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Subretinal space

Amsler s grid abnormalities indicate fluid in subretinal space (Figs. 60-4 and 60-5)... [Pg.943]

FIGURE 60-4. Amsler s grid distortions in the lines of the grid may be caused by subtle changes in central vision due to fluid in the subretinal space. This is the Amsler s grid as it appears to someone with normal vision. (From the National Eye Institute, National Institutes of Health Ref. No. EC03. Accessed online at h ttp //w w w. nei.nih.gov/photo/)... [Pg.944]

Rhegmatogenous retinal detachment (RD) is defined by fluid accumulation in the subretinal space through retinal tear, inducing separation of the neurosensory retina from the retinal pigmentary epithelium (Fig. 1). [Pg.407]

Internal tamponade potency is the capacity to obdurate a dehiscence. It is correlated to the surface pressure of the product used. Schematically, the higher the tension, the stronger the tendency of the fluid to form a single bubble and to remain in the vitreous cavity without running through retinal dehiscences into the subretinal space. As a result, no fluid is passing through retinal dehiscences, which makes retinal reapplication possible. The internal tamponade potency is unrelated to the viscosity of the product. [Pg.409]

Table 1 shows the products used and tested as ocular endotamponades and their characteristics. In addition to the specific density, the interfacial tension against water is also an important parameter for the use. The drainage of subret-inal fluids is achieved, but the interfacial tension prevents the passage of the PFCL into the subretinal space. [Pg.428]

GFP gene under control of CMV to retinal cells by injection into the subretinal space of eyes in rats the GFP gene was efficiently expressed in both photoreceptor cells and retinal pigment epithelium predominant expression in photoreceptor cells was achieved using the rhodopsin promoter. The transduction efficiency was high and photoreceptor cells in >80% of the area of whole retina were expressing GFP (76). Intron-containing constructs have been successfully introduced into recent versions of lentivirus vectors (77). [Pg.344]

Kamei, M., K. Misono, and H. Lewis. 1999. A study of the ability of tissue plasminogen activator to diffuse into the subretinal space after intravitreal injection in rabbits. Am J Ophthalmol 128 739. [Pg.519]

Some of the molecular mechanisms necessary to achieve and maintain immune privilege in the AC also exist in subretinal space. [Pg.53]

There are many retinal diseases for which currently no effective treatment exists. The potential usefulness of rednal transplantation as a heatment option can be explored once the knowledge of the parameters determining the immunologic rejection of allogeneic retinal hansplant and biologic mechanisms of cells transplanted into subretinal space are better known. [Pg.53]

Jiang LQ, Jorquera M, Streilein JW (1993) Subretinal space and vitreous cavity as immunologically privileged sites for retinal allografts. Invest Ophthalmol Vis Sci 34 3347-3354. [Pg.56]

Although the high surface tension of perfluorocarbons allows closure of retinal breaks and prevents them from flowing into the subretinal space, particularly during intraocular manipulation, they can gain entry into the subretinal space, resulting in residues in the eye (15,16). The removal of perfluorocarbons is recommended at the end of surgery, but they can be left in the eye for limited periods of time (17). [Pg.2654]

Pederson, J. E. In Fluid Physiology of the Subretinal Space in Retina, 2nded. Ryan, S. J., Ed. Mosby-Year Book St. Louis, 1994, pp. 1955-1967. [Pg.122]

Pharmacodynamics. Since ranibizumab is delivered via an intravitreal injection, studies were undertaken to determine if the drug could cross the neural retina and access the subretinal space where the CNV lesions are located. A study in rhesus monkeys demonstrated that 25 pg in 50 pL of Fab antibody fragment diffused through the neural retina to the retinal pigment epithelial layer after one hour and persisted in this location for up to seven days (10). The half-life in the vitreous was 3.2 days. These data are consistent with the results of a pharmacokinetic study done by a noninvasive fluorophotometric method that showed that fluorescein-labeled ranibizumab disappeared from the vitreous with a mean terminal half-life of 2.9 days and a mean residence time of 4.2 days (11). [Pg.75]


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See also in sourсe #XX -- [ Pg.74 , Pg.75 ]




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