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Mobile edge computing (MEC), extending computing services from cloud to edge, is recognized as one of key pillars to facilitate real-time services and tackle backhaul bottleneck. However, it is not economically efficient to attach intensive security appliances to every MEC node to defend application-level DDoS attacks and ensure the availability of services. Thus, we explore the elasticity of security defense among MEC nodes by proposing a COoperative DEfense (CODE) framework for MEC, referred to as CODE4MEC. CODE4MEC aims to adapt to traffic changes by coordinating container-carried defensive resources among cooperative MEC nodes in an automatic way. Towards this aim, we propose four control plane functions to enable a life-cycle management for CODE4MEC, namely, CODE triggering, scheduling, coordination and releasing. However, an effective CODE4MEC requires non-trivial algorithmic schemes, in particular for CODE scheduling and coordination functions. We thus design an online combinatorial auction mechanism for real-time CODE scheduling, and prove a tighter performance bound relative to prior arts. As for CODE coordination, a flow-based traffic and context information coordination scheme is proposed to enable classical defense schemes to work properly and efficiently. Finally, using a combination of real testbed and simulation evaluations, we validate the effectiveness of CODE4MEC.

Liver fibrosis results from the formation of fibrous scars of hepatic stellate cells by various chronic liver diseases. Considering that the liver is the most important metabolic organ in the human body, exploring the metabolic characteristics of liver fibrosis is expected to discover new markers and therapeutic targets. In this study, we first used mouse model to verify that both lactate content and histone acetylation levels were significantly increased in hepatic fibrosis mice. At the same time, it was confirmed that activated hepatic stellate cells (HSCs) cocultured with M1 macrophages can promote their transformation into M2 macrophages in hepatic stellate cell line and primary hepatic stellate cells. In addition, the addition of lactic acid to the medium in which M1 cells are cultured can promote their transformation into M2 macrophages. Therefore, we concluded that activated HSCs can promote the transformation of M1 to M2 macrophages through lactate accumulation, thereby causing liver fibrosis.

With the rapid development of information technology and communication technology, several online recovery platforms have introduced offline channels to encourage customers to participate in product acquisition and improve profits. Motivated by this reverse supply chain practice, we develop a game theory model under three scenarios (single offline channel, single online channel, and dual-channel structures) to assess the effect of a newly added offline channel for online recovery platforms and explore the factors that have significant impacts on the dual-channel strategy for recovery platforms. We conduct static analyses to solve the model and perform a numerical study to examine the robustness of the results. The results reveal that a recovery platform can always gain more profit and set lower recovery prices under the dual-channel structure. However, the relatively high shipping cost might cause the recovery platform to recover a smaller quantity under the dual-channel structure compared with the single offline channel structure. In addition, the recovery platform is more likely to adopt a dual-channel structure with low shipping cost, high average hassle cost or hassle cost uncertainty, and less uncertainty on the reservation value. Moreover, the recovery platform can use the price difference between online and offline channels as a tool to split product holders and induce them to choose the most appropriate channel. Our findings highlight the profit and recovery quantity benefits brought by the dual-channel structure, and provide management insights for recovery platforms.

This study assessed the mechanism of tanshinone A in regulating biological characteristics of Hematopoietic Stem Cell (HSC) in liver cirrhosis through targeting of miR-9a-5p. HSC cells were divided into negative control group and stimulated miR-9a-5p inhibitor group. Transfection was performed according to specification of the kit. Expression of miR-9a-5p was assessed with Real-time polymerase chain reaction (PCR). Cell proliferation was tested with flow cytometry (FCM), and α-smooth muscle actin (SMA) and Type I collagen expressions were detected with Western Blot assay. Caspase-3 activity was tested with spectrophotometry, while variation of inflammatory factor was detected with enzyme-linked immunosorbent assay (ELISA). There was higher miR-9a-5p level in HSC induced by Chemokine (C-C motif) ligands 4 (CCL-4). Biological characteristics of HSC induced by CCL-4 was restrained by down-regulation of miR-9a-5p, and presentation quantity of α-SMA and Type I collagen was reduced. So, occurrence of inflammation and migration of HSC could be restrained. The presentation quantity of Type I collagen was reduced with tanshinone A, and expression of miR-9a-5p was reduced. HSC characteristics in liver cirrhosis were affected by tanshinone A probably through regulating miR-9a-5p. It could provide a brand-new selection for treatment on liver cirrhosis.

Over the past few decades, many research efforts have been dedicated to qualitatively and quantitatively evaluate resilience in different domains. As compared with research areas in social science and ecology, the concept of resilience in the engineering domain is relatively new. In the engineering domain, studies on resilience mostly focus on civil infrastructure. It is important to extend the concept of resilience to a broad range of engineering applications. The field environments of complex engineering systems vary with different applications. Even with the same component/system applied in different field environments, the ability, time, and resources required by failure detection, diagnosis, and restoration can be different. Hence, it is critical to introduce a new dimension, random field environment (RFE), into the development of the mathematical model for quantifying resilience. This article first introduces a new definition of resilience and then proposes a general RFE-based multidimensional time-dependent resilience model connecting reliability, vulnerability, and recoverability. Besides, we present a specific RFE-based multidimensional time-dependent resilience model by considering the specified functions of the impact of the RFE on system performance and recovery. Furthermore, we extend the proposed resilience model by incorporating multiple failure paths of complex systems. Finally, we apply the proposed resilience model to vehicular edge computing networks to evaluate the vehicular network resilience with the disruptive events on the communication links.

Our study was aimed to study the mechanism of oxymatrine in regulating the Hematopoietic Stem Cell (HSC) mitochondrial apoptosis and improving prognosis of rats with liver cirrhosis through AMPK signal pathway. The HSC cells were cultivated and identified by IHC method. The inhibition rates for active HSC cells by oxymatrine at several concentrations were as follows; 0.5, 1, 2, 4 and 8 mg/mL, as detected by MTT method. The optimum interfered concentration was confirmed. The condition for apoptosis in HSC cells interfered with oxymatrine at 0.125, 0.25, and 0.5 mg/mL concentrations. The variation of apoptosis in control group and model group was also observed through TEM. The active presentation of AMPK, PAMPK, Caspsase-3 and BCL-2 was detected with RT-PCR. The index of hepatic function in venous blood of rats’ eyeball was tested, and degree of hepatic fibrosis in liver tissue homogenate was also tested. Expression of AMPK/PAMPK, Caspsase-3 and BCL-2 was detected with Western Blot assay. Results showed that, proliferative rate was elevated along with prolonged cultivation duration. The optimum drug interfered concentration was 0.5 mg/mL. The expression of AMPK, PAMPK, Caspsase-3 and BCL-2 in model group was notably higher than in the control group. There was splitting decomposition in cell nucleus and cohesion in cytoplasm after HSC cells were disposed with oxymatrine. The expression of AMPK, Caspsase-3 and BCL-2 was prompted to induce generation of mitochondrial apoptosis, and level of liver function and indicators of hepatic fibrosis were reduced effectively. The prognosis of rats with liver cirrhosis could then be improved.

Background Only a small subset of colon cancer patients with mismatch repair deficiency may also benefit from Immune checkpoint inhibitors (ICIs). New biomarkers correlated with ICIs responsiveness need to be explored. Methods The study data were obtained from TCGA, GEO, cBioPortal, UALCAN, UCSC Xena browser, and CPTAC databases. Protein kinase C beta (PRKCB) was screened via weighted gene co-expression network analysis (WGCNA), survival analysis and differential expression analysis. The biological and immune landscape of PRKCB was explored by performing bioinformatics and immunohistochemical analyses. These findings were used to predict responsiveness to immunotherapy. Results Yellow module in WGCNA, as a hub module, was strongly positively correlated with infiltrated CD8 + T cell and Immune Score. PRKCB was an essential member of the yellow module, downregulated in colon cancer tissue, and associated with poor prognosis. GO, KEGG, REACTOME enrichment analysis showed PRKCB was associated with Cytokine-cytokine receptor interaction, Chemokine signaling pathway, T cell receptor signaling pathway, NF-κB signal pathway, Natural killer cell mediated cytotoxicity, and PD-L1 signaling. Meanwhile, the PRKCB expression was highly positively correlated with the infiltration of the CD4 + T cells, CD8 + T cells, and NK cells. Moreover, the immunohistochemistry analysis of tissue microarray demonstrated that PRKCB expression was positively correlated with infiltrated CD8 + T cell and PD-L1 expression. As expected, the TIDE and SubMap algorithm verified that ICIs could be effective in PRKCB-high patients. Conclusion PRKCB-high was associated with good prognoses in colon cancer patients. PRKCB-high was an indicator of inflamed TIME, which correlated with high responsiveness to immunotherapy in colon cancer patients.

Background: WD repeat domain 12 (WDR12) encodes a member of the WD-repeat protein family, a component of a nucleolar protein complex that affects the maturation of the large ribosomal subunit, which was highly expressed in colorectal cancer (CRC) tissues compared to para-cancerous tissues. However, its function is unclear in CRC. Thus, our goal was to reveal the biological role of WDR12 in the tumorigenesis and development of CRC. Method：To investigate the correlation of gene knockdown with CRC malignancy (proliferative and anti-apoptotic) by performing lentivirus-assisted WDR12 knockdown experiments in HCT116 and SW620 model CRC cell lines and Validated in vivo experiments in nude mice. Then the possible mechanism of the downstream pathway of WDR12 was investigated by ingenuity pathway analysis (IPA). Finally, in vitro experiments explored the relationship between RAC1 and WDR12 in cell proliferation and anti-apoptosis. Result: In-vitro lentivirus-assisted WDR12 gene knockdown experiments in CRC cell lines showed cell proliferation inhibition, decreased cell viability, and promotion of cell apoptosis compared to empty controls. Hereafter, In-vivo tumor formation experiments in nude mice revealed that tumor area, volume, and weight were significantly lower for knockdown WDR12. In addition, Ingenuity Pathway Analysis and Western blot showed that knockdown of WDR12 affected the down-regulation of a series of downstream genes, including RAC1, PLK1, EZH2, and SKP2, which affected cell proliferation, apoptosis, and cell cycle. Functional recovery experiments demonstrated that overexpression of RAC1 recovered the ability of WDR12 to promote cell proliferation and inhibit apoptosis. Conclusion: In conclusion, WDR12 may be a novel oncogenic factor and a therapeutic target in CRC. Meanwhile, RAC1 may be one of the interacting genes in the downstream pathway of WDR12.

For the mobile edge computing network consisting of multiple base stations and resource-constrained user devices, network cost in terms of energy and delay will incur during task offoading from the user to the edge server. With the limitations imposed on transmission capacity, computing resource, and connection capacity, the perslot online learning algorithm is first proposed to minimize the time-averaged network cost. In particular, by leveraging the theories of stochastic gradient descent and minimum cost maximum flow, the user association is jointly optimized with resource scheduling in each time slot. The theoretical analysis proves that the proposed approach can achieve asymptotic optimality without any prior knowledge of the network environment. Moreover, to alleviate the high network overhead incurred during user handover and task migration, a two-timescale optimization approach is proposed to avoid frequent changes in user association. With user association executed on a large time scale and the resource scheduling decided on the single time slot, the a symptotic optimality is preserved. Simulation results verify the effectiveness of the proposed online learning algorithms.

With convenient Internet access and ubiquitous high-quality sensors in end-user devices, a growing number of content consumers are engaging in the content creation process. Meanwhile, mobile edge computing (MEC) can provision distributed computing resources for local data processing. The MEC-enhanced video crowdsourcing application will gather user-generated video contents and collectively distribute them to the viewers of interest. To empower the crowdsourced video streaming at the edge, we investigate how to efficiently transmit data from content generators to the viewers. In particular, for a group of collaborative mobile users willing to share their data with the viewers, the content generation and delivery scheme is designed by considering the cost incurred by the crowdsourcing application. By leveraging the cloud resources available at the wireless base stations, the uploading or downloading server site is chosen for each user. To minimize the system makespan, i.e., the overall data transmission time among the generators and viewers, the user association scheme is also designed to efficiently utilize the diverse wireless radio resources. As compared with traditional centralized/distributed content delivery schemes, the proposed algorithm can improve the cost-effectiveness of distributed radio/cloud resources deployed at the mobile edge.

With the advancements of Software Defined Networking and Network Function Virtualization technologies, users can access the software-based service function chain (SFC), which is composed of multiple sequential virtual network function (VNF) nodes. Although SFC is more flexible and adaptive in terms of design and deployment, the security risks should not be underestimated. At present, there is a lack of security or risk assessment for SFC, and SFC deployments rarely take their security into account. However, vulnerabilities and risks can cause VNF node failure during operation, which can lead to issues such as disruptions in SFC service and user data leakage. This paper proposes the concept of SFC credibility, which quantifies the authenticity, availability, and reliability of the VNF nodes from both time and space dimensions. Then, a hierarchical credibility evaluation model is built such that VNF nodes can be selected for the user based on their trustworthiness. A credibility-based deployment strategy is further designed for SFC and the corresponding VNF forwarding graph. Furthermore, a comparative study with three existing deployment strategies has shown the advantages of the proposed method. The extensive experimental results demonstrate the improved trust degree and the acceptance rate of SFC with a limited budget.

Cerebral ischemic stroke (CIS) remains a primary cause of death worldwide. The current knowledge has identified the implication of microRNAs (miRNAs) in the pathophysiology of CIS. This study investigated the mechanism of miR-302a-3p in nerve repair post CIS.A middle cerebral artery occlusion (MCAO) model was established in mice to simulate CIS. miR-302a-3p expression in brain tissues of MCAO mice was up-regulated by injecting agomiR-302a-3p. Neurological deficits of MCAO mice were evaluated through neurological function score, forelimb placing test, and balance beam walking test. Neuronal damage was measured using Nissl staining. The concentrations of nerve injury-related factors (S100B and GFAP) and the contents of neuroinflammatory factors (TNF-α and IL-1β) in serum were examined using ELISA kits. miR-302a-3p, E2F1, and long non-coding RNA (lncRNA) SNHG3 expressions in brain tissues of MCAO mice were determined using RT-qPCR and Western blot. The binding relationships between miR-302a-3p and E2F1 and E2F1 and SNHG3 were validated using dual-luciferase and ChIP assays, respectively.miR-302a-3p expression was reduced in brain tissues of MCAO mice. miR-302a-3p overexpression increased the number of neurons, decreased the concentrations of S100B and GFAP, reduced the contents of TNF-α and IL-1β, promoted nerve repair, and alleviated CIS-induced brain injury. miR-302a-3p targeted E2F1 expression, and E2F1 activated SNHG3 transcription. E2F1 overexpression or SNHG3 overexpression reversed the effect of miR-302a-3p overexpression on nerve repair in MCAO mice.miR-302a-3p overexpression repressed SNHG3 transcription by targeting E2F1 expression, thereby promoting nerve repair and alleviating CIS.

The demand for bandwidth-intensive and delay-sensitive services is surging daily with the development of 5G technology, resulting in fierce competition for scarce radio resources. Power domain Nonorthogonal Multiple Access (NOMA) technologies can dramatically improve system capacity and spectrum efficiency. Unlike existing NOMA scheduling that mainly focuses on fairness, this paper proposes a power control solution for uplink hybrid OMA and PD-NOMA in dual dynamic environments: dynamic and imperfect channel information together with the random user-specific hierarchical quality of service (QoS). This paper models the power control problem as a nonconvex stochastic, which aims to maximize system energy efficiency while guaranteeing hierarchical user QoS requirements. Then, the problem is formulated as a partially observable Markov decision process (POMDP). Owing to the difficulty of modeling time-varying scenes, the urgency of fast convergency, the adaptability in a dynamic environment, and the continuity of the variables, a Deep Reinforcement Learning (DRL)-based method is proposed. This paper also transforms the hierarchical QoS constraint under the NOMA serial interference cancellation (SIC) scene to fit DRL. The simulation results verify the effectiveness and robustness of the proposed algorithm under a dual uncertain environment. As compared with the baseline Particle Swarm Optimization algorithm (PSO), the proposed DRL-based method has demonstrated satisfying performance.

Osteoporosis is diagnosed based on the results of BMD assessment and/or fragility fractures. Vertebral fracture is the most common fragility fracture. Many vertebral fractures are asymptomatic and are not clinically recognized. Early detection of vertebral fracture may increase diagnosis of osteoporosis. In this study, we performed BMD measurement combined with vertebral fracture assessment (VFA) by DXA for the postmenopausal women receiving the first bone densitometry and studied the impact of VFA on the diagnosis of osteoporosis. A total of 502 postmenopausal women were enrolled in our study. Patients’ age was 66.7 ± 9.5 years. All patients had BMD assessment and VFA by dual-energy X-ray absorptiometry. Genant’s semiquantitative assessment was used. The impact of VFA on the diagnosis of osteoporosis was studied. All parameters of groups were compared using the Chi-squared test. There were 257 patients with T-score ≤−2.5, 202 patients with a T-score between −1 and − 2.5, and 43 patients with BMD within the normal range. There were 162 patients with 345 fractured vertebrae identified by VFA, among which 84% of patients were previously unknown. Osteoporosis or severe osteoporosis was presented in 51.2% patients diagnosed by BMD alone, in 55.2% patients diagnosed by BMD plus fracture history, and in 62.4% of patients diagnosed by BMD plus fracture history and VFA. Severe osteoporosis significantly increased by 17.2% in patients receiving VFA. VFA combined with BMD can detect previously unknown vertebral fractures and increase clinical diagnosis of osteoporosis. It is plausible to speculate that this method should be considered in postmenopausal women for the first BMD assessment.

Leaf angle of maize is a fundamental determinant of plant architecture and an important trait influencing photosynthetic efficiency and crop yields. To broaden our understanding of the genetic mechanisms of leaf angle formation, we constructed a F3:4recombinant inbred lines (RIL) population to map QTL for leaf angle. The RIL was derived from a cross between a model inbred line (B73) with expanded leaf architecture and an elite inbred line (Zheng58) with compact leaf architecture. A sum of eight QTL were detected on chromosome 1, 2, 3, 4 and 8. Single QTL explained 4.3 to 14.2% of the leaf angle variance. Additionally, some important QTL were confirmed through a heterogeneous inbred family (HIF) approach. Furthermore, twenty-four candidate genes for leaf angle were predicted through whole-genome re-sequencing and expression analysis in qLA02-01and qLA08-01 regions. These results will be helpful to elucidate the genetic mechanism of leaf angle formation in maize and benefit to clone the favorable allele for leaf angle. Besides, this will be helpful to develop the novel maize varieties with ideal plant architecture through marker-assisted selection.

Intelligent transportation is an important component of future smart cities, and electric autonomous vehicles (EAVs) are envisioned to be the main form of transportation because EAVs can save energy, protect the environment, and improve service efficiency. With limited vehicle-specific energy storage capacity and overall constraint in the smart grid’s electric load, we propose a novel intelligent management scheme to jointly schedule the travel and charging activities of the EAV fleet in one geographical area. This scheme not only schedules EAVs to meet the passengers’ requests but also explores the matching problem between the energy requirement of EAVs and the deployment of charging piles in smart cities. We minimize the total cruise energy consumption of EAVs under the condition of limited energy supply while guaranteeing the quality-of-service (QoS). Network Calculus (NC) is extended to model the electric traffic flow in this paper. With the real-world electric taxi data in Beijing, simulation results demonstrate that the proposed scheme can achieve substantial energy reduction and remarkable improvements in both the order completion rate and utilization rate of the charging stations.

Objective: The study aimed to explore the role of miR-25 and the notch signaling pathway in the memory capacity and brain tissue of mice with central nervous system (CNS) infections. Methods: A bioinformatics website and the dual-luciferase reporter assay were used to analyze the targeting relationship between miR-25 and Notch1. The mice were randomized into 7 groups (n=10 per group), including the normal group, the model group (lipopolysaccharide at a dose of 500 μg/kg for the model establishment), the NC group, the miR-25 mimic group, the miR-25 inhibitor group, the DAPT group, and the miR-25 inhibitor + DAPT group. qRT-PCR and western blot were used to measure the miR-25, Notch1, and Hes5 expression levels in the hippocampal CA1 region of the mice’s brains, along with the cyclo-oxygenase 2 (COX-2) and inducible nitric oxide synthase (iNOS) levels in the mice’s hippocampi. Results: Compared with the normal mice, the model mice had up-regulated miR-25, COX-2, and iNOS expressions and down-regulated Notch1 and Hes5 expressions, lower superoxide dismutase (SOD) levels in the hippocampi, and higher malondialdehyde (MDA) levels. Compared with the model group, the miR-25 mimic and DAPT groups had down-regulated Notch1 and Hes5 expressions, lower learning and memory capacities and SOD levels, higher MDA levels, and up-regulated COX-2 and iNOS expressions. Conclusion: Down-regulating miR-25 may improve the memory capacity in mice with CNS infections by activating the Notch signaling pathway.