Expression and significant roles of the long non-coding RNA CASC19/miR-491-5p/HMGA2 axis in the development of gastric cancer

BACKGROUND Gastric cancer(GC)is a common malignant tumor,long non-coding RNA and microRNA(miRNA)are important regulators that affect tumor proliferation,metastasis and chemotherapy resistance,and thus participate in tumor progression.CASC19 is a new bio-marker which can promote tumor invasion and metastasis.However,the mechanism by which CASC19 affects the progression of GC through miRNA is not clear.AIM To explore the role of the CASC19/miR-491-5p/HMGA2 regulatory axis in GC.METHODS To explore the expression and prognosis of CASC19 in GC through clinical samples,and investigate the effects of inhibiting CASC19 on the proliferation,migration,invasion and other functions of GC cells through cell counting Kit-8(CCK-8),ethynyldeoxyuridine,Wound healing assay,Transwell,Western blot and flow cytometry experiments.The effect of miR-491-5p and HMGA2 in GC were also proved.The regulatory relationship between CASC19 and miR-491-5p,miR-491-5p and HMGA2 were validated through Dual-luciferase reporter gene assay and reverse transcription PCR.Then CCK-8,Transwell,Wound healing assay,flow cytometry and animal experiments verify the role of CASC19/miR-491-5p/HMGA2 regulatory axis.RESULTS The expression level of CASC19 is related to the T stage,N stage,and tumor size of patients.Knockdown of the expression of CASC19 can inhibit the ability of proliferation,migration,invasion and EMT conversion of GC cells,and knocking down the expression of CASC19 can promote the apoptosis of GC cells.Increasing the expression of miR-491-5p can inhibit the proliferation of GC cells,miR-491-5p mimics can inhibit EMT conversion,and promote the apoptosis of GC cells,while decreasing the expression of miR-491-5p can promote the proliferation and EMT conversion and inhibit the apoptosis of GC cells.The expression of HMGA2 in GC tissues is higher than that in adjacent tissues.At the same time,the expression level of HMGA2 is related to the N and T stages of the patients.Reducing the level of HMGA2 can promote cell apoptosis and inhibit the proliferation of GC cells.Cell experiments and animal experiments have proved that CASC19 can regulates the expression of HMGA2 through miR-491-5p,thereby affecting the biological functions of GC.CONCLUSION CASC19 regulates the expression of HMGA2 through miR-491-5p to affect the development of GC.This axis may serve as a potential biomarker and therapeutic target of GC.

Long noncoding RNAs HAND2-AS1 ultrasound microbubbles suppress hepatocellular carcinoma progression by regulating the miR-873-5p/tissue inhibitor of matrix metalloproteinase-2 axis

BACKGROUND Increasing data indicated that long noncoding RNAs(lncRNAs)were directly or indirectly involved in the occurrence and development of tumors,including hepatocellular carcinoma(HCC).Recent studies had found that the expression of lncRNA HAND2-AS1 was downregulated in HCC tissues,but its role in HCC progression is unclear.Ultrasound targeted microbubble destruction mediated gene transfection is a new method to overexpress genes.AIM To study the role of ultrasound microbubbles(UTMBs)mediated HAND2-AS1 in the progression of HCC,in order to provide a new reference for the treatment of HCC.METHODS In vitro,we transfected HAND2-AS1 siRNA into HepG2 cells by UTMBs,and detected cell proliferation,apoptosis,invasion and epithelial-mesenchymal transition(EMT)by cell counting kit-8 assay,flow cytometry,Transwell invasion assay and Western blotting,respectively.In addition,we transfected miR-837-5p mimic into UTMBs treated cells and observed the changes of cell behavior.Next,the UTMBs treated HepG2 cells were transfected together with miR-837-5p mimic and tissue inhibitor of matrix metalloproteinase-2(TIMP2)overexpression vector,and we detected cell proliferation,apoptosis,invasion and EMT.In vivo,we established a mouse model of subcutaneous transplantation of HepG2 cells and observed the effect of HAND2-AS1 silencing on tumor formation ability.RESULTS We found that UTMBs carrying HAND2-AS1 restricted cell proliferation,invasion,and EMT,encouraged apoptosis,and HAND2-AS1 silencing eliminated the effect of UTMBs.Additionally,miR-873-5p targets the gene HAND2-AS1,which also targets the 3’UTR of TIMP2.And miR-873-5p mimic counteracted the impact of HAND2-AS1.Further,miR-873-5p mimic solely or in combination with pcDNA-TIMP2 had been transformed into HepG2 cells exposed to UTMBs.We discovered that TIMP2 reversed the effect of miR-873-5p mimic caused by the blocked signalling cascade for matrix metalloproteinase(MMP)2/MMP9.In vivo results showed that HAND2-AS1 silencing significantly inhibited tumor formation in mice.CONCLUSION LncRNA HAND2-AS1 promotes TIMP2 expression by targeting miR-873-5p to inhibit HepG2 cell growth and delay HCC progression.

Mechanism and technology study of collaborative support with long and short bolts in large-deformation roadways

Common short bolts of equal length are widely used to support the roofs of roadways in coal mines.However, they are insufficient to keep the roof stable against large deformations, so docking long bolts with high levels of elongation that can adapt to large deformations of the surrounding rock have been adopted. This paper proposes a collaborative support method that uses long and short bolts. In this study,the mechanism of docking long bolts and collaborative support was studied. Numerical simulation, similarity simulation, and field testing were used to analyze the distribution law of the displacement, stress,and plastic failure in the surrounding rock under different support schemes. Compared with the equal-length short bolt support, the collaborative support changed the maximum principal stress of the shallow roof from tensile stress to compressive stress, and the minimum principal stress of the roof significantly increased. The stress concentration degree of the anchorage zone clearly increased. The deformation of the roof and the two sides was greatly reduced, and the subsidence shape of the shallow roof changed from serrated to a smooth curve. The roof integrity was enhanced, and the roof moved down as a whole. Plastic failure significantly decreased, and the plastic zone of the roof was within the anchorage range. The similarity simulation results showed that, under the maximum mining stress,the roof collapsed with the equal-length short bolt support but remained stable with the collaborative support. The collaborative support method was successfully applied in the field and clearly improved the stability of the surrounding rock for a large deformation roadway.

Long non-coding RNA highly up-regulated in liver cancer promotes exosome secretion

BACKGROUND Highly upregulated in liver cancer (HULC) is a long non-coding RNA (lncRNA) which has recently been identified as a key regulator in hepatocellular carcinoma (HCC) progression. However, its role in the secretion of exosomes from HCC cells remains unknown. AIM To explore the mechanism by which HULC promotes the secretion of exosomes from HCC cells. METHODS Serum and liver tissue samples were collected from 30 patients with HCC who had not received chemotherapy, radiotherapy, or immunotherapy before surgery. HULC expression in serum exosomes and liver cancer tissues of patients was measured, and compared with the data obtained from healthy controls and tumor adjacent tissues. The effect of HULC upregulation in HCC cell lines and the relationship between HULC and other RNAs were studied using qPCR and dualluciferase reporter assays. Nanoparticle tracking analysis was performed to detect the quantity of exosomes.RESULTS HULC expression in serum exosomes of patients with HCC was higher than that in serum exosomes of healthy controls, and HULC levels were higher in liver cancer tissues than in tumor adjacent tissues. The expression of HULC in serum exosomes and liver cancer tissues correlated with the tumor-node-metastasis (TNM) classification, and HULC expression in tissues correlated with that in serum exosomes. Upregulation of HULC promoted HCC cell growth and invasion and repressed apoptosis. Notably, it also facilitated the secretion of exosomes from HCC cells. Moreover, qPCR assays showed that HULC repressed microRNA-372-3p (miR-372-3p) expression. We also identified Rab11a as a downstream target of miR-372-3p. Dual-luciferase reporter assays suggested that miR-372-3p could directly bind both HULC and Rab11a. CONCLUSION Our findings illustrate the importance of the HULC/miR-372-3p/Rab11a axis in HCC and provide new insights into the molecular mechanism regulating the secretion of exosomes from HCC cells.

Long noncoding RNA RP4 functions as a competing endogenous RNA through miR-7-5p sponge activity in colorectal cancer

AIM To investigate the role of long noncoding RNA(lnc RNA) RP4 in colorectal cancer.METHODS Lentivirus-mediated lnc RNA RP4 overexpression and knockdown were performed in the colorectal cancer cell line SW480. Cell proliferation, tumor growth, and early apoptosis were evaluated by a cell counting kit-8 assay, an in vivo xenograft tumor model, and annexin V/propidium iodide staining, respectively. Analysis of the lnc RNA RP4 mechanism involved assessment of the association of its expression with mi R-7-5 p and the SH3 GLB1 gene. Western blot analysis was also performed to assess the effect of lnc RNA RP4 on the autophagy-mediated cell death pathway and phosphatidylinositol-3-kinase(PI3 K)/Akt signaling.RESULTS Cell proliferation, tumor growth, and early apoptosis in SW480 cells were negatively regulated by lnc RNA RP4. Functional experiments indicated that lnc RNA RP4 directly upregulated SH3 GLB1 expression by acting as a competing endogenous RNA(ce RNA) for mi R-7-5 p. This interaction led to activation of the autophagy-mediated cell death pathway and de-repression of PI3 K and Akt phosphorylation in colorectal cancer cells in vivo.CONCLUSION Our results demonstrated that lnc RNA RP4 is a ce RNA that plays an important role in the pathogenesis of colorectal cancer, and could be a potential therapeutic target for colorectal cancer treatment.

Analytical models for the penetration of semi-infinite targets by rigid,deformable and erosive long rods

A theoretical study is presented herein on the pen- etration of a semi-infinite target by a spherical-headed long rod for Yp 〉 S, where Yp is the penetrator strength and S is the static target resistance. For Yp 〉 S, depending upon initial impact velocity, there exist three types of penetration, namely, penetration by a rigid long rod, penetration by a deforming non-erosive long rod and penetration by an erosive long rod. If the impact velocity of the penetrator is higher than the hydrodynamic velocity （VH）, it will penetrate the target in an erosive mode; if the impact velocity lies between the hydrodynamic velocity （VH） and the rigid body velocity （VR）, it will penetrate the target in a deformable mode; if the impact velocity is less than the rigid body velocity （VR）, it will penetrate the target in a rigid mode. The critical conditions for the transition among these three penetration modes are proposed. It is demonstrated that the present model predictions correlate well with the experimental observations in terms of depth of penetration （DOP） and the critical transition conditions.

Long noncoding RNA negative regulator of antiviral response contributes to pancreatic ductal adenocarcinoma progression via targeting miR-299-3p

BACKGROUND Pancreatic ductal cancer(PDAC)has high malignancy and poor prognosis.Long noncoding RNAs(lncRNAs)are associated with high levels of malignancy,including PDAC.However,the biological and clinical significance of negative regulator of antiviral response(NRAV)in PDAC is unclear.AIM To study the regulatory role of lncRNA NRAV in PDAC.METHODS GEPIA analyzed lncRNA NRAV and miRNA(miR-299-3p)expression levels in PDAC tissues and measured them in PDAC cells by quantitative measurements in real time.The specific role of NRAV and miR-299-3p in cell proliferation and transfer potential was evaluated by cell formation analysis,Cell Counting Kit-8 and Transwell analysis.The relationship between NRAV and miR-299-3p was studied by predictive bioinformatics,RNA immunoassay,and fluorescence enzyme analysis.In vivo experiments included transplantation of simulated tumor cells under naked mice.RESULTS The expression level of lncRNA NRAV was higher in both tumor tissues and cell lines of PDAC and was negatively associated with the clinical survival of PDAC patients.Functionally,overexpression of NRAV promoted cell proliferation and metastasis of PDAC cells,while knockdown of NRAV reversed these effects.Finally,NRAV was performed as a molecular sponge of miR-299-3p.Moreover,overexpression of miR-299-3p could reverse the promoting effects of NRAV on cell proliferation and metastasis of PDAC cells.CONCLUSION NRAV facilitates progression of PDAC as a molecular sponge of miR-299-3p and may be a potential molecular marker for diagnosis and treatment of PDAC.

Basic Study Long non-coding RNA TP73-AS1 promotes pancreatic cancer growth and metastasis through miRNA-128-3p/GOLM1 axis

BACKGROUND Previous studies have suggested that long non-coding RNAs(lncRNA)TP73-AS1 is significantly upregulated in several cancers.However,the biological role and clinical significance of TP73-AS1 in pancreatic cancer(PC)remain unclear.AIM To investigate the role of TP73-AS1 in the growth and metastasis of PC.METHODS The expression of lncRNA TP73-AS1,miR-128-3p,and GOLM1 in PC tissues and cells was detected by quantitative real-time polymerase chain reaction.The bioinformatics prediction software ENCORI was used to predict the putative binding sites of miR-128-3p.The regulatory roles of TP73-AS1 and miR-128-3p in cell proliferation,migration,and invasion abilities were verified by Cell Counting Kit-8,wound-healing,and transwell assays,as well as flow cytometry and Western blot analysis.The interactions among TP73-AS1,miR-128-3p,and GOLM1 were explored by bioinformatics prediction,luciferase assay,and Western blot.RESULTS The expression of TP73-AS1 and miRNA-128-3p was dysregulated in PC tissues and cells.High TP73-AS1 expression was correlated with a poor prognosis.TP73-AS1 silencing inhibited PC cell proliferation,migration,and invasion in vitro as well as suppressed tumor growth in vivo.Mechanistically,TP73-AS1 was validated to promote PC progression through GOLM1 upregulation by competitively binding to miR-128-3p.CONCLUSION Our results demonstrated that TP73-AS1 promotes PC progression by regulating the miR-128-3p/GOLM1 axis,which might provide a potential treatment strategy for patients with PC.

Synthesis of M1-3xAl2O4:Eu2+x/Dy3+ 2x(M^2+= Sr^2+, Ca^2+ and Ba^2+) phosphors with long-lasting phosphorescence properties via co-precipitation method

The long afterglow fluorescent material of M1-3xAl2O4:Eu2+ x/Dy3+2x(M2+= Sr2+, Ca2+ and Ba2+) phosphors are successfully synthesized by calcining precursor obtained via co-precipitation method at 1300oC for 4 h with reducing atmosphere (20% H2 and 80% N2). The phase evolution, morphology and afterglow fluorescent properties are systematically studied by the various instruments of XRD, FE-SEM, PLE/PL spectroscopy and fluorescence decay analysis. The PL spectra shows that the Sr1-3xAl2O4:Eu2+x/Dy3+ 2x phosphors display vivid green emission at s519 nm (4f65d1!4f7 transition of Eu2+) with monitoring of the maximum excitation wavelength at s334 nm (8S7=2!6IJ transition of Eu2+), among which the optimal concentration of Eu2+ and Dy3+ is 15 at.% and 30 at.%, respectively. The color coordinates and temperature of Sr1-3xAl2O4:Eu2+ x/Dy3+ 2x phosphors are approximately at (s0.27, s0.57) and s6700 K, respectively. On the above basis, the M0:55Al2O4:Eu2+ 0:15/Dy3+ 0:3 (M2+= Ca2+ and Ba2+) phosphors is obtained by the same method. The PL spectra of these phosphors shows the strongest blue emission at s440 nm and cyan emission at s499 nm under s334 nm wavelength excitation, respectively, which are blue shifted comparing to Sr1??3xAl2O4:Eu2+ x/Dy3+ 2x phosphors. The color coordinates and temperatures of M0:55Al2O4:Eu2+ 0:15/Dy3+ 0:3 (M2+= Ca2+ and Ba2+) phosphors are approximately at (s0.18, s0.09), s2000 K and (s0.18, s0.42), s11600 K, respectively. In this work, long afterglow materials of green, blue and cyan aluminates phosphors with excellent properties have been prepared, in order to obtain wide application in the field of night automatic lighting and display.

Long noncoding RNA TNFRSF10A-AS1 promotes colorectal cancer through upregulation of HuR

BACKGROUND Recent studies have emphasized the emerging importance of long noncoding RNAs(lncRNAs)in colorectal cancer(CRC).However,the functions and regulatory mechanisms of numerous lncRNAs in CRC have not been fully elucidated.AIM To explore the functional role and underlying molecular mechanisms of lncRNA TNFRSF10A-AS1 in CRC.METHODS TNFRSF10A-AS1 expression was measured by quantitative real-time polymerase chain reaction in CRC,and the relationship between TNFRSF10A-AS1 levels and the clinicopathological features of CRC patients was analyzed.The effect of TNFRSF10A-AS1 expression on CRC proliferation and metastasis was examined in vitro and in vivo.Mechanistically,we investigated how TNFRSF10A-AS1 is involved in CRC as a competitive endogenous RNA.RESULTS TNFRSF10A-AS1 was expressed at a high level in CRC and the upregulation of TNFRSF10A-AS1 was associated with advanced T grade and tumor size in CRC patients.A functional investigation revealed that TNFRSF10A-AS1 enhanced the proliferation,migration ability and invasion ability of colon cancer cells in vitro and in vivo.A mechanistic analysis demonstrated that TNFRSF10A-AS1 acted as a miR-3121-3p molecular sponge to regulate HuR expression,ultimately promoting colorectal tumorigenesis and progression.CONCLUSION TNFRSF10A-AS1 exerts a tumor-promoting function through the miR-3121-3p/HuR axis in CRC,indicating that it may be a novel target for CRC therapy.

Potential role of long noncoding RNA RP5-881L22.5 as a novel biomarker and therapeutic target of colorectal cancer

BACKGROUND The incidence of colorectal cancer in humans is high,and it is in the top five for cancer-related morbidity and mortality.It is one of the main threats to human health.The function of long noncoding RNAs in tumor occurrence and development has gradually gained attention in recent years.In increasing numbers of studies,researchers have demonstrated that it plays an important role in the pathogenesis of colorectal cancer.AIM To find out if long noncoding RNA RP5-881L22.5 played a role in the pathogenesis of colorectal cancer in relation to the tumor microenvironment.METHODS We analyzed the transcriptome data and clinical data in The Cancer Genome Atlas-colon adenocarcinoma.The CIRBERSORT algorithm was applied to evaluate these tumor-infiltrating immune cells in The Cancer Genome Atlas-colon adenocarcinoma cancer tissue samples.Using the“estimate”package in R,we assessed the tumor immune microenvironment.The expression level of RP5-881L22.5 in tumor tissue and adjacent normal tissue samples from 4 pairs of colorectal cancer patients was determined by quantitative reverse transcription PCR.Colorectal cancer cells were tested for invasiveness using a transwell invasion assay after RP5-881L22.5 expression was knocked down.RESULTS The expression of lncRNA RP5-881L22.5 was related to the clinical characteristics of the tumors,and it was negatively related to the infiltration level of immune cells in the tumor microenvironment and the expression of T cell inhibitory receptors.A major function of its coexpressed mRNA was to regulate tumor immunity,such as the immune response.When quantitative reverse transcription PCR was performed on tumor tissues from 4 pairs of colorectal cancer patients,the results showed that RP5-881L22.5 was highly expressed.Subsequently,knocking down the expression of RP5-881L22.5,the invasiveness of colorectal cancer cell lines was reduced,and the apoptosis rate was increased.CONCLUSION RP5-881L22.5 plays a crucial role in the microenvironment of tumors as well as in the pathogenesis of colorectal cancer.The relationship between RP5-881L22.5 and the tumor immune microenvironment deserves further study.

Non-stationary Buffeting Response Analysis of Long Span Suspension Bridge Under Strong Wind Loading

The non-stationary buffeting response of long span suspension bridge in time domain under strong wind loading is computed. Modeling method for generating non-stationary fluctuating winds with probabilistic model for non-stationary strong wind fields is first presented. Non-stationary wind forces induced by strong winds on bridge deck and tower are then given a brief introduction. Finally,Non-stationary buffeting response of Pulite Bridge in China,a long span suspension bridge,is computed by using ANSYS software under four working conditions with different combination of time-varying mean wind and time-varying variance. The case study further confirms that it is necessity of considering non-stationary buffeting response for long span suspension bridge under strong wind loading,rather than only stationary buffeting response.

星形胶质细胞上调基因-1表达与食管鳞状细胞癌预后的相关性研究

目的：探讨食管鳞状细胞癌组织中星形胶质细胞上调基因-1（AEG-1）的表达情况及其与临床分期、预后的相关性。方法：应用半定量RT-PCR、Western blotting及免疫组织化学技术检测AEG-1基因在食管鳞状细胞癌组织中的表达情况,并与肿瘤临床分期特征及预后进行相关性分析。结果：食管鳞状细胞癌组织中AEG-1 mRNA及蛋白表达量分别为癌旁正常组织的8.2-18.5倍及4.6-13.2倍。76例食管鳞状细胞癌石蜡包埋组织中AEG-1蛋白表达阳性占70例。AEG-1在男性患者中的表达强度强于女性患者,在中晚期病变中的表达强度强于早期病变,另AEG-1表达强度与患者生存时间呈负相关。结论：AEG-1不仅可以用于预测食管癌患者预后,也可能成为一个潜在的基因治疗靶点。

隧道径向锚钉-斜交锚杆复合支护技术研究

基于长短锚杆组合支护理论,提出了一种隧道径向锚钉-斜交锚杆复合支护技术,该技术可提高支护结构的整体抗力,有利于缩小围岩塑性区半径,增加锚杆处于稳定围岩区的长度。为进一步研究锚钉和锚杆的组合长度,将隧道围岩划分为A、B和C三区,并把锚杆作用在围岩体内的剪应力简化为环向边界应力,运用厚壁圆筒弹塑性理论推导了锚钉和锚杆组合长度计算式。实例分析表明,0.8m(锚钉)和3.8m(锚杆)的组合长度可以使隧道塑性区半径降低28%,锚固盲区减小88.8%。可见,在隧道长短锚杆组合支护理论中,该计算方法对围岩锚固体长度参数设计有一定指导意义。

长锚杆/锚索改善深埋大跨度隧道初支结构受力试验研究

针对深埋大跨度软岩隧道拱脚及拱顶处初支开裂、钢架变形过大问题,提出了局部增设长锚杆或锚索的支护技术,以实现对该类隧道初支结构受力的调节改善。基于课题组自主研发的隧道结构性能测试平台,对比分析了同等围岩荷载作用下系统锚杆支护与多类长锚杆/锚索支护方案的初期支护结构受力变形特征,研究了不同环向间距与布设范围的长锚杆/锚索支护效果。研究结果表明:(1)常规支护时,大跨度隧道初期支护整体呈压扁趋势,拱顶内侧与拱脚外侧承受结构最大弯矩而最先开裂,仰拱内侧拉裂后模型加速变形进而引起结构整体失稳破坏;(2)4种增设长锚杆或锚索支护方案下,初支拱顶处结构安全系数分别为常规支护体系的4.59,2.12,1.96,1.80倍,拱脚处结构安全系数分别为常规支护的5.23,2.80,2.34,2.37倍;(3)在拱部120°范围以2 m环向间距布设长锚杆对初支结构内力改善效果最佳,支护点轴向强拉力产生的局部负弯矩组合效应抵消了拱顶处较大正弯矩;(4)不同位置长锚杆/锚索支护力整体呈从拱顶处至拱肩侧先减小后增大的规律。

长螺杆加强型胶合木梁柱节点力学性能

胶合木梁柱螺栓钢填板节点由于抗弯刚度较低,在结构设计中通常被视为铰接。提出了一种长螺杆加强型胶合木梁柱节点,为无支撑或剪力墙的中高层木结构体系中提供较好的刚性连接。设计并加工了3组不同长螺杆直径的节点试件,通过单调加载和往复加载试验探究了节点的抗弯刚度、抗弯承载力、破坏模式及耗能性能。通过ABAQUS有限元软件建立了节点力学模型,模拟结果与试验结果较为吻合,并基于该模型开展了参数分析。结果表明:该节点具有较高的抗弯刚度与抗弯承载力,经过合理构造后节点损伤主要集中在长螺杆,而长螺杆在破坏后易于更换,可提高节点韧性与使用寿命。参数分析结果表明,转动刚度与长螺杆直径及力臂呈正相关。基于试验与模拟的结果,提出了该类节点抗弯刚度及抗弯承载力的计算方法,为其在实际工程中的设计与应用提供参考。

超长外露锚杆无损检测方法的研究与应用

锚杆无损检测技术是利用声波反射原理检测注浆锚杆的注浆饱满度及其埋设长度的一种方法,目前已在各类支护工程中广泛应用。但当锚杆外露长度过长时,其取得的检测结果误差较大,不能准确地反映锚杆的锚固质量。硬梁包水电站地下厂房岩壁吊车梁锚杆外露长度均超过1 m,其锚杆数量多,对钻孔注浆质量要求高,阐述了对如何准确快捷地实施检测,并进行了研究分析与探讨,所取得的经验可供类似工程借鉴。

大断面巷道穿断层破碎带区域支护参数优化数值模拟

目的:合理的支护参数是确保巷道围岩稳定和控制支护成本的关键。本研究以巨龙铜矿大断面排水巷道为研究对象进行支护参数优化。方法:设计了三种支护参数,利用有限元软件进行了数值模拟研究。通过分析不同支护参数下位移、应力及塑性区结果进行支护参数优化。结果:结果表明,锚杆支护能够有效改善围岩应力分布,避免出现应力集中。随着锚杆间距和排距的增大,巷道围岩最大位移增大,当锚杆间距和排距为1000 mm时,巷道围岩位移最大。围岩塑性变形主要发生于巷道肩部和两帮位置。当锚杆间距和排距为1000 mm时,塑性区深度大于锚杆长度。综合数值模拟结果和支护成本,巨龙铜矿大断面排水巷道最优锚杆支护参数为800 mm×800 mm(间距×排距)。意义:研究结果为穿断层破碎带巷道支护设计提供了理论参考。

筒体悬挂结构若干问题分析

以菏泽博物馆新馆项目为背景,从计算方法、构件受力和设计、整体屈服机制等八个方面对筒体悬挂结构体系做了较全面的研究。结果表明:1)计算筒体悬挂结构水平地震作用时无需调整层质量;2)规范底部轴力法、振型分解反应谱法并不适用筒体悬挂结构竖向地震作用计算,考虑最小限值调整后的吊柱设计仍可能偏不安全;3)采用长孔螺栓节点设计能让筒体悬挂结构吊柱在各工况下处于理想轴向拉压受力状态;4)中高烈度区吊柱在大震组合作用下可能受压,有必要复核其受压稳定和承载力;5)吊柱受力在小震阶段为恒、活载控制,大震阶段其恒、活载占比降低,地震逐渐起控制作用;6)合理的吊柱布置除满足建筑条件外,还需兼顾核心筒顶受力,减小筒顶不平衡弯矩;7)核心筒顶上包与否均能实现与屋面悬挂桁架的有效刚性连接;8)合理的筒体悬挂结构屈服机制就是落地核心筒的延性破坏过程,即始于连梁开裂破损,终于筒底墙肢钢筋拉屈、混凝土压溃。

面向大跨度框架桥顶进施工的既有特制道岔便梁扩大应用改造研究

为解决大跨度框架桥顶进施工时加固便梁跨度不足问题,对既有特制道岔便梁接长改造,将旧纵梁两跨端切除、栓接新节段梁,然后利用连接件将D型便梁横梁与接长纵梁连接。建立了改造便梁的有限元模型,对其进行了受力性能分析,最后对改造方案进行了试验验证。受力分析表明螺栓连接、纵梁截面强度和拼接板净截面强度均满足规范要求;现场动应力和动态性能测试结果证明了改造方案可行。提供了一种安全性高、施工简单的大跨度框架桥顶进施工的线路架空加固方案,同时提高了既有特制道岔便梁的利用率,降低了工程费用,具有较高的应用推广价值。