By Jennifer I. Lim (ed.)
Addressing an immense affecting thousands world wide, this resource compiles the main useful and groundbreaking learn at the etiology, evaluation, and remedy of Age-Related Macular Degeneration (AMD). With full-color illustrations all through, this reference explores study developments that experience led to novel treatments that supply sight saving, much less harmful varieties of remedy for exudative AMD, in addition to innovations to avoid the development of non-exudative AMD. With 3 new chapters and expansive volume of part updates, this resource offers the newest reviews on OCT imaging, experimental remedies, new purposes for thermal lasers, and gene remedy for AMD. The resource additionally summarizes reports from present medical trials to stay the premier within the provision of deal with sufferers with this disabling disorder.
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Extra resources for Age-Related Macular Degeneration
Nonspeciﬁc ampliﬁcation mechanisms may also play a role in AMD. Recently, several groups have identiﬁed complement components in drusen (22,182). Fragments of C5 and the MAC were identiﬁed in most specimens, and C3 was present in some. The activation pathway remains unknown. The RPE express speciﬁc and nonspeciﬁc complement inhibitors such as decay accelerating factor and vitronectin to suggest intrinsic defense mechanisms to prevent against complementmediated injury (183). Ocular Immune and Inflammatory Disorders Resulting in Atrophic Retinal Degeneration or CNV Ocular Histoplasmosis Syndrome OHS may represent a condition to suggest a role for infection-triggered immunity as a mechanism for RPE injury and CNV formation.
Also, antigen-speciﬁc immune responses directed against chlamydial HSPs may cross-react with host cellular HSP including those expressed in the retina (128). Similar, but less extensive data have been generated to support a role of CMV infection in atherosclerosis (129–131). A. Several studies have linked serologic evidence of prior CMV infection to atherosclerosis. Although the association is mild, studies have elucidated possible mechanisms for this association such as enhanced scavenging of LDL particles by virally infected endothelial cells.
CFH binds principally to C3b and accelerates the decay of the alternative pathway D3-convertase and participates as a cofactor for the factor-I–mediated proteolytic inactivation of C3b (190). Interestingly, it is the binding of CFH to sialic residues on the cell surface which is critical to its ability to inhibit C3b. CFH also binds to other multiple residues within various bacteria.