Silicone Oil for the management of complicated retinal detachments was introduced by Cibis and associates . Its clinical use was later prohibited in the United States because of significant post-operative complications. Experimental studies indicated that silicone oil might be retino toxic. Scott 2 in Cambridge, for many years continued to advocate the use of Silicone Oil and he slowly convinced retinal surgeons that there might be a place for Silicone Oil in detachment s u r g e r y . Because of a better understanding of vltreoretinal abnormalities and improved surgical techniques, the use of Silicone Oil is now being re-evaluated in many centres including the United States.

No description available.

Primary rhegmatogenous retinal detachment (RRD) is one of the most common ophthalmic emergencies. RRD is caused by a full thickness break in the retina which initiates separation of the neurosensory retina from the underlying retinal pigment epithelium. The subsequent accumulation of fluid within this potential space extends the area of detachment and causes visual loss. Previous assessments of RRD incidence have demonstrated large differences in case definition and methodology, with incidence estimates varying 3-fold geographically and in different time periods. To date there have been no systematic or prospective incidence estimates of primary RRD in the U.K. In this thesis I present the findings of a 2-year epidemiology study that prospectively aimed to recruit all incident cases of primary RRD diagnosed in Scotland. Case recruitment from consenting participants comprised a detailed questionnaire and a blood sample. In this thesis, I present the findings of the Scottish retinal detachment study that examined the incidence, demographic features, temporal incidence trends, as well as clinical and socio-economic associations of primary RRD in Scotland. From the clinical and genetic resource I assembled, I calculated the first population based estimate of the sibling recurrence risk ratio for RRD and designed and assisted in the analysis of the first case-control genome wide association study of this condition. Results from this study have estimated the annual incidence of primary RRD in Scotland to be 12.05 per 100,000 population. Based on this estimate, there are approximately 7,300 new cases annually in the United Kingdom. RRD incidence increases with age, is more common in men and right eyes, and is strongly associated with socio-economic affluence. In addition, using hospital episode data, the overall age-standardised incidence of RRD in Scotland was shown to be steadily increasing since 1987 with an average annual increase of 1.9%. Analysis of the clinical findings highlighted that the majority of RRD cases are caused by more than one retinal break; an important consideration for appropriate surgical management. Ocular trauma, previous cataract surgery, family history, and retinal degeneration are important predisposing features. In addition, over a 2 year period approximately 7% of individuals will suffer a RRD in the fellow eye representing an important risk of bilateral visual loss. Furthermore, I demonstrate that the risk of having an affected sibling with RRD is increased 2-fold given that one sibling has had the condition, substantiating a genetic component to the pathogenesis of this condition. In the final aspect of this thesis I will present the design and analysis of a two stage case-control genome-wide association study examining the role of common genetic variants and selected candidate genes in predisposing to RRD development.

No description available.

No description available.

by Xu Xun. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1994. / Includes bibliographical references (leaves 78-87). / Chapter CHAPTER 1 --- INTRODUCTION --- p.1 / Chapter CHAPTER 2 --- LITERATURE REVIEW --- p.6 / Chapter 2.1 --- Anatomy of retina and vitreous --- p.6 / Chapter 2.2 --- Rhegmatogenous retinal detachment --- p.8 / Chapter 2.2.1 --- Retinal breaks --- p.8 / Chapter 2.2.2 --- Retinal detachment and subretinal fluid --- p.8 / Chapter 2.3 --- Proliferative vitreoretinopathy --- p.9 / Chapter 2.4 --- Total protein in subretinal fluid --- p.11 / Chapter 2.5 --- Fibroblast growth factor --- p.12 / Chapter 2.5.1 --- Structure of b and a FGF and their gene --- p.13 / Chapter 2.5.2 --- Expression of bFGF and aFGF in neuroretinal and pigment epithelial cells --- p.14 / Chapter 2.5.3 --- The FGF receptors --- p.15 / Chapter 2.5.4 --- In vitro biological effect of FGF --- p.15 / Chapter 2.5.5 --- FGF in retinal diseases --- p.16 / Chapter 2.6 --- Cellular study of proliferative vitreoretinopathy --- p.18 / Chapter 2.6.1 --- Experimental study --- p.18 / Chapter 2.6.2 --- Pathogenesis of intravitreal proliferation --- p.20 / Chapter 2.6.3 --- Cellular components of proliferative tissue --- p.20 / Chapter 2.6.4 --- Cellular components of subretinal fluid --- p.22 / Chapter CHAPTER 3 --- MATERIALS AND METHODS --- p.24 / Chapter 3.1 --- Specimens --- p.24 / Chapter 3.2 --- Determination of total protein --- p.24 / Chapter 3.2.1 --- Study population --- p.24 / Chapter 3.2.2 --- Quantitation of total protein --- p.25 / Chapter 3.3 --- Determination of bFGF --- p.27 / Chapter 3.3.1 --- Study population --- p.27 / Chapter 3.3.2 --- Quantitation of bFGF --- p.28 / Chapter 3.4 --- Celular study --- p.30 / Chapter 3.4.1 --- Study population --- p.30 / Chapter 3.4.2 --- Fixation of samples --- p.30 / Chapter 3.4.3 --- Immunocytology --- p.32 / Chapter 3.4.4 --- Examination of autofluorescence --- p.35 / Chapter 3.4.5 --- Hematoxylin and eosin staining --- p.36 / Chapter CHAPTER 4 --- RESULTS --- p.37 / Chapter 4.1 --- Total protein --- p.37 / Chapter 4.1.2 --- Total protein in subretinal fluids --- p.38 / Chapter 4.1.3 --- Total protein in normal vitreous of autopsy and sera of patients --- p.40 / Chapter 4.1.4 --- Relationship of protein level and size of retinal break --- p.40 / Chapter 4.1.5 --- Relationship of protein level and duration of retinal detachment --- p.43 / Chapter 4.1.6 --- Relationship of protein level and degree of PVR --- p.45 / Chapter 4.2 --- Basic FGF in subretinal fluids --- p.47 / Chapter 4.2.1 --- Standard curve for determination of bFGF in SRF --- p.47 / Chapter 4.2.2 --- The levels of bFGF in both SRF and controls --- p.48 / Chapter 4.2.3 --- Levels of bFGF in different degrees of PVR --- p.50 / Chapter 4.2.4 --- Levels of bFGF in SRF of RD with and without previous cryotherapy --- p.54 / Chapter 4.2.5 --- The relationship of level of protein and bFGF --- p.55 / Chapter 4.3 --- Results of cytological examination --- p.57 / Chapter 4.3.1 --- Pigment examingnation by autofluorescence --- p.57 / Chapter 4.3.2 --- Cellular study of subretinal fluids --- p.59 / Chapter 4.3.3 --- Cellular study of subretinal fluid in eyes with prior cryotherapy --- p.62 / Chapter CHAPTER 5 --- DISCUSSION --- p.68 / Chapter 5.1 --- Evaluaton of method for obtaining specimens --- p.68 / Chapter 5.2 --- Total protein of SRF in retinal detachment --- p.69 / Chapter 5.3 --- Basic FGF in subretinal fluids --- p.71 / Chapter 5.4 --- Elevated level of bFGF in eye after cryotherapy --- p.74 / Chapter 5.5 --- Cell components in SRF of PVR --- p.75 / REFERENCES --- p.78

Thesis (M. Phil.)--University of Hong Kong, 2010. / Includes bibliographical references (leaves 116-130). Also available online.

Thesis (M. Phil.)--University of Hong Kong, 2010. / Includes bibliographical references (leaves 116-130). Also available in print.

published_or_final_version / Anatomy / Master / Master of Philosophy

Retinal detachment (RD) is a leading cause of blindness and although final surgical reattachment rate has greatly improved, visual outcome in many macula-off detachments is disappointing, mainly because of photoreceptor cell death. We previously showed that both lutein and Lycium barbarum polysaccharides (LBP) are neuroprotective in a rodent model of ischemia/reperfusion injury. The objective of this study is to investigate lutein and LBP as possible pharmacological adjuncts to surgery. Lutein: Subretinal injections of 1.4% sodium hyaluronate were used to induce RD in Sprague-Dawley rats until their retinae were approximately 70% detached. Daily injections of corn oil (control group) or 0.5mg/kg lutein in corn oil (treatment group) were given intraperitoneally starting 4 hours after RD induction. Animals were euthanized 3 days and 30 days after RD and their retinae were analyzed for photoreceptor apoptosis and cell survival at the outer nuclear layer (ONL) using TUNEL staining and cell counting on retinal sections. Glial fibrillary acidic protein (GFAP) and rhodopsin (RHO) expression were evaluated with immunohistochemistry. Western blotting was done with antibodies against cleaved caspase-3, cleaved caspase-8 and cleaved caspase-9 to delineate lutein’s mechanism of action in the apoptotic cascade. To seek a possible therapeutic time window, the same set of experiment was repeated with treatment commencing 36 hours after RD. When lutein was given 4 hours after RD, there was significantly fewer TUNELpositive cells in ONL 3 days after RD when compared with the vehicle group. Cell counting showed that there were significantly more nuclei in ONL in lutein-treated retinae by day 30. Treatment groups also showed significantly reduced GFAP immunoreactivity and preserved RHO expression. At day 3 after RD, Western blotting showed reduced expression of cleaved caspase-3 and cleaved caspase-8 in the treatment group. No difference was found for cleaved caspase-9. When lutein was given 36 hours after RD similar results were observed. Our results suggest that lutein is a potent neuroprotective agent that can salvage photoreceptors in rats with RD, with a therapeutic window of at least 36 hours. The use of lutein in patients with RD may serve as an adjunct to surgery to improve visual outcomes. LBP: The same RD model was used for the LBP experiment. Phosphate buffered solution (PBS) or LBP in PBS was given orally through a gavage at 1mg/kg and 10mg/kg concentrations. For this experiment, animals were sacrificed 7 days after RD, and only cell counting of the ONL and TUNEL staining were performed. Both sets of results did not produce statistically significant changes with the use of LBP. Our preliminary data for the effect of LBP on retinal detachment shows no significant beneficial effect. / published_or_final_version / Medicine / Master / Master of Research in Medicine