latency, ultra-high reliability, and almost zero service outage. We also discuss major entities in intelligent edge computing and their role in the Tactile Internet. Finally, several potential research challenges in edge intelligence for the Tactile Internet are highlighted.This work was supported in part by the National Natural Science Foundation of China under Grant 61901128, and Agile Edge Intelligence for Delay Sensitive IoT (AgilE-IoT) project (Grant No. 9131-00119B) of Independent Research Fund Denmark (DFF).Mukherjee, M.; Guo, M.; Lloret, J.; Zhang, Q. (2020). Leveraging Intelligent Computation Offloading with Fog/Edge Computing for Tactile Internet: Advantages and Limitations. IEEE Network. 34(5):322-329. https://doi.org/10.1109/MNET.001.200000432232934

The Expression Levels of XLF and Mutant P53 Are Inversely Correlated in Head and Neck Cancer Cells.

XRCC4-like factor (XLF), also known as Cernunnos, is a protein encoded by the human NHEJ1 gene and an important repair factor for DNA double-strand breaks. In this study, we have found that XLF is over-expressed in HPV(+) versus HPV(-) head and neck squamous cell carcinoma (HNSCC) and significantly down-regulated in the HNSCC cell lines expressing high level of mutant p53 protein versus those cell lines harboring wild-type TP53 gene with low p53 protein expression. We have also demonstrated that Werner syndrome protein (WRN), a member of the NHEJ repair pathway, binds to both mutant p53 protein and NHEJ1 gene promoter, and siRNA knockdown of WRN leads to the inhibition of XLF expression in the HNSCC cells. Collectively, these findings suggest that WRN and p53 are involved in the regulation of XLF expression and the activity of WRN might be affected by mutant p53 protein in the HNSCC cells with aberrant TP53 gene mutations, due to the interaction of mutant p53 with WRN. As a result, the expression of XLF in these cancer cells is significantly suppressed. Our study also suggests that XLF is over-expressed in HPV(+) HNSCC with low expression of wild type p53, and might serve as a potential biomarker for HPV(+) HNSCC. Further studies are warranted to investigate the mechanisms underlying the interactive role of WRN and XLF in NHEJ repair pathway

Deadline-Aware Fair Scheduling for Offloaded Tasks in Fog Computing With Inter-Fog Dependency

[EN] A fundamental problem in fog computing networks is how to schedule the deadline-aware offloaded tasks that directly arrive from the end-users and via other fog nodes. The computational resource allocation becomes more challenging when the tasks demand different delay-deadlines. In this letter, we aim to propose a scheduling strategy to maximize the number of the completed tasks within their respective deadlines while making the network strongly stable. We exploit Lyapunov drift-plus-penalty function on the queue length to schedule the tasks in the queues. Subsequently, the scheduling policy decides the amount of task to be offloaded to the underloaded fog nodes to fully utilize the computational resources offered by all fog nodes in the network. Our simulation results reveal that the proposed strategy outperforms the baseline schemes, especially when those tasks have distinct delay-deadlines.This work was supported in part by the National Natural Science Foundation of China under Grants 61901128 and 61672174.Mukherjee, M.; Guo, M.; Lloret, J.; Iqbal, R.; Zhang, Q. (2020). Deadline-Aware Fair Scheduling for Offloaded Tasks in Fog Computing With Inter-Fog Dependency. IEEE Communications Letters. 24(2):307-311. https://doi.org/10.1109/LCOMM.2019.295774130731124

Small molecule-mediated tribbles homolog 3 promotes bone formation induced by bone morphogenetic protein-2.

Although bone morphogenetic protein-2 (BMP2) has demonstrated extraordinary potential in bone formation, its clinical applications require supraphysiological milligram-level doses that increase postoperative inflammation and inappropriate adipogenesis, resulting in well-documented life-threatening cervical swelling and cyst-like bone formation. Recent promising alternative biomolecular strategies are toward promoting pro-osteogenic activity of BMP2 while simultaneously suppressing its adverse effects. Here, we demonstrated that small molecular phenamil synergized osteogenesis and bone formation with BMP2 in a rat critical size mandibular defect model. Moreover, we successfully elicited the BMP2 adverse outcomes (i.e. adipogenesis and inflammation) in the mandibular defect by applying high dose BMP2. Phenamil treatment significantly improves the quality of newly formed bone by inhibiting BMP2 induced fatty cyst-like structure and inflammatory soft-tissue swelling. The observed positive phenamil effects were associated with upregulation of tribbles homolog 3 (Trib3) that suppressed adipogenic differentiation and inflammatory responses by negatively regulating PPARγ and NF-κB transcriptional activities. Thus, use of BMP2 along with phenamil stimulation or Trib3 augmentation may be a promising strategy to improve clinical efficacy and safety of current BMP therapeutics

Enhanced Osteogenesis of Adipose-Derived Stem Cells by Regulating Bone Morphogenetic Protein Signaling Antagonists and Agonists.

UnlabelledAlthough adipose-derived stem cells (ASCs) are an attractive cell source for bone tissue engineering, direct use of ASCs alone has had limited success in the treatment of large bone defects. Although bone morphogenetic proteins (BMPs) are believed to be the most potent osteoinductive factors to promote osteogenic differentiation of ASCs, their clinical applications require supraphysiological dosage, leading to high medical burden and adverse side effects. In the present study, we demonstrated an alternative approach that can effectively complement the BMP activity to maximize the osteogenesis of ASCs without exogenous application of BMPs by regulating levels of antagonists and agonists to BMP signaling. Treatment of ASCs with the amiloride derivative phenamil, a positive regulator of BMP signaling, combined with gene manipulation to suppress the BMP antagonist noggin, significantly enhanced osteogenic differentiation of ASCs through increased BMP-Smad signaling in vitro. Furthermore, the combination approach of noggin suppression and phenamil stimulation enhanced the BMP signaling and bone repair in a mouse calvarial defect model by adding noggin knockdown ASCs to apatite-coated poly(lactic-coglycolic acid) scaffolds loaded with phenamil. These results suggest novel complementary osteoinductive strategies that could maximize activity of the BMP pathway in ASC bone repair while reducing potential adverse effects of current BMP-based therapeutics.SignificanceAlthough stem cell-based tissue engineering strategy offers a promising alternative to repair damaged bone, direct use of stem cells alone is not adequate for challenging healing environments such as in large bone defects. This study demonstrates a novel strategy to maximize bone formation pathways in osteogenic differentiation of mesenchymal stem cells and functional bone formation by combining gene manipulation with a small molecule activator toward osteogenesis. The findings indicate promising stem cell-based therapy for treating bone defects that can effectively complement or replace current osteoinductive therapeutics

Novel link between E2F1 and Smac/DIABLO: proapoptotic Smac/DIABLO is transcriptionally upregulated by E2F1

Deregulated expression of E2F1 not only promotes S-phase entry but also induces apoptosis. Although it has been well documented that E2F1 is able to induce p53-dependent apoptosis via raising ARF activity, the mechanism by which E2F induces p53-independent apoptosis remains unclear. Here we report that E2F1 can directly bind to and activate the promoter of Smac/DIABLO, a mitochondrial proapoptotic gene, through the E2F1-binding sites BS2 (−542 ∼ −535 bp) and BS3 (−200 ∼ −193 bp). BS2 and BS3 appear to be utilized in combination rather than singly by E2F1 in activation of Smac/DIABLO. Activation of BS2 and BS3 are E2F1-specific, since neither E2F2 nor E2F3 is able to activate BS2 or BS3. Using the H1299 ER-E2F1 cell line where E2F1 activity can be conditionally induced, E2F1 has been shown to upregulate the Smac/DIABLO expression at both mRNA and protein levels upon 4-hydroxytamoxifen treatment, resulting in an enhanced mitochondria-mediated apoptosis. Reversely, reducing the Smac/DIABLO expression by RNA interference significantly diminishes apoptosis induced by E2F1. These results may suggest a novel mechanism by which E2F1 promotes p53-independent apoptosis through directly regulating its downstream mitochondrial apoptosis-inducing factors, such as Smac/DIABLO

Quantitative Estimation of Urban PM2.5 Pollution Baseline and Meteorological Resource Endowment Using Machine Learning in Chinese Yangtze River Economic Belt

Considering the influence of baseline values, meteorological conditions, and human activities on PM2.5, quantifying them will facilitate the classification, control, and management of pollution. The machine learning model explained the PM2.5-meteorological nonlinear relationship between PM2.5 and meteorological factors in each city across the Yangtze River Economic Belt, China. Meteorological resource endowments (MRE) are used to quantify the variation on PM2.5 concentration caused by meteorological conditions. Contamination baseline (CB) is used to characterize the lowest limit of anthropogenic impact in PM2.5 contamination without meteorological interference. According to the values of MRE and CB, cities in the Yangtze River economic belt can be divided into four categories (Q1-4). The average value of MRE is −0.41 μg/m3. The average value of CB is 34.05 μg/m3, which is lower than the Chinese Grade II standard (GB 3095-2012). The additional emissions by humans resulted in an increase of 7 μg/m3 in concentration, while the meteorological factors led to a decrease of −0.41 μg/m3. In terms of city classification, Q1 is concentrated in the midstream, and PM2.5 is the most challenging pollutant to control. Q2 is concentrated downstream, with relatively high PM2.5 emissions but favorable meteorological conditions. Q3 is concentrated upstream, and there is surplus environmental capacity even with limited meteorological conditions. Cites in Q4 have the most suitable development potential and exhibit a discrete spatial distribution. The research distinguished various categories of pollution and provided insights into the different characteristics of pollution around the Yangtze River Economic Belt. This information has helped the government classify cities and implement specific policies based on their individual situations