ABSTRACT
As a primary treatment for strabismus, extraocular muscle surgery can achieve the purpose of correcting the eye position, improving the appearance and reconstructing the third-level visual function. Previous studies have found that the vascular density(VD)and thickness of retina increased in the early stage after extraocular muscle surgery, where multiple mechanisms involved. In recent years, with the appearance of detection means such as optical coherence tomography angiography(OCTA), our quantitative understanding of retinal microscopic changes and their mechanisms brought about by traditional extraocular muscle surgery has become more and more profound. The increase of retinal VD in the early postoperative period may be closely related to the recovery of postoperative visual function. However, the related studies are few, and the association between microscopic changes and visual function after extraocular muscle surgery and its mechanism need to be further clarified. This article will review the microscopic changes of retina and their mechanisms after extraocular muscle surgery from multiple perspectives to improve our understanding of the relationship between the mechanism of its influence and visual function, with a view to provide references for the choice of extraocular muscle surgery scheme and related clinical research.
ABSTRACT
Abstract? AIM: To evaluate the efficiency of two different operation ways, vitrectomy and vitrectomy combined with inferior scleral buckling, for a complex kind of retinal detachment.?METHODS:The complex kind of retinal detachment were diagnosed in 100 cases ( 100 eyes ) , with the common features:1)the course of more than 1mo;2) at least one retinal hole located in the inferior marginal retina;3) the detachment of retina was found proliferated, there was at least 1 retinal fold in retinal detachment area. The patients were randomly divided into two groups: the treatment group ( 50 eyes ) who received vitrectomy combined with inferior scleral buckling;the control group ( 50 eyes ) who received vitrectomy without scleral buckling. The retinal anatomic reattachment, visual function recovery, macular central fovea thickness and complications in two groups were observed.? RESULTS: There were 49 eyes ( 98%) with retinal anatomic reattachment in the treatment group while 42 eyes(84%)in control group(χ2=4.2605, P0.05);the macular central fovea thickness was 272 ±32.21μm in the treat group while it was 316 ± 33.46μm(t=12.597,P<0.01).Intraocular pressure in 12 eyes ( 24%) was more than 30mmHg in the treatment group while 4 eyes ( 8%) in control group within 1wk postoperation (χ2=4.7619,P<0.05); intraocular pressure in 100 eyes were controlled below 21mmHg 1mo postoperatively.? CONCLUSION: It is a more effective method to vitrectomy combined with inferior scleral buckling than the single vitrectomy for the special kind of retinal detachment.It can increase the rate of retinal anatomic reattachment and reduce macular edema.
ABSTRACT
Diabetic retinopathy (DR) is one of the common and serious diabetic complications,with a complex nosogenesis.Studies have shown that transforming growth factor-β (TGF-β) participates in the occurrence and development of DR,and Smads protein is able to mediate and activate TGF-β/Smads signal transduction pathway and further involves in the pathogenesis of DR.Smurf is one of the ubiquitin ligases in ubiquitin-proteasome pathway,and it is clarified to regulate TGF-β/Smads signal transduction pathway degradation.At present,the study on the relationship between TGF-β/Smads pathway and DR has made great progress.The role of ubiquitin-proteasome pathway regulating TGF-β/Smads signal transduction pathway in DR is reviewed in this article.
ABSTRACT
Background As one of the most common microvascular complication of diabetes in eyes,diabetic retinopathy (DR) is one of the most important cause of blindness.Nuclear factor-kappa B (NF-κB) is involved in the occurrence and development of the disease through the activation of a series of inflammatory cytokines.Objective The present study was to investigate the effects of peroxisome proliferator-activated receptor-gamma (PPAR-γ) excitomotor,rosiglitazone,on NF-κB expression and apoptosis of the retinal ganglion cells (RGCs) in the retina with diabetes mellitus. Methods Ninety SPF male Wistar rats were randomized into normal control group,diabetic control group and rosiglitazone group.Diabetes mellitus was induced by intraperitoneal injection of 50 mg/kg streptozotocin(STZ).Then 3 mg/kg rosiglitazone was intragastricly administered once per day in the rosiglitazonegroup,and the same volume of saline solution was used at the same way in the normal control group and diabetic control group from 3 days after modeling.The rats were sacrificed and the eye cups specimen was made at 4,8 and 12 weeks after usage of drugs.Retinal histopathological examination was performed by hematine-eosin staining,and expression of NF-κB p65 protein in retina and apoptotic index(AI) of RGCs were detected by immunohistochemistry and TUNEL assay,respectively in different time points mentioned above.The use of the animals complied with the Regulations for the Administration of Affairs Concerning Experimental Animals by State and Technology Commission.Results The blood glucose level was significantly elevated at various time points in the diabetic control group and rosiglitazone group compared with normal control group (P＜0.01 ),and that of the rosiglitazone group was significantly declined in comparison to the diabetic control group (q =0.81,0.82,1.23,P＞ 0.05 ).Normal retinal structure was seen in the normal control group,and edema retinal cell and disorder of retinal layers were exhibited in the diabetic control group.Retinal structure was almost normal in the rosiglitazone group.The NF-κB p65 was expressed weakly in the retina of normal control group,but the expression of NF-κB p65 was significantly elevated in the diabetic control group and rosiglitazone group compared with the normal control group(P＜0.01 ).However,the expression of NF-κB p65(A value)was significantly decreased in the rosiglitazone group compared with diabetic control group at 8 weeks and 12 weeks( q=17.77,15.30,P＜0.01 ).There were a few apoptotic cells in rat retina of the normal control group.Compared with the normal control group,the AI of the diabetic control group and rosiglitazone group was significantly reduced(P＜0.01 ).However,the AI of RGCs in the rosiglitazone group was significantly lower than that of diabetic control group in various time points (q =19.28,27.39,49.92,P＜0.01 ). Conclusions As one of the PPAR-γexcitomotors,rosiglitazone can inhibit apoptosis of RGCs through downregulating the expression of NF-κB in rat retina with diabetes mellitus,indicating a protective effect of rosiglitazone on retina in diabetic rat.