简介:【摘要】C5/C9共聚石油树脂是以石油裂解后的C5、C9为主要原料通过聚合反应得到的,在热熔胶、黏合剂、胶粘剂以及橡胶和轮胎领域有着广阔的应用前景。本文主要通过对在固定床反应装置条件下C5/C9共聚石油树脂的合成方法和技术难点等方面,对整个加氢工艺进行分析。
简介:[摘要] 目的:探究高血压脑出血患者血清免疫球蛋白和补体C3、C4变化价值。方法:纳入40例高血压脑出血患者、40例原发性高血压患者进行探究分析,(时间:2019年01月~2020年01月),对比性探究分析,电脑数组排列分组,对照组(原发性高血压患者,n=40),实验组(高血压脑出血患者,n=40)。分析两组患者免疫球蛋白水平对比(IgG、IgA、IgM)、补体C3、C4水平对比。结果:(1)免疫球蛋白水平对比:组间相较,实验组IgG、IgM,差异明显,(P<0.05);(2)补体C3、C4水平对比:组间对比,实验组1d、7d、14dC3、C4水平,差异明显,(P<0.05)。结论:高血压脑出血患者血清免疫球蛋白和补体C3、C4水平,可直接对患者免疫功能进行反应,为患者后续治疗提供理论依据。
简介:摘 要:SRIO是面向嵌入式系统开发提出的高可靠、高性能、基于包交换的新一代高速互联技术,主要作用以每秒千兆字节性能级别进行芯片到芯片和板对板通信的系统内接口。它作为一种高速数据接口,广泛应用在TI公司C66X系列DSP上,用于DSP与FPGA之间的大块数据传输。本文主要介绍xilinx公司FPGA与TI公司C66X之间SRIO接口开发方法。
简介:AbstractBackground:Macrophages play an important role in renal ischemia reperfusion injury, but the functional changes of macrophages under hypoxia/reoxygenation and the related mechanism are unclear and need to be further clarified.Methods:The effects of hypoxia/reoxygenation on functional characteristics of RAW264.7 macrophages were analyzed through the protein expression detection of pro-inflammatory factors TNF-α and CD80, anti-inflammatory factors ARG-1 and CD206. The functional implications of C-X3-C motif chemokine receptor 1(CX3CR1) down-regulation in hypoxic macrophages were explored using small interfering RNA technology. Significance was assessed by the parametric t-test or nonparametric Mann-Whitney test for two group comparisons, and a one-way ANOVA or the Kruskal-Wallis test for multiple group comparisons.Results:Hypoxia/reoxygenation significantly increased the protein expression of M1-related pro-inflammatory factors TNF-α, CD80 and chemokine C-X3-C motif chemokine ligand 1 (CX3CL1)/CX3CR1 and inhibited the protein expression of M2-related anti-inflammatory factors ARG-1 and CD206 in a time-dependent manner in RAW264.7 cells. However, the silencing of CX3CR1 in RAW264.7 cells using specific CX3CR1-siRNA, significantly attenuated the increase in protein expression of TNF-α (P < 0.05) and CD80 (P < 0.01) and the inhibition of ARG-1 (P < 0.01) and CD206 (P < 0.01) induced by hypoxia/reoxygenation. In addition, we also found that hypoxia/reoxygenation could significantly enhance the migration (2.2-fold, P < 0.01) and adhesion capacity (1.5-fold, P < 0.01) of RAW264.7 macrophages compared with the control group, and CX3CR1-siRNA had an inhibitory role (40% and 20% reduction, respectively). For elucidating the mechanism, we showed that the phosphorylation levels of ERK (P < 0.01) and the p65 subunit of NF-κB (P < 0.01) of the RAW264.7 cells in the hypoxic/reoxygenation group were significantly increased, which could be attenuated by down-regulation of CX3CR1 expression (P < 0.01, both). ERK inhibitors also significantly blocked the effects of hypoxic/reoxygenation on the protein expression of M1-related pro-inflammatory factors TNF-α, CD80 and M2-related anti-inflammatory factors ARG-1 and CD206. Moreover, we found that conditioned medium from polarized M1 macrophages induced by hypoxia/reoxygenation, notably increased the degree of apoptosis of hypoxia/reoxygenation-induced TCMK-1 cells, and promoted the protein expression of pro-apoptotic proteins bax (P < 0.01) and cleaved-caspase 3 (P < 0.01) and inhibited the expression of anti-apoptotic protein bcl-2 (P < 0.01), but silencing CX3CR1 in macrophages had a protective role. Finally, we also found that the secretion of soluble CX3CL1 in RAW264.7 macrophages under hypoxia/reoxygenation was significantly increased.Conclusions:The findings suggest that hypoxia/reoxygenation could promote M1 polarization, cell migration, and adhesion of macrophages, and that polarized macrophages induce further apoptosis of hypoxic renal tubular epithelial cells by regulating of CX3CL1/CX3CR1 signaling pathway.
简介:摘要目的探讨单通道C3-C4导联和平均参考导联新生儿振幅整合脑电图(amplitude-integrated electroencephalogram,aEEG)图形的差异。方法回顾性选择2018年8月至2019年9月南方医科大学南方医院新生儿科收治的脑电图正常的足月儿为研究对象,收集从单通道C3-C4导联和平均参考导联获取的aEEG数据,比较两种不同导联中各通道宽带和窄带的上、下边界振幅,并分析其aEEG波形差异。结果共纳入90例患儿,单通道C3-C4导联的宽、窄带上、下边界振幅及带宽均高于平均参考导联,与平均参考导联9个通道行两两比较,差异均有统计学意义(P<0.05),平均参考导联O1-AV及O2-AV通道识别睡眠-觉醒周期的误判率分别为40.0%、46.7%;在脑电背景活动分析中,90例平均参考导联中有6例宽带下边界振幅<5 μV,导致对脑电背景活动的误判,误判率为6.7%。结论单通道C3-C4导联与平均参考导联获取的aEEG波形模式存在差异,使用平均参考导联获取的aEEG图形进行分析可能导致误判。
简介:摘要目的探讨1例结节性硬化症(tuberous sclerosis complex, TSC)患者可能的遗传学病因。方法应用高通量测序技术、多重连接探针扩增技术和Sanger测序技术对1例疑似结节性硬化症患者行基因变异分析,并在家系其他成员及100名正常对照中进行验证;通过反转录-PCR及Sanger测序技术确定该变异可能导致的mRNA转录变化。结果测序结果显示该家系中先证者发生了TSC2基因的c.2355+1G>C杂合变异,cDNA的序列分析表明该变异导致TSC2基因在第21外显子3′端插入62个碱基序列,这种剪切位点变化导致蛋白翻译提前终止,预测产生截短蛋白。结论TSC2基因c.2355+1G>C变异可能是该患者的致病原因。本研究结果不仅进一步丰富了TSC2基因的变异谱,同时为产前诊断和胚胎植入前遗传学检测的开展提供了理论基础。
简介:【摘要】本文通过分析乙醇偶合制备C4烯烃实验数据,通过控制变量,建立乙醇转化率和C4 烯烃的选择性分别受温度,Co 负载量,Co/SiO2 、 HAP 装料比与乙醇浓度的关系的函数模型,因为所有函数的泰勒展开式都为多项式,所以我们根据数据建立多项式模型,再计算残差,运用多元线性回归分析确定拟合程度最好的模型,并用matlab求解得乙醇转化率和C4 烯烃的选择性最高时的最优模型。
简介:摘 要:随着环保标准的不断提高,面对严峻的环保形势,目前我国对于NOx的污染排放问题也更为重视,正是基于这个背景,兰州石化公司化肥厂动力车间2014年C锅炉实施烟气脱硝工程改造,采用低氮燃烧、选择性非催化还原反应(SNCR)、选择性催化还原反应(SCR)联合脱硝技术,分三段脱除烟气中
简介:摘要目的检测C-X-C基序趋化因子10(CXCL10)在人肝癌组织中的表达水平及其与肝癌患者临床生物学特征和预后的关系,并探讨CXCL10对肝癌细胞增殖和侵袭的作用。方法癌症基因组图谱(TCGA) RNA测序数据库分析CXCL10在配对(n=56)、非配对肝癌组织(n=370)、癌旁正常组织(n=56)的表达水平,根据CXCL10表达水平、生存时间和生存状态获得CXCL10在肝癌的临界值,根据其cutoff值我们将肝癌患者分为CXCL10高表达组和CXCL10低表达组,进一步分析其与肝癌患者临床生物学特征、生存和肿瘤复发的关系。利用小干扰RNA在肝癌HepG2细胞株敲低CXCL10基因,实时定量聚合酶链反应(PCR)和蛋白质印迹法(Western blot)检测CXCL10、增殖细胞核抗原(PCNA)和基质金属蛋白酶(MMP)-2的表达水平。噻唑蓝(MTT)和Transwell检测CXCL10沉默对肝癌细胞增殖和侵袭的影响。两组间比较采用独立t检验。χ2检验分析CXCL10表达与肝癌临床病理学特征的关系;Kaplan-Meier及Cox回归分析CXCL10表达与肝癌患者预后的关系。结果t检验分析结果显示,CXCL10在配对肝癌组织(t=3.677,P<0.01)和非配对肝癌组织的表达水平显著高于癌旁组织(t=4.692,P<0.01);χ2检验显示,其高表达与肝癌患者年龄(χ2=4.680,P<0.05)、性别(χ2=7.993,P<0.01)、肿瘤大小(χ2=7.436,P<0.05)及病理学分级(χ2=6.350,P<0.05)均明显相关,但与其他临床病理学因素无相关(χ2=0.092、0.468,P>0.05);Kaplan-Meier分析显示,CXCL10高表达患者的生存率低于CXCL10低表达患者(χ2=4.672,P<0.05)而肿瘤复发率高于CXCL10低表达患者(χ2=4.672,P<0.05),差异有统计学意义。体外实验显示,CXCL10沉默减少PCNA和MMP-2蛋白表达,抑制肝癌细胞增殖活性。CXCL10沉默组肝癌侵袭细胞数[(51.2±5.4)个]明显低于空载组[(136.3±11.5)个]穿过小室的细胞数(t=2.315,P<0.01),差异有统计学意义。结论CXCL10高表达与肝癌患者年龄、性别、肿瘤大小、病理学分级及不良预后存在明显相关,其沉默能抑制肝癌细胞的增殖和侵袭潜能。
简介:摘要总结1例表现为步态异常的成年型Chediak-Higashi综合征患者的临床资料,并对其溶酶体调节转运蛋白(LYST)基因进行变异分析。应用全外显子测序及Sanger测序验证,同时对其家系成员进行验证。测序结果显示先证者LYST基因存在c.421C>T(p.Arg141*)纯合变异,其父母该位点为杂合携带。查阅人类基因变异数据库未见该变异类型报道,根据美国医学遗传学及基因组学会遗传变异解读指南,c.421C>T变异被判定为致病性变异。