Full-thickness macular hole: a rare complication of neuroretinitis.

is a known infective cause of neuroretinitis. We present a case of neuroretinitis complicated by macular hole in a 22-year-old man. The neuroretinitis was managed with early high-dose intravenous corticosteroid and oral antibiotic.

Nanomembrane-Based, Thermal-Transport Biosensor for Living Cells.

Knowledge of materials' thermal-transport properties, conductivity and diffusivity, is crucial for several applications within areas of biology, material science and engineering. Specifically, a microsized, flexible, biologically integrated thermal transport sensor is beneficial to a plethora of applications, ranging across plants physiological ecology and thermal imaging and treatment of cancerous cells, to thermal dissipation in flexible semiconductors and thermoelectrics. Living cells pose extra challenges, due to their small volumes and irregular curvilinear shapes.

Recessive mutations in DGKE cause atypical hemolytic-uremic syndrome.

Pathologic thrombosis is a major cause of mortality. Hemolytic-uremic syndrome (HUS) features episodes of small-vessel thrombosis resulting in microangiopathic hemolytic anemia, thrombocytopenia and renal failure. Atypical HUS (aHUS) can result from genetic or autoimmune factors that lead to pathologic complement cascade activation.

Bevacizumab for neovascular age related macular degeneration (ABC Trial): multicentre randomised double masked study.

Objectives: To evaluate the efficacy and safety of intravitreous bevacizumab injections for the treatment of neovascular age related macular degeneration.

Design: Prospective, double masked, multicentre, randomised controlled trial.

Setting: Three ophthalmology centres in the United Kingdom.

Inflammatory choroidal neovascular membrane in posterior uveitis-pathogenesis and treatment.

Choroidal neovascular membrane (CNVM) formation is a well-documented sight-threatening complication of posterior segment intraocular inflammation (PSII). The aim of this article is to review the basic and clinical science literature on the pathogenesis of CNVM formation in PSII and to present results of a case series. We searched the literature using the mesh terms- inflammation, CNVM, age-related macular degeneration, immunosuppression, photodynamic therapy, steroids, vascular endothelial growth factors and posterior uveitis.

Angle closure glaucoma and lens subluxation secondary to eye rubbing in a patient with mycosis fungoides.

We report an unusual case of angle closure glaucoma in a patient with the skin lymphoma mycosis fungoides. Constant eye rubbing led to bilateral lens subluxation and uncontrolled intraocular pressure.

Subperiosteal orbital hemorrhage following self-strangulation.

Subperiosteal orbital hematomas are uncommon. The delayed presentation of such an event is described in an anticoagulated patient who attempted self-strangulation. Despite the initial presence of a relative afferent pupillary defect, excellent visual recovery occurred, demonstrating the importance of prompt recognition and treatment.

Changes in the balance of the tissue inhibitor of matrix metalloproteinases (TIMPs)-1 and -3 may promote keratocyte apoptosis in keratoconus.

Keratoconus is a disease in which the central cornea becomes thinned. This could result from corneal stromal cell apoptosis or be induced or perpetuated by the activation of matrix degrading enzymes, particularly members of the matrix metalloproteinase (MMP) family. In some circumstances, the MMP inhibitors TIMP-1 and TIMP-3 exhibit anti-apoptotic and pro-apoptotic properties, respectively.

Matrix bound SFD mutant TIMP-3 is more stable than wild type TIMP-3.

Background: Sorsby's fundus dystrophy (SFD) is a degenerative retinopathy characterised by accumulation of mutant TIMP-3 protein in Bruch's membrane.

Aim: To compare the stability of matrix bound SFD mutant TIMP-3s with wild type TIMP-3.

Methods: COS-7 cells were transfected with plasmids containing wild type, Ser 181, Gly-167, Ser-156, and Tyr-168 TIMP-3 cDNA.

Sorsby's fundus dystrophy mutant tissue inhibitors of metalloproteinase-3 induce apoptosis of retinal pigment epithelial and MCF-7 cells.

C-terminal domain tissue inhibitor of metalloproteinases-3 (TIMP-3) mutations cause the rare hereditary blindness Sorsby's fundus dystrophy (SFD), which involves loss of retinal pigment epithelial (RPE) cells. Since wild-type TIMP-3 causes apoptosis, we investigated whether SFD TIMP-3 might kill RPE and other cells. Plasmid-mediated overexpression of Ser-156, Gly-167, Tyr-168 and Ser-181 SFD mutant TIMP-3 decreased RPE viability to 22+/-8, 20+/-6, 32+/-5, 30+/-12% (SFD mutants all P<0.

Adenovirus mediated gene delivery of tissue inhibitor of metalloproteinases-3 induces death in retinal pigment epithelial cells.

Background: Sorsby's fundus dystrophy (SFD) and age related macular degeneration (ARMD) are retinal diseases associated with a high level of accumulation of mutant and wild type TIMP-3, respectively, in Bruch's membrane. The pathogenic role of TIMP-3 in these diseases is uncertain, but causative mutations have been identified in the TIMP-3 gene of patients with SFD. Recent reports that TIMP-3 causes apoptosis in certain cell types and not in others prompted the authors to investigate whether TIMP-3 causes apoptosis in cultured retinal pigment epithelium (RPE) cells.