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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Ocular permeation and inhibition of retinal inflammation: an examination of data and expert opinion on the clinical utility of nepafenac.

BACKGROUND: The efficacy of topical nonsteroidal anti-inflammatory drugs (NSAIDs) for inflammation in the anterior segment, and pain control after cataract surgery, is well established. However, their effectiveness in the posterior segment has not been as well studied. Nepafenac ophthalmic suspension, 0.1% is a new topical NSAID pro-drug that has been approved by the US Food and Drug Administration (FDA) for the treatment of pain and inflammation after cataract surgery. Preclinical data suggest nepafenac may also provide unique efficacy in the posterior segment. SCOPE: We searched the PubMed database from 1966 to 2005 for various combinations of the search terms 'nepafenac', 'ophthalmic', 'inflammation', 'anterior segment', and 'posterior segment'. We review here the three articles identified in the search, and also include findings from three recent clinical trials. RESULTS: Nepafenac's corneal permeability characteristics are superior to those of ketorolac tromethamine, diclofenac sodium, and bromfenac sodium. Nepafenac is hydrolyzed by intraocular tissues to amfenac, a potent cyclooxygenase inhibitor. In addition to a limited hydrolysis in the cornea, significant bioactivation occurs in the iris/ciliary body and retina/choroid. Nepafenac administration significantly suppresses PGE2 synthesis in the retina/choroid. Topical nepafenac administration also significantly inhibits prostaglandin (PG)-mediated blood-retinal barrier breakdown and concurrent protein extravasation into the vitreous. In these studies, topical ketorolac and diclofenac failed to inhibit these key markers of inflammation. Nepafenac's clinical effectiveness in the posterior segment may be explained by its superior corneal permeation, biodistribution, and bioactivation to amfenac by the target tissues (i.e., iris, ciliary body, retina, and choroid) known to generate PGs. CONCLUSIONS: Nepafenac's ability to inhibit PG synthesis in the retina/choroid following topical administration indicates the drug also targets suppression of PG synthesis in the posterior segment. Nepafenac may therefore have a clinical role in conditions that are caused by PG-mediated vascular leakage, such as anterior chamber inflammation and cystoid macular edema following cataract surgery.[1]


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