Kdm6a-CNN1 axis orchestrates epigenetic control of traumainduced spinal cord microvascular endothelial cell senescence to balance neuroinflammation for improved neurological repair

Cellular senescence assumes pivotal roles in various diseases through the secretion of proinflammatory factors.Despite extensive investigations into vascular senescence associated with aging and degenerative diseases,the molecular mechanisms governing microvascular endothelial cell senescence induced by traumatic stress,particularly its involvement in senescence-induced inflammation,remain insufficiently elucidated.In this study,we present a comprehensive demonstration and characterization of microvascular endothelial cell senescence induced by spinal cord injury(SCI).Lysine demethylase 6A(Kdm6a),commonly known as UTX,emerges as a crucial regulator of cell senescence in injured spinal cord microvascular endothelial cells(SCMECs).Upregulation of UTX induces senescence in SCMECs,leading to an amplified release of proinflammatory factors,specifically the senescenceassociated secretory phenotype(SASP)components,thereby modulating the inflammatory microenvironment.Conversely,the deletion of UTX in endothelial cells shields SCMECs against senescence,mitigates the release of proinflammatory SASP factors,and promotes neurological functional recovery after SCI.UTX forms an epigenetic regulatory axis by binding to calponin 1(CNN1),orchestrating trauma-induced SCMECs senescence and SASP secretion,thereby influencing neuroinflammation and neurological functional repair.Furthermore,local delivery of a senolytic drug reduces senescent SCMECs and suppresses proinflammatory SASP secretion,reinstating a local regenerative microenvironment and enhancing functional repair after SCI.In conclusion,targeting the UTX-CNN1 epigenetic axis to prevent trauma-induced SCMECs senescence holds the potential to inhibit SASP secretion,alleviate neuroinflammation,and provide a novel treatment strategy for SCI repair.

聚酰亚胺/TiO_(2)纳米杂化膜的制备及表征

将间苯二胺,2,2’-双三氟甲基-4,4’-联苯二胺和2,3,3’,4’-联苯四甲酸二酐反应得到可溶性聚酰亚胺(KPI),再把KPI与TiO_(2)溶胶共混,经流延制膜并热亚胺化后得到PI/TiO_(2)纳米杂化膜。通过红外光谱、扫描电镜、透射电镜和能谱仪对PI/TiO_(2)纳米杂化膜的成分、结构和形态进行表征。结果表明,TiO_(2)已成功引入PI基体中,并以纳米尺寸均匀分布。热重分析和拉伸实验表明,TiO_(2)的引入提高了PI/TiO_(2)纳米杂化膜热的稳定性和力学性能。紫外-可见光谱表明,TiO_(2)的掺入并不影响PI/TiO_(2)纳米杂化膜的光学透过率。分别研究了PI/TiO_(2)纳米杂化膜对亚甲基蓝和刃天青的光催化活性。24h内,PI/TiO_(2)(5%)纳米杂化膜对亚甲基蓝的降解率高达96.40%,说明PI/TiO_(2)纳米杂化膜具有极强的光催化活性,能起到光催化效果的主要原因是杂化体系内含有光催化活性的TiO_(2)纳米粒子。PI/TiO_(2)杂化膜具有有效的光催化活性及潜在的抗污染自清洁能力。

相分离法制备聚乳酸/醋酸纤维素三维微-纳米纤维多孔支架及其生物矿化活性

分别以N,N-二甲基甲酰胺、四氢呋喃、乙腈、1,4-二氧六环和N,N-二甲基乙酰胺为溶剂,在无其它添加剂条件下,通过低温淬火、萃取、洗涤和干燥得到聚乳酸(PLLA)/醋酸纤维素(CA)三维微-纳米纤维多孔支架。实验结果表明,以四氢呋喃为溶剂,得到了直径50~350 nm的三维微-纳米纤维多孔结构,该尺寸和结构刚好与天然细胞外基质(50~500 nm)相吻合。采用扫描电镜探讨了淬火时间、淬火温度、聚合物浓度和聚合物比例等条件对纤维支架形貌的影响。通过水接触角、吸水率、力学性能和体外生物活性等测试考察了CA的添加对纤维支架亲水性、力学性能和生物活性的影响。实验结果表明,与纯PLLA纤维支架相比,CA的加入改善了PLLA/CA三维微-纳米纤维多孔支架的亲水性,提高了支架的压缩强度和冲击强度,进而提高了材料的生物活性。PLLA/CA三维微-纳米纤维多孔支架的孔隙率均大于94%,比表面积均大于52 m^(2)/g,说明PLLA/CA三维微-纳米纤维多孔支架为高孔隙率和大比表面积的三维多孔材料。该孔隙率和比表面积为细胞的黏附、迁移、分化、增殖及养料的传输提供了很好的条件。

聚L-乳酸泡沫材料制备及油水分离应用

以聚L-乳酸(PLLA)/四氢呋喃为淬火溶液,通过热致相分离法得到PLLA泡沫材料。泡沫由直径为(45±13)μm的多孔微球组成。以PLLA泡沫材料为油水分离材料,研究其对十二醇、机油、石蜡油和硅油的吸附和油水分离性能。实验结果表明,PLLA泡沫材料的比表面积和孔隙率分别高达13.9m^2/g和97.5%,水接触角(WCA)为141.8°,与普通PLLA流延膜相比水接触角约增加了70°。PLLA泡沫材料对4种油的吸附容量均大于12g/g,为流延膜的14~19倍。吸油容量的增加主要与泡沫材料的高孔隙率和大比表面积,及材料表面和内部的微/纳结构有关。由于超疏水性、亲油性和毛细管效应,PLLA泡沫材料可以快速吸收漂浮在水面上的油层,可作为一种理想的油水分离材料。