miRNA sequencing analysis of healthy and atretic follicles of chickens revealed that miR-30a-5p inhibits granulosa cell death via targeting Beclin1

Background:The egg production performance of chickens is affected by many factors,including genetics,nutrition and environmental conditions.These factors all play a role in egg production by affecting the development of follicles.MicroRNAs(miRNAs)are important non-coding RNAs that regulate biological processes by targeting genes or other non-coding RNAs after transcription.In the animal reproduction process,miRNA is known to affect the development and atresia of follicles by regulating apoptosis and autophagy of granulosa cells(GCs).Results:In this study,we identified potential miRNAs in the atretic follicles of broody chickens and unatretic follicles of healthy chickens.We identified gga-miR-30a-5p in 50 differentially expressed miRNAs and found that gga-miR-30a-5p played a regulatory role in the development of chicken follicles.The function of miR-30a-5p was explored through the transfection test of miR-30a-5p inhibitor and miR-30a-5p mimics.In the study,we used qPCR,western blot and flow cytometry to detect granulosa cell apoptosis,autophagy and steroid hormone synthesis.Confocal microscopy and transmission electron microscopy are used for the observation of autophagolysosomes.The levels of estradiol(E2),progesterone(P4),malondialdehyde(MDA)and superoxide dismutase(SOD)were detected by ELISA.The results showed that miR-30a-5p showed a negative effect on autophagy and apoptosis of granulosa cells,and also contributed in steroid hormones and reactive oxygen species(ROS)production.In addition,the results obtained from the biosynthesis and dual luciferase experiments showed that Beclin1 was the target gene of miR-30a-5p.The rescue experiment conducted further confirmed that Beclin1 belongs to the miR-30a-5p regulatory pathway.Conclusions:In summary,after deep miRNA sequencing on healthy and atretic follicles,the results indicated that miR-30a-5p inhibits granulosa cell death by inhibiting Beclin1.

Quercetin ameliorates oxidative stress-induced senescence in rat nucleus pulposus-derived mesenchymal stem cells via the miR-34a-5p/SIRT1 axis

BACKGROUND Intervertebral disc degeneration(IDD)is a main contributor to low back pain.Oxidative stress,which is highly associated with the progression of IDD,increases senescence of nucleus pulposus-derived mesenchymal stem cells(NPMSCs)and weakens the differentiation ability of NPMSCs in degenerated intervertebral discs(IVDs).Quercetin(Que)has been demonstrated to reduce oxidative stress in diverse degenerative diseases.AIM To investigate the role of Que in oxidative stress-induced NPMSC damage and to elucidate the underlying mechanism.METHODS In vitro,NPMSCs were isolated from rat tails.Senescence-associatedβ-galactosidase(SA-β-Gal)staining,cell cycle,reactive oxygen species(ROS),realtime quantitative polymerase chain reaction(RT-qPCR),immunofluorescence,and western blot analyses were used to evaluated the protective effects of Que.Meanwhile the relationship between miR-34a-5p and Sirtuins 1(SIRT1)was evaluated by dual-luciferase reporter assay.To explore whether Que modulates tert-butyl hydroperoxide(TBHP)-induced senescence of NPMSCs via the miR-34a-5p/SIRT1 pathway,we used adenovirus vectors to overexpress and downregulate the expression of miR-34a-5p and used SIRT1 siRNA to knockdown SIRT1 expression.In vivo,a puncture-induced rat IDD model was constructed,and X rays and histological analysis were used to assess whether Que could alleviate IDD in vivo.RESULTS We found that TBHP can cause NPMSCs senescence changes,such as reduced cell proliferation ability,increased SA-β-Gal activity,cell cycle arrest,the accumulation of ROS,and increased expression of senescence-related proteins.While abovementioned senescence indicators were significantly alleviated by Que treatment.Que decreased the expression levels of senescence-related proteins(p16,p21,and p53)and senescence-associated secreted phenotype(SASP),including IL-1β,IL-6,and MMP-13,and it increased the expression of SIRT1.In addition,the protective effects of Que on cell senescence were partially reversed by miR-34a-5p overexpression and SIRT1 knockdown.In vivo,X-ray,and histological analyses indicated that Que alleviated IDD in a punctureinduced rat model.CONCLUSION In summary,the present study provides evidence that Que reduces oxidative stress-induced senescence of NPMSCs via the miR-34a/SIRT1 signaling pathway,suggesting that Que may be a potential agent for the treatment of IDD.

MiR-125a-5p is Upregulated in Plasma of Residents from An Electronic Waste Recycling Site

The mechanism of health effects caused by organohalogen pollutants, e.g., toxins from electronic waste(e-waste), is poorly understood. We supposed that micro RNAs(mi RNAs), an important post-transcriptional regulator, could play a role in this process. In this study, fasting peripheral blood samples were collected from residents living at an e-waste site in northern China and a nearby reference population. Concentrations of e-waste related organohalogen pollutants in plasma from the exposure group were higher than the corresponding measurement in the reference group. Correspondingly, sixty mi RNAs in plasma showed > 2-fold change between the two groups in microarray analysis. Among them, mi R-125a-5p was confirmed to be upregulated by q RT-PCR and its validated targets were enriched in responses to xenobiotics and cancer related pathways. Furthermore, significant positive correlations were found between levels of mi R-125a-5p in plasma and reactive oxygen species(ROS) in polymorphonuclear neutrophil leukocytes(P < 0.05). These evidences suggested oxidative stress might be an intermediate between e-waste related POPs exposure and alteration of plasma mi RNA.

黄土湿陷过程下埋地油气管道力学行为有限元模拟

针对黄土遇水后湿陷产生陷穴并引起埋地管道悬空这一过程中管道的力学行为,以基于弹塑性地基的黄土湿陷区悬空管道力学模型为基础,从湿陷原因和机理出发,建立三维有限元实体模型,模拟了土体湿陷过程和沉降变形,模拟计算结果与理论值和实测值进行了比对验证;进一步的计算和回归分析得到了管道最大位移、最大von Mises应力与地表土体湿陷沉降量的变化规律,同时也得到了最终湿陷情况下管道的von Mises应力分布和湿陷区范围的影响。结果表明:土体湿陷沉降是管道和土体共同作用的结果,湿陷前期管道与土体一起运动,位移和应力增加较快,而管道下方土体脱离管道产生陷穴后则增长较慢;管道最大位移和土体湿陷沉降量间呈对数函数关系,而管道最大von Mises应力和土体湿陷量呈指数函数关系;湿陷区管段向下弯曲变形会在3个位置形成应力集中区,湿陷区范围增大会引起管道应力和变形的明显增加,且3个区域的最值分布有所不同。

螺旋板换热器密封端盖结构研究

为合理选择螺旋板换热器密封端盖结构,采用有限元分析技术对螺旋板换热器中常用密封端盖结构进行分析对比,并在此基础上对影响变形的相关变量进行研究。结果表明:椭圆形端盖结构、径向加强筋端盖结构、倒锥端盖结构的应力和变形约为单环形加强筋结构的一半,其中倒锥端盖综合性能要好于其它几种;倒锥端盖结构lc/Ra约为0.15、ld/lb约为0.3、角度a约为45°～50°时,倒锥端盖无论是应力还是变形都趋于合理。

高坎桥正交异性钢桥面板的疲劳分析

为了解正交异性钢桥面板的抗疲劳性能,以高坎桥为背景,采用MIDAS/FEA计算该桥桥面板主要构造细节的疲劳应力幅,运用线弹性断裂力学分析方法对横隔板的疲劳扩展寿命进行估算。计算结果表明,钢桥面板、纵肋和横隔板间的连接部位最大应力幅均小于常幅疲劳限值,但其中的横隔板弧形缺口边缘应力集中较严重。通过线弹性断裂力学疲劳分析,横隔板弧形缺口边缘裂纹长度从1mm扩展到临界裂纹尺寸553mm要经过1.23×106次应力循环。

Chlorogenic acid alleviates oxidative damage in hepatocytes by regulating miR-199a-5p/GRP78 axis

Chlorogenic acid(CGA)is a phenylpropanoid compound in chrysanthemum,which has a variety of biological activities.Nevertheless,CGA has not yet been studied concerning oxidative stress in hepatocytes.Our research aims to investigate whether chlorogenic acid can improve hepatic oxidative stress,and further illustrated its detailed mechanism.The results of free radicals measurement and Western blot showed that CGA suppressed the activation of JNK(c-Jun NH2-teminal kinase)signaling pathway by ameliorating endoplasmic reticulum stress in H2O2-treated hepatocytes,thereby eliminating excess intracellular free radicals.In addition,through RT-qPCR,we found that miR-199a-5p down-regulated in H2O2-induced L02 cells,which was restored by CGA.By inhibiting the expression of miR-199a-5p to promote the transcription of GRP78 gene,the antioxidant capacity of CGA was greatly weakened in hepatocytes.Our findings suggest that CGA treatment alleviated the H2O2-induced oxidative stress by targeting miR-199a-5p,thereby ameliorating ER stress and inhibiting JNK phosphorylation for anti-oxidant capacity enhancement.Based on our available results,CGA may be an alternative compound to mitigate hepatic oxidative damage through the miR-199a-5p/GPR78 axis.

模拟全髋关节置换术后两种假体的应力对比分析

对比分析置入解剖型假体和置入传统型假体应力遮挡效应，为临床提供生物力学基础。随机取5个为模拟全髋关节置换术以（北京普鲁士钢研外植入物有限公司）传统型假体置入的股骨组，随机取5个以（德国LINK公司）保留股骨颈解剖型假体置入股骨组。首先在正常股骨标本的各测点上黏贴电阻应变片，进行应变电测量之后，待标本在室温不受力状态下放置24h后，对正常股骨标本分别置入传统型假体、保留股骨颈解剖型假体，分别测出置入传统型假体组和解剖型假体组股骨各测点的应变值，计算各测点的应力值，根据应力遮挡率计算公式，计算应力遮挡率值。置入传统型假体组股骨标本近端1～10号测点应力遮挡率值大于置入解剖型假体组股骨标本近端1～10号测点应力遮挡率值，差异显著（P＜0．05）。解剖型假体和传统型假体具有不同的防应力遮挡效果，保留股骨颈解剖型假体防应力遮挡效果显著。

基于蠕变试验的ZChSnSb11-6应力松弛特性研究

在相同温度下,对巴氏合金ZCh Sn Sb11-6做了蠕变试验,获得合金在Norton形式和指数形式下的稳态蠕变方程,并利用所得系数得到合金在两种形式下应力松弛计算公式。采用ANSYS有限元分析软件模拟巴氏合金ZCh Sn Sb11-6的应力松弛过程,得到松弛过程中的蠕变曲线,并比较了理论与有限元方法计算结果,两种方法相对误差不到0.5%。结果表明:在松弛过程中,Norton形式的蠕变速率比指数形式的蠕变速率小,且相比指数形式,Norton形式下的应力松弛计算公式精度更高,更适合于巴氏合金ZCh Sn Sb11-6.

基于APDL的大规模多物理场间接耦合批处理程序开发

在大规模多物理场间接耦合分析时,求解和后处理流程复杂,批处理命令流编写十分困难。针对这一情况,使用APDL和联合二次开发应用程序可以高效地扩充ANSYS批处理功能。文中提出一种APDL语言和联合开发方法,并设计开发一套大规模多物理场间接耦合批处理程序,用以提高ANSYS批量计算、结果提取和统计的效率,将APDL语言脚本"胶着"特性与强类型语言规范性融合,充分利用APDL二次开发工具和的MFC平台开发程序,更加灵活地控制ANSYS分析流程、数据提取和数据管理,从而提高大规模多物理场间接耦合分析效率。通过300t钢水罐罐壁热-应力间接耦合分析实例验证了所开发的批处理程序的可靠性和高效性。

反应谱理论及其在电阻架抗震分析中的应用

以高压绝缘电阻架为研究对象,基于振型分解反应谱理论,建立了三维梁壳单元有限元分析模型。结合电阻架的动力特性和地震响应谱,并计入结构阻尼对地震反应的影响,进行了电阻架的模态分析和反应谱分析,得到了电阻架在双向水平与扭转地震偶联作用下的位移、速度、加速度响应以及应力。分析结果表明,电阻架位移和速度的最大响应点在最顶层电阻器上,加速度最大的位置在铜管。地震响应的应力评定满足结构强度要求,该方法为电阻架的抗震设计提供了参考及依据。

基于Geostudio的某土石坝稳定性流固耦合分析

选用某土石坝坝体的某一典型剖面,采用GeoStudio软件中的渗流分析模块SEEP/W和应力应变分析模块SIGMA/W,基于比奥固结原理进行坝体稳定性的流固耦合即应力场与渗流场的耦合分析,以较真实地判定坝体在外力作用下的力学响应特性,为找出该土石坝时间-位移曲线异常波动的真正原因提供了依据。

大跨度连续梁桥的地震时程反应分析

运用有限元程序Midas对哈(尔滨)—大(连)铁路客运专线大连至沈阳段营海特大桥主桥大跨预应力混凝土连续梁进行了自振特性分析及地震荷载作用下的时程分析,通过计算得出了连续梁的前十阶的频率、振型,并进一步计算了在地震作用下结构的内力和位移,计算结果显示在罕遇地震作用下墩底可能会出现塑性铰导致桥墩产生塑性变形,为结构安全性的验证提供了可靠的参考数据。

横梁腹板切口形状对正交异性钢桥面板疲劳性能的影响研究

在正交异性钢桥面板中,横梁腹板与纵肋连接部位及横梁腹板切口边缘处较容易发生疲劳开裂,为了弄清横梁腹板切口形状对这两个构造细节疲劳性能的影响规律,采用有限单元法,通过在3种作用下采用不同切口形状的正交异性板各考察点主拉应力或面外应力比率的对比研究,得出以下结论:(1)在剪切作用下,切口形状对纵肋与横梁连接部位的应力影响不大,切口边缘半径对横梁切口边缘拉应力影响很大;(2)在支撑作用下,切口尺寸越大,纵肋与横梁连接部位的应力越大;(3)在面外作用下,切口尺寸越大,横梁对纵肋的面外转动变形约束越小,面外应力比率越小。

基于红外热像显微观测技术的304不锈钢疲劳性能研究

借助红外热像仪和远场视频显微镜研究了304奥氏体不锈钢应力疲劳的温度响应与微观形貌变化规律,运用扫描电镜对试件断口进行微观分析。研究结果表明:载荷幅值对试样表面最大温升有一定影响,试件表面温度变化与微观形貌的演化之间存在相关性。随着应力水平的增加,试样断口裂纹扩展区疲劳条带变窄,瞬断区韧窝增多。

轴间差速器十字轴的疲劳断裂分析与改进

轴间差速器十字轴在受到长期冲击载荷后十字轴的根部容易断裂。经有限元分析得出断裂原因主要是应力集中引起金属疲劳导致的,对轴间差速器十字轴做了相关的材料和设计改进,断裂现象明显减少,使产品使用效率和寿命有了明显提高。

矮塔斜拉桥塔墩梁固结实体分析

以黄龙带矮塔斜拉特大桥为工程背景,利用大型通用有限元软件MIDAS/FEA对塔梁墩固结部位进行详细应力分析。确立6种不利荷载工况后,计算了固结部位的纵向正应力、横向正应力、竖向正应力、主拉应力及主压应力,分析结果表明了该结构部位的应力分布情况,并提出相应的优化处理方案,为设计和施工提供了科学的理论依据。

Investigation on high temperature strengthening and toughening of iron-base superalloy

A new modified A-286 (15Cr-28Ni-1.5Mo-lW-2Ti-Nb-Al) (mass fraction) designated as GH871 is characterized by high strengths but low ductility at 650℃ stress rupture and also high crack propagation rates at 650℃ creep and creep/fatigue interaction conditions. For improvement of ductility and crack propagation behaviour, a primary vacuum induction melting and followed electro-slag refining process (VIM+ESR) has been adopted instead of air melting and electro-slag refining process (AIM+ESR). Vacuum melted GH871 (VIM+ESR) can keep the high strength level of this alloy and improve the ductility and also decrease crack propagation rates by this alloy purification. It is a good combination of strengthening and toughening for the alloy improvement and development.

Compression loading of osteoclasts attenuated micro RNA-146a-5p expression,which promotes angiogenesis by targeting adiponectin

Osteoclastogenesis in alveolar bone induced by compression stress triggers orthodontic tooth movement.Compression stress also stimulates angiogenesis,which is essential for osteoclastogenesis.However,the effects of osteoclastogenesis induced by compression on angiogenesis are poorly understood.In vivo,we found the markers of angiogenesis increased during orthodontic bone remodeling.In vitro,osteoclast-derived exosomes increased proliferation,migration,and tube formation of human umbilical vein endothelial cells(HUVECs),as well as expression of vascular endothelial growth factor and CD31.The promotive effects of exosomes derived from compressed osteoclasts were greater than those derived from osteoclasts without compression.Next,we analyzed changes in the micro RNA transcriptome after compression stress and focused on micro RNA146 a-5 p(mi R-146 a),which was significantly decreased by compression.Transfection of an inhibitor of mi R-146 a stimulated angiogenesis of HUVECs while mi R-146 a mimics repressed angiogenesis.Adiponectin(ADP)was confirmed to be a target of mi R-146 a by dual luciferase reporter assay.In HUVECs treated with exosomes,we detected increased ADP which promoted angiogenesis.Knockdown of ADP in HUVECs reduced the promotive effects of exosomes.Our results demonstrate that the decreased mi R-146 a observed in osteoclasts after compression promotes angiogenesis by targeting ADP,suggesting a novel method to interfere with bone remodeling induced by compression stress.

应力敏感性致密气藏压裂井动态反演新方法

针对致密砂岩气藏的储层特征及渗流机理,建立并求解了考虑储层应力敏感性和裂缝导流能力的致密砂岩气藏压裂井不稳定渗流数学模型,进一步开发出应力敏感性致密砂岩气藏压裂井产能递减典型曲线图版,利用图版拟合可以求取致密砂岩气藏应力敏感储层参数及压裂工艺参数,形成一套快速有效的致密砂岩气藏压裂井动态反演技术及动态产能确定方法。通过苏里格气藏压裂井实例分析,验证了该应力敏感性致密砂岩气藏压裂井动态反演技术方法的可靠性,有助于致密砂岩气藏的高效开发。