Screening for Diabetic Retinopathy Using a Portable, Noncontact, Nonmydriatic Handheld Retinal Camera.

Background: Diabetic retinopathy (DR) is a leading cause of low vision and blindness. We evaluated the feasibility of using a handheld, noncontact digital retinal camera, Pictor, to obtain retinal images in dilated and undilated eyes for DR screening. We also evaluated the accuracy of ophthalmologists with different levels of training/experience in grading these images to identify eyes with vision-threatening DR.

Immunologic graft rejection in descemet's stripping endothelial keratoplasty and penetrating keratoplasty for endothelial disease.

Objective: To evaluate and compare the cumulative incidence and risk factors for first-episode immunologic graft rejection in Descemet's stripping automated endothelial keratoplasty (DSAEK) and penetrating keratoplasty (PK) and to identify potential risk factors for rejection.

Design: Retrospective chart review.

Participants: All patients who underwent PK or DSAEK for endothelial disease at the Department of Ophthalmology, North Shore LIJ, between January 2004 and June 2010.

Soluble vascular endothelial growth factor receptor-1 contributes to the corneal antiangiogenic barrier.

Purpose: Pathological neovascularisation within the normally avascular cornea is a serious event that can interfere with normal vision. Upregulation of vascular endothelial growth factor (VEGF) has been associated with neovascularisation in the eye, suggesting that maintaining low levels of VEGF is important for corneal avascularity and intact vision. This study aims to determine the expression profile and possible contribution of sVEGFR-1 to the corneal avascular barrier.

Flt-1 intraceptor induces the unfolded protein response, apoptotic factors, and regression of murine injury-induced corneal neovascularization.

Purpose: To determine whether Flt24K, a recombinant construct of domains 2 to 4 of VEGFR-1 (Flt) coupled with an endoplasmic reticulum retention signal (KDEL) can bind VEGFR-2 and induce apoptosis, unfolded protein response (UPR), and regression of injury-induced corneal neovascularization.

Methods: Human microvascular endothelial cells were transfected with pCMV.Flt24K and subjected to hypoxia.

Corneal avascularity is due to soluble VEGF receptor-1.

Corneal avascularity-the absence of blood vessels in the cornea-is required for optical clarity and optimal vision, and has led to the cornea being widely used for validating pro- and anti-angiogenic therapeutic strategies for many disorders. But the molecular underpinnings of the avascular phenotype have until now remained obscure and are all the more remarkable given the presence in the cornea of vascular endothelial growth factor (VEGF)-A, a potent stimulator of angiogenesis, and the proximity of the cornea to vascularized tissues. Here we show that the cornea expresses soluble VEGF receptor-1 (sVEGFR-1; also known as sflt-1) and that suppression of this endogenous VEGF-A trap by neutralizing antibodies, RNA interference or Cre-lox-mediated gene disruption abolishes corneal avascularity in mice.