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9 个结果
  • 简介:α-Eleostearicacidandβ-eleostearicacidformedvesiclesinaqueousmediumwhenanethanolsolutionofeleostearicacidwasinjectedrapidlyintoavigorouslyvortexedaqueousphase.Formationofthevesicleswasdemonstratedbyelectronmicroscopicobservationandbromothymolblueencapsulationexperiments.PolymerizationsoftheeleostearicacidsintheformedvesiclescarriedoutbyUVirradiationproducedpoly-α-eleostearicacidandpoly-β-eleostearicacidvesicles.

  • 标签: Eleostearic ACID UV IRRADIATED POLYMERIZATION VESICLE
  • 简介:AbstractExtracellular vesicles (EVs) are anuclear particles composed of lipid bilayers that contain nucleic acids, proteins, lipids, and organelles. EVs act as an important mediator of cell-to-cell communication by transmitting biological signals or components, including lipids, proteins, messenger RNAs, DNA, microRNAs, organelles, etc, to nearby or distant target cells to activate and regulate the function and phenotype of target cells. Under physiological conditions, EVs play an essential role in maintaining the homeostasis of the pulmonary milieu but they can also be involved in promoting the pathogenesis and progression of various respiratory diseases including chronic obstructive pulmonary disease, asthma, acute lung injury/acute respiratory distress syndrome, idiopathic pulmonary fibrosis (IPF), and pulmonary artery hypertension. In addition, in multiple preclinical studies, EVs derived from mesenchymal stem cells (EVs) have shown promising therapeutic effects on reducing and repairing lung injuries. Furthermore, in recent years, researchers have explored different methods for modifying EVs or enhancing EVs-mediated drug delivery to produce more targeted and beneficial effects. This article will review the characteristics and biogenesis of EVs and their role in lung homeostasis and various acute and chronic lung diseases and the potential therapeutic application of EVs in the field of clinical medicine.

  • 标签: Lung diseases Biomarker Lung disease pathogenesis Extracellular vesicles Clinical application
  • 简介:AbstractThe syncytiotrophoblast, a fused single-cell layer between mother and fetus, constitutively releases extracellular vesicles (STBEV) directly into the maternal circulation. STBEV contain a variety of proteins and RNA which can be targeted to specific cells. In preeclampsia, asymptomatic placental oxidative stress is a precursor to later multi-organ dysfunction in the mother. Increased STBEV release in preeclampsia is considered a manifestation of syncytiotrophoblast stress, which may play a key role in signaling between fetus and mother. STBEV release in preeclampsia changes, both in terms of volume and content. In this review, we outline the latest advances in STBEV isolation and detection. We consider evidence for differential STBEV release, protein cargo and RNA content in preeclampsia, highlighting common pitfalls in study design. We summarise studies to date demonstrating STBEV actions on target cells. Ultimately, we consider how STBEV fit into the pathophysiology of the heterogeneous syndrome of preeclampsia. The key unifying concept in early- and late-onset preeclampsia is syncytiotrophoblast stress. We submit that STBEV are the key stress signal in preeclampsia. We believe that further investigation of STBEV release, content, and actions may offer valuable insights into preeclampsia pathophysiology and potential new clinical diagnostics and therapeutic targets.

  • 标签: Biomarkers Diagnostics Extracellular vesicles Placenta Preeclampsia Signalling Stress Syncytiotrophoblast
  • 简介:Vesiclecanbepreparedfromaqueousmixturesofsimplecommerciallyavailable,single-tailedcanonicandanionicsurfactants.Inthiswork,theI3/I1value,Ie/Imvalue,andfluorescencelifetimeofpyreneindifferentsystems(seethepreparationofsamples)weredetermined.Hieessentialaffectingfactorsintheformationofvesiclecanbededucedfromtheobtainedresults.Itshowedthatlargevesiclemustformnaturallybeforesonicationin0.082MoctyltrimethylammoniumbromideandsodiumlauratepH=9.2aqueoussolution.Whileaftersonication,onlysmallvesicleexists,whichcanbeprovedfurtherthroughelectronmicroscope.

  • 标签: VESICLE FLUORESCENCE PROBE PYRENE
  • 简介:无数生物因素被建议了解释早泄(PE)。然而,有精囊(SV)的数据相关PE是稀少的。学习试图评估在SV和PE的尺寸之间的关系。没有PE,代表性的学习与PE和44个志愿者包括了44个门诊病人,并且SV的尺寸被比较。射精的潜伏时间,早泄诊断工具(PEDT),可勃起的Function-15的国际索引,和健康长期的前列腺炎症状的国家研究所索引的自我估计的intravaginal被用于对症状的评价。比作控制组,PE组有SV的显著地更高的吝啬的前面以后的直径(APD)(P<0.001)。SV截止水平的最佳的吝啬的APD是为PE的9.25公里。在PE组,PEDT与SV的吝啬的APD相比与SV9.25公里的吝啬的APD也是更高的<9.25公里。PEDT显著地与SV的吝啬的APD被相关(r=0.326,P=0.031)。精液的血浆蛋白质被集体spectrometry在六PE和六个匹配的控制盒子之间比较,102蛋白质是至少起来调整或下面调整的1.5褶层,这被显示出。在他们之中,GGT1,LAMC1,和应用软件在PE组是显著地更高的。这些结果显示有SV的更大的吝啬的APD的人可能让更高的PEDT得分。SV的Transrectal超声应该与早泄在病人的评估被考虑。SV可能在SV是为有PE和超声变化的病人的治疗的一个潜在的目标。

  • 标签: 超声检查 DIAMETER PEDT 慢性前列腺炎 SVS APD
  • 简介:Theinsectmidgutepitheliumiscomposedofcolumnar,goblet,andregenerativecells.Columnarepithelialcellsarethemostabundantandhavemembraneprotrusionsthatformthebrushbordermembrane(BBM)ontheirapicalside.Theseincreasesurfaceareaavailableforthetransportofnutrients,butalsoprovideopportunitiesforinteractionwithxenobioticssuchaspathogens,toxinsandhostplantallelochemicals.RecentimprovementsinproteomicandbioinfbrmaticstoolsprovidedanopportunitytodeterminetheproteomeoftheT.niBBMinunprecedenteddetail.ThisstudyreportstheidentificationofproteinsfromBBMvesicles(BBMVs)usingsingledimensionpolyacrylamidegelelec?trophoresiscoupledwithmulti-dimensionalproteinidentificationtechnology.Morethan3000proteinswereassociatedwiththeBBMVofwhich697werepredictedtopossesseitherasignalpeptide,atleastonetransmembranedomainoraGPI-anchorsignal.Ofthese,bioinfbrmaticsanalysisandmanualcurationpredictedthat185maybeassociatedwiththeBBMVorepithelialcellplasmamembrane.Thesearediscussedwithrespecttotheirpredictedfunctions,namelydigestion,nutrientuptake,cellsignaling,development,cell-cellinteractions,andotherfunctions.Webelievethistobethemostdetailedproteomicanalysisofthelepidopteranmidgutepitheliummembranetodate,whichwillprovideinformationtobetterunderstandthebiochemical,physiologicalandpathologicalprocessestakingplaceinthelarvalmidgut.

  • 标签: BRUSH BORDER membrane vesicles MIDGUT PROTEOMIC
  • 简介:我们为把坚持、有效的抗菌剂性质合并到广泛地使用的聚合物报导灵巧的策略,poly(甲基methacrylate)(PMMA),由异分子聚合有2-(tert-butylamino)的甲基methacrylate(MMA)在经由原子转移基聚合(ATRP)的一个壶的乙醇methacrylate(TA)。随后自己组装结果poly(甲基methacrylate)-block-poly[(2-tert-butylamino)ethylmethacrylate](PMMA20-b-PTA15)diblock共聚物负担得起明确的水可分散的泡,它能轻易地为有效抑制在医院里在墙上被喷洒并且细菌杀死。1H-NMR和胶化浸透层析(GPC)研究证实了良好共聚物的成功的合成。传播电子显微镜学(TEM),原子力量显微镜学(AFM)和散布的动态光(DLS)学习与狭窄的尺寸分发证明了泡的形成。DLS研究在各种各样的温度揭示了泡的优秀稳定性。抗菌剂测试对克积极、克否定的细菌显示出聚合物泡的有效抗菌剂活动。而且,这策略可以为在许多领域里为灵巧的抗菌剂应用准备大量聚合材料被扩大。

  • 标签: 下线 服务 迁移
  • 简介:在一封初步的信(四面体Lett。2010,51,188),我们报导了二个新基于一种肺结核特效药的四倍的结合氢的主题,这是,二monopodal(1a和1b)和五dipodal(2a,2b和3a3c)从在烃的dipodal主题的超分子的聚合物和泡的芳香的一种肺结核特效药衍生物,和形成。在这份报纸,我们在场有他们在水的媒介的自我装配的行为上的一个重音的这些结合氢的主题的性质上的一幅完整的图画。SEM,AFM,TEM并且荧光灯显微图显示所有dipodal混合物也在极的甲醇和水甲醇(多达50%水)形成泡混合物。控制实验证明1b不在一样的媒介形成泡。到dipodal混合物的溶液的1b的增加禁止后者形成泡的能力。在高集中,3b和3c另外gelate分离溶剂,包括的烃,酉旨,甲醇,和甲醇水混合。集中依赖者SEM调查表明3b和3c的泡熔化形成胶化和3c罐头de总数的胶化reversibly形成泡。

  • 标签: 超分子聚合物 自组装行为 可逆转换 水介质 囊泡 凝胶
  • 简介:AbstractBackground:The use of microRNAs in the therapy of kidney disease is hampered by the difficulties in their effective delivery. Microvesicles (MVs) are known as natural carriers of small RNAs. Our prior research has demonstrated that MVs isolated from mesenchymal stem cells (MSCs) are capable of attenuating kidney injuries induced by unilateral ureteral obstruction and 5/6 sub-total nephrectomy in mice. The present study aimed to evaluate the effects of miR-34a-5p (miR-34a)-modified MSC-MVs on transforming growth factor (TGF)-β1-induced fibrosis and apoptosis in vitro.Methods:Bone marrow MSCs were modified by lentiviruses over-expressing miR-34a, from which MVs were collected for the treatment of human Kidney-2 (HK-2) renal tubular cells exposed to TGF-β1 (6 ng/mL). The survival of HK-2 cells was determined using 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) and Annexin V-Light 650/propidium iodide (PI) assays. The expression levels of epithelial markers (tight junction protein 1 [TJP1] and E-cadherin) and mesenchymal markers (smooth muscle actin alpha (α-SMA) and fibronectin) in HK-2 cells were measured using Western blot analysis and an immunofluorescence assay. In addition, changes in Notch-1/Jagged-1 signaling were analyzed using Western blotting. Data were analyzed using a Student’s t test or one-way analysis of variance.Results:MiR-34a expression increased three-fold in MVs generated by miR-34a-modified MSCs compared with that expressed in control MVs (P < 0.01, t= 16.55). In HK-2 cells, TJP1 and E-cadherin levels decreased to 31% and 37% after treatment with TGF-β1, respectively, and were restored to 62% and 70% by miR-34a-enriched MSC-MVs, respectively. The expression of α-SMA and fibronectin increased by 3.9- and 5.0-fold following TGF-β1 treatment, and decreased to 2.0- and 1.7-fold after treatment of HK-2 cells with miR-34a-enriched MSC-MVs. The effects of miR-34a-enriched MSC-MVs on epithelial-mesenchymal transition (EMT) markers were stronger than control MSC-MVs. The effects of miR-34a-enriched MSC-MVs on these EMT markers were stronger than control MSC-MVs. Notch-1 receptor and Jagged-1 ligand, two major molecules of Notch signaling pathway, are predicted targets of miR-34a. It was further observed that elevation of Notch-1 and Jagged-1 induced by TGF-β1 was inhibited by miR-34a-enriched MSC-MVs. In addition, TGF-β1 exposure also induced apoptosis in HK-2 cells. Although miR-34a-mofidied MSC-MVs were able to inhibit TGF-β1-triggered apoptosis in HK-2 cells, the effects were less significant than control MSC-MVs (control:TGF-β1 :miR-nc-MV:miR-34a-MV = 1.3:0.6:1.1:0.9 for MTT assay, 1.8%:23.3%:9.4%:17.4% for apoptosis assay). This phenomenon may be the result of the pro-apoptotic effects of miR-34a.Conclusions:The present study demonstrated that miR-34a-over-expressing MSC-MVs inhibit EMT induced by pro-fibrotic TGF-β1 in renal tubular epithelial cells, possibly through inhibition of the Jagged-1/Notch-1 pathway. Genetic modification of MSC-MVs with an anti-fibrotic molecule may represent a novel strategy for the treatment of renal injuries.

  • 标签: Micro-vesicles Mesenchymal stem cells miR-34a Epithelial-mesenchymal transition