急性冠脉综合征患者pentraxin-3与纤维蛋白原的变化

目的:了解急性冠脉综合征患者炎性指标pentraxin-3与血栓指标纤维蛋白原(FIB)的变化。方法:回顾性研究35例急性心肌梗死患者、27例不稳定心绞痛患者及15例健康体检者,所有研究对象清晨空腹抽血,检测其血浆pentraxin-3、FIB水平,并进行比较。结果:急性冠脉综合征患者血pentraxin-3、FIB水平明显高于健康体检者,差异显著(P<0.01);急性心肌梗死组高于不稳定性心绞痛组,差异显著(P<0.05)。Pentraxin-3浓度与FIB浓度之间存在正相关关系(P<0.01)。结论:作为炎性指标pentraxin-3与血栓指标纤维蛋白与冠心病发生急性冠脉综合征相关,且两者相辅相成,可能共同促进急性冠脉综合征的发生。

pentraxin-3在急性心肌梗死中的意义

目的研究pentraxin-3在急性心肌梗死中的表达情况及意义。方法回顾性研究2003年1月到2005年9月间急性ST段抬高型心肌梗死患者35例,其中男25例,女10例,平均年龄68.59±11.92岁,诊断标准依据于1979年WHO关于缺血性心脏病的命名诊断标准。急性心肌梗死患者于发病后24h内清晨空腹抽血;另有15例健康体检者,其中男9例,女6例,平均年龄69.87±7.14岁,清晨空腹抽血,检测血浆pentraxin-3水平。所有研究对象均排除感染、肿瘤,全身免疫疾病,严重肝、肾疾病。pentraxin-3检测采用夹心ELISA法,试剂由美国Elixes公司提供。比较两组血浆pentraxin-3水平。所有急性心肌梗死患者于入院当时、6h、12h、24h、48h、72h抽血检测肌酸激酶水平。取其最高值为肌酸激酶峰值。所有急性心肌梗死患者在其入院后2周行超声心动图检查测射血分数。所有数据输入SPSS统计包,计量资料用x±s表示,组间比较用t检验。pentraxin-3与肌酸激酶峰值、射血分数之间行相关分析。结果急性心肌梗死患者血pentraxin-3水平为6.96±2.64μg/L,明显高于健康体检者2.67±0.86μg/mL,差异有显著性(P<0.01)。急性心肌梗死患者肌酸激酶浓度为3844±869ku/L,急性心肌梗死2周后射血分数为42%±7%,pentraxin-3浓度与肌酸激酶峰值之间有正相关关系(r=0.434,P<0.01),与急性心肌梗死2周后射血分数值之间呈负相关关系(r=-0.307,P<0.05)。结论pentraxin-3是一种典型的急性时相蛋白,由多型核巨细胞、血管平滑肌细胞、巨噬细胞、内皮细胞等分泌的组织原型长链pentraxin分子,尤其是在动脉粥样斑块上表达。本研究急性心肌梗死患者pentraxin-3较正常对照组明显升高,说明作为炎症因子pentraxin-3在急性心肌梗死患者中表达明显。pentraxin-3浓度与肌酸激酶峰值之间呈正相关关系,与急性心肌梗死2周后射血分数之间呈负相关关系,说明pentraxin-3与炎症和组织损伤程度成正比。

Pentraxin-3与急性冠状动脉综合征及冠状动脉病变的关系

目的了解急性冠状动脉综合征患者炎性指标pentraxin-3的变化,并了解其与冠状动脉病变之间的关系。方法回顾性研究从2003年7月到2005年9月期间85例急性冠状动脉综合征患者及25例健康体检者,检测其血浆pentraxin-3水平,并进行比较。所有急性冠状动脉综合征患者行选择性冠状动脉造影,了解pentraxin-3与冠状动脉病变之间的关系。结果急性冠状动脉综合征患者血浆pentraxin-3水平,明显高于健康体检者(P<0.01),且急性心肌梗死组高于不稳定性心绞痛组(P<0.01)。A型病变、B型病变、C型病变三种病变类型患者血浆pen-traxin-3差异无显著性。结论作为炎性指标,pentraxin-3与冠心病发生急性冠状动脉综合征密切相关,但与冠状动脉病变类型无明确相关。

急性冠脉综合征患者pentraxin-3与凝血酶活化的纤溶抑制物的变化

目的了解急性冠脉综合征(Acute Coronary Syndrome,ACS)患者炎性指标pentraxin-3与纤溶指标凝血酶活化的纤溶抑制物(Thrombin activatable finolysis inhibitor,TAFI)的变化。方法检测比较102例急性心肌梗死(AMI组)、81例不稳定心绞痛(UAP组)及23例健康体检者(对照组)的血浆pentraxin-3、TAFI水平。结果急性冠脉综合征患者血浆pentraxin-3、TAFI明显高于对照组,差异有统计学意义(P<0.01);AMI组血浆pentraxin-3及TAFI水平高于UAP组,差异有统计学意义(P<0.05)。pentraxin-3浓度与TAFI浓度呈正相关(r=0.17,P<0.05)。结论 pentraxin-3与TAFI共同在ACS的发生发展中起重要作用。

2型糖尿病患者Pentraxin-3与尿白蛋白相关性的研究

目的:分析2型糖尿病患者Pentraxin-3(PTX3)与尿白蛋白的相关性,探讨PTX3在糖尿病肾病中的作用。方法:2型糖尿病患者115例,根据尿白蛋白排泄率(UAER)分成正常白蛋白尿组、微量白蛋白尿组与临床白蛋白尿组,分别检测3组PTX3、血糖、血脂、HS-CRP、γ-谷氨酰转移酶等。结果:微量白蛋白尿组PTX3水平显著高于正常白蛋白尿组(P<0.01),临床白蛋白尿组PTX3水平显著高于正常白蛋白尿组和微量白蛋白尿组(P<0.01),PTX3与UAER呈正相关(r=0.667,P<0.01)。各组间年龄、FPG、TG、GGT、HS-CRP比较差异有统计学意义(P<0.05)。结论:PTX3水平与白蛋白尿相关,PTX3有助于糖尿病肾病的早期诊断。2型糖尿病患者PTX3水平升高是一个重要的危险因素。

帕金森病患者血清pentraxin-3含量变化及其临床意义

目的探讨帕金森病(PD)患者血清中pentraxin-3的变化及其临床意义。方法采用酶联免疫吸附法(ELISA)检测40例健康体检者(对照组)和98例PD患者(PD组)血清pentraxin-3和胶质纤维酸性蛋白(GFAP)水平。并采用Sperman等级相关分析pentraxin-3水平与PD组各因素的相关性。结果 PD组血清pentraxin-3和GFAP浓度均明显高于对照组,差异均有统计学意义(t分别=2.85、2.12,P均<0.05);观察组内血清pentraxin-3浓度与年龄、病程、Hoehn-Yahr分级、UPDRSⅠ、GFAP无相关性(r分别=0.62、0.73、0.49、0.55、0.44,P均>0.05),与UPDRSⅡ、UPDRSⅢ呈正相关(r分别=0.57、0.64,P均<0.05)。结论血清pentraxin-3检测可作为判断帕金森病病情的指标之一。

速度350km/h高速铁路长大下坡地段闭塞分区设置方法研究

通过分析长大下坡道闭塞分区长度对CTCS-3级和后备CTCS-2级列控系统的影响,指出二者对闭塞分区长度的需求完全相反,并针对CTCS-3级列控系统的行车许可回缩、速度突降等问题的产生原因进行分析。阐述坡度、闭塞分区长度与不同列控模式下列车运行速度、追踪间隔时间等要素之间的关系,制定闭塞分区设置的基本原则。检算典型坡度下闭塞分区长度设置的合理区间范围及相应追踪间隔时间,指出坡度超过-30‰后将无法兼顾不同列控等级下的运行速度。设计模拟退火算法,根据闭塞分区设置原则及闭塞分区取值规律,给出压缩求解空间、提高求解效率的方法。以郑万高速铁路长大下坡地段为例,对闭塞分区设置进行优化,在不考虑其他约束的前提下,与设计院优化方案相比,本求解优化方案在确保CTCS-3级控车模式下允许速度可达350 km/h的同时,将CTCS-2级控车模式下的允许速度提高30 km/h,追踪间隔时间压缩23 s。

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.

Synthesis and Luminescence of SrZnO_2∶Eu^(3+), Li^+ Phosphor by Long Wavelength UV Excitation

SrZnO2 ： Eu^3 ＋ , Li^＋ phosphor powder by long wavelength UV excitation was synthesized by conventional solid-state reaction method. XRD and PL were employed to characterize their properties. The resuits show that Eu^3＋ ions preferentially occupy Sr^2＋ asymmetry cationic sites, thus emitting 612 nm red light originated from ^5D0 to ^7F2 transition. The luminescent intensity can be greatly enhanced with incorporation of Li^＋ ions. The excitation efficiency in range of 350 - 400 nm also increases greatly due to incorporating Li ^＋ ions. SrZnO2 ： Eu^3 ＋ , Li^＋ is a promising redemitting phosphor by long wavelength UV excitation.

LncRNA MALAT1通过靶向miR-146a调节PI3K/Akt信号通路影响胃癌细胞的增殖、迁移和侵袭

目的 探究长链非编码RNA(long non-coding RNA,LncRNA)肺腺癌转移相关转录子1(metastasis-associated lung adenocarcinoma transcript 1,MALAT1)通过调节miR-146a对胃癌(gastric cancer, GC)细胞的增殖、迁移和侵袭的影响及其机制。方法 收集GC组织和配对正常胃上皮组织,将GC细胞MNK-45分为空白对照(blank control, BC)组(未转染)、MALAT1 siRNA-NC组(转染MALAT1 siRNA-NC)、MALAT1 siRNA组(转染MALAT1 siRNA)、miR-146a mimics-NC组(转染miR-146a mimics-NC)、miR-146a mimics组(转染miR-146a mimics)、MALAT1 siRNA+miR-146a inhibitor-NC组(共转染MALAT1 siRNA+miR-146a inhibitor-NC)、MALAT1 siRNA+miR-146a inhibitor组(共转染MALAT1 siRNA+miR-146a inhibitor)。定量荧光PCR(qRT-PCR)检测胃组织或细胞中MALAT1、miR-146a表达量;CCK-8法和克隆形成实验检测细胞增殖能力;Transwell法检测细胞侵袭和迁移能力;RNA pull down实验、双荧光素酶报告实验分析MALAT1和miR-146a的结合情况;Western blot检测磷脂酰肌醇3激酶(phosphatidylinositol 3-kinase, PI3K)/蛋白激酶B(protein kinase B,Akt)通路蛋白及c-Myc、基质金属蛋白酶9(matrix metalloproteinase 9,MMP9)蛋白表达量。结果 转染MALAT1 siRNA可明显降低MNK-45细胞的MALAT1表达量,敲低MALAT1或过表达miR-146a可降低细胞活力、克隆能力、迁移和侵袭,增加miR-146a表达,降低PI3Kp85α、PI3Kp85β、c-Myc、MMP9蛋白表达量及p-Akt/Akt水平;MALAT1可结合并靶向下调miR-146a表达;低表达miR-146a可逆转敲低MALAT1对MNK-45细胞增殖、迁移和侵袭的抑制效应。结论 MALAT1可能作为ceRNA吸附并降解miR-146a,敲低MALAT1可上调miR-146a表达,并通过PI3K/Akt通路抑制GC细胞增殖、迁移和侵袭。

Long Non-coding RNA MEG3 Induces Renal Cell Carcinoma Cells Apoptosis by Activating the Mitochondrial Pathway

Summary： This study aimed to examine the effect of long non-coding RNA （LncRNA） MEG3 on the biological behaviors of renal cell carcinoma （RCC） cells 786-0 and the possible mechanism. MEG3 expression levels were detected by RT-qPCR in Rmaor tissues and adjacent non-tumor tissues from 29 RCC patients and in RCC lines 786-0 and SN12 and human embryonic kidney cell line 293T. Plasmids GV144-MEG3 （MEG3 overexpression plasmid） and GV144 （control plasmid） were stably transfected into 786-0 cells by using lipofectamine 2000. Cell viabilities were determined by MTT, cell apoptosis rates by flow cytometry following PE Annexin V and 7AAD staining, apoptosis-related protein expressions by Western blotting, and Bcl-2 mRNA by RT-qPCR in the transfected cells. The results showed that MEG3 was evidently downregulated in RCC tissues （P〈0.05） and RCC cell lines （P〈0.05）. The viabilities of 786-0 cells were decreased significantly after transfection with GV144-MEG3 for over 24 h （P〈0.05）. Consistently, the apoptosis rate was significantly increased in 786-0 cells transfected with GV144-MEG3 for 48 h （P〈0.05）. Furthermore, overexpression of MEG3 could reduce the expression of Bcl-2 and procaspase-9 proteins, enhance the expression of cleaved caspase-9 protein, and promote the release of cytochrome c protein to cytoplasm （P〈0.05）. Additionally, Bcl-2 mRNA level was declined by MEG3 overexpression （P〈0.05）. It was concluded that MEG3 induces the apoptosis of RCC cells possibly by activating the mitochondrial pathway.

血清Pentraxin-3在胃癌诊断中的应用价值

目的研究血清Pentraxin-3(PTX-3)与肿瘤相关糖类抗原(CA)724和CA199在胃癌、胃良性病变患者及健康人群中的水平,探讨其表达在胃癌诊断中的临床应用价值。方法采取电化学发光法检测80例胃癌患者(胃癌组)、80例胃良性病变患者(胃良性病变组)及40例健康者(健康对照组)血清中CA724和CA199水平,采用酶联免疫吸附试验(ELISA)检测所有研究对象血清中PTX-3水平,并分析各指标水平与胃癌患者临床病理参数之间的相关性,同时比较这3项指标联合检测对胃癌的诊断价值。结果胃癌组患者血清中CA724、CA199和PTX-3水平明显高于胃良性病变组(P<0.05)和健康对照组(P<0.01);血清中CA724、CA199和PTX-3水平均与胃癌的TNM分期、分化程度、淋巴结转移与否密切相关(P<0.05)。血清CA724、CA199和PTX-3单独检测时,灵敏度均较低,特异度较高。而多项血清指标联合检测时,CA724+CA199+PTX-3联合检测对于胃癌的诊断效果最佳,其灵敏度为95.00%,特异度为79.17%,准确度为93.00%,约登指数为0.77。结论胃癌患者血清CA724、CA199和PTX-3水平显著增加,可能参与了胃癌的发生、发展,这3项指标的联合检测可以提高临床上胃癌诊断的准确性,具有重要的临床应用价值。

急性缺血性脑卒中患者血清长链非编码RNA母系表达基因3和Zeste同源物增强子-2表达与神经功能损伤的相关性分析

目的探讨长链非编码RNA(lncRNA)母系表达基因3(MEG3)与Zeste同源物增强子-2(EZH2)在急性缺血性脑卒中(AIS)患者血清中的表达水平及其与神经功能损伤之间的关系。方法选取延安市人民医院2021年1月至2022年11月收治的92例AIS患者为脑卒中组,92例健康体检者为对照组,根据NIHSS评分将脑卒中组患者分为致残性损伤组19例,非致残性损伤组73例。采用实时荧光定量聚合酶链式反应、酶联免疫吸附法分别检测血清lncRNAMEG3、EZH2水平。采用Spearman相关分析法进行AIS患者血清lncRNAMEG3、EZH2表达水平与美国国立卫生研究院卒中量表(NIHSS)评分之间的相关性分析;采用多因素Logistic回归分析AIS患者合并神经功能致残性损伤的影响因素,并绘制受试者工作特征(ROC)曲线分析血清lncRNA MEG3、EZH2水平对AIS患者合并神经功能致残性损伤的诊断价值。结果脑卒中组患者血清lncRNA MEG3、EZH2表达水平均高于对照组(t=11.817、11.542,P<0.05)。Spearman相关分析显示,AIS患者血清lncRNA MEG3、EZH2水平与NIHSS评分均呈正相关(r=0.540、0.603,P<0.01)。致残性损伤组体质量指数、吸烟史占比、甘油三酯、总胆固醇、同型半胱氨酸、发病-到院时间(ODT)、lncRNAMEG3、EZH2水平均高于非致残性损伤组(t/χ2=2.103、5.050、9.121、5.585、2.276、5.448、4.638、4.682,P<0.05)。多因素Logistic回归分析显示,甘油三酯、总胆固醇、lncRNA MEG3、EZH2以及ODT均是AIS患者合并神经功能致残性损伤的影响因素(OR=4.853、4.277、2.674、3.052、3.901,P<0.05)。lncRNA MEG3、EZH2联合诊断AIS患者合并神经功能致残性损伤的曲线下面积(AUC)大于lncRNAMEG3以及EZH2单独诊断的AUC(Z=2.626、2.954,P<0.01),敏感度、特异度分别为94.74%、82.15%。结论AIS患者血清lncRNA MEG3、EZH2水平均上升,与AIS患者神经功能损伤程度均正相关,可用作AIS患者合并神经功能致残性损伤的诊断指标,且联合诊断效果更好。

Preparation and Long Persistence Red Luminescence of M_ (0.2)Ca_(0.8)TiO_3∶Pr ^(3+) (M=Mg^(2+), Sr^(2+), Ba^(2+), Zn ^(2+)

M 0.2Ca 0.8TiO 3∶Pr 3+(M=Mg 2+, Sr 2+, Ba 2+, Zn 2+) long persistence red phosphors were prepared by solid state reaction. The influence of the partially replacing Ca 2+ in CaTiO 3 with Mg 2+, Sr 2+, Ba 2+, Zn 2+ on the excitation spectra, the emission spectra and the long persistence properties were studied. The results suggest that certain quantity of Mg 2+, Sr 2+, Ba 2+, Zn 2+ which partially replace Ca 2+ can enhance the luminescent intensity and prolong the afterglow persistence of the samples. The intensity of Mg 0.2Ca 0.8TiO 3∶Pr 3+ is above all of the samples. Take Mg 0.2Ca 0.8TiO 3∶Pr 3+ as the basic sample, the influence of Pr 3+ concentrations (C(Pr 3+)) on the long afterglow properties were also studied. The results suggest that when the C(Pr 3+) is 0.10% (mol fraction) the intensity of the sample is the highest. The excitation spectra of all these samples show broad band spectra ranging from 300～500 nm peaking at about 342 nm. The emission spectra also exhibit a broad band peaking at 613 nm (CaTiO 3∶Pr 3+ is 612 nm). XRD research indicates that the crystalline phases change due to the replacement of divalent metal ions.The research on the thermoluminescence spectra of Mg 0.2Ca 0.8TiO 3∶Pr 3+ indicates that the peak is at 107.35 ℃ and the depth of the trap energy is about 0 852 eV.

Yu Gan Long Ameliorates Hepatic Fibrosis by Inhibiting PI3K/AKT,Ras/ERK and JAK1/STAT3 Signaling Pathways in CCl4-induced Liver Fibrosis Rats

Yu Gan Long(YGL)is a Chinese traditional herbal formula which has been reported to attenuate liver fibrosis for many years and we have explored its anti-fibrotic mechanism through blocking transforming growth factor(TGF-β)in the previous study.But the mechanisms associated with platelet-derived growth factor(PDGF)-BB remain obscure.In this study,we further investigated the mechanism of YGL reducing carbon tetrachloride(CCl4)-induced liver fibrosis in rats.Our results showed that YGL suppressed CCl4-induced upregulation of collagen IV(Col IV),type HI precollagen(PCHI),hyaluronuc acid(HA)and laminin(LN),which are implicated in liver fibrosis.Also,YGL reduced theα-smooth muscle actin(α-SMA)expression,which acts as the indicator of liver fibrosis.Furthermore,YGL decreased the serum levels of hepatic stellate cell(HSC)mitogen PDGF-BB and inflammation cytokines,including TNF-α,IL-1β,IL-6.Markers involved in liver fibrosis,such as Ras,p-Raf-1,p-ERK1/2,p-JNK,p-P38,p-PI3K,p-AKT,p-JAKl,p-STAT3 were downregulated significantly after treatment with YGL.Our results indicated that YGL ameliorated CCl4-induced liver fibrosis by reducing inflammation cytokines production,and suppressing Ras/ERK,PI3K/AKT,and JAK1/STAT3 signaling pathways,which provided further evidence towards elucidation of the anti-fibrotic mechanism of YGL.

Lipopolysaccharide Challenge Induces Long Pentraxin 3 Expression in Mice Independently from Acute Lung Injury

Objective To determine whether the onset of acute lung injury （ALl） induces the up-regulation of pentraxin 3 （PTX3） expression in mice and whether PTX3 concentration in the biofluid can help recognizing sepsis-induced ALI. Methods Wild-type C57BL/6 mice （12-14 weeks old） were randomly divided into 3 groups. Mice in the group 1 （n=12） and group 2 （n=12） were instilled with lipopolysaccharide via intratracheal or intraperitoneal routes, respectively. Mice in the group 3 （n=8） were taken as blank controls. Pulmonary morphological and functional alterations were measured to determine the presence of experimental ALl. PTX3 expression in the lung was quantified at both protein and mRNA levels. PTX3 protein concentration in blood and bronchoalveolar lavage fluid was measured to evaluate its ability to diagnose sepsis-induced ALI by computing area under receiver operator characteristic curve （AUROCC）. Results ALl was commonly confirmed in the group 1 but never in the other groups. PTX3 expression was up-regulated indiscriminately among lipopolysaccharide-challenged mice. PTX3 protein concentration in the biofluid was unable to diagnose sepsis-induced ALl evidenced by its small AUROCC. PTX3 concentration in bronchoalveolar lavage fluid did not correlate with that in serum. Conclusions Lipopolysaccharide challenges induced PTX3 expression in mice regardless of the presence ofALI. PTX3 may act as an indicator of inflammatory response instead of organ injury per se.

Decreased expression of the long non-coding RNA HOXD-AS2 promotes gastric cancer progression by targeting HOXD8 and activating PI3K/Akt signaling pathway

BACKGROUND Long non-coding RNAs(lncRNAs) have been shown to be associated with many tumors. However, the specific mechanism of lncRNAs in the occurrence and development of gastric cancer(GC) has not been fully elucidated.AIM To explore the expression level and molecular mechanism of HOXD-AS2 in GC tissues and cells, and analyze its significance in the prognosis of GC.METHODS Real-time quantitative PCR was used to detect the expression of HOXD-AS2 in 79 pairs of GC tissues and five cell lines. The pc HOXD-AS2 plasmid vector was constructed and transfected into SGC-7901 and SNU-1 GC cells. Matrigel Transwell and wound healing assays were used to confirm the effect of HOXDAS2 on invasion and migration of GC cells. Cell counting kit-8 assay and flow cytometry were used to verify the effect of HOXD-AS2 on the proliferation, cell cycle, and apoptosis of GC cells. The relevant regulatory mechanism between HOXD-AS2 and HOXD8 and PI3K/Akt signaling pathway was verified by Western blot analysis.RESULTS The low expression of lncRNA HOXD-AS2 was associated with lymph node metastasis and tumor-node-metastasis stage in GC. In vitro functional experiments demonstrated that overexpression of HOXD-AS2 inhibited GC cell progression. Mechanistic studies revealed that HOXD-AS2 regulated the expression of its nearby gene HOXD8 and inhibited the activity of the PI3K/Akt signaling pathway.CONCLUSION These results indicate that downregulation of HOXD-AS2 significantly promotes the progression of GC cells by regulating HOXD8 expression and activating the PI3K/Akt signaling pathway. HOXD-AS2 may be a novel diagnostic biomarker and effective therapeutic target for GC.

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.

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.

Long noncoding RNA negative regulator of antiviral response contributes to pancreatic ductal adenocarcinoma progression via targeting miR-299-3p

BACKGROUND Pancreatic ductal cancer(PDAC)has high malignancy and poor prognosis.Long noncoding RNAs(lncRNAs)are associated with high levels of malignancy,including PDAC.However,the biological and clinical significance of negative regulator of antiviral response(NRAV)in PDAC is unclear.AIM To study the regulatory role of lncRNA NRAV in PDAC.METHODS GEPIA analyzed lncRNA NRAV and miRNA(miR-299-3p)expression levels in PDAC tissues and measured them in PDAC cells by quantitative measurements in real time.The specific role of NRAV and miR-299-3p in cell proliferation and transfer potential was evaluated by cell formation analysis,Cell Counting Kit-8 and Transwell analysis.The relationship between NRAV and miR-299-3p was studied by predictive bioinformatics,RNA immunoassay,and fluorescence enzyme analysis.In vivo experiments included transplantation of simulated tumor cells under naked mice.RESULTS The expression level of lncRNA NRAV was higher in both tumor tissues and cell lines of PDAC and was negatively associated with the clinical survival of PDAC patients.Functionally,overexpression of NRAV promoted cell proliferation and metastasis of PDAC cells,while knockdown of NRAV reversed these effects.Finally,NRAV was performed as a molecular sponge of miR-299-3p.Moreover,overexpression of miR-299-3p could reverse the promoting effects of NRAV on cell proliferation and metastasis of PDAC cells.CONCLUSION NRAV facilitates progression of PDAC as a molecular sponge of miR-299-3p and may be a potential molecular marker for diagnosis and treatment of PDAC.