L形冷弯薄壁型钢组合钢管混凝土柱轴压性能

为解决异形钢管混凝土柱阴角对其承载力的影响,提出了用1个冷弯薄壁方钢管和2个U形钢管焊接成L形钢管,内填充混凝土形成L形冷弯薄壁型钢组合钢管混凝土柱形式。设计了5组共10根试件的轴压试验,并开展了有限元参数分析,研究了钢管厚度、U形管外伸长度和钢材强度等参数对构件承载力和延性等力学性能的影响。结果表明:该类试件的主要破坏形态为中上部局部鼓曲破坏,适量增大U形管外伸长度可以提高承载力,但增大到一定程度之后易发生弯扭破坏;承载力和延性随着钢管厚度和钢材强度增大而增加;混凝土强度对构件的初始刚度和峰值荷载的影响都很小,但对曲线下降段的影响较大;试件端部和中部截面阴角处的混凝土应力值比各边中部更大,说明采用U形钢管与方钢管组合的方式改善了阴角处钢管对混凝土约束普遍较弱的问题。基于“统一理论”,给出了两种承载力建议计算公式,与试验结果吻合较好,两种计算方法在0.44~1.94的约束效应系数范围内具有良好的适用性。

甘蓝型油菜BnaSLY1基因进化分析及功能研究

赤霉素调控植物表皮细胞增长、茎叶伸长以及株型建成。拟南芥SLY1属于F-box蛋白,它通过靶向泛素化赤霉素信号转导路径的负向调控因子——DELLA蛋白来影响植物生长发育,然而油菜中BnaSLY1的基因功能尚未揭示。本研究对BnaSLY1进行了表达特征和进化树分析,利用CRISPR/Cas9技术创制了BnaSLY1不同拷贝数的突变体,结合RNA-Seq技术对BnaSLY1的生物学功能及其对油菜生长发育的影响进行了研究。结果表明,甘蓝型油菜Westar中有2个SLY1同源拷贝BnaA01.SLY1和BnaA06.SLY1,它们表达模式基本相同,为组成型表达基因,其蛋白定位在细胞核,且在不同的油菜品种及十字花科植物间序列保守。与对照相比,单突bnaa01sly1和bnaa06sly1开花时间推迟,株高显著降低,而双突bnasly1还表现出深绿色光叶表型,叶片厚度增加,开花期比单突进一步推迟,株高也进一步降低。RNA-Seq结果显示,双突与Westar之间的差异表达基因显著富集在生长素信号转导路径以及蜡质合成通路,多个开花时间相关基因表达也发生显著变化。本研究表明, BnaSLY1除影响植物株高和开花时间等生长发育进程,还影响表皮蜡质合成,为探索赤霉素信号转导路径在甘蓝型油菜生长发育中的重要作用奠定了理论基础。

缺血性脑卒中铁死亡特征基因NFE2L2的鉴定与验证

背景:铁死亡与缺血性脑卒中的发病密切相关,靶向铁死亡是一种治疗缺血性脑卒中有前景的方案,但具体调控靶点尚不明确。目的:通过生物信息学和机器学习方法筛选缺血性脑卒中铁死亡相关特征基因,并通过细胞实验进行验证,探讨铁死亡在缺血性脑卒中的作用。方法:基于GEO数据库和FerrDb数据库选取符合条件的缺血性脑卒中相关数据集和铁死亡表达数据集,通过t检验筛选铁死亡相关差异基因。对铁死亡相关差异基因进行GO功能富集分析与KEGG信号通路富集分析。通过PPI网络分析和机器学习筛选缺血性脑卒中铁死亡的特征基因,利用ROC分析和GSEA分析探究特征基因的准确性和生物功能。然后进行细胞实验,将HT22细胞分为对照组与缺血性脑卒中组,对照组不作任何干预,缺血性脑卒中组加入0.1 mol/L的H_(2)O_(2)干预24 h诱导细胞氧化应激和铁死亡,通过实时荧光定量RT-PCR和Western Blot验证铁死亡的发生和特征基因表达。结果与结论:(1)共获取45个铁死亡相关差异基因,GO和KEGG富集分析发现差异基因与氧化应激、自噬、铁死亡、脂肪细胞因子信号通路和线粒体代谢密切相关。(2)通过PPI网络中的MCODE插件和cytoHubba插件与机器学习中的LASSO算法和SVM-RFE算法共鉴定出1个铁死亡特征基因核因子E2相关因子2(nuclear factor erythroid 2-related factor 2,NFE2L2)。(3)对NFE2L2进行ROC曲线分析,发现在训练集和验证集中构建的诊断预测模型具有良好的准确性与特异性;对NFE2L2进行GSEA分析,发现特征基因通过免疫、炎症反应、氨基酸代谢及神经因子调控等方面参与缺血性脑卒中发病机制的调控。(4)细胞实验的RT-PCR和Western Blot分析表明,与对照组对比,缺血性脑卒中组中的酰基辅酶A合成酶长链家族成员4 mRNA和蛋白表达水平显著增高(P<0.05),谷胱甘肽过氧化物酶4 mRNA和蛋白表达水平显著降低(P<0.05);与对照组对比,缺血性脑卒中组中特征基因NFE2L2 mRNA和蛋白表达水平显著增高(P<0.05)。(5)上述结果证实,缺血性脑卒中与铁死亡密切相关,靶向特征基因NFE2L2可以为研究和治疗缺血性脑卒中提供一定的思路与方向。

基于整车关键尺寸L114的平台架构研究

为了研究最优的整车平台架构策略,本文详细阐述平台架构的概念,定义了架构关键尺寸L114,列举国内某车企基于关键尺寸L114一致的平台拓展尺寸链,并梳理该平台架构乘员舱架构件具体的策略,通过对比分别采取平台车型关键尺寸L113一致与平台车型关键尺寸L114一致时的平台通用化率,发现2种策略的平台通用化率基本一致。同时结合整车安全碰撞策略进行分析,结果表明,若采用关键尺寸L114更具优势,该策略下同平台车型仅需满足高车型的碰撞策略,即可同步满足其他车型的侧碰要求,有效降低平台开发成本。

Effects of P301L-TAU on post-translational modifications of microtubules in human iPSC-derived cortical neurons and TAU transgenic mice

TAU is a microtubule-associated protein that promotes microtubule assembly and stability in the axon.TAU is missorted and aggregated in an array of diseases known as tauopathies.Microtubules are essential for neuronal function and regulated via a complex set of post-translational modifications,changes of which affect microtubule stability and dynamics,microtubule interaction with other proteins and cellular structures,and mediate recruitment of microtubule-severing enzymes.As impairment of microtubule dynamics causes neuronal dysfunction,we hypothesize cognitive impairment in human disease to be impacted by impairment of microtubule dynamics.We therefore aimed to study the effects of a disease-causing mutation of TAU(P301L)on the levels and localization of microtubule post-translational modifications indicative of microtubule stability and dynamics,to assess whether P301L-TAU causes stability-changing modifications to microtubules.To investigate TAU localization,phosphorylation,and effects on tubulin post-translational modifications,we expressed wild-type or P301L-TAU in human MAPT-KO induced pluripotent stem cell-derived neurons(i Neurons)and studied TAU in neurons in the hippocampus of mice transgenic for human P301L-TAU(p R5 mice).Human neurons expressing the longest TAU isoform(2N4R)with the P301L mutation showed increased TAU phosphorylation at the AT8,but not the p-Ser-262 epitope,and increased polyglutamylation and acetylation of microtubules compared with endogenous TAU-expressing neurons.P301L-TAU showed pronounced somatodendritic presence,but also successful axonal enrichment and a similar axodendritic distribution comparable to exogenously expressed 2N4R-wildtype-TAU.P301L-TAU-expressing hippocampal neurons in transgenic mice showed prominent missorting and tauopathy-typical AT8-phosphorylation of TAU and increased polyglutamylation,but reduced acetylation,of microtubules compared with non-transgenic littermates.In sum,P301L-TAU results in changes in microtubule PTMs,suggestive of impairment of microtubule stability.This is accompanied by missorting and aggregation of TAU in mice but not in i Neurons.Microtubule PTMs/impairment may be of key importance in tauopathies.

Loss-of-function mutations of microRNA-142-3p promote ASH1L expression to induce immune evasion and hepatocellular carcinoma progression

BACKGROUND Hepatocellular carcinoma(HCC)has been a pervasive malignancy throughout the world with elevated mortality.Efficient therapeutic targets are beneficial to treat and predict the disease.Currently,the exact molecular mechanisms leading to the progression of HCC are still unclear.Research has shown that the microRNA-142-3p level decreases in HCC,whereas bioinformatics analysis of the cancer genome atlas database shows the ASH1L expression increased among liver tumor tissues.In this paper,we will explore the effects and mechanisms of microRNA-142-3p and ASH1L affect the prognosis of HCC patients and HCC cell bioactivity,and the association between them.AIM To investigate the effects and mechanisms of microRNA-142-3p and ASH1L on the HCC cell bioactivity and prognosis of HCC patients.METHODS In this study,we grouped HCC patients according to their immunohistochemistry results of ASH1L with pathological tissues,and retrospectively analyzed the prognosis of HCC patients.Furthermore,explored the roles and mechanisms of microRNA-142-3p and ASH1L by cellular and animal experiments,which involved the following experimental methods:Immunohistochemical staining,western blot,quantitative real-time-polymerase chain reaction,flow cytometric analysis,tumor xenografts in nude mice,etc.The statistical methods involved in this study contained t-test,one-way analysis of variance,theχ^(2)test,the Kaplan-Meier approach and the log-rank test.RESULTS In this study,we found that HCC patients with high expression of ASH1L possess a more recurrence rate as well as a decreased overall survival rate.ASH1L promotes the tumorigenicity of HCC and microRNA-142-3p exhibits reduced expression in HCC tissues and interacts with ASH1L through targeting the ASH1L 3′untranslated region.Furthermore,microRNA-142-3p promotes apoptosis and inhibits proliferation,invasion,and migration of HCC cell lines in vitro via ASH1L.For the exploration mechanism,we found ASH1L may promote an immunosuppressive microenvironment in HCC and ASH1L affects the expression of the cell junction protein zonula occludens-1,which is potentially relevant to the immune system.CONCLUSION Loss function of microRNA-142-3p induces cancer progression and immune evasion through upregulation of ASH1L in HCC.Both microRNA-142-3p and ASH1L can feature as new biomarker for HCC in the future.

载富血小板血浆水凝胶对L929细胞氧化损伤的保护作用

背景:在慢性创面愈合过程中,活性氧的过量生成可能会损害L929成纤维细胞的功能,从而延缓创面修复,因此保护成纤维细胞免受氧化应激的影响对于促进创面愈合非常重要。目的:评估羧甲基壳聚糖-氧化硫酸软骨素/富血小板血浆(CMC-OCS/PRP)水凝胶对H2O2刺激下L929细胞的保护作用。方法:制备CMC-OCS/PRP水凝胶,表征水凝胶的微观形貌、降解性能、清除H2O2与羟基自由基的能力及生物相容性。取生长状态良好的L929细胞,分5组培养:对照组常规培养,H2O2组加入H2O2,CMC-OCS组加入羧甲基壳聚糖-氧化硫酸软骨素水凝胶浸提液+H2O2,PRP组加入富血小板血浆凝胶浸提液+H2O2,CMC-OCS/PRP组加入羧甲基壳聚糖-氧化硫酸软骨素/富血小板血浆水凝胶浸提液处理+H2O2,每组先加入水凝胶浸提液处理6 h,然后再加入H2O2处理24 h。培养结束后,检测细胞活性氧及丙二醛水平,细胞凋亡、胶原纤维Ⅰ蛋白表达。在加入H2O2的情况下,将上述水凝胶浸提液分别与L929成纤维细胞直接或间接共培养36 h,通过划痕实验、Transwell小室实验检测细胞的迁移能力。结果与结论:①CMC-OCS/PRP水凝胶具有均匀相互关联的多孔结构及良好的降解能力,体外可有效清除H2O2与羟基自由基,并且具有良好的生物相容性;②与对照组比较,H2O2组细胞凋亡率、细胞活性氧与丙二醛水平升高(P<0.05),细胞铺展面积减少(P<0.05),胶原纤维Ⅰ蛋白表达无明显变化(P>0.05);与H2O2组比较,CMC-OCS组、CMC-OCS/PRP组细胞活性氧水平降低(P<0.05),PRP组、CMC-OCS组、CMCOCS/PRP组丙二醛水平降低(P<0.05)、细胞铺展面积增加(P<0.05),CMC-OCS/PRP组细胞凋亡率降低(P<0.05),PRP组、CMC-OCS组、CMCOCS/PRP组胶原纤维Ⅰ蛋白表达增加(P<0.05);③与对照组比较,H2O2组细胞迁移数量减少(P<0.05),迁移面积无明显变化(P>0.05);与H2O2组比较,PRP组、CMC-OCS组、CMC-OCS/PRP组细胞迁移数量、迁移面积均增加(P<0.05),并且以CMC-OCS/PRP组增加最显著;④在氧化应激条件下,CMC-OCS/PRP水凝胶可改善成纤维细胞的迁移能力,抗细胞凋亡并保护细胞伸展功能。

Recombinant chitinase-3-like protein 1 alleviates learning and memory impairments via M2 microglia polarization in postoperative cognitive dysfunction mice

Postoperative cognitive dysfunction is a seve re complication of the central nervous system that occurs after anesthesia and surgery,and has received attention for its high incidence and effect on the quality of life of patients.To date,there are no viable treatment options for postoperative cognitive dysfunction.The identification of postoperative cognitive dysfunction hub genes could provide new research directions and therapeutic targets for future research.To identify the signaling mechanisms contributing to postoperative cognitive dysfunction,we first conducted Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses of the Gene Expression Omnibus GSE95426 dataset,which consists of mRNAs and long non-coding RNAs differentially expressed in mouse hippocampus3 days after tibial fracture.The dataset was enriched in genes associated with the biological process"regulation of immune cells,"of which Chill was identified as a hub gene.Therefore,we investigated the contribution of chitinase-3-like protein 1 protein expression changes to postoperative cognitive dysfunction in the mouse model of tibial fractu re surgery.Mice were intraperitoneally injected with vehicle or recombinant chitinase-3-like protein 124 hours post-surgery,and the injection groups were compared with untreated control mice for learning and memory capacities using the Y-maze and fear conditioning tests.In addition,protein expression levels of proinflammatory factors(interleukin-1βand inducible nitric oxide synthase),M2-type macrophage markers(CD206 and arginase-1),and cognition-related proteins(brain-derived neurotropic factor and phosphorylated NMDA receptor subunit NR2B)were measured in hippocampus by western blotting.Treatment with recombinant chitinase-3-like protein 1 prevented surgery-induced cognitive impairment,downregulated interleukin-1βand nducible nitric oxide synthase expression,and upregulated CD206,arginase-1,pNR2B,and brain-derived neurotropic factor expression compared with vehicle treatment.Intraperitoneal administration of the specific ERK inhibitor PD98059 diminished the effects of recombinant chitinase-3-like protein 1.Collectively,our findings suggest that recombinant chitinase-3-like protein 1 ameliorates surgery-induced cognitive decline by attenuating neuroinflammation via M2 microglial polarization in the hippocampus.Therefore,recombinant chitinase-3-like protein1 may have therapeutic potential fo r postoperative cognitive dysfunction.

Autism spectrum disorder:difficulties in diagnosis and microRNA biomarkers

We performed a PubMed search for microRNAs in autism spectrum disorder that could serve as diagnostic biomarkers in patients and selected 17 articles published from January 2008 to December 2023,of which 4 studies were performed with whole blood,4 with blood plasma,5 with blood serum,1 with serum neural cell adhesion molecule L1-captured extracellular vesicles,1 with blood cells,and 2 with peripheral blood mononuclear cells.Most of the studies involved children and the study cohorts were largely males.Many of the studies had performed microRNA sequencing or quantitative polymerase chain reaction assays to measure microRNA expression.Only five studies had used real-time polymerase chain reaction assay to validate microRNA expression in autism spectrum disorder subjects compared to controls.The microRNAs that were validated in these studies may be considered as potential candidate biomarkers for autism spectrum disorder and include miR-500a-5p,-197-5p,-424-5p,-664a-3p,-365a-3p,-619-5p,-664a-3p,-3135a,-328-3p,and-500a-5p in blood plasma and miR-151a-3p,-181b-5p,-320a,-328,-433,-489,-572,-663a,-101-3p,-106b-5p,-19b-3p,-195-5p,and-130a-3p in blood serum of children,and miR-15b-5p and-6126 in whole blood of adults.Several important limitations were identified in the studies reviewed,and need to be taken into account in future studies.Further studies are warranted with children and adults having different levels of autism spectrum disorder severity and consideration should be given to using animal models of autism spectrum disorder to investigate the effects of suppressing or overexpressing specific microRNAs as a novel therapy.

新疆胡颓子属植物(Elaeagnus)分类探讨

在花果标本定株采集的基础上,对新疆地区胡颓子属植物种类的形态学分类依据进行了探讨,对目前记载的新疆胡颓子属种类进行了整理,共确定新疆地区分布有胡颓子属3种1变种:尖果沙枣(E.oxycarpaSchlecht.)、沙枣(E.angustifoliaL.)、东方沙枣(E.angustifoliavar.orientalis(L.)Kuntze)、大果沙枣(E.moorcroftiiWall.exSchlecht.),并对其中部分种类的特征描述进行了补充。

沙枣(Elaeagnus angustifolia L.)研究现状与展望

沙枣(Elaeagnus angustifolia L.)是胡颓子科胡颓子属的一种小乔木,是一种集生态效益与经济效益于一体的资源植物,是西北地区具有开发利用前景的重要资源。对我国上世纪60年代至今对沙枣的研究文献作一综述,包括沙枣果实、花、叶、果核及树液的成分、木材的理化性质、沙枣的生理生态学特性、引种实验、繁殖方法、品种划分等方面的工作。最后提出了沙枣利用中存在的问题及建议。

沙枣(Elaeagnus angustifolia L.)的胚和胚乳发育

本文报道了沙枣受精前后,胚囊的结构和胚珠、胚囊中组织化学变化,以及胚和胚乳的发育,胚乳母细胞早于受精卵发育。为核型胚乳,胚乳发育早期,胚囊中富含蛋白质,胚胎发育为紫苑型,当多细胞原胚吋,胚乳开始形成细胞壁,胚细胞中含少量淀粉粒和可溶性蛋白质,这时候,胚柄极为发达,心形胚时,胚乳巳全部形成细胞壁,但局限于胚囊边缘,鱼雷形胚时,胚柄开始退化。以后,随着子叶的发育和生长,胚乳渐被吸入,接近成胚期,胚已为发达的子叶所取代,沙枣为无胚乳种子,成胚的子叶发达,于基部外方具一舌状物。

Study on Introduction and Plantation of Elaeagnus angustifolia L.

[Objective] The experiment aimed to explore the possibility of introducing Elaeagnus angustifolia L. in saline land of West Jilin Province for improving local ecological environment. [Method] The Elaeagnus angustifolia L. from Ningxia Province were sown in nursery and practice base of Forestry College in Beihua University to observe their phenophase, growth state, stress resistance and study the relations between survival rate and different cutting medium, grafting methods. [Result] Elaeagnus angustifolia L. could adapt to climate condition in Jilin area and grow well . Among 3 cold-proof measures, there was no freezing injury by soil burial method, although there was 2.8% and 3.9% mortality by covering grassy marshland and winding straw, the cold injury degree was light, so they could go through winter normally. Meanwhile, Elaeagnus angustifolia L. had good saline-alkali tolerance, drought resistance and flood resistance. The successful cutting and graft of Elaeagnus angustifolia L. provided a condition for planting in large-scale and knew the rooting rate of different cutting medium. [Conclusion] Elaeagnus angustifolia L. could be introduced to plant in West Jilin Province.

沙枣（Elaeagnus angustifolia L．）在黄河三角洲盐碱地的应用前景

黄河三角洲是我国三大三角洲之一，总面积达5．4×105 hm2，其中盐碱地面积达70％以上，并且仍在以每年1．3×105 hm2的速度增加．黄河三角洲地区土地盐碱化程度高，夏季降雨集中，春秋季较干旱，这些不利的环境因素导致该地区生态环境比较脆弱，绿化造林难度大，植被覆盖面积小，当地的景观生态系统比较单一．因此，筛选优质抗盐碱树种并建立一套完整的绿化栽培体系，以提高黄河三角洲地区的绿化面积是现在所面临的严峻问题．沙枣由于抗旱耐盐碱成为改良黄河三角洲地区的绿化树种，本文综述了沙枣作为黄河三角洲地区盐碱地绿化树种的应用前景．

沙枣(Elaeagnus angustifolia L.)的大、小孢子发生和雌雄配子发生

小孢子形成为同时型,小孢子在一个四分体中的排列为辐射(两侧)对称。药壁由表皮、药室内壁、中层和绒毡层所组成;成熟时仅由表皮和纤维层所组成;药壁的特点为中层一层和腺质(分泌)绒毡层。花粉粒为三角形和具三孔沟的,释放时为2细胞。大孢子的孢原为1—2个细胞,直接起大孢子母细胞功能。胞质分裂横向,大胞子排列是“直线型”,四分体中合点端大孢子为功能大孢子单核胚囊经过三次有丝分裂形成成熟胚囊(雌配子体)。沙枣的胚囊为蓼型(1卵器,3反足细胞和一个2核的中央细胞)。

沙枣(Elaeagnus angustifolia L.)体内、外胚胎发育的比较研究

本文应用经典制片法和离体培养法。对沙枣体内、外胚胎发育的各阶段做比较研究。主要区别于原胚期:1)、形态发生:体内只有一种方式,即两极分化方式。而离体的有二种方式,即器官发生和胚状体发生途径。2)、胚性细胞起源:体内只一种起源(即起源于受精卵),离体的胚性细胞的起源有三种方式:a由紧邻表皮细胞的单个薄壁细胞产生;b由表皮细胞横分裂产生和c由表皮及其下的薄璧细胞共同参与产生。3)胚性细胞的细胞学特征:体内发生的合子具明显的极性分化,细胞质、淀粉粒和细胞核集中在合点端。它第一次分裂后,顶、基细胞在细胞学特征上具明显区别。而离体条件下的胚性细胞第一次分裂后无典型的顶、基细胞之分。故也缺乏典型的胚柄细胞。胚分化和成熟期。

L型阵水下目标方位和距离联合最大似然估计

空间目标定位是阵列信号处理领域中的研究热点,广泛应用于雷达、声纳、通信、射电天文、医学诊断、地震遥感等众多领域。传统的水下声源定位仅获取目标声源的深度和距离信息,却无法估计目标的方位信息。针对这一问题,在充分考虑水下声传播模型的基础上,利用L型阵列固有的结构特征,将最大似然估计技术应用到水下目标定位,提出一种基于L型水听器阵列的水下目标方位与距离联合最大似然估计算法。研究表明:最大似然估计法可有效突破传统波束形成分辨力“瑞利限”的限制,提高水下目标定位的分辨能力和精度。计算机仿真分析显示,在单目标和相干双目标的场景中,文中所提出的方法均具有更为尖锐的谱峰及更低的旁瓣水平,可对水下目标进行有效的方位角和距离联合估计。

L波段差分干涉SAR卫星严格回归轨道优化设计方法

相比于传统SAR卫星应用方向,我国第一代L波段差分干涉SAR卫星主要用于实现全球精准地表形变测量。为了达到重轨差分干涉优于5 cm的形变测量指标,首先需要解决卫星空间基准轨道高精度回归的工程难题。对此,本文提出一种严格回归轨道优化设计方法,通过地球重力场阶数需求分析建立卫星高阶动力学模型,将J4摄动下修正的太阳同步回归轨道参数作为优化算法初值,以卫星WGS-84坐标系位置、速度回归精度满足收敛阈值为目标,利用启发式多目标进化算法开展轨道参数寻优。仿真试验表明,寻优结果回归精度可达厘米级,优于既定工程指标,并且本文方法有效性和正确性已经过L波段差分干涉SAR卫星在轨验证。

316L不锈钢掺杂SiC环状同轴送粉TIG熔覆层组织结构与性能

TIG熔覆是经济高效的表面修复方法,与传统的预置粉末法相比,同轴送粉法具有优良的适应性,但是试验研究相对较少.自主设计制造了环状同轴送粉TIG熔覆焊枪,与管状同轴送粉TIG熔覆焊枪相比,制造的熔覆层不存在熄弧位置凹坑、焊缝不够平直以及焊缝熔宽不一致等问题,而且具有更高的熔覆效率.结果表明,采用优化的焊接热输入、送粉量和SiC含量参数匹配,在316L不锈钢表面进行环状同轴送粉TIG熔覆,获得了外观优良的单层单道熔覆层、单层多道熔覆层.对熔覆层进行显微硬度测量、微观组织及元素成分分析、宏观电化学腐蚀试验、微区电化学腐蚀试验以及耐磨性能测试,并与母材进行了比对,环状同轴送粉TIG熔覆导入的SiC粉末有效地提升了熔覆层的耐蚀性与耐磨性.

苦瓜皂苷L调控PI3K/AKT通路促进内皮祖细胞增殖能力和内皮功能的实验研究

目的:探讨苦瓜皂苷L对内皮祖细胞(EPC)增殖能力和内皮功能的作用及机制。方法:体外分离、培养、鉴定外周血EPC。使用不同浓度苦瓜皂苷L处理EPC 24 h后,应用细胞计数试剂盒(CCK-8)法检测各组细胞活力。使用AutoDock Tools 5.6软件,分别以磷脂酰肌醇3-激酶(PI3K)和蛋白激酶B(AKT)为受体,以药物分子苦瓜皂苷L为配体采用盲对接法进行分子对接。使用PI3K/AKT抑制剂LY294002和最佳使用浓度的苦瓜皂苷L单独或同时处理EPC 24 h后检测各组细胞活力和磷酸化PI3K(p-PI3K)、磷酸化AKT(p-AKT)及磷酸化内皮型一氧化氮合酶(p-eNOS)表达水平。结果:与对照组比较,苦瓜皂苷L呈剂量依赖性地促进EPC增殖,且40μmol/L的苦瓜皂苷L是最佳药物浓度。与对照组比较,LY294002可下调EPC细胞活力,苦瓜皂苷L可上调细胞活力。与苦瓜皂苷L组比较,共同使用苦瓜皂苷L和LY294002可降低细胞活力。分子对接结果显示,苦瓜皂苷L与PI3K和AKT均存在直接作用,形成稳定的锁钥结构。与对照组比较,LY294002可显著下调p-PI3K、p-AKT和p-eNOS蛋白水平;苦瓜皂苷L可上调p-PI3K、p-AKT和p-eNOS蛋白水平。与苦瓜皂苷L组比较,使用苦瓜皂苷L和LY294002可降低p-PI3K、p-AKT和p-eNOS蛋白水平。结论:苦瓜皂苷L通过PI3K/AKT信号通路靶向调节EPC的增殖能力,进而上调内皮型一氧化氮合酶(eNOS)活化水平以促进EPC内皮功能。