Branch retinal vein occlusion has an incidence of 0.5% to 1.2%. Several risk factors, such as hypertension, hyperlipidemia, diabetes mellitus, thrombophilia and hypercoagulation, systemic and inflammatory diseases, medications, and ocular conditions, have found to be associated with BRVO. The symptoms depended on the site and severity of the occlusion. The average reduction in visual acuity for ischemic BRVO is 20/50 and for nonischemic BRVO is 20/60. Acute BRVO can be detected by fundoscopy, where flame hemorrhages, dot and blot hemorrhages, cotton wool spots, hard exudates, retinal edema, and dilated tortuous veins can be observed. Chronic BRVO would be more subtle and characterized by the appearance of venous collateral formation and vascular sheathing, in addition to complications previously mentioned. Areas of ischemia can be evaluated using fluorescein angiography. The extent of macular edema and the presence of retinal detachment can be detected by fundoscopic examination or fluorescein angiography, although optical coherence tomography is considered to be the best method. As far as complications, the most common is macular edema, followed by retinal neovascularization, vitreous hemorrhage, or retinal detachment.
Coats’ disease is an idiopathic, ophthalmic condition characterized by retinal telangiectasis, intraretinal and subretinal exudation, which can lead to retinal detachment. It is mostly unilateral, progressive and affects mainly males during childhood, although adult cases have also been described. In this review, we make an update of the literature about Coats’ disease, emphasizing on diagnosis and treatment, including the most recent treatment modalities, i.e. anti-vascular endothelial growth factor agents.
Macroautophagy/autophagy is an evolutionarily conserved catabolic pathway whose modulation has been linked to diverse disease states, including age-associated disorders. Conventional and conditional whole-body knockout mouse models of key autophagy genes display perinatal death and lethal neurotoxicity, respectively, limiting their applications for in vivo studies. Here, we have developed an inducible shRNA mouse model targeting Atg5, allowing us to dynamically inhibit autophagy in vivo, termed ATG5i mice. The lack of brain-associated shRNA expression in this model circumvents the lethal phenotypes associated with complete autophagy knockouts. We show that ATG5i mice recapitulate many of the previously described phenotypes of tissue-specific knockouts. While restoration of autophagy in the liver rescues hepatomegaly and other pathologies associated with autophagy deficiency, this coincides with the development of hepatic fibrosis. These results highlight the need to consider the potential side effects of systemic anti-autophagy therapies.
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