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<title cf:type="text"><![CDATA[International Journal of Ophthalmology Press -->Hypothesis]]></title>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[ipRGCs: possible causation accounts for the higher prevalence of sleep disorders in glaucoma patients]]></title>
<link><![CDATA[http://www.ijo.cn/gjyken/article/abstract/20170722]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Sleep accounts for a third of one’s lifetime, partial or complete deprivation of sleep could elicit sever disorders of body function. Previous studies have reported the higher prevalence of sleep disorders in glaucoma patients, but the definite mechanism for this phenomenon is unknown. On the other hand, it is well known by us that the intrinsically photosensitive retinal ganglion cells (ipRGCs) serve additional ocular functions, called non-image-forming (NIF) functions, in the regulation of circadian rhythm, melatonin secretion, sleep, mood and others. Specifically, ipRGCs can directly or indirectly innervate the central areas such as suprachiasmatic nucleus (SCN), downstream pineal gland (the origin of melatonin), sleep and wake-inducing centers and mood regulation areas, making NIF functions of ipRGCs relate to sleep. The more interesting thing is that previous research showed glaucoma not only affected visual functions such as the degeneration of classical retinal ganglion cells (RGCs), but also affected ipRGCs. Therefore, we hypothesize that higher prevalence of sleep disorders in glaucoma patients maybe result from the underlying glaucomatous injuries of ipRGCs leading to the abnormalities of diverse NIF functions corresponding to sleep.]]></description>
<pubDate>2017/7/11 0:00:00</pubDate>
<category><![CDATA[Hypothesis]]></category>
<author><![CDATA[Zhen-Zhen Guo, Shan-Ming Jiang, Li-Ping Zeng, Li Tang, Ni Li, Zhu-Ping Xu and Xin Wei]]></author>
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<atom:name>Zhen-Zhen Guo, Shan-Ming Jiang, Li-Ping Zeng, Li Tang, Ni Li, Zhu-Ping Xu and Xin Wei</atom:name>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Magnetic nanoparticles conjugated with “RPE cell -MCP-1 antibody -VEGF antibody” compounds for the targeted therapy of age-related macular degeneration: a hypothesis]]></title>
<link><![CDATA[http://www.ijo.cn/gjyken/article/abstract/20170525]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Age-related macular degeneration (AMD) is the leading cause of vision loss in the elderly throughout the world. Treatment of AMD utilizing retinal pigment epithelium (RPE) transplantation represents a promising therapy. However, simplex RPE transplantation can only replace the diseased RPE cells, but has no abilities to stop the development of AMD. It has been indicated that oxidization triggers the development of AMD by inducing the dysfunction and degeneration of RPE cells, which results in the upregulation of local monocyte chemotactic protein-1 (MCP-1) expression. MCP-1 induces macrophage recruiment which triggers local inflammation. As a result, the expression of vascular endothelial growth factor (VEGF) is upregulated by MCP-1 mediated inflammation and results in the formation of choroidal neovascularization (CNV). We accordingly propose a targeted therapy of AMD by subretinal transplanting the compound of RPE cell, MCP-1 antibody, and VEGF antibody and using a magnetic system to guide RPE cell compounds conjugated with superparamagnetic iron oxide nanoparticles (SPIONs). Furthermore, SPION-labelled RPE cells can be tracked and detected in vivo by non-invasive magnetic resonance imaging (MRI). This novel RPE cell transplantation methodology seems very promising to provide a new therapeutic approach for the treatment of AMD.]]></description>
<pubDate>2017/5/11 0:00:00</pubDate>
<category><![CDATA[Hypothesis]]></category>
<author><![CDATA[Zhao-Jiang Du,Peng Li and Li Wang]]></author>
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<atom:name>Zhao-Jiang Du,Peng Li and Li Wang</atom:name>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Potential role of Müller cells in the pathogenesis of macropsia associated with epiretinal membrane: a hypothesis revisited]]></title>
<link><![CDATA[http://www.ijo.cn/gjyken/article/abstract/20171119]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Pathophysiological explanations for metamorphopsia associated with retinal pathologies generally focus on photoreceptor organization disruption. However, the retinal microarchitecture is complicated, and we hypothesize that other retinal cells may also be involved. Metamorphopsia has been widely studied in eyes with epiretinal membranes and we revisit the idea that Müller cell displacement causes retinal macropsia. A PubMed query and related article search for the macula ultrastructure under normal and pathological conditions revealed an enormous amount of information, particularly ultrahigh definition optical coherence tomography and other retinal imaging modality studies. Findings of these imaging studies support our hypothesis that Müller cells, and not cone photoreceptors, are primarily responsible for macropsia in eyes with epiretinal membranes. More specifically, we conclude that displacement of Müller cell endfeet, and not photoreceptor cones, is a more likely the explanation for retinal macropsia associated with epiretinal membranes.]]></description>
<pubDate>2017/11/7 0:00:00</pubDate>
<category><![CDATA[Hypothesis]]></category>
<author><![CDATA[Ahmet Colakoglu and Solmaz Balci Akar]]></author>
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<atom:name>Ahmet Colakoglu and Solmaz Balci Akar</atom:name>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[A hypothesis for treating inflammation and oxidative stress with hydrogen sulfide during age-related macular degeneration]]></title>
<link><![CDATA[http://www.ijo.cn/gjyken/article/abstract/20180526]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[Age-related macular degeneration (AMD) is a leading cause of blindness and is becoming a global crisis since affected people will increase to 288 million by 2040. Genetics, age, diabetes, gender, obesity, hypertension, race, hyperopia, iris-color, smoking, sun-light and pyroptosis have varying roles in AMD, but oxidative stress-induced inflammation remains a significant driver of pathobiology. Eye is a unique organ as it contains a remarkable oxygen-gradient that generates reactive oxygen species (ROS) which upregulates inflammatory pathways. ROS becomes a source of functional and morphological impairments in retinal pigment epithelium (RPE), endothelial cells and retinal ganglion cells.  Reports demonstrated that hydrogen sulfide (H2S) acts as a signaling molecule and that it may treat ailments. Therefore, we propose a novel hypothesis that H2S may restore homeostasis in the eyes thereby reducing damage caused by oxidative injury and inflammation. Since H2S has been shown to be a powerful antioxidant because of its free-radicals’ inhibition properties in addition to its beneficial effects in age-related conditions, therefore, patients may benefit from H2S salubrious effects not only by minimizing their oxidant and inflammatory injuries to retina but also by lowering retinal glutamate excitotoxicity.]]></description>
<pubDate>2018/5/11 0:00:00</pubDate>
<category><![CDATA[Hypothesis]]></category>
<author><![CDATA[Akash K George, Mahavir Singh, Rubens Petit Homme, Avisek Majumder, Harpal S Sandhu and Suresh C Tyagi]]></author>
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<atom:name>Akash K George, Mahavir Singh, Rubens Petit Homme, Avisek Majumder, Harpal S Sandhu and Suresh C Tyagi</atom:name>
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