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<title>British Journal of Ophthalmology Original articles - Laboratory science</title>
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<description>British Journal of Ophthalmology RSS feed -- recent Original articles - Laboratory science articles</description>
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<title>British Journal of Ophthalmology</title>
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<title><![CDATA[Aged peripheral retinal lesions originating from the ciliary body sweep away the retinal pigmented epithelium]]></title>
<link>http://bjo.bmj.com/cgi/content/short/96/6/900?rss=1</link>
<description><![CDATA[
<sec><st>Aims</st>
<p>To investigate age-related lesions in the far-anterior retina that migrate from the ciliary body (CB) and how they affect the neural retina and retinal pigmented epithelium (RPE).</p>
</sec>
<sec><st>Methods</st>
<p>One eye from three healthy subjects aged 87, 92 and 93&nbsp;years were used. Retinae were photographed, embedded in resin and then sectioned at 2&nbsp;&mu;m.</p>
</sec>
<sec><st>Results</st>
<p>Multiple elliptically shaped lesions were present in the CB. Larger lesions extended into the peripheral retina. Lesions resulted from deposits that had lenticular qualities. These develop centrally along Bruch's membrane sweeping away the RPE, such that piles of RPE cells were present around the deposits that resulted in retinal atrophy. The internal composition of the deposits revealed large numbers of spherical bodies, unlike those seen in drusen. RPE cells adjacent to these deposits and their underlying lesions became highly irregular, with melanin granules spacing themselves out within the cell and adopting similar orientations. This is a highly distinctive feature.</p>
</sec>
<sec><st>Conclusions</st>
<p>These far-anterior deposits were different in nature from drusen in terms of morphology, composition and origin. They swept away the RPE, exposing the Bruch's membrane and isolating the retina, leading to atrophy. They appeared to originate from the CB and progressed centrally. The deposits may have developed from the ciliary muscle, which would account for their elongated orientation. Their impact on melanin distribution in RPE cells was unexpected and unusual, implying that they release a signal that influences melanin organisation.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Begum, R., Jeffery, G.]]></dc:creator>
<dc:date>2012-05-15T13:21:38-07:00</dc:date>
<dc:identifier>info:doi/10.1136/bjophthalmol-2011-301273</dc:identifier>
<dc:identifier>hwp:master-id:bjophthalmol;bjophthalmol-2011-301273</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Unlocked]]></dc:subject>
<dc:title><![CDATA[Aged peripheral retinal lesions originating from the ciliary body sweep away the retinal pigmented epithelium]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Original articles - Laboratory science</prism:section>
<prism:volume>96</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>900</prism:startingPage>
<prism:endingPage>904</prism:endingPage>
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<title><![CDATA[Toxicity of voriconazole on corneal endothelial cells in an animal model]]></title>
<link>http://bjo.bmj.com/cgi/content/short/96/6/905?rss=1</link>
<description><![CDATA[
<sec><st>Aims</st>
<p>To determine the effect of intracamerally injected voriconazole on corneal endothelial cells in rabbit eyes.</p>
</sec>
<sec><st>Methods</st>
<p>Various concentrations of voriconazole (0%, 0.03%, 0.1%, 0.25%, 0.5% and 1%) were injected intracamerally in 36 eyes of 18 rabbits (six eyes for each concentration). Measurements of endothelial cell counts and central corneal thickness were performed at 30, 60, 90 and 120&nbsp;min after the injection. In each group, five of six corneas were used for the live/dead cell assay; staining with alizarin red and trypan was done. In one cornea from each group, scanning electron microscopy was performed.</p>
</sec>
<sec><st>Results</st>
<p>There was no significant difference in endothelial cell counts and central corneal thickness among the six groups at any time points. The live/dead cell assay revealed no difference in the mean percentage of dead endothelial cells among the six groups (p=0.504). However, scanning electron microscopy revealed blurring of cell border at voriconazole concentrations &ge;0.25%, indicating cell wall damage.</p>
</sec>
<sec><st>Conclusion</st>
<p>Intracameral injection of voriconazole did not induce a significant gross change in rabbit corneal endothelial cells up to a concentration of 1%. However, risk of microstructural damages might exist with a concentration of &ge;0.25%.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Han, S. B., Yang, H. K., Hyon, J. Y., Shin, Y. J., Wee, W. R.]]></dc:creator>
<dc:date>2012-05-15T13:21:38-07:00</dc:date>
<dc:identifier>info:doi/10.1136/bjophthalmol-2011-301129</dc:identifier>
<dc:identifier>hwp:master-id:bjophthalmol;bjophthalmol-2011-301129</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Toxicity of voriconazole on corneal endothelial cells in an animal model]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Original articles - Laboratory science</prism:section>
<prism:volume>96</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>905</prism:startingPage>
<prism:endingPage>908</prism:endingPage>
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