101 Q&A about America 是什么意思啊_百度作业帮
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101 Q&A about America 是什么意思啊
101 Q&A about America 是什么意思啊
101 questions and answers about America101 关于美国的问和答11G101-1图集中60页Δ/hb＞1/6是什么意思？_百度知道
11G101-1图集中60页Δ/hb＞1/6是什么意思？
HB是梁高，要收边的大小。还有那个六分之一，说的是柱子的六分之一吗
还是说的谁的六分之一
上面的三角形我知道是，梁高分之收边大小的意思难道说的就是△除HB的意思吗
我有更好的答案
按默认排序
柱截面要收的尺寸除梁的高度小于等于1/6的情况下，柱的钢筋可以打弯后上升，否则要断开重新插筋
你的意思是，假如梁高是6CM
要收边是1CM
就是1/6＞
梁高的6分之一吗
等于也可以的。是看你柱子要收多少而定的。例子：如果柱子要收50，那你梁高要在300或者300以上。如果柱子要收100，那你梁高要在600或者600以上。
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出门在外也不愁KeywordsEndothelial cells, Rapamycin, Proliferation, Migration, MicroRNAmiR-21, RhoB, Raptor, Rictor
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&&&&&&&&雷帕霉素是一种大环内酯类抗生素。由于雷帕霉素被发现能够抑制血管平滑肌细胞(VSMC)增殖和迁移,故被广泛用于药物涂层支架(DES),从而防止冠状动脉支架植入术后的血管腔再狭窄。然而一个不容忽视的问题是,近来一些临床研究结果显示,与裸金属支架相比,接受雷帕霉素涂层支架植入的患者具有更高的支架内晚期血栓(LST)发生率。产生这一现象的原因被认为是雷帕霉素除了能够抑制VSMC的增殖和迁移外,同样可以抑制血管内皮细胞(VEC)的增殖和迁移能力,从而导致支架丝内皮覆盖不全,进而引起LST。尽管一些方法如延长双联抗血小板治疗、他汀治疗等提示可以改善LST的发生,但其效果、费用及安全性仍不完善。已有一些研究就雷帕霉素抑制VEC的机制做了探讨。雷帕霉素靶点复合物1(mTORCl),是由哺乳动物雷帕霉素靶蛋白(mTOR), mTOR调控相关靶蛋白(Raptor), G蛋白β样蛋白(GβL)三者构成；而mTORC2则由雷帕霉素非敏感mTOR伴侣(Rictor)与mTOR、GβL构成。现有研究发现,一旦与FKBP12结合,雷帕霉素可以直接抑制mTORC1信号通路,进而导致细胞转录、核糖体合成和信号翻译进程的全面停滞,使得内皮细胞周期停止于G0/G1期。mTORC2控制细胞骨架运动,曾一度被认为是雷帕霉素非敏感的。然而近来研究表明,雷帕霉素同样可以抑制mTORC2信号通路,长时间雷帕霉素处理(&24h)可以通过mTORC2-p27kip信号通路抑制内皮细胞迁移。尽管这些研究似乎给出了雷帕霉素抑制内皮细胞增殖和迁移机制的答案,随着时间的推移,更新更深入的机制开始进入我们的视野。微小RNA (microRNA, miR)是一类内源性非编码小RNA,长度一般在19-22个碱基范围内。miR通过与靶基因3’端非编码区域(UTR)结合,降解或抑制靶基因mRNA翻译效率,从而在基因转录水平广泛发挥负性调控的作用。已有报道表明,miR在内皮细胞功能方面扮演着十分重要的角色,诸如增殖、迁移、成血管、凋亡等重要的内皮细胞功能方面,miR均广泛参与。除此以外,越来越多的证据表明,miR与mTORC各成员间也存在调控关系。Uesugi等报道,在口腔癌细胞中,miR-218可作用于Rictor蛋白；Chen等发现在血管内皮细胞中,miR-101介导了层流应切力导致的mTOR蛋白水平下调。这些miR与mTORC成分间的互动关系提示miR可能参与了雷帕霉素对内皮细胞功能的调节。因此,我们提出这一假设：雷帕霉素抑制血管内皮细胞增殖和迁移能力,部分可能通过miR途径实现。研究这一具体机制可进一步深入揭露雷帕霉素作用的机制,并为临床上解决LST这一难题提供新的解决思路。本研究中,我们首先观察了雷帕霉素对人脐静脉内皮细胞(HUVEC)增殖和迁移功能的影响,并筛选出雷帕霉素作用下表达水平显著变化的miR；其次我们研究了该筛选出来的miR在雷帕霉素诱导的HUVEC增殖和迁移抑制中的作用及其机制。以下分两部分对本研究的方法、结果及结论作一简述。1雷帕霉素对人脐静脉内皮细胞增殖、迁移功能的影响及其作用下人脐静脉内皮细胞microRNA的表达差异目的：观察雷帕霉素对人脐静脉内皮细胞增殖、迁移功能的影响,挑选出雷帕霉素抑制内皮细胞增殖、迁移的最佳作用浓度和时间,观察该作用浓度及时间下HUVEC microRNA表达差异并验证确认。方法：培养并扩增HUVEC细胞系,采用1-1000ng/ml雷帕霉素分别作用12-72h,分别用CCK-8试验、EDU吸收试验检测HUVEC增殖能力,划痕实验、改良的Boyden小室迁移试验检测HUVEC迁移能力。检索Pubmed,选择与内皮细胞(EC)增殖与迁移能力有关的miR, qRT-PCR array法筛选雷帕霉素作用下表达水平显著变化的miR,进一步qRT-PCR法验证。结果：CCK-8及EDU吸收实验证实雷帕霉素可剂量时间依赖性地抑制HUVEC增殖,以100ng/ml作用24小时最为显著。划痕实验、改良的Boyden小室迁移试验证实雷帕霉素处理24小时可剂量依赖性的抑制HUVEC迁移能力。qRT-PCR array检测显示100ng/ml雷帕霉素作用24小时可上调miR-21水平。进一步qRT-PCR验证显示miR-21上调与雷帕霉素呈时间剂量依赖性,并于100ng/ml和24h达到峰值。结论：雷帕霉素可抑制HUVEC增殖和迁移能力,并可时间和剂量依赖性地上调HUVEC miR-21水平。2miR-21在雷帕霉素诱导的人脐静脉内皮细胞增殖和迁移抑制中的作用及机制目的：观察miR-21在雷帕霉素诱导的HUVEC增殖和迁移抑制中的作用,并探讨其作用机制。方法：采用miR-21模拟物或抑制剂转染HUVEC从而上调或下调细胞内miR-21水平,分别采用CCK-8试验、EDU染料吸收试验检测HUVEC增殖能力,划痕实验、改良的Boyden小室迁移试验检测HUVEC迁移能力。采用生物信息学方法,检索miR-21作用的可能靶基因,并进一步使用qRT-PCR、western blot及构建包含特定靶基因3’-UTR序列及突变序列的双荧光素酶报告载体质粒与miR-21模拟物共转染293T细胞,验证该基因是否为miR-21靶基因。使用siRNA技术分别下调Raptor和Rictor蛋白,观察其下调是否影响miR-21的表达。结果：使用miR-21抑制剂下调其表达可恢复雷帕霉素抑制的HUVEC增殖和迁移能力,miR-21模拟物可进一步抑制HUVEC增殖和迁移能力,但与雷帕霉素单独处理组相比较无统计学差异。生物信息学检测提示RhoB是miR-21的靶基因。qRT-PCR、western blot检测及双荧光素酶报告载体实验证实RhoB是miR-21的靶基因。Raptor下调可促进miR-21表达,Rictor siRNA不改变miR-21水平。结论：miR-21下调可逆转雷帕霉素抑制HUVEC增殖和迁移的作用,RhoB是miR-21的靶基因,雷帕霉素上调miR-21可能是其抑制Raptor的结果。
&&&&Rapamycin (sirolimus) is a macrocyclic lactone antibiotic. Because it can suppress the proliferation and migration of vascular smooth muscle cells (VSMCs), rapamycin is widely used in drug eluting stents (DES) to prevent in-stent restenosis (ISR) after percutaneous coronary intervention. However, recent clinical trials revealed that patients who received rapamycin-eluting stents implantation presented with higher rates of late stent thrombosis (LST), compared to patients who received bare-metal stents. This is due to the ability of rapamycin to impair the proliferation and migration of vascular endothelial cells, which leads to a delayed re-endothelialization of stent struts. This disadvantage has limited the use of rapamycin in DES.The mechanism of the inhibitory effects of rapamycin on endothelial proliferation and migration has been previously discussed. The mammalian target of rapamycin complex1(mTORC1) is comprised of GβL, mammalian target of rapamycin (mTOR) and Raptor. mTORC2is comprised similarly of G β L and mTOR, though Rictor is substituted for Raptor. Once bound to FKBP12, rapamycin can directly inhibit mTORC1signalling, which leads to a total arrest of transcription, ribosome biogenesis, translation initiation, and stop cell cycle at the G0/G1phase in endothelial cells. mTORC2was once thought to be insensitive to rapamycin and to control th however, later studies revealed that rapamycin could also inhibit mTORC2signalling and that long-term rapamycin treatment (&24h) could impair the mobility of endothelial cells through the mTORC2-p27(kip) pathway. Although all these studies seemed to provide answers to the question of how rapamycin mediated the prevention of endothelial cell proliferation or migration, more recently, new and deeper insights into these mechanisms have been indicated.MicroRNAs (miRNAs, miRs) are a class of endogenous small non-coding RNAs that are approximately19-22bases in length. MiRs can regulate gene expression widely at the post-transcriptional level, mostly by targeting the3’-UTR of mRNAs. miRs have been reported to play large roles in several functions of endothelial cells, including proliferation, migration, angiogenesis, senescence and survival. Recent studies have revealed direct connections between miRs and mTORC. Uesugi et al. reported that miR-218targets the mTORC component Rictor in oral cancer cells. Chen et al. found that miR-101mediates the suppressive effects of laminar shear stress on mTOR expression in vascular endothelial cells. These reports of feedback between miRs and the mTOR complex indicate that miRs may be involved in rapamycin-induced regulation in endothelial cells.Based on these considerations, we hypothesized that miRs may mediate the suppression effect of rapamycin on endothelial proliferation and migration. The research on this topic will not only give new explanations of rapamycin-induced inhibitory effect on angiogenesis, but also provide new insight of methods to solve LST problem. In the present study, we first observed the effect of rapamycin on endothelial proliferation and migration, found out the miR whose expression was deeply affected by rapamycin treatment. Then, we tested the effect of this miR on rapamycin induced suppression of endothelial proliferation and migration, and investigated the mechanism as well. Now we will explain our study by two parts.Part1:Effects of rapamycin on human umbilical vein endothelial proliferation and migration, and the expressive difference of microRNAs under rapamycin treatmentObjective:To investigate the effect of rapamycin on human umbilical vein endothelial proliferation and migration, find out the most effective concentration and treated time of rapamycin on endothelial growth and mobility, and investigate the expressive difference of microRNA under this rapamycin treatment.Methods:HUVEC cell line was purchased and cultured. Various concentration (1-1000ng/ml) of rapamycin were added and treated for different durations (12-72h). The proliferation ability of HUVECs was then detected by using CCK-8test and EDU proliferation assay. Wound healing test as well as Boyden chamber assay were used for detecting the mobility of HUVECs. By searching Pubmed with Mesh words "microRNA" and "endothelial cells", we chose several miRs, evaluating the expression levels of these miRs by qRT-PCR array. miR whose level was changed greatestly was further analyzed and checked by qRT-PCR.Result:Rapamycin treatment could significantly inhibit the proliferation of HUVECs in a time-dose dependent manner, and had a peak at100ng/ml and24h, as revealed by CCK-8test and EDU proliferation assay. Wound healing test as well as Boyden chamber assay revealed that24h rapamycin treatment could suppress the migration of HUVECs in a dose dependent manner. qRT-PCR array showed that among all the tested miRs, only the level of miR-21was significantly upregulated by rapamycin treatment (100ng/ml,24h). Further test confirmed that the expression of miR-21was augmentated by rapamycin treatment in a time-dose depedent manner with a peak at100ng/ml and24h.Conclusion:Rapamycin treatment can inhibit the proliferation and migration of HUVEC, and can upregulate the level of miR-21in a time-dose dependent manner. Part2:Effects and mechanisms of miR-21on rapamycin-induced suppression of endothelial proliferation and migrationObjective:To investigate the Effects and mechanisms of miR-21on rapamycin-induced suppression of endothelial proliferation and migration.Methods:By using miR-21mimic and inhibitor, we upregulation/downregulation the level of miR-21in HUVECs. CCK-8test, EDU proliferation assay, wound healing test and Boyden chamber assay were used for detecting the proliferation and migration of HUVECs respectively. Using bioinformatic method, we found out the putative target gene of miR-21, and confirm this target gene by using qRT-PCR, western blot and luciferase reporter assay. Finally, we knock-down the expression of Raptor or Rictor with siRNA technology, and investigated the level of miR-21after that.Result:Downregulation of miR-21by its inhibitor totally abolished the negative effects of rapamycin on HUVEC proliferation and migration. RhoB was confirmed as a direct target gene of miR-21. Knockdown of Raptor by siRNA mimicked the effects of rapamycin on miR-21expression.Conclusion:Downregulation of miR-21can abolished the negative effects of rapamycin on HUVEC proliferation and migration. RhoB is a direct target gene of miR-21. The upregulation of miR-21induced by rapamycin may be a result of Raptor inhibition.
&&&&&&&&MicroRNA在雷帕霉素诱导的内皮细胞增殖和迁移抑制中的作用及机制致谢5-6中文摘要6-10Abstract10-13主要缩略词表14-16目次16-17前言17-19第一部分 雷帕霉素对人脐静脉内皮细胞增殖、迁移功能的影响及其作用下人脐静脉内皮细胞microRNA的表达差异19-48&&&&引言19-21&&&&1.1 材料与方法21-31&&&&1.2 结果31-41&&&&1.3 讨论41-43&&&&参考文献43-48第二部分 MiR-21在雷帕霉素诱导的人脐静脉内皮细胞增殖和迁移抑制中的作用及机制48-80&&&&引言48-49&&&&2.1 材料与方法49-64&&&&2.2 结果64-75&&&&2.3 讨论75-77&&&&参考文献77-80全文结论80-81综述81-98&&&&参考文献91-98作者简历及在学期间所取得的科研成果98
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