Baoziwan-Majiashan Area of Jiyuan Oilfield Analysis of Reservoir Characteristics and Main Control Factors in Long 4 5 Section

Based on the sheet, scanning electron microscope and high pressure mercury analysis method, this paper takes Jiyuan oilfield-Ma Jia mountain district 4 5 sandstone reservoir as the research object, from the reservoir petrology, pore type and porosity, permeability, the system analyzed the reservoir characteristics and its control factors. The results show that the sandstone in the 4 5 section of Baoziwan-Majiashan area of Jiyuan oilfield is fine in size and high in filling content. The pore types were dominated by intergranular pores and dissolved pores, with a low face rate. The reservoir property is relatively poor, with mean porosity of 11.11% and mean permeability of 1.16 × 10−3 µm2. In the low porous, low otonic background, the development of relatively high pore hypertonic areas. Compaction and cementation should play a destructive role in reservoir properties, and dissolution should play a positive role in reservoir properties. Compaction adjusts the migration of clay minerals and miscellaneous bases in the original sediment in the study area, greatly reducing the porosity and permeability of the reservoir;the development of the cement cement, carbonate cementation and some quartz secondary compounds reduces the storage space;the dissolution effect, especially the secondary dissolution pores of the reservoir, which obviously improves the properties of the reservoir.

ACSL4介导铁死亡及在动脉粥样硬化性心血管病中的潜在作用

背景:铁死亡是一种铁依赖性调节细胞死亡形式,其特征是铁依赖性脂质过氧化,长链酰基辅酶A合酶4参与脂质过氧化底物的形成进而导致铁死亡。近几年研究表明,长链酰基辅酶A合酶4介导铁死亡在动脉粥样硬化性心血管疾病中发挥关键作用。目的:总结长链酰基辅酶A合酶4的结构功能和调控机制及其介导铁死亡的潜在分子机制,阐述长链酰基辅酶A合酶4驱动铁死亡在动脉粥样硬化、缺血性脑卒中和心肌梗死中的应用,以期为治疗动脉粥样硬化心血管疾病提供新的治疗策略。方法:在PubMed数据库检索自建库起至2023年8月收录的相关文献,以“atherosclerosis,ferroptosis,long-chain acyl-coenzyme A synthase 4,ACSL4,glutathione peroxidase 4,ischemic stroke,myocardial infarction,endothelial cell,smooth muscle cells,foam cell”为检索词,最终纳入76篇文献进行综述分析。结果与结论:①长链酰基辅酶A合酶4参与形成多不饱和脂肪酸的辅酶衍生物并将其插入磷脂,为铁死亡发生的核心机制脂质过氧化提供底物;②在长链酰基辅酶A合酶4表达的调节因子中,整合素α6β4、细胞内囊泡转运因子p115、锌脂蛋白A20负调控其表达,同时多种miR通过结合3′-UTR下调其表达,相反长链酰基辅酶A合酶4的表达上调大部分通过转录因子转录调控;③长链酰基辅酶A合酶4依赖性生成含有多不饱和脂肪酸的磷脂是脂质过氧化并执行铁死亡必不可少的必要条件,且长链酰基辅酶A合酶4与谷胱甘肽过氧化酶4作为铁死亡的正负调控因子相互制约,其具体机制仍待进一步研究;④长链酰基辅酶A合酶4介导铁死亡参与动脉粥样硬化、心肌梗死、缺血性脑卒中的病理机制,动脉粥样硬化中内皮细胞损伤与长链酰基辅酶A合酶4介导的铁死亡密切相关,但长链酰基辅酶A合酶4参与泡沫细胞形成、平滑肌细胞表型转化、钙化的研究尚未见报道;⑤长链酰基辅酶A合酶4作为铁死亡的生物标志物和潜在靶点成为研究热点,靶向长链酰基辅酶A合酶4抑制铁死亡可能成为治疗动脉粥样硬化性心血管疾病的新方向,而抑制长链酰基辅酶A合酶4的药物研究较少,未来还需进一步研究。

ACSL4通过AMPK/mTOR通路抑制七氟醚诱导神经元铁死亡机制的实验研究

目的探讨酰基辅酶A合成酶长链家族成员4(acyl-CoA syntbetase long chain family member 4,ACSL4)在七氟醚(sevoflurane,Sev)诱导的神经元细胞损伤中的作用及机制。方法以人神经母细胞瘤SH-SY5Y细胞为研究对象,分别设置对照组(二甲基亚砜,10μmol/L)、Sev组和Sev+铁死亡抑制剂Ferrostatin-1(Fer-1,10μmol/L)组,采用CCK-8法检测细胞活性。体外构建4.1%Sev暴露的术后认知功能障碍模型,按照转染类别分为Ctrol组、Sev组、Sev+si-NC组、Sev+si-ACSL4组和Sev+si-ACSL4+compound C组。采用比色法检测各组细胞中丙二醛(malonaldehyde,MDA)、4-羟基壬烯醛(4-hydroxynonenal,4-HNE)、谷胱甘肽(glutathione,GSH)和Fe2+含量;2’,7’-二氯荧光素二乙酸盐(DCFH-DA)荧光探针检测活性氧水平;实时荧光定量PCR(qRT-PCR)检测ACSL4,谷胱甘肽过氧化酶4(glutathione peroxidase 4,GPX4)和溶质载体家族7成员11(solute carrier family 7 member 11,SLC7A11)mRNA表达;蛋白免疫印迹法(WB)检测ACSL4,GPX4,腺苷酸激活蛋白激酶(adenosine 5’-monophosphate-activated protein kinase,AMPK)、磷酸化(phosphorylated,p)-AMPK,哺乳动物雷帕霉素靶蛋白(mammalian target of rapamycin)mTOR和p-mTOR蛋白表达。结果CCK-8结果显示,Sev组细胞活力(0.41±0.11)较对照组(0.98±0.07)明显降低,Sev+Fer-1组细胞活力(0.83±0.09)较Sev组显著升高,差异具有统计学意义(t=7.572,5.118,均P<0.01)。Sev组细胞中Fe2+,MDA,4-HNE,ROS水平和p-AMPK/AMPK比率以及ACSL4的mRNA和蛋白表达高于Ctrol组(t=5.900,7.421,4.795,13.517,10.825,9.945,11.334),GSH,p-mTOR/mTOR比率以及SLC7A11,GPX4的mRNA和蛋白表达低于Ctrol组(t=20.438,3.551,11.460,12.211,6.845,8.287),差异具有统计学意义(均P<0.05)。Sev+siACSL4组Fe2+,MDA,4-HNE,ROS水平和p-AMPK/AMPK比率以及ACSL4的mRNA和蛋白表达低于Sev+siNC组(t=3.818,3.164,3.054,4.465,13.088,7.918,9.737),细胞活力、GSH含量、p-mTOR/mTOR比率以及SLC7A11,GPX4的蛋白表达高于Sev+si-NC组(t=2.912,7.248,7.574,20.092,5.915),差异具有统计学意义(均P<0.05)。Sev+si-ACSL4+compound C组细胞活力、GSH含量和SLC7A11,GPX4蛋白表达低于Sev+si-ACSL4组(t=4.435,8.521,4.522,8.767),而Fe2+,MDA,4-HNE和ROS水平高于Sev+si-ACSL4组(t=10.046,4.004,2.957,3.752),差异具有统计学意义(均P<0.05)。结论抑制ACSL4表达可通过激活AMPK/mTOR信号通路减轻Sev诱导的SH-SY5Y细胞铁死亡。

胃癌组蛋白H3第4位赖氨酸的三甲基化修饰相关长链非编码RNA预后模型的构建与验证

目的 探索胃癌组蛋白H3第4位赖氨酸的三甲基化(trimethylation of lysine 4 on histone H3,H3K4me3)修饰相关长链非编码RNA(long non-coding RNA,LncRNA)特征,构建相关预后模型并预测胃癌免疫治疗疗效。方法 从癌症基因组图谱数据库下载胃癌相关转录组测序数据和对应的患者临床资料,通过构建H3K4me3相关调节因子基因与LncRNA的共表达网络识别H3K4me3修饰相关LncRNA,并将癌症基因组图谱数据库中370例符合筛选标准的胃癌患者样本(整体组)按1:1随机抽样划分为训练组(n=185)和验证组(n=185)。随后基于单因素Cox回归、Lasoo回归分析构建H3K4me3相关LncRNA预后风险评分模型并进行内部验证。Kaplan-Meier生存分析和受试者操作特征曲线(receiver operating characteristic curve,ROC曲线)被用于验证模型的预测性能。通过单因素和多因素Cox回归分析评估风险评分等临床指标的预后预测价值。结合风险评分、年龄和肿瘤TNM分期构建预测胃癌患者总生存率的列线图模型,ROC曲线与校准图被用于评估列线图的预测准确性。借助共识聚类识别异质性聚类亚群并进行免疫治疗疗效预测。结果 基于共表达网络关系识别了14个具有预后价值的H3K4me3相关LncRNA并构建了相关风险模型及评价体系。根据训练组预后风险评分模型获得的中位风险评分将训练组、验证组和整体组胃癌患者划分为高、低风险,Kaplan-Meier生存曲线显示低风险患者的总体生存情况要优于高风险患者(P<0.05)。此外,该模型在训练组中预测胃癌患者1、3、5年总生存率的曲线下面积(area under curve,AUC)分别为0.708、0.730、0.770,在验证组中分别为0.690、0.648、0.713,而在整体组中分别为0.697、0.670、0.724。多因素Cox回归分析显示基于H3K4me3相关LncRNA构建的风险评分模型是预测胃癌患者预后的独立因素(P<0.001)。构建的列线图预测胃癌患者1、2、3年总生存率的AUC分别为0.727、0.780、0.717,且其校准曲线与理想曲线相接近。基于共识聚类算法进一步识别了2种具有异质性免疫特征的H3K4me3-LncRNA亚群,其中亚组Ⅱ具有更高的免疫细胞浸润水平和更强的免疫应答潜力,并对5-氟尿嘧啶、奥沙利铂等显示出更高的药物敏感性,而亚组Ⅰ则可能对磷脂酰肌醇3-激酶特异性抑制剂具有更高的敏感性。结论 本研究构建了一个H3K4me3-LncRNA风险评分模型以预测胃癌患者的预后,并揭示了其异质性微观特征及在预测免疫治疗疗效方面的潜在价值。

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.

Preparation of Non-Grinding Long Afterglow SrAl_2O_4:Eu^(2+), Dy^(3+) Material by Microwave Combustion Method

The non-grinding long afterglow material SrAl2O4：Eu^2＋ , Dy^3＋ was prepared by combustion method in home mierowave oven direetly, after dispersant, frother, eomburent, and mineralizer were added into the reacting system. XRD analysis showed that the powders were nearly pure SrAl2O4 phase with few other phases, and the size of the grain was 41.1 nm. Fluoreseenee speetrum results indieated that there were 2 exeitation peaks loeated at 345 and 400 nm, and the emission peak loeated at 516 nm, afterglow lasted up to 30 min or more. The mierowave eombustion method has advantages of less time, low temperature and no grinding process, and the material made by the method has good luminescent property.

Effect of mixing process on the luminescent properties of SrAl_2O_4:Eu^(2+),Dy^(3+) long afterglow phosphors

A new mixing method was developed for solid-state reaction synthesis of SrAl2O4:Eu2+,Dy3+ long afterglow phosphors.The morphology and crystal structure of the phosphors were analyzed with scanning electron microscope(SEM) and X-ray diffractometer(XRD).The excitation and emission spectra of the long afterglow phosphors were measured,and the main emission band was around 514 nm.The decay time of the product was measured and compared with the phosphors prepared using dry-mixing method and wet-mixing method.It ...

SrAl_2O_4∶Eu^(2+),Nd^(3+) and Dy^(3+) Long Afterglow Phosphor

The SrAl 2O 4∶Eu 2+ , Nd 3+ and SrAl 2O 4∶Eu 2+ , Dy 3+ long afterglow phosphor were synthesized. Their excitation and emission spectra at different excitation and afterglow characteristics were analyzed after the excitation power was taken off. The effects of Eu 2+ , Dy 3+ , Nd 3+ mole concentrations on phosphorescence characteristics were also discussed. It is crucial to have trapping levels located at a suitable depth related to the thermal release rate at room temperature. The incorporation of Nd 3+ ions as an auxiliary activator into the SrAl 2O 4∶Eu 2+ system causes very intense and long phosphorescence. The response time of SrAl 2O 4∶Eu 2+ , Dy 3+ phosphors is quicker than that of SrAl 2O 4∶Eu 2+ , Nd 3+ . Phosphorescence characteristics of SrAl 2O 4∶Eu 2+, Nd 3+ is much better than those of SrAl 2O 4∶Eu 2+ , Dy 3+ . The integrate area of the excitation spectrum of SrAl 2O 4∶Eu 2+ , Nd 3+ phosphor is larger than that of SrAl 2O 4∶Eu 2+ , Dy 3+ phosphor within the range of 250～360 nm. For phosphorescence characteristics to the system of SrAl 2O 4∶Eu 2+ , Nd 3+ phosphor, the optimum concentration of Nd 3+ trivalent rare earth ions is 0.05 mol.

BRIGHT LONG AFTERGLOW PHOSPHORESCENCE GLASS MADE OF SrAl_(2)O_(4): Eu^(2+), Dy^(3+) AND GLASS FRITS

Bright long afterglow phosphorescence glasses were prepared by using SrAl2O4： Eu^2＋, Dy^3＋ phosphors and suitable glass frits together. The SrAl2O4： Eu^2＋, Dy^3＋ phosphors were initially prepared by the solid reaction method. Three kinds of glass frits were prepared to match the SrAl2O4： Eu^2＋, Dy^3＋ phosphors. Effects of the compositions of the glass frits, the ratios of the phosphors to the frits us well us the firing temperature and firing times on the properties of the samples were discussed. XRD analysis indicated the samples exhibited the typical diffraction peaks of SrAlwO4： Eu^2＋, Dy^3＋. The emission spectra of the samples showed broad bands peaking at 510nm.The excitation spectra of the samples showed broad bands ranging from 300 to 480hm. These are believed due to the 5d4f-4f transitions of Eu^2＋ in the SrAl2O4： Eu^2＋, Dy^3＋ phosphors. The afterglow luminescence of the samples excited by a 40W fluorescence lamp for 30min can be observed in the dark for more lOh with the naked eyes. It can find wide applications in many fields.

Characterization of Y_2O_2S∶Eu ^(3+), Mg^(2+), Ti^(4+) Long-Lasting Phosphor Synthesized by Flux Method

Long-lasting phosphor Y2O2S ： Eu^3＋ , Mg^2＋ , Ti^4＋ was synthesized by a flux method and their luminescence properties were investigated. The result indicates that the unit cell parameter c is linearly increased with the increase of Eu2O3 content in Y2O2S： Eu^3＋ （0.01 ≤ x ≤0.10）. On the other hand, the change of unit cell parameter a is not linear dependence. In the Y2O2S： Eu^3 ＋ crystal structure, Eu^3＋ ions only replaced Y^3 ＋ ions＇ places in which it posited center position of c axis. With the increase of Eu2O3 content, the position of the strongest emission peak changed from 540 nm （5D1→^ 7F2 transition） to 626 nm （^5Do→^7TF2 transition）, and the maximum intensity was obtained when x = 0.09 in Y2O2S： Eu^3＋ （0.01 ≤x ≤0.10）. This is due to the environment of trivalent europium in the crystal structure of Y2O2S. Doping with Mg^2＋ or Ti^4＋. ions alone cannot get the good long-lasting afterglow effect, whereas co-doping with Mg^2 ＋ and Ti^4 ＋ ions and excited with 365 nm ultraviolet light, a strong thermoluminesence peak appeared, red and orange long-lasting phosphorescence （LLP） was also observed and the phosphorescence lasted nearly 3 h in the light perception of the dark-adapted human eye （0.32 mcd·m^-2）. Thus the LLP mechanism was analyzed.

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.

长链脂酰辅酶A合成酶4表达水平对肝癌预后影响的Meta分析

目的评价长链脂酰辅酶A合成酶4(acyl-CoA synthetase long-chain family member 4,ACSL4)对肝癌患者预后的影响。方法系统检索PubMed、Embase、Cochrane Library、Web of science、中国知网、万方医学与维普数据库,检索时间均从建库至2023年2月,收集ACSL4表达对肝癌患者预后影响的队列研究。文献的筛选过程由2名评估员自主完成。将纳入的研究依据纽卡斯尔-渥太华质量评价量表(Newcastle Ottawa Scale,NOS)进行质量评估,提取文献中肝癌患者的临床病理特征、研究的结局指标及HR(95%CI)等相关数据。运用Stata17.0MP软件对文献数据进行统计分析,采用漏斗图与Egger’s检验探讨偏倚风险。结果共纳入6项队列试验(890例肝癌患者)。Meta分析表明,与ACSL4低表达组患者相比,ACSL4高表达组肝癌患者总生存期(overall survival,OS)较短(HR=1.274,95%CI:1.141~1.422,P<0.001);肝癌患者中,男性ACSL4高表达(OR=1.12,95%CI:1.008~1.224,P<0.05)。Egger’s检验表明研究间存在发表偏倚的可能性较小(P=0.055)。ACSL4表达水平与年龄、肿瘤分期、肿瘤大小和肿瘤包膜是否完整以及是否合并肝硬化的相关性无统计学意义(P均>0.05)。结论ACSL4高表达与肝癌患者较短OS的相关性具有统计学意义,但仍需要更多的高质量临床研究进行验证。

Long non-coding RNA CA7-4通过提高细胞自噬水平增强肺癌细胞A594的顺铂耐药

目的分析长链非编码RNA(Long non-coding RNA,LncRNA)CA7-4影响非小细胞肺癌(Non-small cell lung cancer,NSCLC)细胞系A549的顺铂(Cisplatin,DDP)耐药的机制。方法将人NSCLC细胞系A549在不同浓度的DDP中培养,检测细胞活力计算半数抑制浓度(Half maximal inhibitory concentration,IC50)。将A549细胞分为对照组、DDP组、CA7-4组及CA7-4+DDP组,其中CA7-4组及CA7-4+DDP组通过转染CA7-4 pcDNA上调LncRNA CA7-4水平;DDP组和CA7-4+DDP组培养基中加入终浓度为12μM的DDP。检测和比较各组细胞的细胞活力、细胞凋亡率和自噬蛋白LC3Ⅰ、LC3Ⅱ水平。结果DDP可剂量依赖性的抑制A549细胞生长,本研究中IC50值为12μM。DDP组的LncRNA CA7-4水平显著低于对照组,CA7-4组的LncRNA CA7-4水平显著高于对照组,并且CA7-4+DDP组的LncRNA CA7-4显著高于DDP组。DDP组细胞活力明显降低而细胞凋亡率显著升高,CA7-4组的胞活力升高、细胞凋亡率降低,并且CA7-4+DDP组的胞活力显著高于DDP组而细胞凋亡率显著低于DDP组。DDP组LC3Ⅱ/LC3Ⅰ水平低于对照组,CA7-4组的LC3Ⅱ/LC3Ⅰ水平高于对照组,且CA7-4+DDP组的LC3Ⅱ/LC3Ⅰ水平显著高于DDP组。结论LncRNA CA7-4可以通过促进NSCLC细胞系A549的自噬促进细胞活力并抑制细胞凋亡,促进细胞对DDP的耐药性。

A Novel Calix[4]arene Having Long-Chain Monoalkenyl at The Upper Rim

5-1',1'-dimethylundecenyloxyphenylmethyl-11,17,23-tris-1 '',1 ''-dimethylethyl-25,26,27,28-tetrahydroxycalix[4] arene was synthesized from 1,1-dimethylundecenyoxylphenylmethylphenol (3) and bishydroxymethylated p-tert-butylphenol-formaldehyde trimer (7) (3-[3-[3-(Hydroxymethyl)-tert-butylsalicyl-5]-tert-butylsalicy]-5-tert-butyl-2-hydroxybenzyl Alcohol) by '1+3' fragment condensation in dioxane with TiCl4 as condensation agent in 28% yield. It is the first long-chain monoalkenyl substituted calix[4]arene in which the alkenyl was attached to the upper rim of calix[4]arene.

血清LncRNA UCA1、NPASDP4水平与急性脑梗死患者神经功能缺损的关系及对预后的预测价值

目的探讨血清长链非编码核糖核酸尿路上皮癌胚抗原1(LncRNA UCA1)、神经元PAS结构域蛋白4(NPASDP4)水平与急性脑梗死(ACI)患者神经功能缺损的关系及对预后的预测价值。方法选取2021年1月—2023年6月南京大学医学院附属鼓楼医院急诊科收治的ACI患者163例(ACI组),根据美国国立卫生研究院卒中量表(NIHSS)评分分为轻度(n=32)、中度(n=73)、重度缺损亚组(n=58),另选取同期健康体检者65例作为健康对照组。根据ACI患者90 d预后分为不良预后亚组52例、良好预后亚组111例。采用实时荧光定量聚合酶链式反应与酶联免疫吸附法,检测血清LncRNA UCA1与NPASDP4水平。Spearman相关性分析血清LncRNA UCA1、NPASDP4水平与ACI患者NIHSS评分的相关性。多因素Logistic回归分析ACI患者不良预后的因素,受试者工作特征(ROC)曲线分析血清LncRNA UCA1、NPASDP4预测ACI患者不良预后的价值。结果与健康对照组比较,ACI组血清LncRNA UCA1、NPASDP4水平升高(t/P=20.114/<0.001、15.711/<0.001)。血清LncRNA UCA1、NPASDP4水平重度缺损亚组>中度缺损亚组>轻度缺损亚组(F/P=187.914/<0.001、195.031/<0.001)。ACI患者血清LncRNA UCA1、NPASDP4水平与NIHSS评分呈正相关(r/P=0.759/<0.001、0.773/<0.001)。随访90 d,与良好预后亚组比较,不良预后亚组血清LncRNA UCA1、NPASDP4水平升高(t/P=6.963/<0.001、6.515/<0.001)。年龄大、NIHSS评分增加、LncRNA UCA1和NPASDP4升高为ACI患者不良预后的独立危险因素[OR(95%CI)=1.107(1.043~1.176)、1.098(1.049~1.150)、3.479(1.941~6.235)、1.959(1.398~2.745)]。血清LncRNA UCA1、NPASDP4及二者联合预测不良预后的AUC分别为0.777、0.789、0.870,二者联合大于血清LncRNA UCA1、NPASDP4单独预测的AUC(Z/P=3.312/0.001、2.721/0.007)。结论血清LncRNA UCA1表达、NPASDP4水平升高与ACI患者神经功能缺损加重和不良预后密切相关,血清LncRNA UCA1联合NPASDP4水平预测ACI患者不良预后的效能较高。

Crystalline and amorphous metal sulfide composite electrode materials with long cycle life:Preparation and performance of hybrid capacitors

Crystalline@amorphous NiCo_(2)S_(4)@MoS_(2)(v-NCS@MS)nanostructures were designed and constructed via an ethylene glycol-induced strategy with hydrothermal synthesis and solvothermal method,which simultaneously realized the defect regulation of crystal NiCo_(2)S_(4) in the core.Taking advantage of the flexible protection of an amor-phous shell and the high capacity of a conductive core with defects,the v-NCS@MS electrode exhibited high specif-ic capacity(1034 mAh·g^(-1) at 1 A·g^(-1))and outstanding rate capability.Moreover,a hybrid supercapacitor was assembled with v-NCS@MS as cathode and activated carbon(AC)as anode,which can achieve remarkably high specific energy of 111 Wh·kg^(-1) at a specific power of 219 W·kg^(-1) and outstanding capacity retention of 80.5%after 15000 cycling at different current densities.

黄芪糖蛋白干扰lncRNA GAS5/miR-21/TLR4信号轴抑制细胞焦亡改善佐剂性关节炎大鼠心肌损伤

目的基于长链非编码RNA生长停滞特异性转录本5/微小RNA 21/Toll样受体4(lncRNA GAS5/miR-21/TLR4)信号轴探究黄芪糖蛋白(HQGP)对佐剂性关节炎(AA)大鼠心肌损伤的作用及机制。方法将SD大鼠随机分为正常对照组、模型组、甲氨蝶呤(MTX)组、HQGP组,每组6只。复制AA模型,第19天开始给药,连续4周。检测各组AA大鼠足趾肿胀度、关节炎指数(AI),HE染色观察大鼠心肌组织病理变化,透射电镜观察心肌组织超微结构的变化及焦亡小体情况,ELISA检测血清白细胞介素6(IL-6)、IL-18、IL-1β和肿瘤坏死因子α(TNF-α)水平,乳酸脱氢酶(LDH)试剂盒检测心肌组织LDH释放量,实时荧光定量PCR检测心肌组织核因子κB p65(NF-κB p65)、胱天蛋白酶1(caspase-1)、含pyrin结构域核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)、消皮素D(GSDMD)的mRNA以及lncRNA GAS5/miR-21/TLR4信号轴分子的表达,Western blot法检测心肌组织TLR4、NF-κB p65、caspase-1、NLRP3和GSDMD蛋白水平。结果与正常对照组相比,模型组大鼠足趾肿胀度、AI显著升高;大鼠心肌纤维溶解、断裂,肌节结构模糊,心肌纤维排列紊乱,组织间有炎性细胞浸润,线粒体嵴明显断裂稀疏,焦亡小体数量增加;血清促炎细胞因子IL-6、IL-18、IL-1β和TNF-α表达显著升高;心肌组织中GAS5表达显著降低,miR-21表达显著升高,LDH释放量、TLR4、NF-κB p65、caspase-1、NLRP3、GSDMD的mRNA和蛋白表达水平显著升高。与模型组比较,HQGP组大鼠足趾肿胀度、AI和心肌组织病理状态明显改善;血清IL-6、IL-18、IL-1β和TNF-α表达显著降低;心肌组织中GAS5表达显著升高,miR-21表达显著降低,LDH释放量、TLR4、NF-κB p65、caspase-1、NLRP3的mRNA和蛋白表达水平显著降低,GSDMD的mRNA表达降低且蛋白水平显著降低。结论HQGP通过上调lncRNA GAS5抑制miR-21/TLR4信号传导,抑制细胞焦亡,减少促炎细胞因子表达,改善AA大鼠心肌损伤。

长链酯酰辅酶A合成酶4介导铁死亡的发生机制

铁死亡(ferroptosis)是一种铁和脂质过氧化依赖性的程序性死亡方式,触发铁死亡的必要条件是细胞内活性氧物质堆积到致死量。由脂质过氧化反应产生的脂质活性氧会作用于细胞膜上的脂质分子,导致脂质过氧化和膜损伤,因此脂质过氧化是铁死亡的显著特征。长链酯酰辅酶A合成酶4(long-chain acyl-CoA synthetase 4,ACSL4)在调节脂质代谢方面具有关键作用,其主要功能是将多不饱和脂肪酸酯化并插入膜磷脂中,从而加速脂质过氧化的发生并推动铁死亡。ACSL4介导的铁死亡主要受到转录、转录后和翻译后水平上的调控影响,在脂质过氧化依赖性的疾病中发挥着重要作用。本文旨在介绍铁死亡的发生机制,重点阐述了ACSL4受到的上游调控从而介导铁死亡的机制,为研究ACSL4介导铁死亡机制提供理论依据。

铁死亡诱导剂Erastin下调ACSL4抑制肝癌细胞体外增殖

目的分析酯酰辅酶A合成酶长链家族成员4(ACSL4)在肝癌中的表达,探究铁死亡调控ACSL4对癌细胞增殖能力的影响。方法收集肝癌和癌旁正常肝组织临床样本,HE染色病理学鉴定后,微量法检测丙二醛(MDA)含量,RT-qPCR检测ACSL4与增殖细胞核抗原(PCNA)的mRNA表达,Western blotting检测ACSL4与PCNA的蛋白表达。体外培养Huh-7人肝癌细胞,先分为3组:即铁死亡诱导剂Erastin组、抑制剂Fer-1组、以及Erastin与Fer-1联合作用组;其中Erastin或Fer-1组均包含0、20、40、60、80、100μmol/L共6个浓度,然后采用筛选的Erastin浓度80μmol/L+(0、30、60、90μmol/L)Fer-1,筛选Fer-1浓度后再分为3组:对照组、80μmol/L Erastin单独处理组、80μmol/L Erastin+60μmol/L Fer-1联合处理组,均作用48 h。干预ACSL4、PCNA的表达后,平板克隆实验检测细胞增殖能力的改变,微量法检测MDA含量的变化。结果相较于癌旁正常肝组织,肝癌组织中MDA含量降低(P<0.01),ACSL4、PCNA的mRNA和蛋白表达均显著增强(P<0.05);Erastin可抑制ACSL4、PCNA的mRNA和蛋白表达(P<0.01),并抑制细胞增殖(P<0.001)、上调MDA含量(P<0.01);单独使用Fer-1对细胞存活率无影响;但加入Erastin后再应用Fer-1,则可逆转Erastin对ACSL4、PCNA表达(P<0.05),细胞增殖能力的抑制(P<0.001),MDA含量的上调(P<0.05)。结论ACSL4在肝癌中表达增强,Erastin可提高MDA含量、下调ACSL4表达,诱导肝癌细胞铁死亡,抑制癌细胞增殖;Fer-1则可逆转Erastin的上述作用。

LncRNA SNHG4调控牙周膜干细胞成骨分化过程中的miR-152-3p

背景:研究表明长链非编码RNA核仁小RNA宿主基因4(LncRNA SNHG4)参与了多种炎症性疾病的进展,而关于LncRNA SNHG4对牙周炎治疗过程中人牙周膜干细胞成骨分化的影响尚不明确。目的:探讨LncRNA SNHG4通过调节miR-152-3p对人牙周膜干细胞成骨分化的影响。方法:从因正畸需要而拔除的前磨牙牙周膜组织中分离出人牙周膜干细胞,将其进行成骨诱导分化0,7,14 d后,qRT-PCR检测Runt相关转录因子2、骨钙素、LncRNA SNHG4及miR-152-3p表达。取第3代人牙周膜干细胞,将其分为NC组、pcDNA组、pcDNA-SNHG4组、inhibitor NC组、miR-152-3p inhibitor组、pcDNA-SNHG4+mimic NC组、pcDNA-SNHG4+miR-152-3p mimic组,qRT-PCR检测各组人牙周膜干细胞中LncRNA SNHG4、miR-152-3p表达,CCK-8法检测细胞增殖情况;比色法检测碱性磷酸酶活性;茜素红染色检测矿化结节形成情况;Western blot检测Runt相关转录因子2、骨钙素、碱性磷酸酶蛋白表达;双荧光素酶报告基因实验验证LncRNA SNHG4与miR-152-3p的关系。结果与结论:①与成骨诱导0 d比较,成骨诱导7,14 d后人牙周膜干细胞中Runt相关转录因子2、骨钙素、LncRNA SNHG4表达升高,miR-152-3p表达降低(P<0.05);②过表达LncRNA SNHG4或抑制miR-152-3p均可提高人牙周膜干细胞的增殖能力及碱性磷酸酶活性、矿化结节形成量和Runt相关转录因子2、骨钙素、碱性磷酸酶的蛋白表达(P<0.05);miR-152-3p mimic减弱了过表达LncRNA SNHG4对人牙周膜干细胞成骨分化的促进作用;LncRNA SNHG4与miR-152-3p存在靶向关系;③结果表明,过表达LncRNA SNHG4可能通过抑制miR-152-3p促进人牙周膜干细胞成骨分化。