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Stephen Ryan Retina Pdf [UPDATED]

Features sweeping content updates, including new insights into the fundamental pathogenic mechanisms of age-related macular degeneration, advances in imaging including OCT angiography and intraoperative OCT, new therapeutics for retinal vascular disease and AMD, novel immune-based therapies for uveitis, and the latest in instrumentation and techniques for vitreo-retinal surgery.

stephen ryan retina pdf

Includes more than 50 video clips (35 new to this edition) highlighting the latest surgical techniques, imaging guidance, and coverage of complications of vitreoretinal surgery. New videos cover Scleral Inlay for Recurrent Optic Nerve Pit Masculopathy, Trauma with Contact Lens, Recurrent Retinal Detachment due to PVR, Asteroid Hyalosis, and many more.

Dr. Peter Wiedemann is Professor of Ophthalmology at Leipzig University. He is a vitreoretinal specialist whose expertise includes complex vitreoretinal surgery and macular disorders. Dr. Wiedemann earned his medical degree at Erlangen University, Germany. He started ophthalmic research at the Doheny Eye Institute, Los Angeles, with Dr. Stephen Ryan and completed residency and fellowship in ophthalmology at Cologne University with Prof. Klaus Heimann. In his research Dr. Wiedemann studies retinal and macular disorders and Müller cells pathophysiology. He has authored over 500 peer reviewed publications in ophthalmology and is co-editor of the textbook Ryan ́s Retina. He is a member of the German National Academy of Sciences Leopoldina, the German Ophthalmological Society, the American Academy of Ophthalmology and the Club Jules Gonin. He is also a Fellow of the Academia Ophthalmologica Internationalis (AOI), the European Academy of Ophthalmology, and a Board Member of the International Council of Ophthalmology (ICO).

Finally, artificial intelligence and the problem of segmentation in automated imaging are considered. The practicing retinologist is regularly confronted with symptoms from border areas, not only with internal medicine but also with neuro-ophthalmological differential diagnoses. In an overlapping area, symptoms can originate not only from the retina but also from superordinate central nervous structures. I would recommend a future edition to include a chapter that leads from symptom to diagnosis, such as phosphenes, glare, flare, palinopsia, and visual snow.

Vascular diseases of the retina are a major cause of blindness among all age groups. Edited and written by internationally well-known experts, this state-of-the-art comprehensive overview of basic and clinical science will enhance the understanding of retinal vascular disease and help in the evaluation of current and future treatment approaches for the clinician. The well-structured and highly illustrated text is divided into the following three main sections:Pathogenesis of retinal vascular diseaseGeneral concepts in the diagnosis and treatment of retinal vascular diseasePathology, clinical course and treatment of retinal vascular diseaseReader-friendly through:Step-by-step explanation of all treatment proceduresRichly illustrated by clinical image series including illustrated single case follow-upThis unique textbook-atlas also includes topics which are not currently found in other retinal disease textbooks, such as case reports and clinical follow-ups. General ophthalmologists, retina specialists as well as ophthalmologists in training will find this book highly stimulating and useful for their daily practice.

The obscured visualization of the fundus and the formation of these small gas bubbles in the vitreous cavity often preclude the use of immediate complementary postoperative laser therapy that sometimes is necessary and may conceal complications such as new retinal breaks and subretinal gas or hemorrhage as well as the central retinal artery status [8].

To describe the longitudinal changes in retinal neovascularization elsewhere (NVE) as observed on optical coherence tomography angiography (OCTA) in proliferative diabetic retinopathy (PDR) treated by panretinal photocoagulation (PRP).

Diabetic retinopathy (DR) is the leading cause of visual impairment and blindness in the working population [1]. DR is responsible for vision loss in 12.6% of diabetic patients and it tends to occur in young patients in Asian countries [1]. Proliferative diabetic retinopathy (PDR), characterized by retinal neovascularization at the disc (NVD) or elsewhere in the retina (NVE), is the most common form [2]. Panretinal photocoagulation (PRP) has been the standard treatment for PDR during the past several decades. Although anti-VEGF agents have demonstrated a positive effect in regressing retinal neovascularization in recent years, PRP is still recommended by 98% of retina specialists as the primary management of PDR [3]. In China, treatment with repeated injections of anti-VEGF agents is impractical in many patients because they are not covered by medical insurance, but the cost-effectiveness and relatively long duration of efficacy make PRP a sound and sensible choice for these patients.

In the present study, we sought to explore the short-term and long-term effects of PRP in regressing retinal NV, and OCTA was performed to quantify and monitor the NVE changes over time in response to the PRP treatment.

The inclusion criteria included treatment-naïve patients with newly diagnosed PDR and NVE, and those who were confirmed by both FFA and OCTA. To reduce bias, each patient chose one eye for observation during this study. The exclusion criteria were as follows: NVE outside the OCTA scan range; NVD (retinal neovascularization at the disc); other causes of NVE, such as retinal vein occlusion; fibrovascular proliferation with retinal traction; fibrosis, scarring, atrophy and hard exudates with central involvement; diabetic macular oedema (DME) involving the central macula; and a previous history of optic neuropathy or uncontrolled glaucoma.

Multiple clinical observations suggest that genetic factors may in part determine the severity of many angiogenesis-dependent diseases. Among patients with coronary artery disease, decreased formation of collateral vessels is associated with decreased levels of hypoxia-induced vascular endothelial growth factor (VEGF) mRNA, after normalizing for age, sex, diabetes, smoking, and hypercholesterolemia.6 The incidence of proliferative diabetic retinopathy is elevated in specific nonwhite populations after accounting for duration and control of diabetes.7 Among those with age-related macular degeneration, vision loss due to choroidal neovascularization is more prevalent in white compared to black populations after adjusting for age, sex, and smoking habits.8 Experiments among inbred strains of mice suggest that the heterogeneity of the extent of angiogenesis in response to exogenous growth factor stimulation is determined by genetic factors.9 In addition, strain-related differences in retinal angiogenesis between rat strains have been demonstrated.10, 11 This suggests that genetic factors which influence the heterogeneity of the angiogenic response may in part determine the severity of a wide spectrum of angiogenesis-dependent diseases.

We evaluated the influence of genetic background on retinal angiogenesis using a murine model of proliferative retinopathy. Here, we establish the first evidence of strain-dependent oxygen-induced retinal angiogenesis in multiple strains of mice: CD-1 (outbred), and C57BL/6J, AKR, DBA, and 129S3/SvIM (inbred). We have further characterized hypoxia-induced pro- and antiangiogenic responses in C57BL/6J and 129S3/SvIM mouse strains. Similarly, these inbred strains were previously identified, and confirmed in our laboratory,18 to have divergently low (C57BL/6J) and high (129S3/SvIM) angiogenic responses in the corneal micropocket assay.9, 19 Gene expression was determined for VEGF and Ang-2, ligands potently induced by hypoxia, and collaborative stimulators of angiogenesis.20, 21, 22 Strain-related influences were also determined for PEDF and TSP-1, potent natural inhibitors of angiogenesis previously implicated in retinal neovascularization.15, 23, 24, 25 Elucidation of strain-related differences in the regulation of pro- and antiangiogenic growth factor responses during angiogenesis may provide insight into determination of angiogenic phenotype and subsequently, prediction of susceptibility to angiogenesis-dependent diseases.

Retinal angiogenesis was precisely characterized following 5 days hypoxia (P17) using lectin histochemistry, the time at which a maximal neovascular response is reached in this model.26 All exposed animals exhibited vascular tufts protruding past the ILM into the vitreous space, denoted as intravitreal neovascularization (Figure 1). In addition, larger retinal vessels were observed within the retina and deep to the ILM, termed intraretinal neovascularization. In contrast, P17 control animals showed no intravitreal neovascularization, and smaller, more regularly spaced, intraretinal vessels were present. No difference in retinal tissue thickness was observed between exposed animals compared to those of developmental controls.

The influence of genetic background on hypoxia-induced retinal angiogenesis was evaluated using multiple strains of mice which were chosen to represent previously reported low, intermediate, and high angiogenic responders to bFGF in the corneal micropocket assay.9, 18 Integrated vascularized surface area from oxygen-induced flat-mounted retinal specimens following 5 days hypoxia (P17) was quantified using endothelial-specific FITC-GSLI by 3D reconstruction confocal microscopy (Figure 2). Neovascularization in 129S3/SvIM and DBA genetic backgrounds was increased 2.2-, and 1.7-fold, respectively, compared to C57BL/6J mice (P

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