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https://www.selleckchem.com/products/pacritinib-sb1518.html Non-arteritic anterior ischemic optic neuropathy (NAION) is characterized by the progressive and irreversible death of retinal ganglion cells (RGCs) which is caused by the insufficient blood supply to the optic nerve (ON) head. At present, hormone therapy is used to reduce optic edema, followed by nerve nutrition therapy to protect the ON. However, no surgical or medical therapy has proven to be beneficial consistently in treating NAION. Vincamine is an alkaloid extracted from the Apocynaceae Vinca plant. Vincamine and its derivatives acting as cerebral vasodilators can easily cross the blood-brain barrier, improve the metabolism of ischemic tissue and protect the neuron. In this study, we aimed to investigate the potential neuroprotection of Vincamine in the photodynamic induced rat model of NAION (rAION), to evaluate its effects and possible mechanisms. We found that Vincamine can rescue RGC death and reduce the number of apoptotic cells. The protection of Vincamine might play through the PI3K/Akt/eNOS signaling pathway. Therefore, Vincamine can be an effective therapy method for NAION. To report a case of bilateral choroidal effusion after laser capsulotomy. A healthy 85 years old white woman was referred to our hospital with a diagnosis of posterior capsule opacification in the left eye. The patient was treated with laser capsulotomy and oral acetazolamide was administered after the procedure. The day after, the patient visited the emergency room complaining bilateral blurred vision. A myopic shift and peripheral choroidal detachment was noted in both eyes. Discontinuation of acetazolamide and treatment with topical steroid and cyclopentolate resulted in a significant improvement in visual acuity and the complete resolution of the choroidal detachment in 1 week. To the best of our knowledge, this is the first reported case of choroidal detachment and acute transient myopia following the administration o

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