System Structure Risk Metric Method Based on Information Flow

Part 5: Modelling and SimulationInternational audienceThe measurement of structure risk aims to analysis and evaluate the not occurred, potential, and the objectively exist risk in system structure. It is an essential way to validate system function and system quality. This paper proposes the risk metric model and algorithm based on information flow and analysis risk trend between traditional tree structure and network-centric structure

MsPrompt: Multi-step Prompt Learning for Debiasing Few-shot Event Detection

Event detection (ED) is aimed to identify the key trigger words in unstructured text and predict the event types accordingly. Traditional ED models are too data-hungry to accommodate real applications with scarce labeled data. Besides, typical ED models are facing the context-bypassing and disabled generalization issues caused by the trigger bias stemming from ED datasets. Therefore, we focus on the true few-shot paradigm to satisfy the low-resource scenarios. In particular, we propose a multi-step prompt learning model (MsPrompt) for debiasing few-shot event detection, that consists of the following three components: an under-sampling module targeting to construct a novel training set that accommodates the true few-shot setting, a multi-step prompt module equipped with a knowledge-enhanced ontology to leverage the event semantics and latent prior knowledge in the PLMs sufficiently for tackling the context-bypassing problem, and a prototypical module compensating for the weakness of classifying events with sparse data and boost the generalization performance. Experiments on two public datasets ACE-2005 and FewEvent show that MsPrompt can outperform the state-of-the-art models, especially in the strict low-resource scenarios reporting 11.43% improvement in terms of weighted F1-score against the best-performing baseline and achieving an outstanding debiasing performance

Performing MapReduce on Data Centers with Hierarchical Structures

Data centers are created as distributed information systems for massive data storage and processing. The structure of a data center determines the way that its inner servers, links and switches are interconnected. Several hierarchical structures have been proposed to improve the topological performance of data centers. By using recursively defined topologies, these novel structures can well support general applications and services with high scalability and reliability. However, these structures ignore the details of some specific applications running on data centers, such as MapReduce, a well-known distributed data processing application. The communication and control mechanisms for performing MapReduce on the traditional structure cannot be employed on the hierarchical structures. In this paper, we propose a methodology for performing MapReduce on data centers with hierarchical structures. Our methodology is based on the distributed hash table (DHT), an efficient data retrieval approach on distributed systems. We utilize the advantages of DHT, including decentralization, fault tolerance and scalability, to address the main problems that face hierarchical data centers in supporting MapReduce. Comprehensive evaluation demonstrates the feasibility and excellent performance of our methodology

CCL21/CCR7 Promotes G2/M Phase Progression via the ERK Pathway in Human Non-Small Cell Lung Cancer Cells

C-C chemokine receptor 7 (CCR7) contributes to the survival of certain cancer cell lines, but its role in the proliferation of human non-small cell lung cancer (NSCLC) cells remains vague. Proliferation assays performed on A549 and H460 NSCLC cells using Cell Counting Kit-8 indicated that activation of CCR7 by its specific ligand, exogenous chemokine ligand 21 (CCL21), was associated with a significant linear increase in cell proliferation with duration of exposure to CCL21. The CCL21/CCR7 interaction significantly increased the fraction of cells in the G2/M phase of the cell cycle as measured by flow cytometry. In contrast, CCL21/CCR7 had no significant influence on the G0/G1 and S phases. Western blot and real-time PCR indicated that CCL21/CCR7 significantly upregulated expression of cyclin A, cyclin B1, and cyclin-dependent kinase 1 (CDK1), which are related to the G2/M phase transition. The expression of cyclin D1 and cyclin E, which are related to the G0/G1 and G1/S transitions, was not altered. The CCL21/CCR7 interaction significantly enhanced phosphorylation of extracellular signal-regulated kinase (P-ERK) but not Akt, as measured by Western blot. LY294002, a selective inhibitor of PI3K that prevents activation of the downstream Akt, did not weaken the effect of CCL21/CCR7 on P-ERK. Coimmunoprecipitation further confirmed that there was an interaction between P-ERK and cyclin A, cyclin B1, or CDK1, particularly in the presence of CCL21. CCR7 small interfering RNA or PD98059, a selective inhibitor of MEK that disrupts the activation of downstream ERK, significantly abolished the effects of exogenous CCL21. These results suggest that CCL21/CCR7 contributes to the time-dependent proliferation of human NSCLC cells by upregulating cyclin A, cyclin B1, and CDK1 potentially via the ERK pathway

Overexpression of CARMA3 in Non-Small-Cell Lung Cancer Is Linked for Tumor Progression

We aimed to investigate the clinical significance of the expression of novel scaffold protein CARMA3 in non-small-cell lung cancer (NSCLC) and the biological function of CARMA3 in NSCLC cell lines. We observed moderate to high CARMA3 staining in 68.8% of 141 NSCLC specimens compared to corresponding normal tissues. The overexpression of CARMA3 was significantly correlated with TNM stage (P = 0.022) and tumor status (P = 0.013). CARMA3 upregulation also correlated with a shorter survival rate of patients of nodal status N0 (P = 0.042)as well as the expression of epidermal growth factor receptor (EGFR) (P = 0.009). In EGFR mutation positive cases, CARMA3 expression was much higher (87.5%) compared to non-mutation cases (66.1%). In addition, we observed that knockdown of CARMA3 inhibits tumor cell proliferation and invasion, and induces cell cycle arrest at the boundary between the G1 and S phase. We further demonstrated a direct link between CARMA3 and NF-κB activation. The change of biological behavior in CARMA3 knockdown cells may be NF-κB-related. Our findings demonstrated, for the first time, that CARMA3 was overexpressed in NSCLC and correlated with lung cancer progression, EGFR expression, and EGFR mutation. CARMA3 could serve as a potential companion drug target, along with NF-kB and EGFR in EGFR-mutant lung cancers

Autonomous motion and control of lower limb exoskeleton rehabilitation robot

Introduction: The lower limb exoskeleton rehabilitation robot should perform gait planning based on the patient’s motor intention and training status and provide multimodal and robust control schemes in the control strategy to enhance patient participation.Methods: This paper proposes an adaptive particle swarm optimization admittance control algorithm (APSOAC), which adaptively optimizes the weights and learning factors of the PSO algorithm to avoid the problem of particle swarm falling into local optimal points. The proposed improved adaptive particle swarm algorithm adjusts the stiffness and damping parameters of the admittance control online to reduce the interaction force between the patient and the robot and adaptively plans the patient’s desired gait profile. In addition, this study proposes a dual RBF neural network adaptive sliding mode controller (DRNNASMC) to track the gait profile, compensate for frictional forces and external perturbations generated in the human-robot interaction using the RBF network, calculate the required moments for each joint motor based on the lower limb exoskeleton dynamics model, and perform stability analysis based on the Lyapunov theory.Results and discussion: Finally, the efficiency of the APSOAC and DRNNASMC algorithms is demonstrated by active and passive walking experiments with three healthy subjects, respectively

TrkB is highly expressed in NSCLC and mediates BDNF-induced the activation of Pyk2 signaling and the invasion of A549 cells

<p>Abstract</p> <p>Background</p> <p>Aberrant regulation in the invasion of cancer cells is closely associated with their metastatic potentials. TrkB functions as a receptor tyrosine kinase and is considered to facilitate tumor metastasis. Pyk2 is a non-receptor tyrosine kinase and integrates signals in cell invasion. However, little is known about the expression of TrkB in NSCLC and whether Pyk2 is involved in TrkB-mediated invasion of A549 cells.</p> <p>Methods</p> <p>The expression of TrkB was investigated in NSCLC by immunohistochemical staining. Both HBE and A549 cells were treated with BDNF. The expression of TrkB, Pyk2 and ERK phosphorylations were assessed by western blot. Besides, A549 cells were transfected with TrkB-siRNA or Pyk2-siRNA, or treated with ERK inhibitor where indicated. Transwell assay was performed to evaluate cell invasion.</p> <p>Results</p> <p>40 cases (66.7%) of NSCLC were found higher expression of TrkB and patients with more TrkB expression had significant metastatic lymph nodes (p = 0.028). BDNF facilitated the invasion of A549 cells and the activations of Pyk2 in Tyr402 and ERK. However, the effects of BDNF were not observed in HBE cells with lower expression of TrkB. In addition, the increased Pyk2 and ERK activities induced by BDNF were significantly inhibited by blocking TrkB expression, so was the invasion of A549 cells. Knockdown studies revealed the essential role of Pyk2 for BDNF-induced cell invasion, since the invasion of A549 cells was abolished by Pyk2-siRNA. The application of ERK inhibitor also showed the suppressed ERK phosphorylation and cell invasion.</p> <p>Conclusion</p> <p>These data indicated that higher expression of TrkB in NSCLC was closely correlated with lymph node metastasis, and BDNF probably via TrkB/Pyk2/ERK promoted the invasion of A549 cells.</p

CCL21/CCR7 Prevents Apoptosis via the ERK Pathway in Human Non-Small Cell Lung Cancer Cells

Previously, we confirmed that C-C chemokine receptor 7 (CCR7) promotes cell proliferation via the extracellular signal-regulated kinase (ERK) pathway, but its role in apoptosis of non-small cell lung cancer (NSCLC) cell lines remains unknown. A549 and H460 cells of NSCLC were used to examine the effect of CCL21/CCR7 on apoptosis using flow cytometry. The results showed that activation of CCR7 by its specific ligand, exogenous chemokine ligand 21 (CCL21), was associated with a significant decline in the percent of apoptosis. Western blot and real-time PCR assays indicated that activation of CCR7 significantly caused upregulation of anti-apoptotic bcl-2 and downregulation of pro-apoptotic bax and caspase-3, but not p53, at both protein and mRNA levels. CCR7 small interfering RNA significantly attenuated these effects of exogenous CCL21. Besides, PD98059, a selective inhibitor of MEK that disrupts the activation of downstream ERK, significantly abolished these effects of CCL21/CCR7. Coimmunoprecipitation further confirmed that there was an interaction between p-ERK and bcl-2, bax, or caspase-3, particularly in the presence of CCL21. These results strongly suggest that CCL21/CCR7 prevents apoptosis by upregulating the expression of bcl-2 and by downregulating the expression of bax and caspase-3 potentially via the ERK pathway in A549 and H460 cells of NSCLC