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group_2_presentation_3_-_glaucoma [2019/04/06 04:57]
pateln25 [REFERENCES]
group_2_presentation_3_-_glaucoma [2019/04/06 05:27] (current)
pateln25 [Future Treatment: Gene Therapy]
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 There are also risk factors associated with primary open-angle glaucoma. African people have a prevalence up to 5 times higher than other ethnic groups of developing glaucoma (Cook & Foster, 2012). You risk of developing glaucoma exponentially increases with age. Particularly,​ Hispanics have a more pronounced increased risk of developing glaucoma with age compared to other ethnic groups (Cook & Foster, 2012). Additionally,​ having a thin cornea and/or a large optic disc diameter has shown to increase one's risk for glaucoma. Other factors associated with higher risk is low physical activity, having cardiovascular disease, and hypertension (Cook & Foster, 2012). There are also risk factors associated with primary open-angle glaucoma. African people have a prevalence up to 5 times higher than other ethnic groups of developing glaucoma (Cook & Foster, 2012). You risk of developing glaucoma exponentially increases with age. Particularly,​ Hispanics have a more pronounced increased risk of developing glaucoma with age compared to other ethnic groups (Cook & Foster, 2012). Additionally,​ having a thin cornea and/or a large optic disc diameter has shown to increase one's risk for glaucoma. Other factors associated with higher risk is low physical activity, having cardiovascular disease, and hypertension (Cook & Foster, 2012).
  
-<box 25% round | > {{ :​wiki:​omd_apr_3801.jpg?​250 ​ |}} </box| Figure 2: Projected estimates of people affected by glaucoma. (Retrieved from:)>+<box 25% round | > {{ :​wiki:​omd_apr_3801.jpg?​250 ​ |}} </box| Figure 2: Projected estimates of people affected by glaucoma. (Retrieved from: Glaucoma, 2019)>
  
  
 ====== SYMPTOMS ====== ====== SYMPTOMS ======
-Glaucoma, also known as the "​silent thief" of sight, rarely causes symptoms until optic-nerve-fiber damages occurs, creating scotomas. The condition can develop in one or both eyes. Clinical features vary with the form of glaucoma. At first, there are no symptoms. Vision stays normal, and there is no pain. As the disease progresses, a person may notice the side vision gradually failing. That is, objects in front may still be seen clearly, but objects to the side may be missed. As glaucoma remains untreated, the person may miss objects to the side and out of the corner of their eye. Without treatment, the person will slowly lose their peripheral side vision. Over time, straight-ahead vision may decrease until no vision remains. ​ The following are the most common features seen in most forms of glaucoma (Naklha2007).+Glaucoma, also known as the "​silent thief" of sight, rarely causes symptoms until optic-nerve-fiber damages occurs, creating scotomas. The condition can develop in one or both eyes. Clinical features vary with the form of glaucoma. At first, there are no symptoms. Vision stays normal, and there is no pain. As the disease progresses, a person may notice the side vision gradually failing. That is, objects in front may still be seen clearly, but objects to the side may be missed. As glaucoma remains untreated, the person may miss objects to the side and out of the corner of their eye. Without treatment, the person will slowly lose their peripheral side vision. Over time, straight-ahead vision may decrease until no vision remains. ​ The following are the most common features seen in most forms of glaucoma (Naklha2007).
  
 **Pain and Redness:** Rapid increase in pressure to very high levels leads to eye pain and redness. ​ **Pain and Redness:** Rapid increase in pressure to very high levels leads to eye pain and redness. ​
  
-**Blurred Vision/​Visual Field Loss:** This occurs as a result of damages to the retinal nerve fibers leading to arcuate scotoma, an inferior nerve-fiber-bundle defect. Central vision is spared initially and the person is unable to notice the defect. Vision may still be perfect even at the terminal stage of glaucomatous field loss (tunnel vision) (Naklha2007).+**Blurred Vision/​Visual Field Loss:** This occurs as a result of damages to the retinal nerve fibers leading to arcuate scotoma, an inferior nerve-fiber-bundle defect. Central vision is spared initially and the person is unable to notice the defect. Vision may still be perfect even at the terminal stage of glaucomatous field loss (tunnel vision) (Naklha2007).
  
-**Elevated Interaocular Pressure:** Pressure and severity of glaucomatous damage determines the rate at which elevated intraocular oressure causes optic nerve damage. In general, pressures of 20 to 30mm Hg usually causes damage over several years, but pressures of 40 to 50mm Hg can lead to rapid visual loss and also deteriorate retinovascular occlusion (Naklha2007).+**Elevated Interaocular Pressure:** Pressure and severity of glaucomatous damage determines the rate at which elevated intraocular oressure causes optic nerve damage. In general, pressures of 20 to 30mm Hg usually causes damage over several years, but pressures of 40 to 50mm Hg can lead to rapid visual loss and also deteriorate retinovascular occlusion (Naklha2007).
  
-**Rainbow-Colored Rings or Halos Perceived Around Lights and Cloudy Cornea:** Endothelial cells are continuously removing fluid to keep the cornea transparent. When pressure rises, the cornea becomes waterlogged,​ causing visual acuity to decrease and forming halos around lights (Naklha2007).+**Rainbow-Colored Rings or Halos Perceived Around Lights and Cloudy Cornea:** Endothelial cells are continuously removing fluid to keep the cornea transparent. When pressure rises, the cornea becomes waterlogged,​ causing visual acuity to decrease and forming halos around lights (Naklha2007).
  
-Other clinical symptoms that have been observed in association with the different forms of glaucoma due to the rapid buildup of intraocular pressure include nausea and vomiting, headaches, cataract, photophobia,​ blepharospasm (involuntary blinking or spasm of the eyelids), strabismus (misalignment of the eyes), epiphoria (excessive tearing), and amblyopia (lazy eye) (Naklha2007).+Other clinical symptoms that have been observed in association with the different forms of glaucoma due to the rapid buildup of intraocular pressure include nausea and vomiting, headaches, cataract, photophobia,​ blepharospasm (involuntary blinking or spasm of the eyelids), strabismus (misalignment of the eyes), epiphoria (excessive tearing), and amblyopia (lazy eye) (Naklha2007).
  
 <box 50% round | > {{ :​wiki:​life_sci_4m03_-_presentation_3_glaucoma_5.jpg?​500 |}} </box| Figure 3: General symptoms of glaucoma.>​ <box 50% round | > {{ :​wiki:​life_sci_4m03_-_presentation_3_glaucoma_5.jpg?​500 |}} </box| Figure 3: General symptoms of glaucoma.>​
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 ===== Future Treatment: Gene Therapy ===== ===== Future Treatment: Gene Therapy =====
    
-There has been a lot of recent research on the use of gene therapy as a means of treating glaucoma. The idea behind gene therapy is to introduce an exogenous gene into a cell in order to modify its activity. Gene therapy is not used to fix defective genes, but to introduce a new gene which down or up-regulates a function of the receiving cell. This is accomplished through the use of inactivated (i.e., they do not express any other activity except the one of the gene of interest and its promoter) vectors (typically, viruses) that are unable to replicate (Fogagnolo & Rossetti, 2011).+There has been a lot of recent research on the use of gene therapy as a means of treating glaucoma.{{ :​wiki:​small-dna-gene_b.gif?​250|}} ​The idea behind gene therapy is to introduce an exogenous gene into a cell in order to modify its activity. Gene therapy is not used to fix defective genes, but to introduce a new gene which down or up-regulates a function of the receiving cell. This is accomplished through the use of inactivated (i.e., they do not express any other activity except the one of the gene of interest and its promoter) vectors (typically, viruses) that are unable to replicate (Fogagnolo & Rossetti, 2011).
  
 In a study conducted by Borrás and colleagues (2001), they investigated the effects of treating the eyes of monkeys with a protein, adenoviral vector expressing rat non-muscle caldesmon fused to green fluorescent protein. After 24-48 hours, trabecular meshwork cells had a change in activity and GFP-caldesmon was hyper-expressed. As a result, aqueous humour outflow was increased by 50%. In another study by Borrás and colleagues (2010), they evaluated the effects of an adenoviral vector carrying the gene of metalloproteinase 1 when injected on living sheep before and after the induction of corticosteroid ocular hypertension leading to intraocular pressure. Sheep were chosen because they have a high corticosteroid response on intraocular pressure. In sheep with high eye pressure, the injection achieved pressure reductions up to 70% in 24 hours. In eyes with normal pressure, pre-injection protected against the increase in IOP which was induced by the continuous application of the corticosteroid for 5 days. In a study conducted by Borrás and colleagues (2001), they investigated the effects of treating the eyes of monkeys with a protein, adenoviral vector expressing rat non-muscle caldesmon fused to green fluorescent protein. After 24-48 hours, trabecular meshwork cells had a change in activity and GFP-caldesmon was hyper-expressed. As a result, aqueous humour outflow was increased by 50%. In another study by Borrás and colleagues (2010), they evaluated the effects of an adenoviral vector carrying the gene of metalloproteinase 1 when injected on living sheep before and after the induction of corticosteroid ocular hypertension leading to intraocular pressure. Sheep were chosen because they have a high corticosteroid response on intraocular pressure. In sheep with high eye pressure, the injection achieved pressure reductions up to 70% in 24 hours. In eyes with normal pressure, pre-injection protected against the increase in IOP which was induced by the continuous application of the corticosteroid for 5 days.
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