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目的 观察单次9 h高压氧(hyp erbaric oxygen,HBO)治疗对局灶性脑梗死大鼠凋亡诱导因子 (apoptosis-inducing factor,AIF)、线粒体膜电位(mitochondrial membrane potential,MMPo)的影响,探讨 HBO治疗的神经保护作用。 方法 108只SD大鼠制作永久性大脑中动脉闭塞模型,随机分为对照组和HBO组,每组各54只。造 模成功3 h后,HBO组实行HBO干预,压力0.2 MPa持续9 h,对照组呼吸常压空气。采用Garcia评分评估 大鼠神经功能,比较两组造模后13 h、24 h和72 h神经功能改善情况,并在各时间点检测大鼠缺血半 暗带脑组织凋亡细胞数、线粒体和细胞核AIF表达及MMPo水平。 结果 ①神经功能评分:HBO组13 h(P <0.001)、24 h(P =0.04)神经功能评分改善比对照组更明显。 ②凋亡细胞数:HBO组13 h、24 h凋亡细胞数较对照组更少(均P <0.001)。③AIF在线粒体和细胞核的 表达:13 h、24 h、72 h各时间点HBO组AI F在线粒体的表达均较对照组多(均P <0.001);各时间点HBO 组AIF在细胞核的表达均较对照组少(均P <0.001)。④MMPo:各时间点HBO组MMPo均高于对照组(均 P <0.001)。 结论 HBO治疗可改善大鼠神经功能,稳定MMPo,抑制AIF由线粒体向细胞核转移可能是其神经保 护作用的机制之一。  相似文献   
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The aim of this paper is to present a method to produce macroporous thin membranes made of poly (ethyl acrylate-co-hydroxyethyl acrylate) copolymer network with varying cross-linking density for cell transplantation and prosthesis fabrication. The manufacture process is based on template techniques and anisotropic pore collapse. Pore collapse was produced by swelling the membrane in acetone and subsequently drying and changing the solvent by water to produce 100 microns thick porous membranes. These very thin membranes are porous enough to hold cells to be transplanted to the organism or to be colonized by ingrowth from neighboring tissues in the organism, and they present sufficient tearing stress to be sutured with surgical thread. The obtained pore morphology was observed by Scanning Electron Microscope, and confocal laser microscopy. Mechanical properties were characterized by stress–strain experiments in tension and tearing strength measurements. Morphology and mechanical properties were related to the different initial thickness of the scaffold and the cross-linking density of the polymer network. Seeding efficiency and proliferation of mesenchymal stem cells inside the pore structure were determined at 2 h, 1, 7, 14 and 21 days from seeding.  相似文献   
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Daily exposure to sunlight is known to affect the structure and function of the epidermal basement membrane (BM), as well as epidermal differentiation and epidermal barrier function. The aim of this study is to clarify whether the inhibition of BM‐degrading enzymes such as heparanase and matrix metalloproteinase 9 (MMP‐9) can improve the epidermal barrier function of facial skin, which is exposed to the sun on a daily basis. 1‐(2‐hydroxyethyl)‐2‐imidazolidinone (HEI) was synthesized as an inhibitor of both heparanase and MMP‐9. HEI inhibited not only the BM damage at the DEJ but also epidermal proliferation, differentiation, water contents and transepidermal water loss abnormalities resulting from ultraviolet B (UVB). This was determined in this study by the use of UVB‐induced human cultured skins as compared with the control without HEI. Moreover, topical application of HEI improved epidermal barrier function by increasing water content and decreasing transepidermal water loss in daily sun‐exposed facial skin as compared with non‐treated skins. These results suggest that the inhibition of both heparanase and MMP‐9 is an effective way to care for regularly sun‐exposed facial skin by protecting the BM from damage.  相似文献   
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评估玻璃体切割联合内界膜剥除对糖尿病性黄斑水肿(DME)的疗效。方法:回顾性病例对照研究。2014年6月至2017年1月间因糖尿病视网膜病变合并玻璃体积血或增殖病变于温州医科大学附属眼视光医院杭州院区行玻璃体切割手术治疗,且术前或术中经光学相干断层扫描(OCT)检查确诊合并DME的患者31例(33眼)纳入研究。16例(18眼)术中联合内界膜剥除作为剥膜组,15例(15眼)仅接受玻璃体切割手术治疗者作为对照组。所有手术均由同一医师主刀完成。术后1、3个月随访时复查OCT,对比观察黄斑中心厚度(CMT)和视力的术后变化情况。随访中CMT和最佳矫正视力(BCVA)比较采用重复测量方差分析,组间CMT和BCVA比较采用独立样本t检验。结果:手术前,手术后1、3个月2组间比较LogMAR视力总体差异有统计学意义(F=15.93,P<0.001)。术后 1个月时剥膜组BCVA高于对照组(t=2.55,P=0.02),但术后3个月时2组间差异无统计学意义(t=0.82, P=0.42)。手术前,手术后1、3个月CMT总体差异无统计学意义(F=2.85,P=0.065)。术后1、3个月时,剥膜组的CMT均低于对照组,2组间差异均有统计学意义(t=2.24,P=0.03;t=3.79,P=0.001)。术后1个月时,剥膜组有效(与术前比CMT减少20%以上)、无效(变化不超过20%)及恶化(增厚超过 20%)的例数分别为8、6、4例,术后3个月时则分别为11、5、2例,与对照组相比,术后1个月时组间差异无统计学意义(Z=-1.687,P=0.092),术后3个月时剥膜组DME改善有效比例明显高于对照组,组间差异有统计学意义(Z=-2.177,P=0.029)。结论:对于非牵拉性DME,内界膜剥除有助于术后早期DME消退。  相似文献   
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Background

Rosacea is a chronic inflammatory skin condition whose etiology has been linked to mast cells and the antimicrobial peptide cathelicidin LL-37. Individuals with refractory disease have demonstrated clinical benefit with periodic injections of onabotulinum toxin, but the mechanism of action is unknown.

Objectives

To investigate the molecular mechanism by which botulinum toxin improves rosacea lesions.

Methods

Primary human and murine mast cells were pretreated with onabotulinum toxin A or B or control. Mast cell degranulation was evaluated by β-hexosaminidase activity. Expression of botulinum toxin receptor Sv2 was measured by qPCR. The presence of SNAP-25 and VAMP2 was established by immunofluorescence. In vivo rosacea model was established by intradermally injecting LL-37 with or without onabotulinum toxin A pretreatment. Mast cell degranulation was assessed in vivo by histologic counts. Rosacea biomarkers were analyzed by qPCR of mouse skin sections.

Results

Onabotulinum toxin A and B inhibited compound 48/80-induced degranulation of both human and murine mast cells. Expression of Sv2 was established in mouse mast cells. Onabotulinum toxin A and B increased cleaved SNAP-25 and decreased VAMP2 staining in mast cells respectively. In mice, injection of onabotulinum toxin A significantly reduced LL-37-induced skin erythema, mast cell degranulation, and mRNA expression of rosacea biomarkers.

Conclusions

These findings suggest that onabotulinum toxin reduces rosacea-associated skin inflammation by directly inhibiting mast cell degranulation. Periodic applications of onabotulinum toxin may be an effective therapy for refractory rosacea and deserves further study.  相似文献   
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