The mechanisms for mutual interactions between microglial cell and Müller cell in ischemic retinopathy / 中华眼底病杂志

Ischemic retinopathy,resulting in multiple lesions like microvasculature damage,inflammation and neovascularization,is a major contributor of vision damage.In these pathological changes,retinal glia cannot be ignored in the development of retinopathy.They constitute a highly versatile population that interacts with various cells to maintain homeostasis and limit disease.Therefore,glial activation and gliosis are strikingly ubiquitous responses to almost every form of retinal disease.Both of microglial cells and Müller cells are major intrinsic retinal glial cells and they are in close relationship,which means they can influence each other,make joint action or even become interdependent.They exhibit morphological and functional changes to have an impact on degree of retinal injury through different responses,which mediated by glial cells are important not only for course of disease progression,but also for the maintenance of neuronal and photoreceptor survival.Thus,defining the mechanisms that underlie communications between microglial cells and Miller cells could enable the development of more selective therapeutic targets,with great potential clinical applications.

Role of autophagy in angiogenesis of retinal vascular endothelial cells under hypoxia condition / 中华实验眼科杂志

Objective To study the role of autophagy in proliferation,migration and tube formation of retinal vascular endothelial cells (RVECs) under the condition of hypoxia in vitro.Methods Mouse RVECs were isolated from 50 C57BL/6J mice primarily cultured using explant culture method,and the cells were identified by immunofluorescence of CD34.Well cultured RVECs were divided into normal control group,hypoxia control group and hypoxia+ 3-methyladenine (3-MA) group.The cells in the normal control group were cultured in the normal environment for 24 hours,and the cells in the hypoxia control group were cultured 1％ O2 environment for 24 hours,and the cells in the hypoxia+3-MA group were pretreated with 5 mmol/L 3-MA for 4 hours and then exposed to 1％ O2 environment for 24 hours.Microtubule-related protein 1 light chain 3 (LC3-Ⅱ/LC3-Ⅰ) and Beclin-1 protein contents in the cells were detected by Western blot analysis;the ultrastructure of autophagosome was examined under the transmission electron microscope.The proliferation,migration and tube formation of the cells were detected by Click-iTEdU kit,scratch assay and matrigel,respectively.Results Primarily culture cells grew well with the cobblestone-like appearance 5-7 days after culture and showed positive response for CD34.The autophagosome number was increased in the hypoxia control group compared with the hypoxia+3-MA group and normal control group.The LC3-Ⅱ/LC3-Ⅰ ratio was 0.243 ± 0.030,0.658 ± 0.032 and 0.405 ± 0.095;the relative expression of Beclin-1 protein in the cells was 0.260±0.040,0.650±0.071 and 0.461±0.089;the proliferation rate of the cells was (45.93± 6.39) ％,(22.74± 2.35) ％ and (24.12 ± 3.59) ％;the scratch healing rate of the cells was (36.02 ± 5.84) ％,(57.26±11.98) ％ and (18.16±9.73) ％;the number of tube formation was 29.20±6.10,41.40±4.04 and 22.00± 2.92 in the normal control group,hypoxia control group and hypoxia + 3-MA group,respectively,with significant differences among the groups (F =35.86,23.53,34.28,21.12,23.27;all at P＜0.01).Compared with the normal control group,the ratio of LC3-Ⅱ/LC3-Ⅰ and the expression of Beclin-1 protein,scratch healing rate and the number of tube formation were significantly increased,and the proliferation rate was significantly reduced in the hypoxia control group (all at P ＜ 0.05).Compared with the hypoxia control group,the ratio of LC3-Ⅱ/LC3-Ⅰ and the expression of Beclin-1 protein,scratch healing rate and the number of tube formation were significantly decreased in the hypoxia + 3-MA group.Conclusions Hypoxia environment activates autophagy of mouse RVECs,which enhances the migration and tube formation abilities of the cells.3-MA inhibits the angiogenesis abilities of mouse RVECs.

Bilateral Profound Visual Loss As a Consequence of Leukaemia – A Case Report

An 18-year-old Malay gentleman was noted to have profound bilateral blurred vision for one month duration, associated with loss of weight, appetite, low grade fever and abdominal distension. Visual acuity on presentation was 6/60 on the right, counting finger on the left with no afferent pupillary defect. Anterior segments were unremarkable. Vitreous cells were occasional bilaterally. Fundus revealed multiple choroidal and sub-retinal Roth spots with areas of pre-retinal and intra-retinal haemorrhages, involving the macula in the left eye. Vessels were dilated and tortuous in all quadrants of the right eye. Many areas of capillary fall out at peripheral retina were demonstrated in fundus fluorescein angiogram. Further systemic and laboratory review confirmed the diagnosis of CML and chemotherapy was initiated. Both eye ischaemic retinopathy secondary to CML was confirmed and scatter pan retinal photocoagulation was performed bilaterally. Good improvement in vision noted during subsequent follow up to 6/24 on the right, 6/60 on the left. High levels of suspicion and accurate early recognition of fundus changes are vital in these types of cases to ensure the institution of prompt treatment.

Ischemic Retinopathy Due to Suspicious Gentamicin Retinal Toxicity after Primary Repair of Scleral Laceration

PURPOSE: To report a case of ischemic retinopathy due to suspicious gentamicin retinal toxicity after primary repair of a scleral laceration. CASE SUMMARY: A 45-year-old man presented to our department with decreasing vision in his right eye after ocular trauma. Best corrected visual acuity (BCVA) was 0.02 in the right eye and slit lamp examination revealed scleral laceration. Both intravenous and topical antibiotics (10% cefazolin and 2% gentamicin) were immediately administered. On intraoperative examination, a scleral laceration located 5 mm to 11 mm from nasal limbus, prolapsed vitreous body and partial division of medial rectus muscle were observed. After irrigation with gentamincin 0.2% around the wound, primary repair was performed. On postoperative day 3, fundus examination revealed a retinal break, barrier laser was performed. On postoperative day 4, diffuse retinal edema with intraretinal hemorrhage was observed as well as, superonasal ghost vessels. Subsequently, fluorescein angiography showed diffuse leakage of retinal vessels and a nonperfusion area at the periphery, especially on the nasal side. As vitreous opacity became worse, the patient underwent pars plana vitrectomy with endolaser. One month later, vitreous cavity was clearer and best visual acuity was 0.2. CONCLUSIONS: Large doses of intraocular gentamicin ccan cause retinal toxicity. Increased gentamicin application through a scleral laceration may lead to toxic antibiotic levels. When a scleral laceration wound irrigation is performed, precautions are necessary to prevent retinal ischemia associated with gentamicin toxicity.

A study protocol on the situational analysis on the current practice of screening and treatment of Retinopathy of Prematurity (ROP)

Objective@#The study protocolaims to provide an overview of the current practice of screening and treatment of ROP in the selected, to estimate the proportion of childhood blindness due to ROP and assess the number of premature babies at risk for ROP.@*Methods@#The study protocol is a descriptive, cross sectional study design using survey questionnaire to be sent out to pediatric ophthalmologists, vitreo-retina specialists and division heads of the neonatal intensive care units of different hospitals in a selected area. Student records and medical abstracts from local schools for the blind will be obtained and will be reviewed. All qualitative data will be reported by frequency distribution and percentages. Extrapolation on the proportion of ROP in the area will be done. @*Conclusion@#Results from the study can show an overview of the current situation of ROP in a selected area and provide the framework for recommendations for programs aimed providing criteria for timely screening and treatment of ROP to prevent complications such as childhood visual impairment and blindness in the country.

Clinical analysis of fundus fluorescein angiography in Takayasu arteritis / 眼科研究

Background Takayasu arteritis is a non specificity inflammation of aorta and its branch.The incidence of Takayasu arteritis is low and its ocular secondary disease is rare.The correct diagnosis of Takayasu arteritis is very important for its early treatment in clinic.Objective This study is to analyze the fundus findings and characteristic of fundus fluorescein angiography (FFA) of Takayasu retinopathy.Methods The FFA and clinical data of 12 patients (24 eyes) with Takayasu arteritis were retrospectively reviewed.Written informed consent was obtained from all the patients before and initiation of any study protocol.Results In 12 patients,chronic ischemic retinopathy was found in 15 eyes of 9 patients.The arm to retina circulation time(A RCT) prolonged to (19.20±2.95) s in 5 eyes,and the retinal circulation time (RCT) delayed to 10.62±6.15 s in 5 eyes.Peripapillary arteriovenous anastomosis was found in 2 eyes of 2 patients.Macular arch ring was incomplete in 6 eyes of 4 patients.Eight patients (14 eyes) had telangiectasis and microaneurysm,and 2 eyes of 2 patients presented neovascularization on the disc or elsewhere.In 12 patients,hypertensive retinopathy was found in 4 eyes of 3 patients,showing narrow retinal artery,arteriosclerosis,hemorrhage,cotton wool spots and hard exudates.Ten patients were diagnosed as Takayasu arteritis before FFA examination,and 2 patients were determinedly diagnosed after FFA was performed.Conclusion The main features of Takayasu retinopathy are hypertensive retinopathy and chronic ischemic retinopathy.It is important for ophthalmologist to correctly recognize the clinical features of TA.

Intravitreal Bevacizumab (Avastin) Treatment of Neovascular Glaucoma in Ocular Ischemic Syndrome

We report a case of ocular ischemic syndrome accompanied by neovascular glaucoma that was successfully treated with Bevacizumab. A 70-year-old male patient diagnosed with neovascular glaucoma of the left eye 3-4 years prior complained of continuous left eye pain and declining visual acuity despite receiving the latest treatment methods. At the time of admission the patient had no light perception in the left eye and his intraocular pressure was 30 mmHg. Anterior segment and fundus examinations revealed neovascularization of the iris and stenosis of the retinal vessel. Hypofluorescence of the choroid and retinal vessels was observed on fluorescence fundus angiography. Left internal carotid artery stenosis was observed on a brain MRI. Despite being treated with eye solution and oral medication, intraocular pressure was not controlled. After 7 days, we performed an intravitreal Bevacizumab 1.25 mg/0.05mL injection. One day after the intravitreal Bevacizumab injection, the neovascularization had nearly regressed and intraocular pressure was 30 mmHg. Intravitreal Bevacizumab injection produced regression of neovascularization and proved effective for treatment of neovascular glaucoma in this case of ocular ischemic syndrome.

Intravitreal Bevacizumab (Avastin) Treatment of Neovascular Glaucoma in Ocular Ischemic Syndrome

We report a case of ocular ischemic syndrome accompanied by neovascular glaucoma that was successfully treated with Bevacizumab. A 70-year-old male patient diagnosed with neovascular glaucoma of the left eye 3-4 years prior complained of continuous left eye pain and declining visual acuity despite receiving the latest treatment methods. At the time of admission the patient had no light perception in the left eye and his intraocular pressure was 30 mmHg. Anterior segment and fundus examinations revealed neovascularization of the iris and stenosis of the retinal vessel. Hypofluorescence of the choroid and retinal vessels was observed on fluorescence fundus angiography. Left internal carotid artery stenosis was observed on a brain MRI. Despite being treated with eye solution and oral medication, intraocular pressure was not controlled. After 7 days, we performed an intravitreal Bevacizumab 1.25 mg/0.05mL injection. One day after the intravitreal Bevacizumab injection, the neovascularization had nearly regressed and intraocular pressure was 30 mmHg. Intravitreal Bevacizumab injection produced regression of neovascularization and proved effective for treatment of neovascular glaucoma in this case of ocular ischemic syndrome.

Two Cases of Ischemic Retinopathy due to Intravitreal Gentamicin Toxicity after Vitrectomy

Retinal toxicity secondary to intravitreal injection of gentamicin for the purpose of prophylaxis or treatment of endophthalmitis was reported infrequently and it was thought to be caused by an error in the intravitreal injection technique or by faulty dilution of gentamicin. After vitrecotomy, we experienced two cases of ischemic retinopathy secondary to intravitreal injection of gentamicin for prevention of endopthalmitist.