TFT-LCD面板高温Cell Gap预警重力Mura

重力Mura是TFT-LCD行业顽固不良,其形成原因为Cell Gap均匀性差导致透光率不均,在视觉上呈现出色不均现象。为解决传统监控方式重力Mura不易拦截的缺陷,基于重力Mura形成原理,本文通过探究液晶量对Cell Gap的影响,Cell Gap变化的敏感区间,不同液晶量面板在高温条件下其Cell Gap随加热时间的变化趋势以及不同位置Cell Gap差异性,总结出通过高温Cell Gap变化趋势预警重力Mura的模型,为行业内预防重力Mura提供了一种全新思路。

Up-Regulation of the Gap Junction Intercellular Communication by Tea Polyphenol in the Human Metastatie Lung Carcinoma Cell Line

Our previous study has proven that tea polyphenol has a role in lung neoplasms. The present communication was to investage the anti-proliferation effect of tea polyphenol on the PG cells, which was a high metastatic human lung carcinoma cell line, by 3-(4,5)-dimethylthiahiazo(-z-y1)-3,5-diphenytetrazoliumromide (MTT) cell viability assay, and to study the change of intracellular calcium concentration, connexin43 (Cx43) expression, gap junctional intercellular communication (GJIC) and cell cycle distribution after the tea polyphenol treatment by laser scanning confocal microscopy and flow cytometry. The results showed that 1) tea polyphenol could kill the PG cells in a dose-depent manner via inhibiting the PG cell proliferation and blocking the PG cell cycle progression staying in G0/G1 phase and not transfering in S and G2/M phases to reduce the PG cell proliferation index;2) the increases of intracellular calcium concentration, GJIC and Cx43 expression were related with the tea polyphenol doses. The data suggested that tea polyphenol could inhibit the growth of PG cells, which mechanism was associated with the up-regulation of GJIC.

液晶面板中Cell-Gap不均匀性的建模分析

本文讨论液晶显示的性能,主要是指液晶单元间隙（Cell gap）的变化,其变化是产生Mura的最根本原因。本文借鉴国际上一些有关液晶面板Cell gap的研究经验,以介绍美国康宁公司的研究成果为主,总结了一套具有适用性的研究模型。该数学模型包括液晶显示的光透性,人的感知度以及实用性。本文举例分析并介绍了该模型在液晶面板设计和制造实践中的应用。

Inhibitory Effects of Rap1GAP Overexpression on Proliferation and Migration of Endothelial Cells via ERK and Akt Pathways

Rapl is expressed in human umbilical vein endothelial cells （HUVECs）. Rapl-GTPase activating protein （RaplGAP）, with its specific target, Rapl, has been shown to be important in the regulation of many physiological and certain pathological processes. In this study, we investigated the effect of RaplGAP expression on endothelial cell function, or, more specifically, proliferation and migration of endothelial cells. HUVECs were transfected with pcDNA3.1 （empty vector）, pcDNA3.1 containing Flag-tagged-RaplGAP or Myc-tagged-RaplN17. The proliferation, migration and tube formation were examined and compared among the 3 groups. Expression of Rapl, RaplGAP, extracellular signal-regulated kinase （ERK）, phospho-ERK, Akt, phosphor-Akt was detected by Western blotting. The results showed that the proliferation, migration and tube formation were significantly reduced in RaplGAP- and RaplN17-transfected HUVECs as compared with empty vector-transfected control. These changes were coincident with increased expression of Rap 1GAP and decreased expression of activated Rap l, phospho-ERK and -Akt. After treatment of Rap l GAP-transfected HUVECs with a stimulator of Rapl guanine-nucleotide-exchange factor （RaplGEF） 8CPT-2＇OMe-cAMP, it was found that Rapl activity was decreased as compared with empty vector-transfected control. Pretreatment of HU- VECs with an ERK inhibitor PD98059 or a PI3K inhibitor LY294002 prior to stimulation not only blocked 8CPT-2＇OMe-cAMP-induced phosphorylation of ERK and Akt, but also significantly reduced cell proliferation and migration. Finally, we examined the effect of vascular endothelial growth factor （VEGF） on HUVECs overexpressing RaplGAP. VEGF-stimulated Rapl activity, phosphorylation of ERK and Akt, cyclin D1 expression and cell proliferation were repressed in HUVECs overexpressing RaplGAP as compared to empty vector-transfected Control. Taken together, our findings demonstrate that RaplGAP/Rapl and their downstream effectors regulate proliferation and migration of HUVECs via ERK and Akt pathways.

Cell cycle dependent regulation of gap junction coupling and apoptosis in GFSHR-17 granulosa cells

Recent results have shown that the level of gap junction coupling could modulate the induction of apoptotic reactions. We previously observed that 1H-[1,2, 4]Oxadiazole[4,3-a]quinoxalin-1-one (ODQ), a block- er of guanylyl cyclase, inhibited gap junction coupling and thereby promoted activation of characteristic apoptotic reactions such as chromatin condensation, DNA strand breaking, and formation of blebs in GFSHR-17 granulosa cells, the in vitro model for granulosa cells of the maturing ovular follicle. In the present report, we focus on the effects of ODQ with respect to the cell cycle in GFSHR-17 granulosa cells. In synchronised GFSHR-17 granulosa cells, the double whole-cell patch-clamp technique revealed that gap junction conductance in mitotic cells was reduced in comparison to cells in interphase. This reduction of gap junction conductance correlated with a reduction of non-phosphorylated Cx43 in mitotic cells. We compared the stimulation of apoptotic reactions by ODQ between cells in mitosis and in interphase. We observed that the induction of both chromatin condensation and DNA strand breaking by ODQ was increased in mitotic cells, as compared to cells in interphase. The effects of ODQ were not observed in He-La cells that do not express connexins. The results in- dicate that reduction of gap junction coupling in mitotic GFSHR-17 granulosa cells depends on phosphor- rylation of Cx43 and raises the sensitivity to stimulation of apoptosis. We propose that gap junction coupling is involved in regulation of apoptosis of granulosa cells in maturing ovular follicle.

Study on roles of gap junctional intercellular communication in low dose parat hyroid hormones-induced bone anabolism in vitro

AIM:To investigate mediating and regulatory effects of osteoblastic gap juncti onal intercellular communication(GJIC) on low-dose parathyroid hormones(PTH)-s timulated bone formation activities in vitro.METHODS:Rat calvarial osteoblasts ( ROBs) in cultures were divided into three groups according to the different mode of exposure.Group A: vehicle (sodium acetate, SA)-treated group; Group B:1×10-8 mol/L hPTH(1-34) intermittent exposure group;Group C:1×10-8 mol/L hPTH(1-34) +1×10-7mol/L TPA exposure group.48 h incubation cycles in three groups were repeated for eight times.GJIC and mineralized bone nodules formation in thr ee groups were detected using Lucifer Yellow (LY) scrape loading dye transfer (S LDT) and mineralized nodule staining together with nodule index,respectively. RE SULTS:At various measuring time points of SA×6 h in group A,PTH×6 h in group B ,PTH×6 h+1 h in group B and PTH×6 h+TPA×1 h in group C,LY(+) cell numbers were 6.8±2.5,19.5±6.5,14.0±3.6 and 5.7±2.4,respectively.Diffusion and transf er of LY fluorescent probe was much more noticeably discerned in group B than in group A and C(P< 0.01).Mineralized bone nodule indices were 45.2±12.5, 88.0±1 5.3 and 38.5±17.9 in group A,B and C respectively.Bone formation activity was m uch better revealed in group B than in group A and C (P< 0.01),whereas no statis tically significant difference of bone formation activities were found in group A compared with group C(P=0.465).CONCLUSION:Mediations and regulations of the co ordinating signals in osteoblastic network via GJIC essentially contribute to PT H-stimulated bone anabolism.However,disruption of GJIC not only hinders osteobl astic intercellular coordination but also frustrates PTH-induced bone formation activities in vitro.Therefore,GJIC may evidently play important roles in regula tions on low-dose PTH-induced bone formation.

Phenotypic changes of Schwann cells on the proximal stump of injured peripheral nerve during repair using small gap conduit tube

Dedifferentiation of Schwann cells is an important feature of the response to peripheral nerve injury and specific negative myelination reg- ulators are considered to have a major role in this process. However, most experiments have focused on the distal nerve stump, where the Notch signaling pathway is strongly associated with Schwann cell dedifferentiation and repair of the nerve. We observed the phenotypic changes of Schwann cells and changes of active Notch signaling on the proximal stump during peripheral nerve repair using small gap conduit tubulization. Eighty rats, with right sciatic nerve section of 4 mm, were randomly assigned to conduit bridging group and control group （epineurium suture）. Glial fibrillary acidic protein expression, in myelinating Schwann cells on the proximal stump, began to up-reg- ulate at 1 day after injury and was still evident at 5 days. Compared with the control group, Notchl mRNA was expressed at a higher level in the conduit bridging group during the first week on the proximal stump. Hesl mRNA levels in the conduit bridging group significantly increased compared with the control group at 3, 5, 7 and 14 days post-surgery. The change of the Notch intracellular domain shared a simi- lar trend as Hesl mRNA expression. Our results confirmed that phenotypic changes of Schwann cells occurred in the proximal stump. The differences in these changes between the conduit tubulization and epineurium suture groups correlate with changes in Notch signaling. This suggests that active Notch signaling might be a key mechanism during the early stage of neural regeneration in the proximal nerve stump.

Mechanism of changes in gap junctional intercellular communication in myocardial cells after burns

Objective: To explore the pathophysiological mechanism of the changes in gap junctionalintercellular communication (GJIC) in the myocardial cells after burns. Methods: After the myocardial cellswere cultured and injured with hypoxia and burn serum, the GJIC in the cells was detected with scrapeloading and dye transfer. Meanwhile, the viability, cytosolic free Ca2+ concentration and Ca2+ influx of themyocardial cells were determined. Results: The cytosolic free Ca2+ concentration and the cellulartransmembrane Ca2+ influx were significantly increased but the viability of the cells markedly decreased afterthe injury. The LY fluorescence reached 4 rows of cells from the scrape line in the normal myocardial cells.The GJIC was blocked at the first hour after hypoxia or hypoxia and burn serum injury. The LY fluorescencewas limited to the primary loads cells at the sixth hour after hypoxia and the third hour after hypoxia andburn serum injury. Conclusion: The function of GJIC in the myocardial cells is to maintain high ordersynchronous contraction of the myocardium. After burns, the runaway calcium homeostasis and impairmentof GJIC function would be accused to be the pathological basis for myocardial heterogeneous behavior.

Effect of the gap junction blocker 1-heptanol on chondrogenic differentiation of mouse bone marrow mesenchymal stem cells in vitro

Objective：To investigate the effect of the gap junction blocker 1-heptanol on the in vitro chondrogenic differentiation of mouse bone marrow mesenchymal stem cells（MSCs） following induction by GDF-5. Methods：MSCs were isolated from mouse bone marrow and cultured in vitro. After 3 passages cells were induced to undergo chondrogenic differentiation with recombinant human GDF-5（100 ng/ml）, with or without 1-heptanol（2.5 la mol/L）. The effect of 1-heptanol on MSCs proliferation was investigated using the MTT assay. Type II collagen mRNA and protein were examined by RT-PCR and immunocytochemistry respectively, and the sulfate glycosaminoglycan was assessed by Alcian blue dye staining. Connexin43（Cx43） protein was examined by western blotting. Results：GDF-5 induced proliferation and chondrogenic differentiation of MSCs. While 1-heptanol treatment had no effect on this proliferation, it inhibited the expression of both type II collagen mRNA and protein. The Alcian blue staining revealed that 1-heptanol also inhibited the deposition of the typical cartilage extracellular matrix promoted by recombinant GDF-5. Western blotting demonstrated that 1-heptanol had no effect on the expression of Cx43. Conclusion：These results suggest that mouse bone marrow MSCs can be differentiated into a chondrogenic phenotype by GDF- 5 administration in vitro. While the gap junction blocker, 1-heptanol, did not reduce gap junction Cx43, these intercellular communication pathways clearly played an important functional role in GDF-5-induced cartilage differentiation.

活化的巨噬细胞对大鼠晶状体损伤后视神经损伤修复的影响

目的:探讨活化的巨噬细胞对大鼠晶状体损伤后视神经损伤修复的影响。方法:选用普通级成年健康Wistar大鼠45只,随机平均分为3组:正常对照组不做任何处理;NC组给予视神经横断性损伤;NC+LP组先给予视神经横断性损伤,再给予晶状体损伤。术后第7、14、21天每组分别处死大鼠5只,免疫组化染色方法检测视网膜组织中ED-1的表达,免疫荧光法检测GAP-43的表达。结果:术后第7、14、21天,正常对照组及NC组视网膜中均未见ED-1阳性细胞;NC+LP组ED-1阳性细胞计数分别为(58.27±4.79)、(45.39±5.13)、(21.17±3.40),第7天时表达最强,之后降低(P<0.001)。术后第7天NC组神经节细胞层可见少量GAP-43表达,高于正常对照组,之后表达降低;NC+LP组各时间点GAP-43表达均大于NC组(P<0.05),术后第14天表达最强(P<0.05)。结论:激活巨噬细胞可促进晶状体损伤后视神经轴突再生。

电针预处理抑制脑缺血后神经胶质细胞缝隙连接通讯功能及其作用机制

目的:探讨电针预处理对脑缺血后神经胶质细胞缝隙连接通讯功能的影响及其作用机制。方法:将96只雄性大鼠随机分为4组,即假手术组(A组)、大脑中动脉闭塞模型(MCAO)组(B组)、电针预处理+MCAO组(C组)及缝隙连接抑制剂甘珀酸(CBX)+MCAO组(D组),每组各24只。A组大鼠不接受MCAO模型构建;B组大鼠仅接受MCAO模型构建;C组大鼠于电针治疗3周后,接受MCAO模型构建;D组大鼠于术前2 h预先侧脑室注射10μL CBX(5μg/μL),接受MCAO模型构建。分别于再灌注12 h、再灌注3 d进行取材,每次每组取12只大鼠。采用免疫荧光双标法观察星形胶质细胞上Cx43表达情况,采用Western blot法检测缺血半暗区神经胶质细胞缝隙连接通讯相关蛋白(Cx43、p-Cx43-S368、p-Cx43-S262、GFAP、PKC、Neun、eNOS、AT1R)表达情况。结果:Cx43主要表达于星形胶质细胞膜表面及突起部位。再灌注12 h,B组、C组、D组Cx43、GFAP荧光强度均高于A组(P<0.05)。再灌注3 d,B组、C组、D组Cx43、GFAP荧光强度均高于A组(P<0.05);C组、D组Cx43、GFAP荧光强度均低于B组(P<0.05)。再灌注12 h,B组、C组、D组Cx43、p-Cx43-S368、p-Cx43-S262、GFAP、PKC、AT1R均高于A组(P<0.05),NeuN、eNOS均低于A组(P<0.05)。再灌注3 d,B组、C组、D组Cx43、p-Cx43-S368、p-Cx43-S262、GFAP、PKC、AT1R均高于A组(P<0.05),NeuN、eNOS均低于A组(P<0.05);C组、D组Cx43、p-Cx43-S368、p-Cx43-S262、GFAP、PKC、AT1R均低于B组(P<0.05),NeuN、eNOS均高于B组(P<0.05)。结论:电针预处理可能通过调节神经胶质细胞缝隙连接通讯相关蛋白的表达,促进脑缺血后神经血管重构,发挥脑保护作用。

神经元-胶质细胞缝隙连接与神经环路的相互作用

间隙连接(gap junction,GJ)也称为缝隙连接,广泛存在于神经元及胶质细胞之间,能够连接相邻细胞并介导相邻细胞间电信号的传递。而这种存在于神经元间,能够介导胞间电信号传递的GJ通道,亦可称为电突触。间隙连接蛋白(connexins,Cxs)是构成GJ的分子基础,在不同的神经元及胶质细胞上都有着不同程度的表达。GJ的存在能够介导神经元以及神经胶质细胞间的不同功能建立,进一步去影响各类成熟神经环路的建立,其对于研究神经精神类疾病发病机制有一定意义。该篇综述联系有关于GJ以及不同Cxs对神经元和不同神经胶质细胞作用的影响,去讨论GJ与神经环路之间的关系,为治疗神经精神疾患提供新的研究思路。

少突胶质细胞对PC12细胞GAP-43表达的影响

目的 研究少突胶质细胞与神经元相互作用时神经元ＧＡＰ－４３的表达。方法 用分离培养的少突胶质细胞及其细胞碎片分别作用于培养的ＰＣ１２细胞，于不同作用时相点在观察ＰＣ１２细胞突起变化的同时检测ＰＣ１２细胞内 ＧＡＰ－４３ ｍＲＮＡ的表达。结果 对照组ＰＣ１２细胞ＧＡＰ－４３ｍＲＮＡ有较高的表达，在给予少突胶质细胞处理后早期，其表达水平即显著降低（Ｐ＜０．０５），一直到处理１２ ｈ，其表达水平仍无明显的回复。结论 少突胶质细胞可能通过产生抑制性物质抑制神经元 ＧＡＰ－４３的表达进而抑制中枢神经系统损伤轴突的再生。

添加剂提高宽带隙钙钛矿太阳电池的性能

该文研究聚对苯乙烯磺酸钠(PSS)对宽带隙钙钛矿薄膜及电池的影响。研究发现PSS添加剂可改善宽带隙钙钛矿薄膜的形貌,提升结晶度并减少缺陷态密度,这有利于抑制混合卤素宽带隙钙钛矿薄膜的相分离问题。J-V测试结果表明钝化后的宽带隙钙钛矿太阳电池性能得到明显提升。在掺有PSS的宽带隙钙钛矿太阳电池中,开路电压最高可达1.23 V,效率最高可达20.54%,并且相分离被抑制后的封装钙钛矿太阳电池稳定性显著改善,在一个太阳连续光照500 h后,电池效率仍可保持在初始效率的81.9%(氮气环境,温度40℃)。

细胞之间线粒体转移的主要途径、主要作用及主要调控机制

背景:线粒体功能障碍导致细胞衰老凋亡,可加重组织损伤。细胞之间线粒体转移促进损伤细胞恢复线粒体功能,有助于治疗线粒体相关疾病。目的:综述细胞之间线粒体转移的作用及调控机制。方法:检索中国知网和PubMed数据库2014-2024年关于细胞之间线粒体转移的文献,以“线粒体转移,隧道纳米管,缝隙连接,微囊泡,细胞融合”为中文检索词,以“Mitochondrial transfer,Tunneling nanotubes,gap junctions,microvesicles,cell fusion”为英文检索词,最终共纳入74篇文献进行分析。结果与结论:①总结了细胞之间线粒体转移的4个主要途径:包括隧道纳米管、缝隙连接、细胞融合和微囊泡。②梳理了细胞之间线粒体转移的主要作用,包括物质交换、信息传递、改善宿主细胞线粒体功能、抑制氧化应激、提高细胞增殖活力及抗炎抗衰老等。③总结了细胞之间线粒体转移的主要调控机制,包括Miro 1促进隧道纳米管形成和线粒体转移、隧道纳米管转移线粒体依赖宿主细胞环状ADP核糖水解酶表达、氧化应激环境诱导隧道纳米管形成、缝隙连接具有Ca^(2+)依赖性、缝隙连接蛋白43影响缝隙连接形成、激活Ras1蛋白和肌动蛋白有助于细胞融合、肌动蛋白和Rab6参与调控线粒体出胞、激活肌动蛋白和NAD+-CD38-cADPR-Ca^(2+)信号通路促进线粒体入胞等。④在细胞信号传导蛋白、细胞动力学相关蛋白及氧化应激环境的影响下,细胞通过隧道纳米管、缝隙连接、微囊泡及细胞融合进行线粒体转移。⑤线粒体转移是细胞之间物质交换和信息交流的重要途径,与疾病的发生发展息息相关,可为治疗线粒体相关疾病提供新的思路,但对细胞间线粒体转移的作用及调控机制仍需进一步探究。

1,1’-磺酰基双(2-甲基-1H-咪唑)对宽带隙钙钛矿太阳电池性能的影响

对倒置结构,带隙为1.68 eV的钙钛矿太阳电池光吸收层掺杂1,1’-磺酰基双(2-甲基-1H-咪唑),以改善钙钛矿薄膜质量,提高太阳电池性能。空间电荷限制电流(SCLC)测试结果表明,掺杂后的钙钛矿薄膜的缺陷密度明显降低;稳态光致发光光谱(PL)结果表明,掺杂后的钙钛矿薄膜的非辐射复合被显著抑制;最终太阳电池的开路电压达到1.17 V,光电转换效率达到21.42%,在氮气环境下储存1000 h后,未封装的太阳电池仍能保持初始效率的96%,稳定性显著提高。

缝隙介导干细胞治疗缺血性卒中的研究进展

缺血性卒中仍是当今世界主要的死亡原因之一。传统的治疗方法存在时间窗狭窄的问题,且治疗后卒中幸存者往往存在神经功能缺损症状。干细胞疗法可以通过增强大脑可塑性来减少神经系统后遗症,而缝隙连接在脑发育过程中对细胞的增殖、迁移和分化是必不可少的,利用小分子(如葡萄糖)通过缝隙连接在干细胞与血管内皮细胞之间的转移构成了干细胞治疗缺血性卒中的重要机制。本文干细胞疗法通过缝隙连接介导治疗缺血性卒中的研究进展进行综述,主要总结了间充质干细胞、造血干细胞、神经干细胞与胚胎干细胞的细胞来源、作用机制以及研究成果,以便深入挖掘干细胞疗法治疗卒中的新思路,以期为临床治疗提供辅助。

膜极距电解槽改造后事故分析

电解槽膜极距改造后,运行电流密度提高,给电解系统带来安全风险。介绍金川集团化工新材料有限责任公司的2次事故。提出加强操作人员的操作精细度,强化电解槽安装过程,保证电解槽安全稳定运行。

基于全无机CsPbBr_(3)钙钛矿太阳能电池的光电性能研究

钙钛矿太阳能电池具有制作工艺简单和光电转换效率高等优点,成为光伏领域研究的热点。而全无机钙钛矿太阳能材料CsPbBr_(3)具有较强的稳定性,是具有竞争力的钙钛矿光吸收材料。主要利用SCAPS-1D软件构建了FTO/TiO_(2)/CsPbBr_(3)/Cu2ZnSnS4(CZTS)/Ag平面异质结结构。研究了全无机钙钛矿材料CsPbBr_(3)厚度和带隙对钙钛矿太阳能电池的影响。

基于PI3K/AKT通路探讨左归丸改善卵巢衰老大鼠卵巢生殖干细胞干性的机制

目的基于磷脂酰肌醇3激酶/蛋白激酶B(PI3K/AKT)通路探讨左归丸通过缝隙连接蛋白43(Cx43)磷酸化改善卵巢衰老大鼠卵巢生殖干细胞(OSCs)干性的机制。方法将8周龄雌性SD大鼠随机分为正常组、模型组、脱氢表雄酮(DHEA)组、左归丸组,每组6只。采用环磷酰胺腹腔注射15 d复制卵巢衰老大鼠模型。模型复制结束后,DHEA组大鼠灌胃DHEA 8.1 mg·kg^(-1),左归丸组大鼠灌胃左归丸1.85 g·kg^(-1),每日1次,连续30 d。采用HE染色法观察大鼠卵巢组织病理变化及各级卵泡计数;ELISA法检测大鼠血清抗缪勒管激素(AMH)、卵泡刺激素(FSH)、雌二醇(E_(2))水平;Western Blot法检测卵巢组织中相关蛋白(PCNA、MVH、Oct4、Cx43、p-Cx43、EGFR、AKT、p-AKT)的表达水平。结果与正常组比较,模型组大鼠体质量明显下降(P<0.05),卵巢湿质量明显降低(P<0.05),始基卵泡数显著减少(P<0.01);血清FSH水平显著升高(P<0.01),E_(2)、AMH水平呈下降趋势(P>0.05);卵巢组织中Oct4、MVH、PCNA、EGFR、p-AKT/AKT、p-Cx43(Ser368)/Cx43、Cx43蛋白表达水平均明显降低(P<0.05,P<0.01)。与模型组比较,左归丸组大鼠体质量明显升高(P<0.05),卵巢湿质量、卵巢指数均显著升高(P<0.01),始基卵泡数显著增加(P<0.01);血清E2水平明显升高(P<0.05);卵巢组织中Oct4、MVH、PCNA、EGFR、p-AKT/AKT、p-Cx43(Ser368)/Cx43、Cx43蛋白水平表达均显著升高(P<0.05,P<0.01)。结论左归丸可能通过维持OSCs干性改善卵巢衰老,其作用机制与PI3K/AKT信号通路及缝隙连接蛋白磷酸化相关。