By Jennifer I. Lim (ed.)
Addressing a tremendous situation affecting hundreds of thousands around the globe, this resource compiles the main sensible and groundbreaking study at the etiology, evaluation, and remedy of Age-Related Macular Degeneration (AMD). With full-color illustrations all through, this reference explores examine developments that experience ended in novel cures that provide sight saving, much less harmful different types of remedy for exudative AMD, in addition to techniques to avoid the development of non-exudative AMD. With 3 new chapters and expansive volume of part updates, this resource offers the newest experiences on OCT imaging, experimental remedies, new purposes for thermal lasers, and gene treatment for AMD. The resource additionally summarizes stories from present medical trials to stay the top of the line within the provision of deal with sufferers with this disabling disorder.
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Extra info for Age-Related Macular Degeneration
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. Antigen-Specific Immunity The potential importance of antigen-speciﬁc immune mechanisms in atherosclerosis is illustrated by the observation of accelerated atherosclerosis in heart transplant patients who experience vascular injury associated with mild, chronic allograft rejection (93).
A complete overview is beyond the scope of this chapter, especially since no evidence exists that all of these cellular effectors participate in AMD. Thus, this section will focus only upon leukocyte subsets potentially relevant to AMD, including monocytes, basophils/mast cells and B lymphocytes/antibodies. Monocytes and Macrophages The monocyte (the circulating cell) and the macrophage (the tissue-inﬁltrating equivalent) are important effectors in all forms of immunity and inﬂammation (4). Monocytes are relatively large cells (12–20 mm in suspension, but up to 40 mm in tissues) and trafﬁc through many normal sites.
Typically, the histology is dominated by neutrophils and monocytes, but at low level of activation minimal cellular inﬁltration may be observed. Many types of glomerulonephritis and vasculitis are thought to represent this mechanism. Immune Complexes with Cell-Surface Antigen If an antigen is associated with the external surface of the plasma membrane, antibody binding might activate the terminal complement cascade to induce cell injury via formation of specialized pore-like structures called the MAC.
Age-Related Macular Degeneration by Jennifer I. Lim (ed.)