AG490

摘要： 目的 探讨JAK2/STAT3通路抑制剂AG490及DNA甲基化抑制剂5-Aza对血小板源性生长因子-BB(PDGF-BB)诱导的大鼠肺动脉平滑肌细胞(PASMCs)增殖的影响及意义.方法 采用CCK8检测不同浓度AG490及5-Aza对PDGF-BB诱导PASMCs增殖的影响;将细胞分为对照组(正常的PASMCs)、0μM组(予30 μg/L PDGF-BB孵育48h)和25μM/1μM组、50μM/3μM组、100μM/5μM组(25μM/1μM组、50μM/3μM组、100μM/5μM组分别给予25/1、50/3、100/5μmol/L AG490/5-Aza共同孵育细胞).采用RT-qPCR检测IL-6、GATA6、JAK2及STAT3 mRNA表达水平;Western blot检测GATA6、p-JAK2及p-STAT3蛋白的表达.结果 与对照组比较,0μM AG490组IL-6、JAK2、STAT3mRNA表达均增加,GATA6mRNA及蛋白水平降低,p-JAK2/JAK2和p-STAT3/STAT3表达升高(P＜0.05).与0μM AG490组比较,25、50、100μM AG490组细胞增殖减少,IL-6、JAK2和STAT3mRNA的表达均降低,GATA6mRNA及蛋白表达升高,p-JAK2/JAK2水平降低(均P＜0.05),50和100μM组中p-STAT3/STAT3水平降低(均P＜0,05);与0μM 5-Aza组相比,1μM、3μM、5μM 5-Aza组细胞增殖减少,IL-6mRNA表达降低,GATA6蛋白、p-STAT3/STAT3表达增高,p-JAK2/JAK2水平降低(均P＜0.05),JAK2、STAT3mRNA水平无显著差异(P＞0.05);3μM和5μM 5-Aza组中GATA6mRNA表达增高(P＜0.05).结论 AG490及5-Aza对PDGF-BB诱导的PASMCs增殖具有抑制作用,该作用可能与阻断JAK2/STAT3信号通路,抑制IL-6调节GATA6启动子甲基化有关.

摘要： 目的 研究JAK2/STAT3信号转导通路在子宫内膜异位症(EMS)发展过程中的作用.方法 将60只大鼠随机分为假手术组、模型组、JAK2/STAT3通路抑制剂组(AG组),每组20只.模型组、AG组大鼠通过自身子宫内膜移植建立EMS模型.AG组造模前给予AG4901 mg/kg,手术后给予AG4904 mg/kg,每周2次,连续4周;模型组给予生理盐水.处理结束后记录各组大鼠异位内膜体积,计算异位内膜生长抑制率,HE染色观察病理改变;蛋白质印迹法(Western blot)检测内膜组织中p-JAK2、JAK2、p-STAT3、STAT3蛋白表达水平.结果 治疗后AG组异位内膜组织生长发育不良,异位内膜体积明显小于模型组,异位内膜生长的抑制率为65.66％.Western blot结果显示,EMS模型大鼠异位内膜病灶中JAK2、STAT3总蛋白及其磷酸化水平(p-JAK2/JAK2、p-STAT3/STAT3)明显高于假手术组;而AG组大鼠异位内膜病灶中JAK2、STAT3总蛋白及其磷酸化水平明显低于模型组.结论 JAK2/STAT3通路在EMS发病过程中可能发挥了重要作用,而抑制JAK2/STAT3信号通路则能够对EMS的治疗产生积极作用.

摘要： 目的 :在本研究中,采用单剂量腹腔注射奥沙利铂诱发急性神经病理性疼痛为模型,观察p-STAT3信号分子的激活情况,并探讨JAK/STAT信号通路抑制剂AG490对该疼痛模型的影响.方法 :利用大鼠机械性缩足反射阈值(paw withdrawal threshold,PWT)和冷热刺激甩尾潜伏期(tail withdrawal latency,TWL)检测大鼠的疼痛行为学变化;采用免疫印记法和免疫荧光法检测大鼠脊髓p-STAT3的表达.结果:与对照组比较,奥沙利铂注射后第1～5天PWT和TWL(冷)显著性缩短(P<0.05),TWL(热)未见明显改变;脊髓p-STAT3的表达显著性增加(P<0.05).与奥沙利铂组比较,AG490组PWT和TWL(冷)显著性延长(P<0.05),而脊髓p-STAT3的表达显著性减少(P<0.05).结论:p-STAT3参与了奥沙利铂致急性神经病理性疼痛的形成,并且AG490可缓解奥沙利铂导致的急性神经病理性疼痛.%Objective: To investigate the activation of spinal phosphorylated STAT3 (p-STAT3) in the model of oxaliplatin-induced acute neuropathic pain in rats and observe the analgesic effect of AG490 in this pain model. Methods: Paw withdrawal threshold (PWT) and tail withdrawal latency (TWL) were used to detect the me-chanical and thermal nociceptive behaviors. The expression of p-STAT3 was detected by western blotting and immunofluorescence. Results: PWT and TWL were significantly decreased after the treatment of oxaliplatin in rats (P < 0.05 vs. control group). At the same time, the expression of p-STAT3 in the spinal cord was significant-ly increased in oxaliplatin group, compared with the control group (P < 0.05). Instead, compared with oxaliplatin group, in AG490 group, the PWT and TWL were significantly increased and the expression of p-STAT3 in the spinal cord was significantly decreased. Conclusion: The p-STAT3 may be involved in the formation of oxal-iplatin-induced acute neuropathic pain, which could be alleviated by AG490.

摘要： 目的 测定蛋白酪氨酸激酶2/信号转导和转录激活因子3(JAK2/STAT3)、信号通路特异性拮抗剂α-氰基-(3,4-羟基)N-苄苯乙烯胺(AG-490)对大鼠脑出血周围组织血管内皮生长因子165(VEGF165)、磷酸化蛋白酪氨酸激酶2(P-JAK2)、磷酸化信号转导和转录激活子3(P-STAT3)表达的影响,分析VEGF165与P-JAK2、P-STAT3的相关性,探讨VEGF165对大鼠脑出血后的神经保护作用是否由JAK2/STAT3信号通道介导.方法 将健康雄性Sprague-Dawley(SD)大鼠75只随机分为假手术组、脑出血组和AG-490组.采用大鼠自体血注入法建立脑出血模型;各组按造模成功后时间分为6h、24 h、48 h、72 h、7d5个亚组,比较各组大鼠进行神经功能缺损评分(NSS);免疫组化染色检测血肿周围VEGF165表达,采用Western blotting检测大鼠血肿周围脑组织P-JAK2、P-STAT3的表达.结果 脑出血组和AG-490组VEGF165、P-JAK2、P-STAT表达均高于假手术组(P＜0.05),并于造模后48 h达高峰(P＜0.05);AG-490组VEGF165、P-JAK2、P-STAT表达较脑出血组低(P＜0.05);脑出血组VEGF165的表达与神经功能的缺损评分呈负相关(r=-0.511,P＜0.05),VEGF165与P-JAK2、P-STAT3的表达呈正相关(r=0.562,P＜0.05;r=0.479,P＜0.05).结论 VEGF165对大鼠脑出血后的神经保护作用可能是由JAK2/STAT3途径介导.

摘要： 目的 探讨酪氨酸激酶(JAK)-信号转导及转录激活因子(STAT)信号转导通路阻断剂α-氰基-(3,4-羟基)N-苄苯乙烯胺(AG490)对肺癌Lewis细胞增殖、凋亡的影响及作用机制.方法 不同浓度AG490(0、20、40、80、160μmol/L)作用于肺癌Lewis细胞24、48 h,噻唑蓝(MTT)实验观察各组细胞的增殖情况,流式细胞术检测0、40、80μmol/L组细胞凋亡率,Western印迹检测0、80μmol/L组细胞STAT3、STAT5、Survivin蛋白表达.结果 AG490作用24和48 h,与0μmol/L组相比,20、40、80、160μmol/L组细胞的增殖抑制率显著升高(P0.05).作用24和48 h时,40、80μmol/L组细胞凋亡率显著高于0μmol/L组(P<0.05),80μmol/L组显著高于40μmol/L组;40、80μmol/L组作用24 h的细胞凋亡率显著低于48 h(P<0.05).80μmol/L组细胞中STAT3、STAT5、Survivin的表达量均显著低于0μmol/L组(P<0.05).结论 一定浓度和时间范围内,AG490可显著抑制细胞的增殖,促进其凋亡,阻断JAK-STAT通路中STAT3、STAT5蛋白的表达水平,进而降低其下游凋亡抑制蛋白Survivin的表达可能是其作用机制之一.

摘要： Objective To study the effect of Jak2-STAT3 pathway on cell proliferation,migration,mineralization and bone defect healing via simulating Jak2-STAT3 pathway inhibitor AG490 to bone marrow mesenchymal stem cells (BMSC) and bone defect mice models.Methods The effect of AG490 on BMSC proliferation was measured by MTT (methyl thiazolyl tetrazolium) assay.Regulation of AG490 on BMSC migration was tested by scratch assay and transwell assay.The BMSC migration related gene,matrix metalloproteinase (MMP)-7,MMP-9 and CXC subfamily receptor 4 (CXCR4),regulated by AG490 was studied by real-time PCR.Western blotting was adopted to analyze the regulation of Jak2-STAT3 phosphorylation through the simulation of AG490.The alizarin red staining and alkaline phosphatase (ALP)activity assay were performed to measure the effect of AG490 on BMSC mineralization and osteogenic differentiation.Mice femur bone defect models were built to analyzed the effect of AG490 on bone remodeling.Results AG490 significantly suppressed the migration rate of BMSC at 1 d and 2 d in the experiment group [(12.42±7.50) ％,(41.8±2.6)％] compared with the control group [(55.5±9.9)％,(86.9±8.7)％] in scratch assay (P=0.000,P=0.000),the number of migrated BMSC in the experiment group (22.8±5.9) was significantly suppressed compared with the control group (58.3±6.6) in Transwell assay (P=0.000).The expression of MMP-7,MMP-9 and CXCR4 were significantly downregulated in experiment group [(0.5±0.1),(0.1±0.1) and (0.35±0.07)] compared with the control group [(1.1±0.1),(1.06±0.33),(1.08±0.13)] (P=0.0003,P=0.000 and P=0.000).Also,the phosphorylation of Jak2-STAT3 was downregulated by AG490 in western blotting.After BMSCs were osteogenic induced for 14 days,the formation of mineralized nodule and the ALP activity of BMSC is significantly suppressed in experiment group (8.0±2.1) compared with the control group (35.7± 1.8)(P=0.0005).AG490 suppressed the bone defects healing,the expression level of phosphorylated Jak2 and phosphorylated STAT3,and the number of alkaline phosphatase positive cell at defect area in vivo is lower in experiment group than the control group.AG490 suppressed the relatively bone density at the defect area significantly (P=0.0004) at 5th week after the surgery.Conclusions AG490 could suppress proliferation,migration and mineralization to of BMSCs regulate bone defect healing via inhibiting Jak2-STAT3 pathway.%目的 探讨Jak2-STAT3信号通路抑制剂AG490对骨髓间充质干细胞(bone marrowmesenchymal stem cell,BMSC)迁移、矿化及骨缺损愈合的调控机制.方法 应用甲基噻唑基四唑(methyl-thiazolyl tetrazolium,MTT)实验、细胞划痕实验及Transwell实验检测AG490对小鼠来源的原代BMSC增殖和迁移能力的调控.荧光定量PCR和蛋白质印迹法研究AG490调控BMSC增殖和迁移的相关基因及通路机制.通过茜素红染色及碱性磷酸酶活性实验探究AG490对BMSC矿化及成骨向分化能力的影响.构建小鼠股骨缺损模型,研究AG490对骨缺损愈合的影响及机制.结果 细胞划痕实验中第1、2天实验组[(12.42±7.50)％,(41.8±2.6)％]的细胞迁移率均显著小于对照组[(55.5±9.9)％,(86.9±8.7)％](P=0.006,P=0.005),Transwell实验中实验组[(22.8±5.9)个]中单位视野细胞迁移数显著少于对照组[(58.3±6.6)个](P=0.000).实验组MMP-7(0.5±0.1)、MMP-9 (0.1 ±0.1)及CXCR4 (0.35±0.07)的相对基因表达量均显著少于对照组[(1.1±0.1),(1.06±0.33),(1.08±0.13)] (P=0.0000,P=0.0003,P=0.0000).蛋白质印迹法结果中实验组磷酸化Jak2、磷酸化STAT3的蛋白表达在AG490的作用下与对照组相比受到明显抑制.BMSC矿化诱导14d后,实验组的碱性磷酸酶相对活性(8.0±2.1)较对照组(35.7±1.8)受到显著抑制(P=0.0005),实验组较对照组矿化结节小且数量较少.体内实验中,术后第5周时,实验组的相对骨密度显著低于对照组(P=0.0004).HE染色及免疫组化染色可见实验组中骨缺损断端处磷酸化Jak2、磷酸化STAT3和碱性磷酸酶阳性细胞较对照组稍多.结论 AG490可通过抑制Jak2-STAT3信号通路抑制BMSC的增殖、迁移和矿化,从而调控骨缺损愈合.

摘要： Objective To investigate the effects of JAK inhibitors on the inflammatory response of lung tissue and the activation of JAK/STAT signaling transduction pathway in lung injury induced by traumatic shock tissue in rabbits by establishing the rabbits model.Methods The rabbit model of lung injury induced by traumatic shock was established.The rabbits were divided into three groups: control group, model group and AG490 group.The pathological findings were observed by hematoxylin-eosin staining.ELISA kit was used to detect the expression of IL-6 in serum.The expressions of CC16, JAK2 and STAT3 mRNA and protein were detected by RT-PCR and Western blotting, respectively.Results Inflammatory cell infiltration was observed in parts of lung of model group, and decreased in AG490 group.The levels of IL-6, IL-1, TNF-α in serum were increased in model group and getting down in AG490 group.The protein levels of CC16, JAK2 and STAT3 in model group were significant higher than those in control group, and their levels represented a downward trend in AG490 group.The expressions of these genes represented the same trend as the protein.Conclusion AG490 can alleviate the inflammation and lung injury induced by traumatic shock by inhibiting the JAK/STAT3 signaling pathway.%目的 本研究将JAK抑制剂AG490应用于兔创伤性休克致肺损伤动物模型,探索JAK抑制剂对兔创伤性休克致肺损伤中肺组织炎症反应的影响.方法 建立兔创伤性休克致肺损伤动物模型;HE染色检测肺组织损伤状况;ELISA检测血清中IL-6、IL-1、TNF-α的表达情况;蛋白免疫印迹实验观察肺组织中CC16、JAK2和STAT3蛋白的表达情况;RT-PCR实验观察肺组织中Clara 细胞分泌蛋白(Clara cell secretion protein, CC16)、JAK2和STAT3基因的表达情况.结果 HE染色结果显示,与对照组比较,模型组出现明显炎性细胞浸润,而AG490组的炎症反应则减轻;ELISA结果显示,血清中IL-6、IL-1、TNF-α因子的表达在模型组升高,分别从(99.64±6.33)、(65.42±6.71)、(76.95±8.41)pg/mL,上升到(675.39±26.42)、(498.77±21.58)、(703.82±32.67)pg/mL,差异有统计学意义(P<0.05);而AG490组则比模型组下降,分别为(278.51±11.69)、(202.34±18.36)、(257.65±14.18)pg/mL;蛋白免疫印迹实验可见模型组CC16、JAK2和STAT3的蛋白表达与对照组比较均明显升高,且差异有统计学意义,而AG490阻断JAK/STAT信号通路后,CC16、JAK2和STAT3的蛋白表达均明显下降;RT-PCR实验结果表明,模型组CC16、JAK2和STAT3的基因表达和AG490阻断组CC16、JAK2和STAT3的基因表达趋势与蛋白表达相一致.结论 AG490可以通过抑制JAK/STAT3信号通路缓解创伤性休克所致肺损伤的发生,并且可以抑制肺部炎症反应.

摘要： AIM:To investigate whether angiotensin (1-7) [Ang-(1-7)] protects human umbilical vein endo-thelial cells (HUVECs) against high glucose-induced injury by inhibiting JAK/STAT signaling pathway .METHODS:The cell viability was examined by CCK-8 assay.The expression levels of JAK2, STAT3, p-JAK2, p-STAT3, cleaved caspase-3 and endothelial nitric oxide synthase ( eNOS) were detected by Western blot .The number of apoptotic cells was observed by photofluorography with Hoechst 33258 nuclear staining.The intracellular levels of reactive oxygen species (ROS) were tested by DCFH-DA staining followed by photofluorography .RESULTS:Expose of the HUVECs to high glucose (40 mmol/L) for different time significantly increased phosphorylation level of JAK 2 which reached the peak at 24 h.The protein level of p-STAT3 significantly increased at 24~48 h and reached the peak at 36 h.The expression of cleaved caspasep-3 was signifi-cantly up-regulated at 12~24 h, and the expression of eNOS gradually decreased at 3~48 h with prolongation of time .Pre-treatment of the HUVECs with Ang-(1-7) at 2μmol/L or AG490 (an inhibitor of JAK/STAT pathway) at 20μmol/L for 0.5 h before exposure of the cells to high glucose for 24 h markedly attenuated high glucose-induced injury of the HUVECs , by in-creasing the cell viability and eNOS expression , and decreasing the apoptotic cells , ROS production and cleaved caspase-3 expression.Furthermore, pretreatment with Ang-(1-7) for 0.5 h also decreased the protein levels of p-JAK2 and p-STAT3.CONCLUSION:Ang-(1-7) protects the HUVECs against high glucose-induced injury by inhibiting JAK/STAT signaling pathway .%目的:研究血管紧张素(1-7)[Ang-(1-7)]能否通过抑制JAK/STAT信号通路对抗高糖诱导的人脐静脉内皮细胞(HUVECs)损伤.方法:CCK-8检测细胞存活率;Western blot法检测内皮细胞JAK2、STAT3、p-JAK2、p-STAT3、cleaved caspase-3和内皮型一氧化氮合酶(eNOS)的蛋白水平;Hoechst 33258染色荧光显微镜照相法检测内皮细胞凋亡数量;DCFH-DA染色荧光显微镜照相法检测内皮细胞内活性氧簇(ROS)的水平.结果:应用高糖(40 mmol/L)处理HUVECs 12~48 h能明显上调JAK2的磷酸化水平,于24 h达最高峰;在24~48 h能明显上调STAT3的磷酸化水平,于36 h最高;在12~24 h能明显上调cleaved caspase-3的表达,在3~48 h随着时间延长,eNOS的表达逐渐降低.2μmol/L的Ang-(1-7)或20μmol/L的JAK/STAT通路抑制剂AG490预处理0.5 h可显著抑制由高糖引起的内皮细胞损伤,表现为p-STAT3、p-JAK2及cleaved caspase-3蛋白水平降低、细胞存活率及eNOS表达升高,细胞凋亡数量和胞内ROS生成减少.结论:Ang-(1-7)能通过抑制JAK/STAT通路对抗高糖诱导的人脐静脉内皮细胞损伤.

摘要： Objective To explore the effect of JAK / STAT3 signaling pathway inhibitor AG490 in traumatic shock induced kidney damage. Methods A total of 30 New Zealand rabbits were divided into control group, model group and AG490 treatment group,with 10 rats in each group. Rabbits were made traumatic shock and kidney damage in model group and AG490 treatment group. To detect the expression of STAT3,Kim-1 and TGF-β1 in kidney tissues via real-time quantitative PCR and western blot. Results Compared with control group,renal creatinine and urea nitrogen levels in model group were significantly higher than those in the control group(P<0. 05);compared with the model group,serum creatinine and blood urea nitrogen levels in AG490 treatment group were significantly lower(P<0. 05);compared with the control group,levels of expression of STAT3 and TGF-β1 mRNA protein in kidney tissue in the model group were significantly increased ( P<0. 05);compared with the model group,STAT3 and TGF-β1 mRNA and protein expression level in AG490 treatment group were significantly reduced(P<0. 05). Conclusion AG490 may be blocked by TGF-β1 activated in JAK/STAT3 signaling pathway,thereby inhibiting the development of traumatic shock and kidney damage.%目的：探讨JAK/STAT3抑制剂AG490对创伤性休克致兔肾损伤的影响。方法将30只健康新西兰兔分为对照组、模型组与AG490治疗组,每组10只。模型组与AG490治疗组兔建立创伤性休克致肾损伤动物模型。通过实时荧光定量聚合酶链反应( Real-time PCR)和蛋白质印迹法( Western-blot)检测肾组织中STAT3、Kim-1、TGF-β1的表达情况。结果与对照组比较,模型组肾组织肌酐与尿素氮水平显著高于对照组,差异有统计学意义(P<0．05)；与模型组比较,AG490治疗组肌酐与尿素氮水平显著降低,差异有统计学意义(P<0．05)；与对照组比较,模型组脏组织中STAT3、TGF-β1的mRNA与蛋白表达水平显著升高,差异有统计学意义(P<0．05)；与模型组比较,AG490治疗组STAT3、TGF-β1的mRNA与蛋白表达水平显著降低,差异有统计学意义(P<0．05)。结论 JAK/STAT3抑制剂可能通过TGF-β1来阻断JAK/STAT3信号通路的激活,进而抑制创伤性休克肾损伤发展。

摘要： 目的:研究p-STAT3的活化在结肠癌中的表达与Snail、MMP2的相关性,及其在离体细胞实验中激活受抑后对结肠癌细胞迁移能力的影响并探讨其机制.方法:免疫组织化学染色检测p-STAT3与Snail、MMP2的表达及其相关性,分析三者与TNM分期、远处转移、淋巴结转移及分化程度之间的关系;MTT实验筛选AG490对增殖无影响的浓度和时间,并用该浓度和时间进行后续实验;采用Western blot法检测AG490抑制p-STAT3活化后STAT3、Snail、MMP2蛋白表达情况;划痕实验观察p-STAT3活化受抑后,结肠癌细胞迁移情况.结果:免疫组织化学染色结果表明,p-STAT3的表达与Snail、MMP2均存在相关性,且均与淋巴结转移相关(P0.05). STAT3 expression was not significantly changed when p-STAT3 expression was inhibited by AG490. Meanwhile, the expression levels of Snail and MMP2 were down-regulated, and the migration ability of colorectal cancer cells was significantly reduced. Conclusion: p-STAT3 promotes colorectal cancer metastasis by regulating the process of epithelial-mesenchymal transition.

摘要： 本发明涉及一种Ag合金膜形成用溅射靶、Ag合金膜、Ag合金反射膜、Ag合金导电膜及Ag合金半透明膜，该Ag合金膜形成用溅射靶的特征在于，具有如下组成：0.2原子％以上2.0原子％以下的Sb、0.05原子％以上1.00原子％以下的Mg，余量由Ag和不可避免杂质构成。

摘要： 本发明涉及Ag球、Ag芯球、助焊剂涂布Ag球、助焊剂涂布Ag芯球、焊料接头、成形焊料、焊膏、Ag糊剂以及Ag芯糊剂。提供即使含有一定量以上的Ag以外的杂质元素也α射线量少且球形度高的Ag球。为了抑制软错误并减少连接不良，将U的含量设为5ppb以下，将Th的含量设为5ppb以下，将纯度设为99.9％以上且99.9995％以下，将α射线量设为0.0200cph/cm2以下，将Pb或Bi任一者的含量、或者Pb和Bi的总含量设为1ppm以上，将球形度设为0.90以上。

摘要： 本发明的Ag合金溅射靶具有如下组分：含有0.1原子％以上且3.0原子％以下范围内的Sn、1.0原子％以上且10.0原子％以下范围内的Cu，且余量由Ag及不可避免的杂质构成。并且，本发明的Ag合金膜具有如下组分：含有0.1原子％以上且3.0原子％以下范围内的Sn、1.0原子％以上且10.0原子％以下范围内的Cu，且余量由Ag及不可避免的杂质构成。

摘要： 本发明涉及一种单罐合成Ag‑Ag2S/CdS异质结构的方法，属于功能纳米结构材料制备领域。本方法首先将碘化银、镉的前驱体和油胺混合，在140‑170oC下加热一定时间，即可得到Ag‑Ag2S/CdS异质复合纳米结构。由本发明制备方法所得的Ag‑Ag2S/CdS异质复合结构呈方块状结构，形态均匀，单分散性好，直径为13~19nm，异质复合结构能在固体基底上有序组装。本发明涉及制备方法单罐单步进行，无需中间加料，工艺简单，操作方便，重复性好，可望大规模工业化生产。这种多组分异质复合纳米结构材料兼具银、硫化银、硫化镉的性能，在光电、催化、生物标记等领域具有很好的应用前景。

摘要： 本发明公开了可低温烧结的一种近零谐振频率温度系数的低介电常数微波介质陶瓷Ag3LiTi2O6及其制备方法。（1）将纯度为99.9%（重量百分比）以上的AgNO3、Li2CO3和TiO2的原始粉末按Ag3LiTi2O6的组成称量配料；（2）将步骤（1）原料湿式球磨混合12小时，球磨介质为蒸馏水，烘干后在800°C大气气氛中预烧6小时；（3）在步骤（2）制得的粉末中添加粘结剂并造粒后，再压制成型，最后在850~880°C大气气氛中烧结4小时；所述的粘结剂采用质量浓度为5%的聚乙烯醇溶液，聚乙烯醇的添加量占粉末总质量的3%。本发明制备的陶瓷在850~880°C烧结良好，介电常数达到28.7～29.4，其品质因数Qf值高达53000-57000GHz，谐振频率温度系数近零，在工业上有着极大的应用价值。

摘要： 本发明涉及一种Ag合金膜形成用溅射靶、Ag合金膜、Ag合金反射膜、Ag合金导电膜及Ag合金半透明膜，该Ag合金膜形成用溅射靶的特征在于，具有如下组成：0.2原子％以上2.0原子％以下的Sb、0.05原子％以上1.00原子％以下的Mg，余量由Ag和不可避免杂质构成。

摘要： 本发明的Ag合金溅射靶具有如下组分：含有0.1原子％以上且3.0原子％以下范围内的Sn、1.0原子％以上且10.0原子％以下范围内的Cu，且余量由Ag及不可避免的杂质构成。并且，本发明的Ag合金膜具有如下组分：含有0.1原子％以上且3.0原子％以下范围内的Sn、1.0原子％以上且10.0原子％以下范围内的Cu，且余量由Ag及不可避免的杂质构成。

摘要： 本发明涉及Ag球、Ag芯球、助焊剂涂布Ag球、助焊剂涂布Ag芯球、焊料接头、成形焊料、焊膏、Ag糊剂以及Ag芯糊剂。提供即使含有一定量以上的Ag以外的杂质元素也α射线量少且球形度高的Ag球。为了抑制软错误并减少连接不良，将U的含量设为5ppb以下，将Th的含量设为5ppb以下，将纯度设为99.9％以上且99.9995％以下，将α射线量设为0.0200cph/cm2以下，将Pb或Bi任一者的含量、或者Pb和Bi的总含量设为1ppm以上，将球形度设为0.90以上。

摘要： 本发明公开了可低温烧结的一种近零谐振频率温度系数的低介电常数微波介质陶瓷Ag3LiTi2O6及其制备方法。（1）将纯度为99.9%（重量百分比）以上的AgNO3、Li2CO3和TiO2的原始粉末按Ag3LiTi2O6的组成称量配料；（2）将步骤（1）原料湿式球磨混合12小时，球磨介质为蒸馏水，烘干后在800°C大气气氛中预烧6小时；（3）在步骤（2）制得的粉末中添加粘结剂并造粒后，再压制成型，最后在850~880°C大气气氛中烧结4小时；所述的粘结剂采用质量浓度为5%的聚乙烯醇溶液，聚乙烯醇的添加量占粉末总质量的3%。本发明制备的陶瓷在850~880°C烧结良好，介电常数达到28.7～29.4，其品质因数Qf值高达53000-57000GHz，谐振频率温度系数近零，在工业上有着极大的应用价值。

摘要： 本发明提供了一种抗菌AG涂布液组合物，所述组合物包括丙烯酸预聚物、丙烯酸酯类单体、功能性因子；其中，相对于100重量份的功能性因子，所述丙烯酸预聚物的含量为50‑600重量份，所述丙烯酸酯类单体的含量为30‑300重量份；所述功能性因子为有机改性的无机金属氧化物。该抗菌AG涂布液组合物制备获得的抗菌AG书写膜在具有防眩功能的同时，又具有良好的抗菌作用。