Idiopathic macular hole (IMH) refers to full thickness defects of retina in macular area with no clear reasons. The management of IMH includes vitrectomy combined with internal limiting membrane (ILM) peeling and pharmacological vitreolysis. But ILM peeling may damage the inner retina; novel techniques, such as inverted ILM flap technique and foveola non-peeling ILM surgery, autologous ILM transplantation had made the method of ILM peeling more diversified with less damage. Pharmacological vitreolysis targeting fibronectin and laminin is considered to work in a two-step mechanism, involving both vitreoretinal separation and vitreous liquefaction. Furthermore, IMH judgment and prognosis indicators like ellipsoid zone, macular hole index, hole formation factor, diameter hole index and tractional hole index based on spectral domain optical coherence tomography enriched the assessment of macular hole diameter, depth and shape. How to make full use of new interventions to reduce the incidence of macular hole and obtain a better visual acuity with closed holes is an important direction for future research.
ObjectivesTo evaluate the therapeutic effect of argon laser photocoagulation combined with intravitreous injection of triamcinolone acetonide (TA) on ischemic central retinal vein occlusion (CRVO).MethodsArgon laser photocoagulation combined with intravitreous injection of TA was performed on 17 patients (17 eyes) with CRVO between December 2003 and July 2004.ResultsDuring the follow-up of 4-10 months, the visual acuity improved in 16 patients, including alleviated or even disappeared cystoid macular edema (CME) in 5, and recurred macular edema in 5 with decreased visual acuity after 3 months. Six patients had increased ocular pressure after intra-ocular injection which alleviated after treated suitably. No neovascularization in angle or secondary neovascular glaucoma was found.ConclusionArgon laser photocoagulation combined with intravitreous injection of TA may improve the visual acuity and reduce complications in ischemic CRVO, though macular edema may recur in some cases. (Chin J Ocul Fundus Dis, 2005,21:224-225)
Objective To investigate the effect of topical treatment with antisense oligonucleotides（ASON）targeting tumor necrosis factor-alpha;（TNF-alpha;）on the pathological process of experimental herpes simplex virus type-Ⅰ（HSV-Ⅰ）induced chorioretinitis in mouse eye. Methods Fifty BALB/c mice were randomly divided into experimental and control group（twenty five mice in each group）.HSV chorioretinitis model was induced in each mouse by inoculating 1times;105 plaque-forming units （pfu） of HSV-Ⅰ（KOS strain）into anterior chamber of the right eye.In experimental group，Fluorescein isothiocyanate （FITC）-labeled ASON targeting TNF-alpha; 2 mu;l were injected sub-conjunctiva in the left eye1day before and 1 and 4 days after the infection;while phosphate buffer solution was injected in the same way in control group.The inflammation changes of the eyes in the 2 groups were observed and the clinical grades were assessed according to the extends of anterior-chamber inflammation，vasodilatation of cornea and iris，formation of cataract，and vitreous opacity. All of the mice were executed 10 days after the infection and were observed histologically. The contents of TNF-alpha; in retina and choroid were measured by enzyme-linked immunobsorbent assay（ELISA）. Results After the infection，acute inflammation appeared in the right eyes in both groups. The inflammation of the left eyes in experimental group was significantly milder than which in the control group.Twelve left eyes had necrotic chorioretinitis in different degrees in the control group while 2 left eyes had mild chorioretinitis in the experimental group. The difference of the number of inflammatory cells between the 2 groups was statistically significant in retina，choroid，and ciliary body（P＜0.05）and was not obvious in anterior chamber，vitreous cavity，and iris（P＞0.05）.The content of TNF-alpha; in choroid and retina was（60plusmn;1.25）pg in the experimental group and（305plusmn;1.03）pg in the control group（P＜0.05）. Conclusions TNF-alpha; ASON treating HSV-Ⅰinduced chorioretinitis may reduce the content of TNF-alpha; in affected mice eyes and decrease the inflammatory reaction. (Chin J Ocul Fundus Dis, 2006, 22: 245-248)
ObjectiveTo observe the influence of down-regulation of HtrA1 expression by small interfering RNA on light-injured human retinal pigment epithelium (RPE) cells. MethodsCultured human RPE cells(8th-12th generations)were exposed to the blue light at the intensity of (2000±500) Lux for 6 hours to establish the light injured model. Light injured cells were divided into HtrA1 siRNA group, negative control group and blank control group. HtrA1 siRNA group and negative control group were transfected with HtrA1 siRNA and control siRNA respectively. The proliferation of cells was assayed by CCK-8 method. Transwell test was used to detect the invasion ability of these three groups. Flow cytometry was used to detect the cell cycle and apoptosis. The expression of HtrA1 and vascular endothelial growth factor (VEGF)-A was detected by real time-polymerase chain reaction and Western blot respectively. ResultsThe mRNA and protein level of HtrA1 in the light injured cells increased significantly compared to that in normal RPE cells (t=17.62, 15.09; P<0.05). Compared with negative control group and blank control group, the knockdown of HtrA1 in HtrA1 siRNA group was associated with reduced cellular proliferation (t=6.37, 4.52), migration (t=9.56, 12.13), apoptosis (t=23.37, 29.08) and decreased mRNA (t=17.36, 11.32, 7.29, 4.05) and protein levels (t=12.02, 15.28, 4.98, 6.24) of HtrA1 and VEGF-A. Cells of HtrA1 siRNA group mainly remained in G0/G1 phase, the difference was statistically significant (t=6.24, 4.93; P<0.05). ConclusionKnockdown of HtrA1 gene may reduce the proliferation, migration capability and apoptosis of light-injured RPE cells, and decrease the expression of VEGF-A.