Cyclophotocoagulation with an illuminated laser probe under a noncontact wide-angle retinoscope: A modified technique of ciliary body photocoagulation.

PURPOSE: This study aimed to investigate the efficacy of cyclophotocoagulation with an illuminated laser probe under a noncontact wide-angle retinoscope in treating refractory glaucoma. METHODS: Eleven patients (11 eyes) with refractory neovascular glaucoma were treated with ciliary body photocoagulation. Preoperative and postoperative corrected visual acuity, intraocular pressure (IOP), ophthalmofundoscopy, B-ultrasound and ultrasound biomicroscopy, optical coherence tomography, and fundus fluorescein angiography were performed. RESULTS: Preoperative IOP ranged from 45 to 58 mmHg (mean 51.9 mmHg). At postoperative 1, 3, and 6 months, the IOPs ranged between 16 and 33 mmHg (mean 27.1 mmHg), 14-28 mmHg (mean 20.6 mmHg), and 14-28 mmHg (mean 18.5 mmHg), respectively. IOP at the last follow-up (range 7-12 months) was 15-24 mmHg (mean 18.8 mmHg). An average of 63.8% decrease in postoperative IOP was found in these patients with no associated complications. The postoperative fibrotic exudate, anterior chamber hyphema, and exudative choroidal detachment were all well-managed and resolved. No patients experienced intraocular lens deviation or dislocation, hypotonia oculi, atrophy of eyeball, retinal detachment, endophthalmitis, or sympathetic ophthalmia. CONCLUSION: Cyclophotocoagulation with an illuminated laser probe under a noncontact wide-angle retinoscope is a safe and effective technique for the treatment of neovascular glaucoma.

Unilateral endogenous fungal endophthalmitis after esophageal cancer surgery: a case report.

BACKGROUND: This study reports a case of Unilateral Endogenous Fungal Endophthalmitis After Esophageal Cancer Surgery. CASE PRESENTATION: One patient presented with a month-long loss of vision in his left eye, he had surgery for esophageal cancer 2 months earlier. The patient underwent cataract surgery (by phacoemulsification) in the left eye combined with 25-gauge vitrectomy and silicone oil tamponade. The microbiological culture pointed to infection with Candida albicans. At 3-month follow-up, the unaided visual acuity of left eye was 0.02 and corrected visual acuity was 0.2. In addition, there was no recurrence of the endophthalmitis within 1 year of the surgery. CONCLUSION: The early diagnosis of endogenous fungal endophthalmitis is difficult, and the disease is very likely to be misdiagnosed as uveitis. It is therefore critical to improve awareness of this condition and to reduce the incidence of its misdiagnosis.

HSV­TK/GCV can induce cytotoxicity of retinoblastoma cells through autophagy inhibition by activating MAPK/ERK.

Retinoblastoma is an severe ophthalmic disease and the most common type intraocular malignant tumor, particularly in infants. Currently, few drugs and therapies are available. Gene therapy has been considered to be a potential treatment to cure cancer effectively and Herpes simplex virus type 1 thymidine kinase/ganciclovir (HSV­TK/GCV) is one type of suicide gene therapy that has been extensively studied. Numerous in vitro and in vivo studied have shown that this system can kill tumor cells, including liver and lung cancer cells. GCV is used as an antiviral drug, and the thymidine kinase, HSV­TK can phosphorylate GCV to GCV­TP, a competitive inhibitor of DNA synthesis, instead of guanine­5'­triphosphate in the process of DNA synthesis. This process prevents DNA chain elongation causing cell death via apoptosis. However, the toxic effects of HSV­TK/GCV on retinoblastoma cells remain unknown, and the molecular mechanisms of its therapeutic effects have not been fully elucidated. Our results suggest that HSV­TK/GCV can significantly cause the death of retinoblastoma cell lines, HXO­RB44 and Y79. Further studies have reported that this cell death is induced by the inhibition of autophagy by activating the MAPK/ERK (mitogen­activated protein kinase/ERK) signaling pathway. The mTOR inhibitor Torin1 can partially block the toxic effects of HSV­TK/GCV on HXO­RB44 cells. The above results demonstrate that the mechanism undertaken by HSV­TK/GCV to exhibit therapeutic effects mechanism may inhibit autophagy by activating MAPK/ERK. The findings of the present study may provide novel insight for the exploration of HSV­TK/GCV in the treatment of retinoblastoma.

Metformin inhibits development of diabetic retinopathy through inducing alternative splicing of VEGF-A.

Previous studies have shown that metformin, an AMP-activated protein kinase activator widely prescribed for type 2 diabetes, is especially beneficial in cases of diabetic retinopathy (DR) with undetermined mechanisms. Here, we used a streptozotocin-induced diabetes model in mice to study the effects of metformin on the development of DR. We found that 10 weeks after STZ treatment, DR was induced in STZ-treated mice, regardless treatment of metformin. However, metformin alleviated the DR, seemingly through attenuating the retina neovascularization. The total vascular endothelial cell growth factor A (VEGF-A) in eyes was not altered by metformin, but the phosphorylation of the VEGF receptor 2 (VEGFR2) was decreased, which inhibited VEGF signaling. Further analysis showed that metformin may induce VEGF-A mRNA splicing to VEGF120 isoform to reduce its activation of the VEGFR2. These findings are critical for generating novel medicine for DR treatment.