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In this paper, we study big data-driven Cyber–Physical Systems (CPS) through cloud platforms and design scheduling optimization algorithms to improve the efficiency of the system. A task scheduling scheme for large-scale factory access under cloud–edge collaborative computing architecture is proposed. The method firstly merges the directed acyclic graphs on cloud-side servers and edge-side servers; secondly, divide the tasks using a critical path-based partitioning strategy to effectively improve the allocation accuracy; then achieves load balancing through reasonable processor allocation, and finally compares and analyses the proposed task scheduling algorithm through simulation experiments. The experimental system is thoroughly analysed, hierarchically designed, and modelled, simulated, and the experimental data analysed and compared with related methods. The experimental results prove the effectiveness and correctness of the worst-case execution time analysis method and the idea of big data-driven CPS proposed in this paper and show that big data knowledge can help improve the accuracy of worst-case execution time analysis. This paper implements a big data-driven scheduling optimization algorithm for Cyber–Physical Systems based on a cloud platform, which improves the accuracy and efficiency of the algorithm by about 15% compared to other related studies.

GITRL/GITR signaling pathway plays an important role in allergy, inflammation, transplantation and autoimmunity. However, its role in asthma remains unclear. Thus, the present study aimed to investigate changes in this pathway and observe the therapeutic effect of its blocking on asthma. By using house dust mite-induced asthma model, changes of GITRL/GITR and its downstream molecules MAPKs (e.g., p38 MAPK, JNK and Erk) and NF-κB were observed. After that, GITRL in lung of mice was knocked down by recombinant adeno-associated virus to observe the impact on its downstream molecules and assess the therapeutic effect on asthma. These results showed that GITRL/GITR and its downstream molecules MAPKs/NF-κB were activated in asthmatic mice. This activation was suppressed after GITRL knockdown, and allergic airway inflammation and airway hyperresponsiveness were alleviated. These results demonstrate that GITRL/GITR-MAPKs/NF-κB signaling pathway participates in the pathogenesis of asthma. Blockade of GITRL/GITR signaling pathway exhibits protective effects in a mouse model of house dust mite-induced allergic asthma.

Background Glucocorticoid-induced tumor necrosis factor receptor family-related protein ligand (GITRL) plays an important role in tumors, autoimmunity and inflammation. However, GITRL is not known to modulate the pathogenesis of allergic asthma. In this study, we investigated whether regulating GITRL expressed on dendritic cells (DCs) can prevent asthma and to elucidate its mechanism of action. Methods In vivo, the role of GITRL in modulating house dust mite (HDM)-induced asthma was assessed in adeno-associated virus (AAV)-shGITRL mice. In vitro, the role of GITRL expression by DCs was evaluated in LV-shGITRL bone marrow dendritic cells (BMDCs) under HDM stimulation. And the direct effect of GITRL was observed by stimulating splenocytes with GITRL protein. The effect of regulating GITRL on CD4+ T cell differentiation was detected. Further, GITRL mRNA in the peripheral blood of asthmatic children was tested. Results GITRL was significantly increased in HDM-challenged mice. In GITRL knockdown mice, allergen-induced airway inflammation, serum total IgE levels and airway hyperresponsiveness (AHR) were reduced. In vitro, GITRL expression on BMDCs was increased after HDM stimulation. Further, knocking down GITRL on DCs partially restored the balance of Th1/Th2 and Th17/Treg cells. Moreover, GITRL stimulation in vitro inhibited Treg cell differentiation and promoted Th2 and Th17 cell differentiation. Similarly, GITRL mRNA expression was increased in the peripheral blood from asthmatic children. Conclusions This study identified a novel role for GITRL expressed by DCs as a positive regulator of CD4+ T cells responses in asthma, which implicates that GITRL inhibitors may be a potential immunotherapy for asthma.

This paper presents an artificial intelligence (AI) method for the evolution prediction of surface scratching in sheet metals subjected to contact sliding. Ball-on-disk sliding was employed, and ball diameter, normal load, surface roughness, sliding cycles and the maximum scratching depth in the metal sheet were taken as the fuzzy variables to assess the contributions of individual variables to the surface damage. To improve the prediction accuracy, the quantum-behaved particle swarm optimisation (QPSO) algorithm was further developed and utilised to refine the fuzzy model by optimising the membership functions of the fuzzy variables. It was found that this AI technique, which integrates the fuzzy set theory with the improved QPSO algorithm, can accurately, reliably and efficiently predict the surface scratching evolution, which is otherwise impossible to be implemented.

For the biogas pressurized water scrubbing process, a plant-level optimizing control system based on the enhanced non-dominated sorting genetic algorithm (NSGA-II) is researched in this paper. According to the technological requirements of the biogas pressurized water scrubbing process, a steady state simulation system is established using Aspen Plus to analyze the constraint domain of the manipulated variables and optimize the operational variables. Under the multi-objective function of the total operating cost and purification effect, the Pareto optimal solutions with the constraints of feasible region of several variables are obtained using the NSGA-II algorithm. A plant-level dynamic control scheme is designed based on the optimal operating variables, and tested using the Aspen Dynamic simulation system. At last a pilot experimental device is developed based on the above optimized operating variables and the control scheme for the biogas pressurized water scrubbing process. The experimental results show that the system has good dynamic response performance, such as the removal rate of CO2 is greater than 99.8% under various disturbances.

Aims: To investigate the expression levels of serum interleukin-17 (IL-17) and interleukin-27 (IL-27) in children with bronchial asthma and to correlate these expression levels with lung function i...

Normally, smooth muscle cells (SMCs) are localized in the tunica media of the vasculature, where they take responsibility for vascular contraction and extracellular matrix (ECM) generation. SMCs also play a significant role in obedience and elastic rebound of the artery in response to the haemodynamic condition. However, under pathological or stressed conditions, phenotype switching from contractile to synthetic state or other cell types will occur in SMCs to positively or negatively contribute to disease progression. Various studies demonstrated that functional changes of SMCs are implicated in several cardiovascular diseases. In this review, we present the function of vascular SMCs (VSMCs) and the involved molecular mechanisms about phenotype switching, and summarize the roles of SMCs in atherosclerosis, hypertension, arterial aneurysms and myocardial infarction, hoping to obtain potential therapeutic targets against cardiovascular disease in the clinical practices.

Miscarriage, the spontaneous loss of a pregnancy before the fetus achieves viability, is a common complication of pregnancy. Decidualization plays a critical role in the implantation of the embryo. To search for molecular factors underlying miscarriage, we explored the role of long noncoding RNAs (lncRNAs) in the decidual microenvironment, where the molecular crosstalk at the feto–maternal interface occurs. By integrating RNA-seq data from recurrent miscarriage patients and decidualized endometrial stromal cells, we identified H19, a lncRNA that exhibits paternally imprinted monoallelic expression in normal tissues, as the most upregulated lncRNA associated with miscarriage. Aberrant upregulation of H19 lncRNA was observed in decidual tissues derived from patients with spontaneous miscarriage as well as decidualized endometrial stromal cells. The maternally imprinted fetal mitogen Igf2, which is usually reciprocally co-regulated with H19 in the same imprinting cluster, was also upregulated. Notably, both genes underwent loss of imprinting, as H19 and IGF2 were actively transcribed from both parental alleles in decidual tissues. Mechanistically, this loss of imprinting in decidual tissues was associated with the loss of the H3K27m3 suppression marker in the IGF2 promoter, CpG hypomethylation at the central CTCF binding site in the imprinting control center (ICR) that is located between IGF2 and H19, and the loss of CTCF-mediated intrachromosomal looping. These data provide the first evidence that aberrant control of the ICR epigenotype-intrachromosomal looping-H19/IGF2 imprinting pathway may be a critical epigenetic risk factor in the abnormal decidualization related to miscarriage. Funding: This work was supported by the National Key RD and the Biomedical Research Service of the Department of Veterans Affairs (BX002905). Declaration of Interest: No potential conflicts of interest exist. Ethical Approval: Ethical approval for this study was provided by the Research Ethics Board of the First Hospital of Jilin University, and written informed consent was obtained from all patients prior to sample collection.

Nitrate is usually the main pollution factor in the river water and groundwater environment because it has the characteristics of stable properties, high solubility and easy migration. In order to ensure the safety of water supply and effectively control nitrate pollution, it is very important to accurately identify the pollution sources of nitrate in freshwater environment. At present, as the most accurate source analysis method, isotope technology is widely used to identify the pollution sources of nitrate in water environment. However, the complexity of nitrate pollution sources and nitrogen migration and transformation in the water environment, coupled with the isotopic fractionation, has changed the nitrogen and oxygen isotopic values of nitrate in the initial water body, resulting in certain limitations in the application of this technology. This review systematically summarized the typical δ15N and δ18O-NO3− ranges of NO3− sources, described the progress in the application of isotope technique to identify nitrate pollution sources in water environment, analyzed the application of isotope technique in identifying the migration and transformation of nitrogen in water environment, and introduced the method of quantitative source apportionment. Lastly, we discussed the deficiency of isotope technique in nitrate pollution source identification and described the future development direction of the pollution source apportionment of nitrate in water environment.

Xijiao Dihuang Tang (XJDHT) is a classical formula of traditional Chinese medicine constituted of Cornu Bubali, Rehmannia glutinosa (Gaertn.) DC., Paeonia lactiflora Pall., and Paeonia suffruticosa Andrews. It was first mentioned in the medical classic “Beiji Qianjin Yaofang” written by Simiao Sun in Tang Dynasty. It shows very strong antipyretic and anticoagulant effects and has been clinically applied to treat various type of blood loss, purple and black spots, heat stroke, and glossitis. Kawasaki disease (KD) is considered as a kind of acute febrile illness in children with systemic vasculitis as the main lesions. The aim of this research is to clarify whether XJDHT can play a protective role in KD. A mouse model of Candida albicans water-soluble fraction (CAWS)–induced coronary arteritis and a KD cell model with tumor necrosis factor (TNF)-α induction were employed to investigate the potential effect and mechanism of XJDHT on coronary artery injury in KD. Data showed that XJDHT remarkably alleviated the coronary artery injury of KD mice, as evidenced by reduced inflammation and downregulated expression of pro-inflammatory cytokines interleukin (IL)-1β and TNF-α. In vitro investigation showed that XJDHT could promote cell proliferation, inhibit cell apoptosis, and improve mitochondrial functions. Subsequent studies demonstrated that XJDHT rescued endothelial cell injury by PI3K/Akt-NFκB signaling pathway. Component analysis of XJDHT detected thirty-eight chemically active ingredients, including paeoniflorin, albiflorin, and paeoniflorigenone, which in in vitro experiments exhibited significant rescue effects on TNF-α–mediated endothelial cell injury. Our findings demonstrated that XJDHT mitigated coronary artery injury of KD through suppressing endothelial cell damage via PI3K/Akt-NFκB signaling.

Neutrophils are rapidly recruited from the peripheral blood to the inflammatory site to initiate inflammatory response against pathogenic infections. The process to recruit neutrophils must be properly regulated since the abnormal accumulation of neutrophils can cause organ damage and dysfunction. The acute respiratory distress syndrome (ARDS)/acute lung injury (ALI) is a common cause of respiratory failure that is characterized by the infiltration of neutrophils and epithelial integrity disruption. Indeed, recent studies suggest a pathogenic role of neutrophils in the clinic severity of the coronavirus disease 2019 (COVID-19) ARDS. The chemokine CXCL1, which is rapidly induced by inflammatory stimuli, plays a key role in neutrophil influx during lung inflammation. The molecular basis ofCxcl1induction is not fully understood. Here we report that TET1, a member of the ten eleven translocation (TET) methylcytosine dioxygenase protein family, displays a striking specificity in the regulation of gene expression in macrophages. RNA sequencing (RNA-seq) analysis showed thatTet1disruption significantly altered the expression of only 48 genes that includeCxcl1and several other genes known to be important for cell migration and trafficking in bone marrow derived macrophages (BMDMs) in response to LPS stimulation. TET1 regulates the induction ofCxcl1by facilitating the DNA demethylation of theCxcl1promoter. InTet1−/−mice, the induction ofCxcl1was suppressed, resulting in defective neutrophil recruitment to the lung during LPS-induced acute lung injury. Our results identify a novel epigenetic mechanism that selectively controlsCxcl1induction and neutrophil recruitment during acute lung injury.Key PointsTET1 has a striking specificity in macrophage gene regulation and controlsCxcl1induction by inflammatory stimuli via DNA demethylationNeutrophil recruitment is defective inTet1deficient mice during acute lung injury

Purpose: To compare the efficacy and safety of robotic-assisted simple prostatectomy and open simple prostatectomy for large benign prostatic hyperplasia.Methods: We systematically searched the Cochrane Library, PubMed, Embase, and Science databases for studies published through December 2020. Controlled trials on RASP and OSP for large prostates were included. The meta-analysis was conducted with the Review Manager 5.4 software.Results: A total of seven studies with 3,777 patients were included in the analysis. There were no significant differences in IPSS (WMD, 0.72; 95%CI: −0.31, 1.76; P = 0.17), QoL (WMD, 0.00; 95%CI: −0.39, 0.39; P > 0.99), Qmax (WMD, 1.88; 95% CI: −1.15, 4.91; P = 0.22), or PVR (WMD, −10.48; 95%CI: −25.13, 4.17; P = 0.16) among patients undergoing RASP and OSP. However, compared with patients who underwent OSP, patients who underwent RASP had a shorter LOS (WMD, −2.83; 95%CI: −3.68, −1.98; P < 0.001), less EBL (WMD, −304.68; 95% CI: −432.91, −176.44; P < 0.001), a shorter CT (WMD, −2.61; 95%CI: −3.94, −1.29; P < 0.001), and fewer overall complications (OR, 0.30; 95% CI: 0.16, 0.57; P < 0.001). Nevertheless, RASP was associated with a longer OT (WMD, 59.69, 95% CI: 49.40, 69.98; P < 0.001).Conclusion: The results of the current study demonstrated that RASP provided similar efficacy to those of OSP in the treatment of large prostate, while maintaining better security. Our findings indicate that RASP is a feasible and effective alternative to OSP.

Kawasaki disease (KD) is an acute vasculitis of pediatric populations that may develop coronary artery aneurysms if untreated. It has been regarded as the principal cause of acquired heart disease in children of the developed countries. Interleukin (IL)-37, as one of the IL-1 family members, is a natural suppressor of inflammation that is caused by activation of innate and adaptive immunity. However, detailed roles of IL-37 in KD are largely unclear. Sera from patients with KD displayed that IL-37 level was significantly decreased compared with healthy controls (HCs). QRT-PCR and western blot analyses showed that the expression level of IL-37 variant, IL-37b, was remarkably downregulated in human umbilical vein endothelial cells (HUVECs) exposed to KD sera-treated THP1 cells. Therefore, we researched the role of IL-37b in the context of KD and hypothesized that IL-37b may have a powerful protective effect in KD patients. We first observed and substantiated the protective role of IL-37b in a mouse model of KD induced by Candida albicans cell wall extracts (CAWS). In vitro experiments demonstrated that IL-37b alleviated endothelial cell apoptosis and inflammation via IL-1R8 receptor by inhibiting ERK and NFκB activation, which were also recapitulated in the KD mouse model. Together, our findings suggest that IL-37b play an effective protective role in coronary endothelial damage in KD, providing new evidence that IL-37b is a potential candidate drug to treat KD.

Pyroptosis is a form of programmed necrosis, and is morphologically and mechanistically unique form of programmed cell death compared to others, such as apoptosis and autophagic cell death. More specifically, pyroptosis features gasdermin family-mediated membrane pore formation and subsequent cell lysis, as well as release of pro-inflammatory intracellular contents including IL-1β, IL-18 and HMGB1. Mechanistically, pyroptosis is driven by two main signaling pathways - one mediated by caspase-1 and the other by caspase-4/5/11. Recent studies show that pyroptosis is implicated in several cardiovascular diseases. In this review, we summarize recent scientific discoveries of pyroptosis's involvement in atherosclerosis, myocardial infarction, diabetic cardiomyopathy, reperfusion injury and myocarditis. We also organized new and emerging evidence suggesting that pyroptosis signaling pathways may be potential therapeutic targets in cardiovascular diseases.

Spectral clustering is one of the most popular clustering approaches and has been applied in Hyperspectral Image (HSI) clustering well. However, most of these methods are not suitable for large scale HSI. In this paper, based on anchor graph and spatial information, we propose a novel method, called fast spectral clustering based on spatial information (FSCS), which could deal with large scale HSI and have better performance in user's accuracy, average accuracy, overall accuracy and so on. Firstly, based on the physical characteristic of HSI, FSCS algorithm combines the spatial information with spectral information, and uses the spatial nearest points to reconstructs the center point and reveal the local spatial structure. As a result, the correlation of pixels is strengthened and the clustering accuracy is improved. Secondly, the new adjacency matrix is constructed based on anchor graph and thus computational complexity is reduced significantly. Finally, in order to avoid tuning the heat-kernel parameter, the parameter-free strategy is adopted in FSCS. Experiments demonstrate the efficiency and effectiveness of the proposed FSCS algorithm.

Background:The progression of liver disorders is frequently associated with inflammatory bowel disease through the gut-liver axis. However, no direct evidence showed the mechanisms of ulcerative colitis (UC) in the development of liver fibrosisper se. Thus, this study aimed to evaluate the effects of UC on liver fibrosis and its potential mechanism in the experimental model.Methods:Male C57BL/6 mice were allocated into five groups (n= 10 per group) to receive either drinking water (control), 2% dextran sulfate sodium (DSS), olive oil, carbon tetrachloride (CCl4) or DSS + CCl4for 4 cycles. Blood was collected for biochemical analysis. Colons were excised for the evaluation of colon length and morphological score. Liver, colon, and mesenteric lymph nodes (MLNs) were collected for histopathological staining, expression analysis, and bacterial translocation assay to evaluate the inflammation, fibrosis, the activation of hepatic stellate cells (HSCs), and gut barrier function.Results:DSS caused severe colitis in mice treated or treated with CCl4, as evident from the elevation of disease activity index (DAI), histological abnormalities, and increased pro-inflammatory cytokines (TNF-α, IFN-γ, and IL-17A). Histopathological staining revealed that DSS treatment aggravated the CCl4-induced extracellular matrix deposition, liver fibrosis, and inflammation in mice. Additionally, biochemical and expression analysis indicated the DSS treatment caused the increase of hydroxyproline and pro-inflammatory cytokines, as well as the abnormal liver function indexes in CCl4-induced mice. Gut barrier function was impaired in DSS- and DSS + CCl4-treated mice, manifesting as the increase in bacterial translocation and lipopolysaccharide level, and the reduction in tight junction proteins (occluding, claudin-1 and ZO-1) expression. Further, the activations of HSCs and TLR4 signaling pathway were observed after DSS + CCl4treatment, presenting with the increase in expression of α-SMA, vimentin, TGF-β, collagen type I, collagen type II, TIMP-2, TLR4, TRAF6, and NF-κB p65, and a decrease in GFAP and MMP-2 expression.Conclusion:The present study verified that UC aggravated CCl4-induced liver injury, inflammation, and fibrosis in mice through the gut-liver axis. Gut barrier dysfunction in UC leads to bacterial translocation and elevated lipopolysaccharide, which may promote the activation of TLR4 signaling and HSCs in the liver.

Abstract: The small-molecular inhibitors targeted JAks (JAK inhibitors), could modulate the cytokines-mediated signaling via JAK-STAT pathway, which plays a important role in immune regulation and cell proliferation. The JAK inhibitors are previously designed and synthesized to treat diseases involved with hematologic and immune system. Increasing evidence shows that they are quite effective in atopic dermatitis (AD), alopecia areata (AA), psoriasis, vitiligo, and other autoimmune-induced dermatologic conditions. Currently, many JAK inhibitors possessing anti-vitiligo activity are being investigated in laboratory and clinically. In this view, we would like to summarize so we review the applications of these inhibitors with emphasis on profile of vitiligo, clinical efficacy, dosages, development of new candidates and adverse events through available literatures.

Studies have reported the vital role of nerves in tumorigenesis and cancer progression. Nerves infiltrate the tumor microenvironment thereby enhancing cancer growth and metastasis. Perineural invasion, a process by which cancer cells invade the surrounding nerves, provides an alternative route for metastasis and generation of tumor-related pain. Moreover, central and sympathetic nervous system dysfunctions and psychological stress-induced hormone network disorders may influence the malignant progression of cancer through multiple mechanisms. This reciprocal interaction between nerves and cancer cells provides novel insights into the cellular and molecular bases of tumorigenesis. In addition, they point to the potential utility of anti-neurogenic therapies. This review describes the evolving cross-talk between nerves and cancer cells, thus uncovers potential therapeutic targets for cancer.

Disagreement exists between theory and experiment when we study surface plasmon resonance (SPR) of gold film with graphene. We attribute this large shift in SPR angle to the rough gold film and wrinkled graphene layer.

Liquid suspensions of carbon nanotubes, graphene and transition metal dichalcogenides have exhibited excellent performance in optical limiting. However, the underlying mechanism has remained elusive and is generally ascribed to their superior nonlinear optical properties such as nonlinear absorption or nonlinear scattering. Using graphene as an example, we show that photo-thermal microbubbles are responsible for optical limiting as strong light scattering centers: graphene sheets absorb incident light and become heated up above the boiling point of water, resulting in vapor and microbubble generation. This conclusion is based on the direct observation of bubbles above the laser beam as well as a strong correlation between laser-induced ultrasound and optical limiting. In situ Raman scattering of graphene further confirms that the temperature of graphene under laser pulses rises above the boiling point of water but still remains too low to vaporize graphene and create graphene plasma bubbles. Photo-thermal bubble scattering is not a nonlinear optical process and requires very low laser intensity. This understanding helps us to design more efficient optical limiting materials and understand the intrinsic nonlinear optical properties of nanomaterials.

Tunnel lining cavities are a common problem that may affect the bearing capacity of the tunnel-supporting structure, as well as the tunnel service life. The impact echo (IE) method can be used to detect voids behind tunnel linings. For a long tunnel, the surrounding rocks/soils are inhomogeneous and anisotropic, with parameters that vary with tunnel mileages. It is interesting to analyse whether alterations of the soil parameters affect the non-destructive test results. A laboratory experiment was performed in this study, in which voids behind a concrete plate, representing the tunnel lining, were designed to model the ineffective contact between the soil and the tunnel. The IE method was employed to inspect the existence of the void using different signal analysis approaches in the time, frequency and time&ndash, frequency domains. Furthermore, the fractal box-counting dimension was calculated for the purpose of quantitative evaluation. Different soil parameters and void sizes were considered, and finally, a finite element model was built and parameter analysis was accomplished using the software ABAQUS. The results demonstrated that: (1) A comprehensive analysis of vibration signals in the time, frequency and time&ndash, frequency domains was useful for identifying voids, while the box-counting dimension was useful for evaluating voids quantitatively. (2) Soils with large density and Young&rsquo, s modulus differences had a certain influence on void detection, while those with large water content and Poisson&rsquo, s ratio differences had little influence. (3) The box-counting dimension value was stable within the area where the void existed behind the tunnel, when the detection point was beyond twice that of the void dimension, it was difficult to locate the void.

Although low‐dose radiation (LDR) possesses the two distinct functions of inducing hormesis and adaptive responses, which result in immune enhancement and tumor inhibition, its clinical applications have not yet been elucidated. The major obstacle that hinders the application of LDR in the clinical setting is that the mechanisms underlying induction of tumor inhibition are unclear, and the risks associated with LDR are still unknown. Thus, to overcome this obstacle and elucidate the mechanisms mediating the antitumor effects of LDR, in this study, we established an in vivo lung cancer model to investigate the participation of the immune system in LDR‐induced tumor inhibition and validated the pivotal role of the immune system by impairing immunity with high‐dose radiation (HDR) of 1 Gy. Additionally, the LDR‐induced adaptive response of the immune system was also observed by sequential HDR treatment in this mouse model. We found that LDR‐activated T cells and natural killer cells and increased the cytotoxicity of splenocytes and the infiltration of T cells in the tumor tissues. In contrast, when immune function was impaired by HDR pretreatment, LDR could not induce tumor inhibition. However, when LDR was administered before HDR, the immunity could be protected from impairment, and tumor growth could be inhibited to some extent, indicating the induction of the immune adaptive response by LDR. Therefore, we demonstrated that immune enhancement played a key role in LDR‐induced tumor inhibition. These findings emphasized the importance of the immune response in tumor radiotherapy and may help promote the application of LDR as a novel approach in clinical practice.

A novel method of layout optimization.Pareto optimal layout of multistatic radar.Available volume is proposed as performance metric.Pareto optimal results based on dynamic game.Low computational complexity. Layouts influence the performance of location accuracy greatly in multistatic radar. The layout in classical regular shape may not be an excellent choice. In this paper, Pareto optimal layout of multistatic radar is proposed based on dynamic game theory. The available volume associated with the Cramer-Rao lower bound (CRLB) of location accuracy is proposed as the utility metric to evaluate the performance of the layout. Simulation results show that different initial layouts may lead to different final layouts. Although these final layouts are different they are all Pareto optimal and similar in performance.

Background Despite the availability of multiple treatment strategies, patients with advanced colon carcinoma (CC) have poor prognoses. The aim of this study was to evaluate the efficacy and safety of natural killer (NK) cell therapy in combination with chemotherapy in patients with locally advanced CC. Methods We assessed the cytotoxicity of NK cells to CC cells (CCs) and CC stem cells (CSCs) pre-treated with 5-fluorouracil or oxaliplatin in vitro. Then, an open-label cohort study was conducted with locally advanced CC patients who had received radical resection. Patients received either NK cell therapy combined with chemotherapy (NK cell group, 27 patients) or pure chemotherapy (control group, 33 patients). Progression-free survival (PFS), overall survival (OS) and adverse effects were investigated. Results Chemotherapy sensitized CCs and CSCs to NK cell cytotoxicity through regulation of NK cell–activating/inhibitory receptor ligands. Poorly differentiated CCs were more susceptible to NK cells than well-differentiated ones. In the cohort study, the 5-year PFS and OS rates in the NK cell group were significantly higher than those in the control group (51.1% versus 35%, P = 0.044; 72.5% versus 51.6%, P = 0.037, respectively). Among patients with poorly differentiated carcinomas and low expression of human leukocyte antigen (HLA)-1, the median PFS in the NK cell group versus the control group was 23.5 versus 12.1 months (P = 0.0475) and 33.1 versus 18.5 months (P = 0.045), respectively. No significant adverse reactions were reported. Conclusion NK cell therapy in combination with chemotherapy in locally advanced CC prevented recurrence and prolonged survival with acceptable adverse effects, especially for poorly differentiated carcinomas.

Background Asthma exacerbations commonly lead to unplanned health care utilization and are costly. Early identification of children at increased risk of asthma exacerbations would allow a proactive management approach. Objective We evaluated common asthma risk factors to predict the probability of exacerbation for individual children aged 0-21 years using data from the electronic medical record (EMR). Methods We analyzed longitudinal EMR data for over 3000 participants with asthma seen at Cincinnati Children's Hospital Medical Center over a 7-year period. The study population was divided into 3 age groups: 0-4, 5-11, and 12-21 years. Each age group was divided into a derivation cohort and a validation cohort, which were used to build a risk score model. We predicted risk of exacerbation in the next 12 months, validated the scores by risk stratum, and developed a clinical tool to determine the risk level based on this model. Results Risk model results were confirmed with validation cohorts by calendar year and age groups. Race, allergic sensitization, and smoke exposure were each important risk factors in the 0-4 age group. Abnormal spirometry and obesity were more sensitive predictors of exacerbation in children >12 years. For each age group, a higher expanded score was associated with a higher predicted probability of an asthma exacerbation in the subsequent year. Conclusion This asthma exacerbation prediction model, and the associated clinical tool, may assist clinicians in identifying children at high risk for exacerbation that may benefit from more aggressive management and targeted risk mitigation.

// Yijing Zhao 1 , Naifei Chen 1 , Yu Yu 1 , Lili Zhou 1 , Chao Niu 1 , Yudi Liu 1 , Huimin Tian 1 , Zheng Lv 1 , Fujun Han 1 and Jiuwei Cui 1 1 Cancer Center, The First Hospital of Jilin University, Changchun, 130021, China Correspondence to: Jiuwei Cui, email: cuijw@jlu.edu.cn Keywords: MICA, MICB, prognosis, cancer, meta-analysis Received: August 02, 2017 Accepted: September 22, 2017 Published: October 03, 2017 ABSTRACT Purpose: MHC class I chain related-proteins A (MICA) and B (MICB) are natural killer group 2D ligands that mediate tumor surveillance. Several studies have suggested that MICA/B levels predict clinical outcomes in patients with cancer; however, this remains contentious. Here, we present a systematic review and meta-analysis of available studies of the prognostic value of MICA/B in cancer. Materials and Methods: We searched PubMed, Embase, Clinicaltrials.gov, and Cochrane Library to identify studies published from inception to July 2017 that assessed MICA/B in patients with cancer. The hazard ratio (HR) and 95% confidence interval (CI) of MICA/B were extracted for overall survival (OS) analysis. Results: A total of 19 studies comprising 2,588 patients with 10 different types of cancer were included in the study. Low sMICA/B levels were found associated with significantly longer OS (HR = 1.65, 95% CI [1.42–1.92], P < 0.00001). Patients with cancers of digestive system that exhibited high MICA/B expression had significantly longer OS in (HR = 0.56, 95% CI [0.39–0.80], P = 0.002) compared with those with lower MICA/B expression ( I 2 = 35%, P = 0.18). Conclusions: Serum soluble MICA/B represents a potential prognostic marker in various human cancers. High cell-surface MICA/B expression in cancers of the digestive system was found associated with increased survival.

Smart machining has tremendous potential and is becoming one of new generation high value precision manufacturing technologies in line with the advance of Industry 4.0 concepts. This paper presents some innovative design concepts and, in particular, the development of four types of smart cutting tools, including a force-based smart cutting tool, a temperature-based internally-cooled cutting tool, a fast tool servo (FTS) and smart collets for ultraprecision and micro manufacturing purposes. Implementation and application perspectives of these smart cutting tools are explored and discussed particularly for smart machining against a number of industrial application requirements. They are contamination-free machining, machining of tool-wear-prone Si-based infra-red devices and medical applications, high speed micro milling and micro drilling, etc. Furthermore, implementation techniques are presented focusing on: (a) plug-and-produce design principle and the associated smart control algorithms, (b) piezoelectric film and surface acoustic wave transducers to measure cutting forces in process, (c) critical cutting temperature control in real-time machining, (d) in-process calibration through machining trials, (e) FE-based design and analysis of smart cutting tools, and (f) application exemplars on adaptive smart machining.

Multiple myeloma (MM) is an incurable hematological malignancy, although bortezomib has markedly improved its outcomes. Growing clinical evidence indicates that enhancing induced natural killer (NK) or γδ T cells for infusion is useful in the treatment of MM. However, whether combination treatment with bortezomib and induced NK and γδ T cells further improves outcomes in MM, and how the treatments should be combined, remain unclear. Herein, we found that low-dose bortezomib did not suppress the viability of induced NK and γδ T cells, but did induce MM cell apoptosis. Importantly, low-dose bortezomib increased the expression of NKG2D and DNAM-1 ligands on MM cells, which sensitized the multiple myeloma cells to lysis by induced NK and γδ T cells. Our results suggested that combination treatment with low-dose bortezomib and induced NK or γδ T cells had a synergistic cytotoxic effect on MM cells. This study provided a proof of principle for the design of future trials and investigation of this combination therapeutic strategy for MM treatment.

Tip-enhanced quantum plasmonics enables simultaneous nanoscale imaging and picoscale control of trions in monolayer WS2., Monitoring and controlling the neutral and charged excitons (trions) in two-dimensional (2D) materials are essential for the development of high-performance devices. However, nanoscale control is challenging because of diffraction-limited spatial resolution of conventional far-field techniques. Here, we extend the classical tip-enhanced photoluminescence based on tip-substrate nanocavity to quantum regime and demonstrate controlled nano-optical imaging, namely, tip-enhanced quantum plasmonics. In addition to improving the spatial resolution, we use the scanning probe to control the optoelectronic response of monolayer WS2 by varying the neutral/charged exciton ratio via charge tunneling in Au-Ag picocavity. We observe trion “hot spots” generated by varying the picometer-scale probe-sample distance and show the effects of weak and strong coupling, which depend on the spatial location. Our experimental results are in agreement with simulations and open an unprecedented view of a new range of quantum plasmonic phenomena with 2D materials that will help to design new quantum optoelectronic devices.

Kawasaki disease (KD) is the most common cause of pediatric cardiac disease in developed countries, and can lead to permanent coronary artery damage and long term sequelae such as coronary artery aneurysms. Given the prevalence and severity of KD, further research is warranted on its pathophysiology. It is known that endothelial cell damage and inflammation are two essential processes resulting in the coronary endothelial dysfunction in KD. However, detailed mechanisms are largely unknown. In this study, we investigated the role of pyroptosis in the setting of KD, and hypothesized that pyroptosis may play a central role in its pathophysiology. In vivo experiments of patients with KD demonstrated that serum levels of pyroptosis-related proteins, including ASC, caspase-1, IL-1β, IL-18, GSDMD and lactic dehydrogenase (LDH), were significantly increased in KD compared with healthy controls (HCs). Moreover, western blot analysis showed that the expression of GSDMD and mature IL-1β was notably elevated in KD sera. In vitro, exposure of human umbilical vein endothelial cells (HUVECs) to KD sera-treated THP1 cells resulted in the activation of NLRP3 inflammasome and subsequent pyroptosis induction, as evidenced by elevated expression of caspase-1, GSDMD, cleaved p30 form of GSDMD, IL-1β and IL-18, and increased LDH release and TUNEL and propidium iodide (PI)-positive cells. Furthermore, our results showed that NLRP3-dependent endothelial cell pyroptosis was activated by HMGB1/RAGE/cathepsin B signaling. These findings were also recapitulated in a mouse model of KD induced by Candida albicans cell wall extracts (CAWS). Together, our findings suggest that endothelial cell pyroptosis may play a significant role in coronary endothelial damage in KD, providing novel evidence that further elucidates its pathophysiology.

The hyperspectral image (HSI) clustering can extract valuable clustering information and be used to classify the ground truth, monitor environment and so on. Spectral clustering is one of the most popular clustering approaches. The algorithm has been applied in HSI clustering well and has drawn massive attentions. However, most of these methods do not take advantage of spatial information of HSI, which can strengthen the correlation of pixels and increase the accuracy. In this paper, based on the physical characteristics of HSI, a new approach is proposed, called hyperspectral image clustering based on spatial information and spectral clustering (SISC). Combining both spatial window and spectral factor, the algorithm makes use of joint spatial-spectral information, and reconstructs the center point and reveals the local spatial structure by using the spatial nearest points. Experimental results with widely-used hyperspectral data indicate that SISC has a better performance in hyperspectral image clustering.

Background/Aims: Diabetic non-healing skin ulcers represent a serious challenge in clinical practice, in which the hyperglycemia-induced disturbance of angiogenesis, and endothelial dysfunction play a crucial role. Resveratrol (RES), a silent information regulator 1 (SIRT1) agonist, can improve endothelial function and has strong pro-angiogenic properties, and has thus become a research focus for the treatment of diabetic non-healing skin ulcers; however, the underlying mechanism by which RES regulates these processes remains unclear. Therefore, the present study was intended to determine if RES exerts its observed protective role in diabetic wound healing by alleviating hyperglycemia-induced endothelial dysfunction and the disturbance of angiogenesis. Methods: We investigated the effects of RES on cell migration, cell proliferation, apoptosis, tube formation, and the underlying molecular mechanisms in 33 mM high glucose-stimulated human umbilical vein endothelial cells (HUVECs) by semi-quantitative RT-PCR, western blot analysis, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining, and immunofluorescence in vitro. We further explored the role of RES on endothelial dysfunction and wound healing disturbance in db/db mice by TUNEL staining, immunofluorescence, and photography in vivo. Results: We observed an obvious inhibition of hyperglycemia-triggered endothelial dysfunction and a disturbance of angiogenesis, followed by the promotion of diabetic wound healing via RES, along with restoration of the activity of the hyperglycemia-impaired SIRT1 signaling pathway. Pretreatment with EX-527, a SIRT1 inhibitor, abolished the RES-mediated endothelial protection and pro-angiogenesis action, and then delayed diabetic wound healing. Furthermore, examination of the overexpression of forkhead box O1 (FOXO1), a transcription factor substrate of SIRT1, in HUVECs and db/db mice revealed that RES activated SIRT1 to restore hyperglycemia-triggered endothelial dysfunction and disturbance of angiogenesis, followed by the promotion of diabetic wound healing in a c-Myc-dependent manner. Pretreatment with 10058-F4, a c-Myc inhibitor, repressed RES-mediated endothelial protection, angiogenesis, and diabetic wound healing. Conclusion: Our findings indicate that the positive role of RES in diabetic wound healing via its SIRT1-dependent endothelial protection and pro-angiogenic effects involves the inhibition of FOXO1 and the de-repression of c-Myc expression.

Despite successful modeling of graphene as a 0.34-nm thick optical film synthesized by exfoliation or chemical vapor deposition (CVD), graphene induced shift of surface plasmon resonance (SPR) of gold films has remained controversial. Here we report the resolution of this controversy by developing a clean CVD graphene transfer method and extending Maxwell-Garnet effective medium theory (EMT) to 2D materials. A SPR shift of 0.24 is obtained and it agrees well with 2D EMT in which wrinkled graphene is treated as a 3-nm graphene/air layered composite, in agreement with the average roughness measured by atomic force microscope. Because the anisotropic built-in boundary condition of 2D EMT is compatible with graphene's optical anisotropy, graphene can be modelled as a film thicker than 0.34-nm without changing its optical property; however, its actual roughness, i.e., effective thickness will significantly alter its response to strong out-of-plane fields, leading to a larger SPR shift., 18 pages, 5 figures

Postsurgical relapse remains a common issue for resectable gastric cancer (GC). Here, we investigated the efficacy and safety of an adjuvant treatment combining chemotherapy with cellular immunotherapy (CIT) using autologous natural killer cells, γδT cells, and cytokine‐induced killer cells in the treatment of stage II/III GC. A pilot prospective cohort study was conducted in 169 patients with stage II/III GC who had undergone gastrectomy with D2 lymph node dissection. Patients were assigned into two groups according to the patient choice of treatment, including chemotherapy alone (chemo) or chemotherapy combined with CIT (chemo/CIT). Disease‐free survival (DFS), overall survival (OS), and adverse events were evaluated. Univariate and multivariate Cox models were used to analyze the impact of chemo/CIT on DFS and OS. Kaplan–Meier analysis with the log‐rank test was used to compare the clinical outcome between two groups. Three‐year DFS rate was 60.6% and 74.7% (P = 0.036) and 3‐year OS rate was 64.9% and 83% (P = 0.051) for the chemo and chemo/CIT group, respectively. TNM stage and chemo/CIT were independent prognostic factors for both DFS (for TNM stage, P

The monolithic integration of electronics and photonics has attracted enormous attention due to its potential applications. A major challenge to this integration is the identification of suitable materials that can emit and absorb light at the same wavelength. In this paper we utilize unique excitonic transitions in WS2 monolayers and show that WS2 exhibits a perfect overlap between its absorption and photoluminescence spectra. By coupling WS2 to Ag nanowires, we then show that WS2 monolayers are able to excite and absorb surface plasmons of Ag nanowires at the same wavelength of exciton photoluminescence. This resonant absorption by WS2 is distinguished from that of the ohmic propagation loss of silver nanowires, resulting in a short propagation length of surface plasmons. Our demonstration of resonant optical generation and detection of surface plasmons enables nanoscale optical communication and paves the way for on-chip electronic–photonic integrated circuits.

How does religious diversity in host countries affect the corporate social responsibility (CSR) decoupling between CSR reporting adoption (i.e., the likelihood of issuing CSR reporting) and CSR imp...

The no. 11 coal seam in the deep area of Hancheng mining area is mining in recent years, which is threatened by the water inrush from the Ordovician limestone aquifer. Coal-floor water inrush is governed by the water abundance of coal-floor aquifer, the water-resisting performance of coal-floor aquitard, and the pathway connecting the water source and the working face. To make an accuracy risk assessment of water inrush from the no. 11 coal seam floor, a GIS-based vulnerability index method (VIM) is adopted for its superior comprehensive consideration of more controlling factors, powerful spatial analysis, and intuitively display functions. This study firstly established an index system including the water pressure of the coal-floor aquifer, the unit water inflow, the thickness, the core recovery percentage, the thickness ratio of brittle rocks to ductile rocks, the thickness of effective aquitard, and the accumulated length of faults and folds, of which the former six indexes governed the water abundance of the coal-floor aquifer which was combined with the last two factors to determine the risk of coal-floor water inrush. Secondly, the thematic map of each controlling factor is established by GIS using the geological prospecting data, and the weight of each factor is determined by the analytic hierarchy process (AHP) after consulting the expert review panel. At last, a vulnerability index is obtained and used to assess the risk of coal-floor water inrush of the no. 11 coal seam. The risk of water inrush of the no. 11 coal seam of the study area was ranked to three zones: the southeastern shallow area in red color is the dangerous zone, the wide northwestern area in green color is the safe zone, and the transition area in yellow color is the moderate-risk zone. Compared with the actual water-inrush incidents, the risk assessment result was verified to achieve an accuracy of 82.35%, which is proved to be a dependable reference for the prevention and controlling of coal-floor water inrush of the no. 11 coal seam in Hancheng mining area.

Background A variety of extra-intestinal manifestations (EIMs), including hepatobiliary complications, are associated with inflammatory bowel disease (IBD). Mesenchymal stem cells (MSCs) have been shown to play a potential role in the therapy of IBD. This study was designed to investigate the effect and mechanism of MSCs on chronic colitis-associated hepatobiliary complications using mouse chronic colitis models induced by dextran sulfate sodium (DSS). Methods DSS-induced mouse chronic colitis models were established and treated with MSCs. Severity of colitis was evaluated by disease activity index (DAI), body weight (BW), colon length and histopathology. Serum lipopolysaccharide (LPS) levels were detected by limulus amebocyte lysate test (LAL-test). Histology and liver function of the mice were checked correspondingly. Serum LPS levels and bacterial translocation of mesenteric lymph nodes (MLN) were detected. Pro-inflammatory cytokines including tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), interleukin-1β (IL-1β), interleukin-17A (IL-17A), Toll receptor 4 (TLR4), TNF receptor-associated factor 6 (TRAF6) and nuclear factor kappa B (NF-κB) were detected by immunohistochemical staining, western blot analysis and real-time PCR, respectively. Results The DSS-induced chronic colitis model was characterized by reduced BW, high DAI, worsened histologic inflammation, and high levels of LPS and E. coli. Liver histopathological lesions, impaired liver function, enhanced proteins and mRNA levels of TNF-α, IFN-γ, IL-1β, IL-17A, TLR4, TRAF6 and NF-κB were observed after DSS administration. MSCs transplantation markedly ameliorated the pathology of colon and liver by reduction of LPS levels and proteins and mRNA expressions of TNF-α, IFN-γ, IL-1β, IL-17A, TLR4, TRAF6 and NF-κB. Conclusions MSCs can improve chronic colitis-associated hepatobiliary complications, probably by inhibition of enterogenous endotoxemia and hepatic inflammation through LPS/TLR4 pathway. MSCs may represent a novel therapeutic approach for chronic colitis-associated hepatobiliary complications.

Objective: To investigate the correlations among airway inflammation, airway epithelial injury and airway hyperresponsiveness (AHR) in asthmatic mice treated with dexamethasone. Methods: Female BALB/c mice were sensitized with intraperitoneal and hypodermic injections of ovalbumin (OVA) and aluminum on days 0, 7 and 14, challenged with OVA starting on day 21 for 10 days, and treated with dexamethasone via intraperitoneal injection starting on day 28 for 3 days. Female C57BL/6 mice were treated intranasally with house dust mite (HDM) on days 1 and 14, challenged intranasally with HDM on days 21, 23, 25, 27 and 29, and treated with sivelestat (a selective neutrophil elastase inhibitor) via intraperitoneal injection after each challenge. Following the final challenge, enhanced pause (Penh) and differential cell counts in the broncho-alveolar lavage fluid were measured and the correlations were analyzed. Results: Compared with OVA-challenged BALB/c mice, the counterpart mice treated with dexamethasone showed reduced Penh and shedding of airway epithelial cells. In addition, we found that Penh 50 (an indicator of AHR) had positive correlations with airway neutrophils and shedding of airway epithelial cells, but no correlation with eosinophils, lymphocytes or macrophages. Moreover, shedding of airway epithelial cells had positive correlations with airway neutrophils, but no correlation with eosinophils, lymphocytes or macrophages. Further, sivelestat decreased Penh 50 and shed airway-epithelial cells in HDM-challenged C57BL/6 mice. Conclusions: Collectively, our findings suggest that airway neutrophils and excessive shedding of airway epithelial cells, but not eosinophils, lymphocytes or macrophages, may be involved in AHR in asthmatic mice treated with dexamethasone.

Background aims Despite the availability of multiple treatment strategies, patients with gastric carcinoma (GC) have a dismal prognosis. The aim of this study was to evaluate the efficacy and safety of cellular immunotherapy (CIT) with the use of autologous natural killer cells, γδT cells and cytokine-induced killer cells in combination with chemotherapy in patients with GC. Methods In this open-label pilot cohort study, patients were treated with the combination therapy (chemo/CIT group) or chemotherapy alone (control group). Progression-free survival (PFS), overall survival (OS), quality of life (QOL) and adverse events were investigated. Results Fifty-eight patients were analyzed, 30 in the chemo/CIT group and 28 in the control group. The median PFS of the chemo/CIT group was significantly longer compared with the control group ( P = 0.021). In subgroup analysis, in patients with stage III GC, node-positive metastasis or poorly differentiated carcinoma, the 2-year PFS rate in chemo/CIT versus control groups was 62.5% versus 26.7% ( P = 0.022), 50% versus 27.3% ( P = 0.016) and 56.3% versus 28.6% ( P = 0.005), respectively. The median OS in either group has not yet been reached, and there was no significant difference in OS between the groups. The QOL was improved in the patients treated with chemo/CIT compared with the control group. CIT was well tolerated and not related to any significant adverse events. Conclusions A combination of CIT and chemotherapy for patients with GC was safe, improved QOL, and might prevent recurrence, especially in GC patients with advanced stage, poorly differentiated carcinoma or lymph node metastasis.

The objective of this paper is to evaluate the impact of the parasitic capacitor to the Gallium-Nitride (GaN) based high-electron-mobility transistor (HEMT). Because of the high switching frequency operation, the parasitic inductor has caught a lot of attention when the GaN HEMT is applied in the high power applications. However, the impact of parasitic capacitor to the GaN HEMT is not discussed in literatures. A prototype circuit is built and tested to evaluate the impacts of parasitic capacitor to the GaN HEMT performance. The results show that the parasitic capacitor can induce voltage spike and damage the GaN HEMT.

The continuous conduction mode (CCM) boost power factor corrector (PFC) has the advantages of low current ripple and low electromagnetic interference. However, due to its high output voltage and CCM operation, the switching frequency will be limited by the reverse recovery loss. In order to achieve higher power density, the switching frequency must be increased. Therefore, the Gallium-Nitride high electron mobility transistor (GaN HEMT) is adopted to replace the conventional Si-based components. As the switching frequency increased, the design of energy storage components of the PFC need to be developed. The design criteria for the energy storage components upon the practical application are developed in this paper. The simulation and hardware implement results are presented to verify the performance of the prototype circuit. Also, some comparisons of experimental results between using GaN HEMT and conventional Silicon-based Metal-Oxide-Semiconductor Field-Effect Transistor (Si-based MOSFET) will be discussed.

The voids behind the tunnel lining, as one of the tunnel diseases, can influence the tunnel service life. For existing running tunnels, it is essential to evaluate the effect of the void condition. In this paper, the impact-echo method was employed to check the voids. Firstly, a tunnel-soil coupled finite element model was built. Then, an impact excitation was applied on the tunnel lining. The responses beside the impact locations were compared for the conditions with different sizes of void and without voids behind the tunnel lining. The responses of the conditions with various impact locations were also be contrasted. The signals were analysed in time domain, frequency domain, and time-frequency domain. In addition, the dynamic stiffness of the tunnel-soil structure and fractal box-counting dimensions of the vibration response were calculated as well. By analysing these responses, the results suggest that the existence of void induce a dominant frequency, lower resistivity to deformation and lower attenuate velocity. With the increase of the size of the void, the features of response are more obvious.

With the explosive growth of smartphones and cloud computing, mobile cloud, which leverages cloud resource to boost the performance of mobile applications, becomes attrac- tive. Many efforts have been made to improve the performance and reduce energy consumption of mobile devices by offloading computational codes to the cloud. However, the offloading cost caused by the cloud platform has been ignored for many years. In this paper, we propose Rattrap, a lightweight cloud platform which improves the offloading performance from cloud side. To achieve such goals, we analyze the characteristics of typical of- floading workloads and design our platform solution accordingly. Rattrap develops a new runtime environment, Cloud Android Container, for mobile computation offloading, replacing heavy- weight virtual machines (VMs). Our design exploits the idea of running operating systems with differential kernel features inside containers with driver extensions, which partially breaks the limitation of OS-level virtualization. With proposed resource sharing and code cache mechanism, Rattrap fundamentally improves the offloading performance. Our evaluation shows that Rattrap not only reduces the startup time of runtime environments and shows an average speedup of 16x, but also saves a large amount of system resources such as 75% memory footprint and at least 79% disk capacity. Moreover, Rattrap improves offloading response by as high as 63% over the cloud platform based on VM, and thus saving the battery life.

This study was designed to evaluate the gastroprotective effect of Kangfuxin (KFX), a Chinese patent medicine constituent isolated from American cockroach, on ethanol-induced gastric ulcer in mice and to elucidate the potential mechanisms of the effect involved. According to the results, mice treated with alcohol appeared obvious gastric mucosal injury, while treatment with Cimetidine (a positive control) and KFX significantly relieved the damage, along with decreased oxidative stress and apoptosis indexes. Subsequently, we conducted a label-free quantitative proteomic (LFQ) and found that NF-κB and PI3K/AKT signaling pathway participated in gastroprotective effect of KFX. Furthermore, Western blot analysis revealed that KFX treatment inhibited the expression of TNF-α, IL-1β, greatly reduced the phosphorylation level of IκB and repressed the nuclear translocation of NF-κB p65, which demonstrated that KFX inhibited the activation of NF-κB pathway. Meanwhile, the PI3K/AKT pathway was also involved in regulating the anti-inflammation effect. These findings define for the first time that the gastroprotective effects of KFX against gastric ulcer can be attributed to its role in NF-κB inhibition.

We study optical transmission and reflection of graphene flakes suspended in liquid with external magnetic fields in both experiment and simulation. We show that graphene flakes controlled by magnetic fields can be used for display.

We study the resonant wavelength of nanograting structures covered by a dielectric medium. We find that the resonant wavelength oscillates as the thickness of the thin dielectric layer increases due to the cavity formed by the dielectric layer. The amplitude of this oscillation in the resonant wavelength is small when the minimum reflection occurs in the nanograting structure. For a plasmonic sensor covered by a dielectric medium, a small oscillation in the resonant wavelength as the thickness of the dielectric medium changes is preferred. We also study the impact of a rounded corner on the resonant wavelength and find that the rounded corners with a small radius of r effectively reduce the nanogroove depth by about 0.2 r. Results from the finite-difference time-domain (FDTD) method agree very well with the phase-matching condition, using parameters calculated from the rigorous coupled-wave analysis (RCWA) method. These results will lead to a better understanding of the accuracy of plasmonic sensors covered by dielectric media.

The objective of this study is to identify the expression status and clinical implications of lipase member H (LIPH) in breast cancer in order to develop strategies for breast cancer management. LIPH expression status was detected in 346 breast cancer specimens by immunohistochemistry. The relationship between LIPH expression, clinico-pathological parameters, and prognosis of breast cancer was determined. LIPH expression was higher in breast cancer specimens than in paracarcinoma tissues (P=0.01). In total, 64.74% (224/346) of breast cancer samples had high expression of the LIPH protein. LIPH was related to tumor size, histological grade, lymph node metastasis, and distant metastasis (P=0.073, 0.001, 0.001, and 0.001, respectively). Furthermore, individuals with high LIPH expression had a significantly higher rate of distant metastasis and poorer disease-specific survival than those with no or low LIPH expression (P=0.01). A Cox regression test indicated that the LIPH protein was an independent prognostic factor (P=0.001). LIPH was differentially expressed in breast cancer individuals and is an independent prognostic factor for breast cancer as well as a potential target for its management.

A void behind the lining in a tunnel is considered to be a critical condition as it can significantly impair the tunnel service life. In this study, we adopted the impact-echo (IE) method to detect the voids. We designed two test conditions (tunnel lining with and without a void) for our experiments performed in a laboratory environment. The influences of void size and impact-void position were analysed using numerical simulations. The vibration response signals were analysed in the time, frequency, and time&ndash, frequency domains using various signal analysis approaches. The results were comparatively analysed to determine the best approach for void detection. The study helped establish that a tunnel void can be evaluated through the vibration energy (amplitude and duration) in the time domain, the resonance frequency and dynamic stiffness in the frequency domain, and the energy distribution in time&ndash, frequency domain. The wavelet transform analysis is the most appropriate method to observe the energy flow during the state changing and the dynamic stiffness method can determine the void position precisely.

e18502 Background: Philadelphia chromosome is an independent prognostic factor in B-cell acute lymphoblastic leukemia (B-ALL). Due to the emergence of TKIs resistance such as imatinib, new methods are yet to be explored. Toll-like receptor 9 (TLR9) agonists have been used in many cancers as immune adjuvants, due to the immune effects as well as direct effects. However, the effect of TLR9 agonists on Ph(+) B-ALLs remain unknown. Methods: Expression levels in primary B-ALL cells from 41 patients in our hospital were determined by real-time quantitative PCR and correlated to clinicopathological factors. WST-1 cell viability assay and flow cytometry were used to confirm the biological behaviors of proliferation, cell cycle arrested, apoptosis, and surface molecules expression in Ph(+) B-ALL cell line. GST pull-down, western blot, and relevant inhibitors were used to detect the mechanism of the monotherapy and combination therapy. All data were analyzed using SPSS 24.0 software. Results: Expression of TLR9 in 19 patients with Ph chromosome was higher than that in 22 patients with the normal chromosome (Median: 0.10 vs. 0.03, P= 0.047). Sup-B15, one of imatinib resistance Ph(+) B-ALL cell line, showed no proliferation suppression, no cell cycle arrested and no apoptosis after CpG 685 stimulation. However, the combination use of CpG 685 and imatinib significantly increased apoptotic cells and upregulated the expression of CD40, MHC class Ⅰ and PD-L1. By comparing the downstream signaling pathway of TLR9 in B-ALL cell lines, Sup-B15 also promoted apoptosis through P38/P53/BAX signaling pathway as other B-ALLs. After imatinib pre-treatment, the inhibition of BAX activation by BCR-ABL kinase as well as C-MYC was exposed, and the resistance of CpG 685 was reversed. In addition, CpG 685 downregulated miR-21, further upregulated PTEN, and ultimately reversed the drug resistance of imatinib which caused by BCR-ABL1-independent AKT phosphorylation in Ph(+) B-ALL. Conclusions: The combinational use of imatinib and CpG 685 to treat B-ALL cells can reverse the drug resistance when applied alone. This method can not only kill Ph(+) B-ALL directly, but also increase the immunogenicity and enhance the recognition by CD8+ T cells. Besides, due to the increasing of PD-L1, adding PD-L1 antibody with imatinib and CpG ODNs in Ph(+) B-ALL warrants more data before moving into clinical practice.