Bilateral, Simultaneous Central Serous Chorioretinopathy in Association With Oral Contraception Use.

This report describes a case of bilateral, simultaneous central serous chorioretinopathy (CSCR) in a young woman on oral contraceptive pills (OCP). A 21-year-old woman with a negative past medical history presented with sudden onset of bilateral decreased vision shortly after starting OCP. Comprehensive ocular examination revealed bilateral central serous chorioretinopathy (CSCR), confirmed on retinal optical coherence tomography (OCT) and intravenous fluorescein angiography.

A Rare Case of Vomiting-Induced Retrobulbar Hemorrhage.

Retrobulbar hemorrhage may result in sudden accumulation of blood in the retrobulbar space which can lead to an orbital compartment syndrome. This potentially blinding condition is characterized by a rapid increase in intra-orbital pressure. While most commonly associated with orbital trauma, it may rarely occur with Valsalva events in patients on anticoagulants.

Poststreptococcal keratouveitis associated with group C streptococcus pharyngitis.

Purpose: To report the first case of poststreptococcal syndrome uveitis (PSU) in association with group C streptococcus (GCS).

Patients And Methods: Chart review of a 24-year-old man who presented with bilateral ocular redness, pain, and photophobia for 5 days and "white rings" around his eyes for a duration of 3 days. The patient further reported fever and sore throat in the preceding week.

A novel calpain inhibitor for treatment of transient retinal ischemia in the rat.

After an acute ischemia/reperfusion of the rat retina, the activation of cytotoxic proteases, including calpain, results in necrosis and apoptosis of retinal ganglion cells resulting in their degeneration. Using a systemically administered calpain inhibitor that crosses the blood-retinal barrier would provide for novel systemic intervention that protects the retina from acute injury and loss of function. Herein, we study a novel calpain peptide inhibitor, cysteic-leucyl-argininal (CYLA), in an in-vivo rat model of retinal ischemia to determine functional protection using electroretinography.

Branch retinal artery occlusion and non-ischemic central retinal vein occlusion due to hyperhomocysteinemia in a 14-year-old child.

A 14-year-old girl presented with sudden, painless loss of vision in the left eye. Complete ophthalmologic examination including fluorescein angiography revealed an impending central vein occlusion and a branch retinal artery occlusion inferotemporally. One month later, there was a non-ischemic central retinal vein occlusion of the same eye.

Necroptosis, a novel form of caspase-independent cell death, contributes to neuronal damage in a retinal ischemia-reperfusion injury model.

Unlabelled: Necroptosis is programmed necrosis triggered by death receptor signaling. We investigated whether necroptosis contributes to neuronal damage and functional impairment in a model of retinal ischemia.

Methods: Sprague-Dawley rats were subjected to raised intra-ocular pressure for 45 min and received intravitreal injections of the specific necroptosis inhibitor, Nec-1, its inactive analogue (Nec-1i) or vehicle.

Deleterious role of TNF-alpha in retinal ischemia-reperfusion injury.

Purpose: Tumor necrosis factor (TNF)-alpha is a mediator of neuronal cell death and survival in ischemia-reperfusion injury. This study was conducted to further elucidate the role of TNF-alpha and its receptor in an in vivo model of retinal ischemia-reperfusion injury by investigating its effects on retinal histopathology and function.

Methods: Retinal ischemia-reperfusion injury was performed on p55 and p75 knockout (KO) mice and Sprague-Dawley rats using the high intraocular pressure

Method: The temporal expression of TNF-alpha was ascertained with immunohistochemical staining.

EDG receptors as a potential therapeutic target in retinal ischemia-reperfusion injury.

LPA (lysophosphatidic acid) specific endothelial differentiation gene (EDG) receptors have been implicated in various anti-apoptotic pathways. Ischemia of the brain and retina causes neuronal apoptosis, which raises the possibility that EDG receptors participate in anti-apoptotic signaling in ischemic injury. We examined the expression of EDG receptors in a model of retinal ischemia-reperfusion injury and also tested LXR-1035, a novel analogue of LPA, in the rat following global retinal ischemic injury.

Ischemic preconditioning attenuates apoptotic cell death in the rat retina.

Purpose: Ischemic preconditioning (IPC) protects the rat retina against the injury that ordinarily follows prolonged ischemia. It has been shown that release of adenosine, de novo protein synthesis, and mediators, such as protein kinase C and K(ATP) channels, is required for IPC protection. However, the molecular mechanisms of neuroprotection by IPC are unknown.

Erythropoietin administration protects retinal neurons from acute ischemia-reperfusion injury.

Erythropoietin (EPO) plays an important role in the brain's response to neuronal injury. Systemic administration of recombinant human EPO (rhEPO) protects neurons from injury after middle cerebral artery occlusion, traumatic brain injury, neuroinflammation, and excitotoxicity. Protection is in part mediated by antiapoptotic mechanisms.