By Jennifer I. Lim (ed.)
Addressing a huge affecting thousands world wide, this resource compiles the main useful and groundbreaking examine 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 ended in novel cures that provide sight saving, much less harmful sorts of therapy for exudative AMD, in addition to concepts to avoid the development of non-exudative AMD. With 3 new chapters and expansive quantity of part updates, this resource provides the newest reports on OCT imaging, experimental remedies, new purposes for thermal lasers, and gene remedy for AMD. The resource additionally summarizes reports from present scientific trials to stay the choicest within the provision of deal with sufferers with this disabling disorder.
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Extra info for Age-Related Macular Degeneration
Source: From Refs. 146, 147. capillaries and epithelial cells. If enough glomeruli are involved, renal impairment occurs. In some ways, glomerulosclerosis resembles geographic atrophy in AMD (Fig. 6). The response to injury hypothesis has been thoroughly evaluated for renal hypertension, a major cause of glomerulosclerosis (141–145,148). The hemodynamic injury hypothesis proposes that glomerular capillary hypertension causes excessive ﬂow through the glomerulus or hydraulic stretching of the capillary wall to activate injury responses in glomerular cells.
The susceptible host could not have possibly evolved receptors for recognition to these new viral mutations. However, these new mutations do serve as “antigens” which stimulate an adaptive antigen-speciﬁc immune response by the host to the virus. The antigen-speciﬁc response recognizes the virus in question and not other organisms (such as the polio virus). Amplification Mechanisms for Both Forms of Immunity Although innate or antigen-speciﬁc immunity may directly induce injury or inﬂammation, in most cases, these effectors initiate a process that must be ampliﬁed in order to produce overt clinical manifestations.
The hemodynamic injury hypothesis proposes that glomerular capillary hypertension causes excessive ﬂow through the glomerulus or hydraulic stretching of the capillary wall to activate injury responses in glomerular cells. The humoral hypothesis proposes that hypertensionassociated hormones or cytokines associated with low grade systemic inﬂammation induced by hypertensive vascular injury, activate cellular injury responses. In either case, the injured endothelium, podocytes and mesangial cells demonstrate abnormal production and turnover of collagen and other matrix molecules, leading to collagenous thickening of the matrix with degeneration of the glomerulus (148–150).