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5
Date Added: Oct 30, 2021
Date Added: Oct 30, 2021
Childhood glaucoma is a treatable cause of blindness provided it is recognized, diagnosed, and treated in time [1]. WHO has estimated that it is responsible for blind years (second only to cataract) [2]. Although congenital glaucoma is a rare disease in terms of prevalence among ophthalmic diseases (0.01% to 0.04%) [3], it accounts for 4.2% to 5.0% of blindness in the pediatric population [4,5] and 2% to 15% of individuals in blind institutions. Prompt diagnosis and surgical treatment can prevent blindness in most of these infants. Preservation of any vision during a child’s formative years is important, to avoid a lifetime of blindness. The fundamental pathophysiology of all childhood glaucoma, regardless of the cause, is impaired outflow through the trabecular meshwork, causing an increased intraocular pressure, which leads to optic neuropathy, ocular enlargement, and corneal changes including corneal edema, haab’s striae, or opacity; this could be due to a developmental abnormality (nonacquired) or due to acquired causes such as trauma, surgery, inflammation, etc. It is clear that childhood glaucoma per se is an umbrella term that comprises a vast variety of diseases including those that occur at birth, those that are developmental in nature but manifest later, and those that are due to acquired causes [6]. It is imperative to know exactly what condition one is dealing with, because the treatment and prognosis depends largely on what the underlying disease is. There has been a growing interest in childhood glaucoma in recent years, probably partly due to greater survival of small infants with the developments in neonatal care and the greater dissemination of modern ophthalmic care to hitherto underdeveloped regions. Unlike adult glaucoma, the management of childhood glaucoma is difficult owing to the varied nature and prognosis of the disease and the need of ensuring normal visual development of the immature growing eye. Pediatric glaucoma is difficult to classify because children often present with a variety of ocular or systemic findings frequently attributable to underlying genetic defects. The management of childhood glaucoma has improved in many ways, which include better classification methods and understanding of the disease, newer diagnostic modalities, improvements in anesthesia procedures, and surgical treatment options that have improved significantly since goniotomy was first described by Barkan [7] and trabeculotomy was first described by Burian and Smith [8,9]. Because of rapid developments in molecular biology techniques, it is now much easier to understand the pathophysiology of the disease by unraveling the underlying genetic abnormality. In this chapter the authors look at recent advancements seen in the world of childhood glaucoma. This would include the development of a novel unified classification system, newer surgical procedures, and the exciting potential of genetic research in this condition.
Paper
6
Date Added: Jun 3, 2021
Date Added: Jun 3, 2021
Macrophage aging is pathogenic in diseases of the elderly, including age-related macular degeneration (AMD), a leading cause of blindness in older adults. However, the role of microRNAs, which modulate immune processes, in regulating macrophage dysfunction and thereby promoting age-associated diseases is underexplored. Here, we report that microRNA-150 (miR-150) coordinates transcriptomic changes in aged murine macrophages, especially those associated with aberrant lipid trafficking and metabolism in AMD pathogenesis. Molecular profiling confirmed that aged murine macrophages exhibit dysregulated ceramide and phospholipid profiles compared with young macrophages. Of translational relevance, upregulation of miR-150 in human peripheral blood mononuclear cells was also significantly associated with increased odds of AMD, even after controlling for age. Mechanistically, miR-150 directly targets stearoyl-CoA desaturase-2, which coordinates macrophage-mediated inflammation and pathologic angiogenesis, as seen in AMD, in a VEGF-independent manner. Together, our results implicate miR-150 as pathogenic in AMD and provide potentially novel molecular insights into diseases of aging.
38
Date Added: Oct 30, 2020
Date Added: Oct 30, 2020
Purpose: The objective of this study was to map the distribution and density of the three major components of the classical scotopic “night vision” pathway (rods, rod bipolar, and AII amacrine cells) in postmortem human retinas.Methods: Four postmortem donor eyes (male and female, aged 44–56 years) were used to cut vertical sections through the temporal horizontal meridian. The sections were processed for immunohistochemistry and imaged using high-resolution multichannel confocal microscopy. Rods, rod bipolar, and AII amacrine cells were counted along the temporal horizontal meridian. Two additional retinas were used for intracellular injections.Results: Rod peak density is close to 150,000 cells/mm2 at 4 to 5 mm (15° to 20°) eccentricity, declining to below 70,000 cells/mm2 in peripheral retina. Rod bipolar density is lower but follows a similar distribution with peak density near 10,000 cells/mm2 between 2 and 4 mm (7° to 15°) eccentricity declining to below 4000 cells/mm2 in peripheral retina. The peak density of AII amacrine cells (near 4000 cells/mm2) is located close to the fovea, at 0.5- to 2 mm-eccentricity (2° to 7°) and declines to below 1000 cells/mm2 in the periphery. Thus, convergence between rods and AII cells increases from central to peripheral retina.
Paper