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The performance of concrete slurry is a very important factor in the construction engineering. In this paper, based on silane modification, the molecular structure of polycarboxylic superplasticizer was optimized. The siloxane group with reactivity with cement-based materials was introduced, so as to improve the water reducing performance of water reducing agent. The molecular structure of the new superplasticizer was characterized by FIIR, 1HNMR and GPC. The adsorption of the water-reducing agent on the surface of cement particles was determined by TOC. The results show that superplasticizer with silane can obviously improved the working performance of the mortar, but also had obvious fluidity retention ability. Because the introduction of silane significantly increased the adsorption amount of water reducing agent molecules in cement particles. At the same time, the introduction of silane decreased the mechanical properties of hardened cement mortars in 1d, because it delayed hydration. However, there was no negative effect on the mechanical properties after 3d, and even the flexural strength of 28d was increased by 13%-37%.

Sepsis-associated encephalopathy (SAE) is a serious and common complication of sepsis. To study the ferroptosis in the pathogenesis of SAE and demonstrate the protection effect of ferroptosis resistance, cognitive function, neurological deficits, blood-brain barrier integrity and neuroinflammation were detected. SAE model was established by cecal ligation and puncture (CLP) in mice and an in vitro model was created by introducing LPS to HT22 cells. Ferroptosis inducer Fe-citrate (Fe) and ferroptosis inhibitor ferrostatin-1 (Fer-1) was post-treated in the models, respectively. SAE caused ferroptosis, as evidenced by an increase in reactive oxygen species (ROS), iron content and malondialdehyde (MDA) and a decrease in glutathione (GSH) level, as well as changes in the expression of ferroptosis-related proteins as acyl-CoA synthetase long-chain family member 4 (ACSL4), glutathione peroxidase 4 (GPX4), and cystine-glutamate antiporter (SLC7A11), and harmed mitochondrial function. In contrast, inhibiting ferroptosis with Fer-1 attenuated ferroptosis. Meanwhile, Fer-1 attenuated neurologic severity score, learning and memory impairment, Fluoro-Jade C (FJC) staining, and decreased Evans Blue (EB) extravasation, microglia activation and TNF-α and IL-1β production following SAE. The benefit of Fer-1 was diminished by ferroptosis inducer Fe. In addition, Fer-1 up-regulated the nuclear factor erythroid-2-related factor 2 (Nrf2)/ heme oxygenase-1(HO-1) signaling axis both in vivo and in vitro. In conclusion, our study revealed that Fer-1 might inhibit feroptosis in neurons by triggering the Nrf2/OH-1 pathway, thereby providing a therapeutic solution for SAE.

LZTR1 is associated with several diseases, including liver cancer, childhood cancer, and schwannomas. However, LZTR1’s role in colon cancer and its mechanism of action have not been reported. The colon cancer tissues and adjacent tissues were collected to measure the expression of LZTR1 by Real time PCR. Colon cancer SW620 cell lines were cultured and randomly divided into control group and LZTR1 group followed by analysis of LZTR1 expression by real time PCR, cell proliferation by MTT assay, Caspase3 activity, Bcl-2 and Bax level by Real time PCR, cell invasion by Transwell chamber; NF-κB/VEGF expression by Western blot. LZTR1 expression was significantly reduced in colon cancer tissues compared to adjacent tissues (P P κB and VEGF (P κB/VEGF signaling pathway.

With the increase in working time, the geometric errors of a Horizontal Machining Center (HMC) will also increase under load, temperature, and wear conditions, decreasing the machining accuracy. As HMC is a high-accuracy machine tool with a high nonlinear system, there is a complex coupling relationship between errors. Therefore, how to thoroughly evaluate the ability of a machine tool to maintain its machining accuracy with the extension of working time is an important way for HMC to control its machining quality. In this paper, this ability is defined as machining accuracy reliability, that is, under specified conditions, the machine tool can work normally to achieve the corresponding machining accuracy ability. To solve this problem, a new analysis method is proposed for evaluating machining accuracy reliability based on the nonlinear correlation between errors. The nonlinear relationship between machining accuracy and errors was determined using multibody modeling technology. The effect of interaction between errors on machining accuracy reliability was analyzed by introducing and calculating partial correlation coefficients. Finally, the method was validated using a four-axis machine tool.

The concept of time-averaged motion is introduced to analyze the coupled ship maneuvering and seakeeping problem. Based on this concept, new equations of ship motion, referred to as time-averaged equations, are proposed for ship maneuvering prediction in waves. The present work is to describe and verify the new method. For the latter, the maneuverability of container ship S-175 in regular waves is predicted by solving the equations, where forces and wave-induced high-frequency motions are approximated by means of a modeling approach. The results are compared with available experimental data. It is indicated that the new method is very promising because satisfactory agreements are found between predictions and experiments. In addition, the influences of wave-induced high-frequency motions on maneuverability are analyzed and discussed.

Objective Tumour necrosis factor-α-induced protein 8-like 2 (TIPE2) has strong anti-inflammatory properties. However, it is unknown whether increased TIPE2 is protective against lipopolysaccharide (LPS)-induced ALI. In the current study, we aimed to investigate whether increased TIPE2 can exert protective effects in a mouse model of ALI induced by LPS. Methods We administered TIPE2 adeno-associated virus (AAV-TIPE2) intratracheally into the lungs of mice. Three weeks later, ALI was induced by intratracheal injection of LPS into BALB/c mice. Twenty-four hours later, lung bronchoalveolar lavage fluid (BALF) was acquired to analyse cells and protein, arterial blood was collected for arterial blood gas analysis and the determination of pro-inflammatory factor levels, and lung issues were collected for histologic examination, transmission electron microscopy (TEM), TUNEL staining, wet/dry (W/D) weight ratio analysis, myeloperoxidase (MPO) activity analysis and blot analysis of protein expression. Results We found that TIPE2 overexpression markedly mitigated LPS-induced lung injury, which was evaluated by the deterioration of histopathology, histologic scores, the W/D weight ratio, and total protein expression in the BALF. Moreover, TIPE2 overexpression markedly attenuated lung inflammation, as evidenced by the downregulation of polymorphonuclear neutrophils (PMNs) in the BALF, lung MPO activity, and pro-inflammatory cytokine levels in the serum. Moreover, TIPE2 overexpression not only dramatically prevented LPS-induced pulmonary cell apoptosis in mice but also blocked LPS-activated JNK phosphorylation and NF-κB p65 nuclear translocation. Conclusions Our study shows that the increased expression of AAV-mediated TIPE2 in the lungs of mice inhibits acute inflammation and apoptosis and suppresses the activation of NF-κB and JNK in a murine model of ALI.

Acute lung injury (ALI) is a critical syndrome that is associated with high morbidity and mortality rates. The activation of the Fas/Fas ligand (FasL) signaling pathway may be an important pathophysiological mechanism during ALI development. Penehyclidine hydrochloride (PHC) has been revealed to exhibit anti-apoptotic properties and may attenuate the observed systemic inflammatory response. The present study was performed to elucidate the molecular mechanism of PHC in the regulation of the Fas/FasL signaling pathway in rats with ALI. An ALI rat model was constructed by inducing blunt chest trauma and hemorrhagic shock (T/HS), with PHC administration prior to or following T/HS. At 6 h following T/HS, blood samples and lung tissues were collected. Western blotting, arterial blood gas analysis, ELISA, hematoxylin and eosin staining, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining and biochemical indicator analysis were performed to determine the degree of lung injury and the key signaling pathways associated with lung damage. The results indicated that the administration of PHC following T/HS effectively attenuates lung injury by improving pulmonary oxygenation, decreasing histopathological damage, decreasing polymorphonuclear neutrophil count and decreasing Fas, FasL, caspase-8, caspase-3, tumor necrosis factor-α, interleukin (IL)-6 and IL-1β expression. The results indicated that PHC exhibits anti-apoptotic functions and exerts protective effects in ALI rats induced by T/HS, which may be attributed to the inhibition of the Fas/FasL signaling pathway.

Endoplasmic reticulum (ER) stress and mitochondrial dysfunction play a pivotal role in the pathological process of sepsis-induced acute lung injury (ALI). Quercetin has been proved to exert anti-inflammation in ALI. This study aimed to explore the protection mechanism of quercetin against sepsis-induced ALI via suppressing ER stress and mitochondrial dysfunction. Cecal ligation and puncture (CLP) mouse model was established to mimic sepsis, and LPS was used to stimulate murine lung epithelial (MLE-12) cells. We observed that quercetin ameliorated pulmonary pathological lesion and oxidative damage in sepsis-induced mice. In LPS-stimulated MLE-12 cells, quercetin could inhibit the level of ER stress as evidenced by decreased mRNA expression of PDI, CHOP, GRP78, ATF6, PERK, IRE1α and improve mitochondrial function, as presented by increased MMP, SOD level and reduced production of ROS, MDA. Meanwhile, transcriptome analysis revealed that quercetin upregulated SIRT1/AMPK mRNA expression. Furthermore, we used siRNA to knockdown SIRT1 in MLE-12 cells, and we found that SIRT1 knockdown could abrogate the quercetin-elicited antioxidation in vitro. Therefore, quercetin could protect against sepsis-induced ALI by suppressing oxidative stress-mediated ER stress and mitochondrial dysfunction via induction of the SIRT1/AMPK pathways.

Background: Sepsis has emerged as a life-threatening condition and acute respiratory distress syndrome (ARDS) induced by sepsis has added more massive destruction for the limitation of effective prevention and therapy. However, well-described studies of analysis-based researches especially bioinformatics analysis on revealing specific targets and underlying molecular mechanisms of sepsis and sepsis-induced ARDS (sepsis/ARDS) still remain limited and delayed despite the era of data-driven medicine. This study might provide a novel insight into the pathophysiology of sepsis/ARDS. Methods: Weight gene co-expression network based on data from the public database was constructed and followed by functional enrichment analysis. By performing differential expression analysis, least absolute shrink and selection operator (LASSO) method and multivariable logistic regression analysis, candidate biomarkers were identified. risk nomogram and various machine learning algorithms were employed to develop diagnostic prediction models, which were then assessed and validated by receiver operating characteristic (ROC) curve analysis. Analysis of marker gene expressions and immune cell infiltration was performed to further evaluate their correlations during the development of sepsis/ARDS. Findings: 2 key modules and 36 hub genes were identified and extensive immune-involved enrichment was significantly associated with sepsis/ARDS. 4 biomarkers (SIGLEC9, TSPO, CKS1B and PTTG3P) were identified as candidate biomarkers and a 4-gene-based prediction model were then developed and proved to be of great efficiency and performance for sepsis/ARDS. The expressions of both SIGLEC9 and TSPO were regulated significantly and exhibit a notable correlation with the stages of sepsis/ARDS. CD4 memory T cells, mast cells and monocytes might be involved in the process of sepsis/ARDS. Besides, SIGLEC9 and TSPO were significantly correlated with the infiltration of the above immune cells. Interpretation: Our study identified 4 genes, SIGLEC9, TSPO, CKS1B and PTTG3P, and established 4-gene-based prediction model for sepsis/ARDS. The relevant gene co-expression network and immune signatures might provide comprehensive insights into integrated analysis for efficient risk prediction, relatively accurate genetic diagnosis and potential immune-mediated molecular intervention of sepsis/ARDS. Funding: The present study was supported by grants from the National Natural Science Foundation of China (NO. 81970722, 81901952 and 82172144). Declaration of Interest: The authors declared no conflict of interest in the study.

Large ocean waves with large wave height may destroy the ship’s structure, whereas it is difficult to predict the nonlinear dynamic strength in the large waves. In this study, we used a nonlinear simulation based on boundary element method (BEM)-finite element method (FEM) and a collapse experiment of ship model to study dynamic ultimate strength and dynamic course of collapse of ship structure, the collapse test was performed in regular tank wave. Besides, a simulation method for nonlinear dynamic ship strength was proposed to predict and compare the results of collapse test. A collapsed model consisting of a plastic hinge and two ship strips is designed. Subsequently, we performed the nonlinear simulation of the ultimate strength of ship model induced by tank wave. Wave loads were calculated following potential theory and BEM. Next, ship structural FEM model was modeled, the ship pressure was transferred to ship wet surface elements, and inertia force was exerted as well. Finally, the nonlinear dynamic strength calculation of ship model was performed in accordance with nonlinear FEM. A four-point-bending test adopted displacement controlling method was designed to obtain the hysteresis characteristic of the elastoplastic hinge. Hysteretic test and simulation analysis was performed to determine post-ultimate bending moment. Time-domain computational results including rotation angle history and vertical bending moment are close to collapse test results so that the two methods are verified. This study verifies that structural nonlinearities of ship structure induced by wave loads could be predicted.

The aim of the present study was to investigate the effect of penehyclidine hydrochloride (PHC) pretreatment on mice with lipopolysaccharide (LPS)‑induced acute lung injury (ALI) and its possible underlying mechanisms. Mice were randomly separated into six groups: i) Sham group; ii) LPS group; iii) LPS + PHC group; iv) tumor necrosis factor a‑induced protein 8‑like protein 2 (TIPE2) group; v) LPS + TIPE2 group; and vi) LPS + TIPE2 + PHC group. The ALI model was induced using LPS through intratracheal injection. The mice received adenovirus gene to induce the overexpression of TIPE2. After mice were sacrificed, lung injury indices were assessed, and arterial blood, bronchoalveolar lavage fluid and lung tissues were collected for subsequent assays. Expression levels of related proteins were detected by using western blotting. It was found that compared with the sham group, the mice treated with LPS showed increased lung injury and dysfunctions of gas exchange. However, these trends were significantly ameliorated in the LPS + PHC group. Evaluation of protein expression in lung tissues showed that the increased expression of nuclear NF‑κB p65 and p‑c‑Jun N‑terminal kinase (JNK) induced by LPS were suppressed in the LPS + PHC group and the expression of TIPE2 was increased. The mice that received adenovirus gene to induce TIPE2 overexpression could also showed protective effects compared with the mice in the LPS group. However, the expression of TIPE2 decreased rather than increased in LPS group. In the mice pretreated with PHC, the expression of TIPE2 increased in mice with LPS‑induced ALI. To conclude, PHC pretreatment could inhibit the occurrence of inflammation and apoptosis in LPS‑induced ALI. This process may be related to the activation of TIPE2 and the inhibition of NF‑κB and JNK signaling pathway in the lungs of mice.

Background Oxycodone is a synthetic opioid receptor agonist that exerts antinociceptive activity via κ-, μ- and δ-opioid receptors (KOR, MOR and DOR, respectively). Activation of MOR has been reported to provide protection against acute lung injury (ALI). We hypothesized that pretreatment with oxycodone would attenuate lung injury at the level of alveolar tight junctions (TJs) and aquaporins (AQPs) and investigated this possibility in a two-hit model of ALI induced by lipopolysaccharide (LPS) and mechanical ventilation (MV). Method Male Sprague Dawley rats and A59 cells were divided into 6 groups: the control group, ALI group, oxycodone-pretreated group, and oxycodone/κ-, μ-, or δ-opioid receptor antagonist-pretreated groups. The rats were pretreated with oxycodone 30 min before intravenous injection of LPS and then allowed to recover for 24 h prior to MV, establishing a two-hit model of ALI. The cells were similarly treated with oxycodone (with or without antagonists) 30 min after exposure to lipopolysaccharide. The cells were cyclically stretched 24 h later to mirror the in vivo MV protocol. Results Oxycodone alleviated the histological lung changes in the rats with ALI and decreased pulmonary microvascular permeability both in vivo and in vitro. Oxycodone upregulated the expression of claudin-5, ZO-1, AQP1, and AQP5 but downregulated the expression of TNF-α, IL-1β, TLR4, NF-κB, MMP9, and caspase-3 and suppressed endothelial apoptosis in vivo and in vitro. These protective effects of oxycodone were partly eliminated by KOR and MOR antagonists but not by DOR antagonists. Conclusion Oxycodone pretreatment appears to act via κ- and μ-opioid receptors to ameliorate LPS- and MV-induced lung injury by suppressing inflammation and apoptosis, and this protective effect might be mediated through the inhibition of the TLR4/NF-κB pathways.

Aims The purpose of the present study was to investigate the possible role of TIPE2 on acute lung injury (ALI) induced by myocardial ischemia/reperfusion (MIR) in diabetic rats. Methods Sprague-Dawley (SD) rats were randomly separated into four groups: control+sham (C + sham); control+MIR (C + MIR); diabetes+sham (D + sham); diabetes+MIR (D + MIR). Diabetes was induced using streptozotocin. Eight weeks after diabetes induction, MIR was conducted. At 2 h after MIR, myocardial injury indices were assessed; arterial blood, bronchoalveolar lavage fluid (BALF) and lung tissues were collected for corresponding detection. Results Rats subjected to MIR showed serious ALI (estimated via pathological changes, lung injury score and Wet/Dry weight ratio), lung inflammation and pulmonary cell apoptosis compared with sham groups, especially in D + MIR group. Evaluation of protein expression in lung tissues showed that p-JNK and nuclear NF-κB p65 protein levels were higher in D + MIR group as compared with C + MIR group. Besides, either hyperglycemia or MIR can significantly upregulate TIPE2 protein levels. Conclusions In conclusion, diabetic lungs are more susceptible to MIR. TIPE2 may involve in this pathological process, possibly through regulation of inflammation, oxidative stress and apoptosis.

Surface damages usually occur in concrete structures. In order to restore the functions and prolong the service life of concrete structures, their surface damages should be repaired in time. This paper reviews the main requirements for repair materials for concrete structures and the most used inorganic repair materials, such as cement-based materials, alkali-activated materials and polymer modified inorganic repair materials. Moreover, techniques to characterize and even improve the interfaces between these repair materials and concrete substrate are summarized. Cement-based material has the advantages of good mechanical properties and consistency with concrete substrate while having the problems of high shrinkage and low flexibility. Polymer modified materials were found as having lower shrinkage and higher flexural strength. Increasing the roughness or humidity of the surface, adding fibers and applying interfacial agents can improve the bond strength between cement-based repair materials and concrete substrates. All of these repair materials and techniques can help to build a good interfacial bonding, and mechanisms of how they improve the interface are discussed in this article. These are of great importance in guaranteeing the effectiveness of the repair of the concrete surface and to guide the research and development of new repair materials.

A single wave of extreme height can damage ship structures in the ocean by generating buckling midship, thus destabilizing the ship girder and causing rupture. The probability of such an extreme wave is low in reality. On the one hand, it is very costly to recreate a real ship test for the study of extreme wave conditions. On the other hand, it is difficult to carry out tests on a scale model in tank waves, because such waves are too small to damage the ship model. In this paper, a hydroelasto-buckling experiment is performed on a ship model to study the dynamic ultimate strength of the ship and dynamic course of collapse of the structure. Thus far, no method of simulation has been proposed to study this problem because the dynamic ultimate strength of the ship involves strong coupling between the nonlinearity in the ship structure and waves. Here, a hydroelasto-buckling ship model is first designed, and a test programme is determined. A buckling hinge that can collapse under the load of the tank wave is used to connect two ship girders with a hinge joint. Then, a number of single tank waves are generated by changing their wave patterns to simulate an extreme ocean wave. The dynamic rotation angle, bottom water press and acceleration at midship are measured in the experiment. Importantly, the relationship between structural response and wave patterns is analyzed. The structural response involves encountering the VBM/rotation deformation induced by the wave load and whipping the VBM/rotation deformation induced by natural structural oscillations. It is found that the ultimate strength of the ship girder can be generated by both encountering waves and the structural flutter response caused by changing wave height. Lastly, the midship water pressure and acceleration are also analyzed to discuss the influence of a large deformation of the ship structure on the fluid load. Some conclusions are presented in the paper.

The aim of the present study was to investigate whether TIPE2 participates in the protective actions of dexmedetomidine (DEX) in a mouse model of sepsis-induced acute lung injury (ALI). We administered TIPE2 adeno-associated virus (AAV-TIPE2) intratracheally into the lungs of mice. Control mice were infected with an adeno-associated virus expressing no transgene. Three weeks later, an animal model of caecal ligation-perforation (CLP)-induced sepsis was established. DEX was administered intravenously 30 min after CLP. Twenty-four hours after sepsis, lung injury was assayed by lung histology, the ratio of polymorphonuclear leukocytes (PMNs) to total cells in the bronchoalveolar lavage fluid (BALF), myeloperoxidase (MPO) activity, BALF protein content and the lung wet-to-dry (W/D) weight ratio. Proinflammatory factor levels in the BALF of mice were measured. The protein expression levels in lung tissues were analysed by Western blotting. The results showed that DEX treatment markedly mitigated sepsis-induced lung injury, which was characterized by the deterioration of histopathology, histologic scores, the W/D weight ratio and total protein levels in the BALF. Moreover, DEX markedly attenuated sepsis-induced lung inflammation, as evidenced by the decrease in the number of PMNs in the BALF, lung MPO activity and proinflammatory cytokines in the BALF. In addition, DEX dramatically prevented sepsis-induced pulmonary cell apoptosis in mice, as reflected by decreases in the number of TUNEL-positive cells, the protein expression of cleaved caspase-9 and cleaved caspase 3 and the Bax/Bcl-2 ratio. In addition, evaluation of protein expression showed that DEX blocked sepsis-activated JNK phosphorylation and NF-κB p65 nuclear translocation. Similar results were also observed in the TIPE2 overexpression group. Our study demonstrated that DEX inhibits acute inflammation and apoptosis in a murine model of sepsis-stimulated ALI via the upregulation of TIPE2 and the suppression of the activation of the NF-κB and JNK signalling pathways.

Background Previous studies showed that GTS-21, a selective alpha 7 nAchR agonist, can trigger anti-inflammatory effects and improve the survival of septic animals. However, whether GTS-21 affects autophagy responses remains unclear. Here, we tested the hypothesis that GTS-21 ameliorates sepsis-induced hepatic injury by modulating autophagy in mice. Method C57BL/6 male mice were randomly separated and categorized into four groups: the sham group, and CLP group subjected to caecal ligation and puncture (CLP, a model of polymicrobial sepsis). The CLP + GTS-21 group was administered GTS-21 immediately after CLP challenge. α-Bungarotoxin (an alpha 7 nAchR antagonist) was injected before CLP was performed, and then, after CLP challenge, GTS-21 was administered to α-BGT + CLP + GTS-21 group. The hepatic tissue and blood samples were harvested 6 h after the operation. Results CLP challenge increased TNF-α and IL-6 production, and hepatic enzyme alanine aminotransferase and aspartate transaminase levels. CLP also elevated the expression of hepatic LC3-II, sequestosome-1/p62, Atg7 and Atg5. The administration of GTS-21 inhibited pro-inflammatory cytokine production and hepatic enzymatic marker expression, promoted the expression of LC3-II, Atg7, Atg5, and decreased the expression of p62, which could be reversed by α-BGT treatment. Conclusion Our findings suggested that α7nAchR is involved in diminishing hepatic damage by inhibiting inflammatory responses and improving autophagy in mice with polymicrobial sepsis.

In recent years, unmanned surface vehicles have emerged in an endless stream, and more and more special functions have been given. The unmanned surface vehicles has experienced explosive growth in China, and in addition to military applications, the civilian market has also shown strong demand. In this paper, we discussed the relevant researches and constructions in China, and we summed up the trends of development and application related to the unmanned surface vehicle in China. Meanwhile, the studies on the unmanned surface vehicles for design, perception, navigation control, modular design and so on are reviewed. We proposed the in-depth research strategy and combined application suggestions of unmanned surface vehicles, also prospected the future development direction and market prospect of unmanned surface vehicles.

The problem of ship motions in waves can be seen as a coupled problem of manoeuvring and seakeeping. The former is a low-frequency motion problem in terms of time scale of ship motion, whereas the latter is relatively a high-frequency motion problem. They can be separately predicted by solving a group of low-frequency ship motion equations and a group of high-frequency ship motion equations. However, the theoretical basis behind both usual groups of motion equations may be questionable. In our previous study, a time-averaged method was introduced to derive the pure low-frequency ship motion equations in regular waves. The new equations have a few additional terms which are the mean inertial forces and moments due to wave-induced high-frequency motions, compared with the usual equations. The low-frequency ship motion equations were then solved to predict ship manoeuvring in waves by means of a modelling approach. It has been demonstrated that these additional terms are non-negligible for manoeuvring prediction, if amplitudes of high-frequency motions are large enough, e.g. in the condition of long wave length and large wave amplitude. In this study, we will give out the more complete pure low-frequency ship motion equations in regular waves and some new explanations. The pure high-frequency ship motion equations are also derived by subtracting the pure low-frequency ship motion equations from transient ship motion equations. On the aspect of manoeuvring prediction, there are two improvements, as compared with before. One is that the mean inertial forces and moments due to second-order high-frequency motions are retained in the pure low-frequency motion equations. The other is that the effect of longitudinal ship speed is taken into account in the modelling approach. As will be shown, the prediction accuracy is improved.

Hexagon Enclosed Platform (HEP) provides life accommodation, ship docking and marine replenishment for many ocean-going vessels in deep ocean. The HEP is composed of six trapezoidal floating modules connected by six rigid connectors and has characteristic of heteromorphic mat-type so that its hydroelastic response is critical. Therefore, this paper proposes a FMRC (Flexible modulus Rigid Connector) HEP model and studies its hydroelastic response by means of numerical simulations and model experiment. Firstly, a scaled model of HEP which is also made up of six trapezoidal structural modules constructing with a steel layer and foam layer is designed and fabricated for model experiment. Secondly, the model experiment of HEP is performed in a number of tank waves. Thirdly, 3D hydroelasticity method is used to calculate the load and structural responses of HEP model. Finally, numerical results and experimental results involving frequency-domain and time-domain results are obtained and compared, and the structural response mechanism of FMRC HEP is analysed. It is found that experimental results and numerical results have accordant matching and hydroelastic response of HEP is generated indeed based on research results. The research results and conclusions obtained in the paper are used to guide conceputal design of a HEP structure.

More and more successful applications of RANS tool to obtain hydrodynamic derivatives or coefficients for ship manoeuvring prediction have been reported in recent years. However, to obtain all required hydrodynamic derivatives from pure RANS simulations will be very time-consuming due to many cases, especially considering dynamic ship motions in water surface and real rotating propeller with dynamic grid approach. This might be one of the limiting factors to apply RANS tool for ship manoeuvring prediction widely, although the relevant numerical methods have been demonstrated to be of acceptable accuracy in many respects. So that, it is quite necessary to explore the appropriate strategies when applying RANS tool for ship manoeuvring prediction, consequently balancing prediction accuracy and time cost as far as possible. In this study, we use the own expanded RANS solver to simulate a series of captive model tests for the oil tanker KVLCC2. Assumptions of double-body flow and body force propeller are introduced during the simulations, in order to reduce computational time. Hydrodynamic derivatives are determined by regression analysis to the computed hydrodynamic forces, and free-running turning test and zig-zag test are simulated by using these derivatives. The RANS method and the whole procedure of manoeuvring prediction are described in this article. The main purpose is to check the applicability of the expanded RANS solver, and to confirm the effectiveness of whole procedure of manoeuvring prediction. It shows that the derivatives from RANS, can be used for manoeuvring prediction, at least for KVLCC2, and the present strategy of ship manoeuvring prediction is quite promising in the respect of the balance of prediction efficiency and accuracy.

The motions and added resistance for KVLCC2 models in head regular waves are predicted by using the expanded RANS solver on OpenFOAM platform. The computed added resistance consists of not only the added resistance due to pure hydrodynamic effect, that is obtained by integrating pressure and viscous stress over hull surface, but also the mean inertia forces due to the surge acceleration and the coupled motion of heave and pitch. Various conditions, i.e. ship speed, wave height, scale ratio, and spring stiffness are considered during the computations, and their influences on the components of added resistance and wave-induced motions are analyzed. The computed results show that spring stiffness, wave height, and scale effects have very little influences on heave and pitch for Froude number 0.142. However, the added resistance due to pure hydrodynamic effect and the total added resistance are affected considerably by wave height and scale ratio. The computed mean inertia force based on first-order heave and pitch is almost equal to the one based on the original result of heave and pitch, indicating the first-order heave and pitch play a major role in the contribution. The computed added resistances with the contribution of mean inertia forces and the first-order heave and pitch RAOs agree well with the available experimental data in general, demonstrating the present computations are effective and reliable. Moreover, this study supports the conclusion that the mean inertia forces, especially the one due to the coupled heave and pitch, should be accounted for when determining added resistance, for the purpose of comparing computed results with experimental data which usually does contain the inertia effects.

Renal ischemia-reperfusion (rI/R) is a risk factor for acute lung injury (ALI). Alveolar macrophages (AMs) activation mediated by rI/R-induced ALI is one of the pathogeneses associated with the development of ALI. In rI/R, α2-adrenergic receptor agonists have been indicated to be effective in decreasing urea nitrogen concentrations. In this study, we explored the underlying pathogenesis of the clinically obtainable α2-adrenergic receptor agonist dexmedetomidine (DEX) in protecting against rI/R -mediated AMs activation. We incubated AMs with the serum of sham and rI/R rats in the presence or absence of various concentrations of DEX. We used an enzyme-linked immunosorbent assay to detect the secretion levels of GSH, LDH, IL-18, IL-1β, and HMGB1 in the culture supernatant. We employed real-time polymerase chain reaction to assess the expression of NOX-4 mRNA, and western blotting to observe the protein levels of NOX-4, the NLRP3 inflammasome, AMPK, and eNOS. In addition, we used immunofluorescence to analyze ROS and MMP activity. Incubation of AMs with DEX suppressed rI/R-mediated cellular LDH production and ROS release. DEX also abolished the rI/R-mediated decrease in the activity of GSH and increased the levels of the rI/R-related NADPH oxidase protein NOX-4. Furthermore, DEX reduced the amelioration of the mitochondrial potential induced by rI/R. Our study showed that DEX inhibits rI/R-mediated levels of the NLRP3 inflammasome proteins ASC, NLRP3, HMGB1 and p20, and ameliorates rI/R-mediated AMPK signaling inactivation. Therefore, DEX reduces the levels of two mediators that are activated by the NLRP3 inflammasome: IL-18 and IL-1β. Finally, our study established that DEX mitigates the rI/R-mediated decrease in eNOS, demonstrating its protective functions against AMs activation. In conclusion, our study demonstrated that the protective action of DEX in AMs is induced through amelioration of HMGB1-NLRP3 inflammasome-AMPK signaling. Our results suggest that the anesthetic reagent DEX exerts beneficial effects to ameliorate rI/R-induced ALI.

Gastric cancer (GC) is the fourth most frequently occurring cancer and the second most common cause of cancer‑associated mortality worldwide. An increasing number of studies have reported that microRNAs (miRNAs/miRs) contribute to the regulation of GC development and progression. Therefore, investigation of the miRNAs involved in the development of GC may result in identification of an effective therapeutic target for patients with this malignancy. miR‑18b has been reported to be aberrantly expressed in several types of human cancer. However, the expression pattern, biological role and specific functional mechanism of miR‑18b in GC remains to be elucidated. In the present study, reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) analysis revealed that miR‑18b was significantly upregulated in GC tissues and cell lines compared with normal gastric tissues and the human gastric epithelial immortalized cell line GES‑1, respectively. High miR‑18b expression was significantly associated with lymph node metastasis, invasive depth and the Tumor Node Metastasis stage of patients with GC. Additionally, functional assays indicated that the inhibition of miR‑18b attenuated cell proliferation and invasion in GC. Furthermore, Kruppel‑like factor (KLF)‑6 was identified as a direct target gene of miR‑18b in GC, from the results of bioinformatics analysis, a luciferase reporter assay, RT‑qPCR and western blot analysis. An inverse association was observed between miR‑18b and KLF6 mRNA levels in GC tissues. KLF6 knockdown partially abrogated the effects of miR‑18b inhibition on GC cell proliferation and invasion. Therefore, miR‑18b/KLF6 targeted therapy may provide a promising treatment for patients with GC.