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Objective To investigate the effects of knocking down Racl gene (ras-related C3 botulinum toxin substrate 1) by small hairpin RNA (shRNA) on retinal neovascularization in a mouse model of oxygen-induced retinopathy (OIR). Methods One hundred and eight 7-day-old C57BL/6J mice were divided into three groups randomly. The OIR was induced by Smith protocol in 2 groups. OIR mice received an intravitreal injection of Racl-shRNA plasmid or the nonsense plasmid in the gene-intervention group and control group respectively at the age of postnatal day 11 (P11). Non-OIR mice also received an intravitreal injection of Racl-shRNA plasmid at P11 as the blank-intervention group which lived in the normoxic environment. Retinal neovascularization was investigated on flat-mounts after fluorescence angiography at P15 and P17. Endothelial cell nuclei breaking through the internal limiting membrane were counted on pathological section at P17. The expression of Racl and NF-κB p65 subunit was measured by immuohistochemistry, Western blot, real-time polymerase chain reaction (RT-PCR) and in situ hybridization. Results Compared with the blank-control group, the level of Racl mRNA in the geneintervention group decreased obviously(t=4.5, P = 0. 001 ); the retinal non-perfusion areas, fluorescence leakage, neovascularization and the number of endothelial cell nuclei breaking through the internal limiting membrane were reduced significantly(t = 6. 521, P< 0. 001) ; the level of NF-κB p65 nuclear translocation decreased(t= 16. 008, P<0. 001)while the expression of NF-κB p65 mRNA was reduced obviously(t=3. 354, P=0. 006), which was positively correlated with the expression of Ratl mRNA (P=0. 012).Conclusion Intravitreal injection of Racl-shRNA with liposome in mice can effectively inhibit the expression of Racl, and inhibit the retinal neovascularization under relative hypoxia via blocking the ROS-NF-κB pathway. 相似文献
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Objective To investigate the effects of knocking down Racl gene (ras-related C3 botulinum toxin substrate 1) by small hairpin RNA (shRNA) on retinal neovascularization in a mouse model of oxygen-induced retinopathy (OIR). Methods One hundred and eight 7-day-old C57BL/6J mice were divided into three groups randomly. The OIR was induced by Smith protocol in 2 groups. OIR mice received an intravitreal injection of Racl-shRNA plasmid or the nonsense plasmid in the gene-intervention group and control group respectively at the age of postnatal day 11 (P11). Non-OIR mice also received an intravitreal injection of Racl-shRNA plasmid at P11 as the blank-intervention group which lived in the normoxic environment. Retinal neovascularization was investigated on flat-mounts after fluorescence angiography at P15 and P17. Endothelial cell nuclei breaking through the internal limiting membrane were counted on pathological section at P17. The expression of Racl and NF-κB p65 subunit was measured by immuohistochemistry, Western blot, real-time polymerase chain reaction (RT-PCR) and in situ hybridization. Results Compared with the blank-control group, the level of Racl mRNA in the geneintervention group decreased obviously(t=4.5, P = 0. 001 ); the retinal non-perfusion areas, fluorescence leakage, neovascularization and the number of endothelial cell nuclei breaking through the internal limiting membrane were reduced significantly(t = 6. 521, P< 0. 001) ; the level of NF-κB p65 nuclear translocation decreased(t= 16. 008, P<0. 001)while the expression of NF-κB p65 mRNA was reduced obviously(t=3. 354, P=0. 006), which was positively correlated with the expression of Ratl mRNA (P=0. 012).Conclusion Intravitreal injection of Racl-shRNA with liposome in mice can effectively inhibit the expression of Racl, and inhibit the retinal neovascularization under relative hypoxia via blocking the ROS-NF-κB pathway. 相似文献
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眼底影像技术在过去十年间飞速发展。原有的成像技术更新换代,新型成像技术层出不穷,相关的研发投入、设备使用量和论文发表量均迅猛增长,同时向多技术联合、融合人工智能和大数据以及设备轻巧化和自动化等方向发展。但眼底影像繁荣的背后也存在眼底知识体系规范化重塑、学术传播均衡性和独立性、"多模式影像"概念误读、新兴技术的有效性和适用性验证、临床影像研究创新、原始技术创新和技术储备以及面向未来的眼底影像数据集成与分析系统等诸多挑战。 相似文献
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[目的]观察病理性近视黄斑病变荧光素眼底血管造影(FFA)的图像特征,分析不同类型黄斑病变及其影响因素.[方法]回顾性分析病理性近视黄斑病变患者251例451只眼的临床资料.根据其临床特点及FFA特征将病理性近视黄斑病变分为6种类型:(1)漆样裂纹;(2)脉络新生血管(CNV);(3)漆样裂纹性黄斑出血;(4)Fuchs斑;(5)黄斑萎缩;(6)黄斑裂孔.分析年龄、性别、屈光度及矫正视力与各类型黄斑病变的关系.[结果]年龄、近视屈光度及矫正视力在不同类型病理性近视黄斑病变之间差异均有统计学意义(年龄:F=29.734,P<0.001;屈光度:F=22.259,P<0.001;矫正视力:F=5.932,P<0.001).Logistic回归分析显示,随年龄增加,CNV及黄斑萎缩构成比均呈上升趋势[比值比(OR)=1.034,95%可信区间(CI)=1.019~1.049,P<0.001;OR=1.054,95%CI=1.031~1.076,P<0.001];而漆样裂纹性黄斑出血则呈下降趋势(OR=0.906,95%CI=0.876~0.937,P<0.001);CNV及黄斑裂孔随近视屈光度增加而构成比呈下降趋势(OR=1.233,95% CI=1.136~1.338,P<0.001;OR=1.554,95% CI=1.185~2.038,P<0.001),黄斑萎缩呈上升趋势(OR=0.762,95%CI=0.705~0.824,P<0.001).各类型黄斑病变可造成不同程度的视力损害,CNV对视力损害程度较重(OR=1.835,95%CI=1.180~2.854,P=0.007),漆样裂纹则较轻(OR=0.506,95%CI=0.328~0.782,P=0.002).[结论]病理性近视黄斑病变根据FFA可分为6大类型,CNV及黄斑萎缩随年龄增长而增加,漆样裂纹黄斑出血则随之减少,CNV及黄斑裂孔随近视屈光度增高而减少,黄斑萎缩则随之增加;病变类型不同,最佳矫正视力不同. 相似文献
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视网膜出血在临床上依据所沉积的不同层次间隙可分为玻璃体出血、玻璃体下出血、内界膜下出血、视网膜浅层出血、视网膜深层出血、视网膜下出血和视网膜色素上皮下出血等七类。掌握不同类型视网膜出血的表现特征对疾病的诊断、鉴别诊断与指导治疗有重要价值。(眼科,2009,18:221—224) 相似文献
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目的 观察息肉样脉络膜血管病变(PCV)静止性息肉样灶的吲哚青绿血管造影(ICGA)特征.方法 回顾分析36例有静止性息肉样灶的PCV患者37只眼的临床资料.其中,11只眼随访了9~29个月,平均随访时间(12.3±5.5)个月.所有患眼均进行视力、眼压、裂隙灯显微镜、散瞳眼底检查,以及眼底彩色照相、荧光素眼底血管造影、ICGA检查.以ICGA检查早期发现囊袋样强荧光和晚期荧光渗漏或者着染者确定为活动性息肉样灶;ICGA检查发现囊袋样稍强荧光,晚期逐渐消退或者呈“冲刷”样表现者确定为静止性息肉样灶.以吲哚青绿开始注射至静止性息肉样灶开始显影的时间定为静止性息肉样灶的显影时间.根据临床和ICGA表现,将静止性息肉样灶分为无症状组、萎缩瘢痕组、结合组.对比观察各组的临床和影像特征以及随访观察眼底及病灶变化情况.结果 37只眼中,静止性息肉样灶的显影时间为8.2~27.0 min,平均显影时间(15.5±4.8) min.无症状组5只眼,占13.5%.眼底检查无出血、渗出、视网膜色素上皮脱离(PED)和(或)神经上皮脱离.ICGA检查有静止性息肉样灶显影.萎缩瘢痕组8只眼,占21.6%.眼底检查患眼黄斑区均有萎缩灶和(或)瘢痕灶,无出血、渗出、视网膜PED和(或)神经上皮脱离.ICGA检查显示其静止性息肉样灶位于萎缩灶或瘢痕灶边缘.结合组24只眼,占64.9%.眼底检查均无萎缩、瘢痕灶,其中10只眼有视网膜下出血,15只眼有视网膜渗出,10只眼有视网膜PED,4只眼有视网膜神经上皮脱离.ICGA检查显示静止性息肉样灶和活动性息肉样灶共存.随访的11只眼中,3只眼静止性息肉样灶完全消退,占27.3%;2只眼静止性息肉样灶部分消退,占18.2%;6只眼静止性息肉样灶无明显改变,占54.5%.结论 PCV的静止性息肉样灶主要在ICGA造影的中晚期显影,可出现于无症状眼、萎缩瘢痕眼以及与活动性息肉样灶共存眼等3种情况,其中与活动性息肉样灶共存是其主要形式. 相似文献