Swept-Source OCT Angiography Identifies Choroidal Neovascularization Arising From a Choroidal Nevus.

Swept-source optical coherence tomography angiography (SS-OCTA) was used to diagnose choroidal neovascularization (CNV) arising from a choroidal nevus. A 61-year-old woman initially presented with submacular hemorrhage. She was diagnosed with neovascular age-related macular degeneration (AMD) and received three injections of bevacizumab (Avastin; Genentech, South San Francisco, CA). At a follow-up visit, SS-OCTA showed that the CNV appeared to arise from an adjacent choroidal nevus. This is the first report of using SS-OCTA to diagnose CNV associated with a choroidal nevus masquerading as neovascular AMD. [Ophthalmic Surg Lasers Imaging Retina. 2018;49:360-363.].info:eu-repo/semantics/publishe

Swept-Source OCT Angiography Identifies Choroidal Neovascularization Arising From a Choroidal Nevus

Swept-source optical coherence tomography angiography (SS-OCTA) was used to diagnose choroidal neovascularization (CNV) arising from a choroidal nevus. A 61-year-old woman initially presented with submacular hemorrhage. She was diagnosed with neovascular age-related macular degeneration (AMD) and received three injections of bevacizumab (Avastin; Genentech, South San Francisco, CA). At a follow-up visit, SS-OCTA showed that the CNV appeared to arise from an adjacent choroidal nevus. This is the first report of using SS-OCTA to diagnose CNV associated with a choroidal nevus masquerading as neovascular AMD. [Ophthalmic Surg Lasers Imaging Retina. 2018;49:360-363.].info:eu-repo/semantics/publishe

Primary Baerveldt Shunt Implantation: Outcomes and Complications

<p><b>Article full text</b></p> <p><br></p> <p>The full text of this article can be found here<b>.</b> <a href="https://link.springer.com/article/10.1007/s40123-016-0056-4">https://link.springer.com/article/10.1007/s40123-016-0056-4</a></p><p></p> <p><br></p> <p><b>Provide enhanced content for this article</b></p> <p><br></p> <p>If you are an author of this publication and would like to provide additional enhanced content for your article then please contact <a href="http://www.medengine.com/Redeem/”mailto:[email protected]”"><b>[email protected]</b></a>.</p> <p><br></p> <p>The journal offers a range of additional features designed to increase visibility and readership. All features will be thoroughly peer reviewed to ensure the content is of the highest scientific standard and all features are marked as ‘peer reviewed’ to ensure readers are aware that the content has been reviewed to the same level as the articles they are being presented alongside. Moreover, all sponsorship and disclosure information is included to provide complete transparency and adherence to good publication practices. This ensures that however the content is reached the reader has a full understanding of its origin. No fees are charged for hosting additional open access content.</p> <p><br></p> <p>Other enhanced features include, but are not limited to:</p> <p><br></p> <p>• Slide decks</p> <p>• Videos and animations</p> <p>• Audio abstracts</p> <p>• Audio slides</p

In Vivo Serial Imaging of Regenerating Corneal Nerves after Surgical Transection in Transgenic Thy1-YFP mice

After surgical transection, corneal nerves regenerate to achieve normal density but do not readopt the normal arrangement. Myelinated nerve fibers also regenerate along with nociceptive nerve fibers in the central corneal stroma

Ocular Surface Extracellular DNA and Nuclease Activity Imbalance: A New Paradigm for Inflammation in Dry Eye Disease

PURPOSE. We determined whether nucleases are deficient in the tear fluid of dry eye disease (DED) patients, and whether this causes extracellular DNA (eDNA) and neutrophil extracellular trap (NET) accumulation in the precorneal tear film, thus causing ocular surface inflammation. METHODS. Exfoliated cells adhered to Schirmer test strips were collected on glass slides, and immunofluorescence confocal microscopy was used to evaluate neutrophils, eDNA, NETs, and their molecular components. Similar experiments were performed with mucoid films collected from the inferior conjunctival fornix or bulbar conjunctiva. We used quantitative PCR to evaluate eDNA signaling pathways and inflammatory cytokine expression. We also determined the amount of ocular surface eDNA and evaluated tear fluid nuclease activity. RESULTS. eDNA, NETs, and neutrophils were present on the ocular surface in DED patients and abundant in mucoid films. NETs consisted of eDNA, histones, cathelicidin, and neutrophil elastase. Tear fluid nuclease activity was decreased significantly in DED patients, whereas the amount of eDNA on the ocular surface was increased significantly. Expression of genes downstream of eDNA signaling, such as TLR9, MyD88, and type I interferon, as well as the inflammatory cytokines interleukin-6 and tumor necrosis factor-a, was significantly increased in DED patients. CONCLUSIONS. Extracellular DNA production and clearance mechanisms are dysregulated in DED. Nuclease deficiency in tear fluid allows eDNA and NETs to accumulate in precorneal tear film, and results in ocular surface inflammation. These findings point to novel therapeutic interventions in severe DED based on clearance of eDNA, NETs, and other molecular components from the ocular surface. Although DED pathogenesis is not understood fully, inflammation has a prominent role in DED symptom development and amplification. 2 The current paradigm suggests that ocular surface inflammation is triggered by surface epithelium stress caused by tear hyperosmolarity. Inflammation is sustained by activated antigen-presenting cells (APCs) and T-cells via the afferent and efferent limbs of the adaptive immune system. 3,4 The immunopathologic events that sustain the systemic adaptive immune response in DED have been characterized. 2-4 However, the mechanisms that activate the adaptive immune response are understood poorly. Ocular surface epithelial stress is a key initial event, and a major source of innate cytokines and chemokines that can damage epithelial cells and activate APCs. Tear hyperosmolarity is recognized as an important stressor. However, tear replacement to decrease osmolarity provides limited therapeutic benefit. Therefore, additional stressors may activate DED ocular surface inflammation, and link the innate and adaptive immune mechanisms. The ocular surface epithelium undergoes continuous, dynamic turnover, 5,6 which is increased in DED patients. 7 Superficial corneal cells are shed into the precorneal tear film. From th