TES prolongs the survival of photoreceptors and delays the decrease of retinal function in RCS rats. Although further investigations are necessary before using TES on patients, these findings indicate that TES may be a therapeutic treatment for some patients with diseases of the photoreceptors such as retinitis pigmentosa.

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Our technique for STS with an intrascleral microelectrode array is safe in rabbit eyes, and EEPs were elicited by current densities that did not induce tissue damage. These results suggest that STS via intrascleral multichannel electrodes is a feasible method for stimulating the retina.

These data are the first to demonstrate that VEGF and NO may play an important role in the development of pterygium and to identify VEGF and NO in the epithelium of pterygium. We hypothesize that environmental stress, such as ultraviolet irradiation and local inflammation stimulate the elaboration of NO and VEGF, resulting in the conjunctival fibrovascular ingrowth characteristic of pterygium.

Fluoroquinolones have activity against normal aerobic flora of the ocular surface. Normal ocular flora, especially gram-positive species, has low resistance to the fourth-generation fluoroquinolones -- gatifloxacin and moxifloxacin.

Osteopontin (OPN) is an adhesive glycoprotein linked to a variety of pathophysiological processes. We investigated whether OPN might act as an opsonin in the diseased brain by studying the postischemic expression and localization of OPN mRNA and protein in a rat model of ischemic stroke. In addition, we characterized the subcellular localization of OPN protein in the ischemic brain core. Induction of OPN mRNA occurred in activated microglia/macrophages in the ischemic core on days 3-7 after reperfusion and this was sustained up to day 28, at least. OPN protein was synthesized and secreted by brain macrophages, which first surrounded damaged striatal white matter tracts and then infiltrated into them. Punctate OPN-immunoreactive profiles were scattered throughout the infarction core except in white matter bundles. Electron microscopy showed the localization of OPN protein along the membranes lining what appeared to be the debris of dead neurons. These were located in the extracellular space and within the cytoplasm of brain macrophages, indicating that the OPN protein accumulated selectively on the surface of dead cells, most of which were phagocytosed subsequently by brain macrophages. However, no significant induction of OPN occurred in degenerating striatal white matter tracts or in brain macrophage-engulfed axonic or myelin debris. These data suggest that OPN secreted by brain macrophages in this rat model of stroke might be involved in the phagocytosis of fragmented cell debris and possibly not in the phagocytosis of axonic or myelin debris.

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