To evaluate the change in subfoveal choroidal thickness between active and quiescent phases of Behcet's posterior uveitis and compare this with the healthy population using enhanced depth imaging optical coherence tomography (EDI-OCT). Thirty eyes from 30 patients with Behcet's posterior uveitis (mean age, 47.03 ± 11.01 years) were retrospectively enrolled in the study. Their subfoveal choroidal thickness was measured using EDI-OCT in the active and quiescent phases of Behcet's uveitis, and compared with the age, sex, and spherical equivalent-matched healthy population. Changes in retinal vascular leakage on fluorescein angiography (FA) were correlated with the changes in subfoveal choroidal thickness. Mean subfoveal choroidal thickness in the acute phase of Behcet's uveitis was significantly greater than that in the quiescent phase (398.77 ± 155.59 μm versus 356.72 ± 141.09 μm; P = 0.004). Subfoveal choroidal thickness in the quiescent phase was also significantly greater than that of the healthy population (259.96 ± 65.16 μm; P < 0.0001). There was a statistically significant association between the change in subfoveal choroidal thickness and the change in vascular leakage revealed by FA (ρ = 0.381, P = 0.046). Subfoveal choroidal thickness in the uninvolved fellow eyes of patients with unilateral Behcet's uveitis was also evaluated and it was significantly greater than that of the healthy population (n = 13 eyes; P = 0.001) CONCLUSIONS: This study found choroidal thickening during the active phase of Behcet's posterior uveitis. Subfoveal choroidal thickness during the quiescent phase was also significantly greater than in normal eyes. The degree of reduction in choroidal thickening was significantly correlated with improvement in retinal vascular leakage as revealed by FA.

Purpose. To investigate the correlation of choroidal thickness (CT) with ocular perfusion pressure (OPP) in young, healthy subjects using enhanced depth imaging optical coherence tomography (EDI-OCT). Methods. A single horizontal section and a single vertical section of EDI-OCT scans in each eye of 69 young, healthy subjects were obtained at the macula. CT was measured at the fovea, and up to 3 mm, at intervals of 0.5 mm, away from the fovea in the superior, inferior, nasal, and temporal choroid. Univariable and multivariable analyses were performed to assess the association of CT with OPP while axial length (AL), refractive error (RE), sex, and/or body mass index (BMI), were taken into consideration. Results. Mean subfoveal CT was 307.03 ± 91.27 μm (mean age, 22.3 ± 3 years; mean axial length, 25.35 ± 1.14 mm; mean refractive error, −3.89 ± 2.02 diopters; mean OPP, 44.18 ± 5.49 mm Hg). Multivariable regression analysis showed that in eyes with <6 diopters of myopia, subfoveal CT (325.92 ± 88.46 μm) changed most significantly in association with RE and mean OPP (β = 25.941, P < 0.001; β = −3.551, P = 0.042, respectively; adjusted R² = 0.249). In subjects with myopia of >6 diopters, subfoveal CT (225.17 ± 49.37 μm) was significantly thinner (P < 0.0001), and a significant correlation with OPP was not observed (P > 0.05). Conclusions. In vivo subfoveal CT as measured by EDI-OCT was significantly associated with OPP in young, healthy subjects when adjusted for RE, suggesting that subfoveal CT may be indirectly indicative of subfoveal ocular perfusion status. This association was not observed in subjects with high myopia.

Purpose. To introduce a tonicity response gene regulator, NFAT (nuclear factor of activated T-cell)-5 and determine its expression mechanism and specific roles in human limbal epithelial cell (HLECs) subjected to hyperosmolar stress. methods. NFAT5 expression was determined in various hyperosmolar conditions in HLECs by RT-PCR and Western immunoblot analyses. NFAT5 translocation during hyperosmolar stress was observed by immunocytochemistry. NFAT5-related signal transduction activity was measured on the basis of inhibition of NF-κB (nuclear factor-κB), and MAPK activity. TNF-α and IL-1β, -6, and -8 levels were determined after inhibition of NFAT5 and/or NF-κB. Hyperosmotic apoptotic cell death, with or without inhibition of NFAT5, was measured by flow cytometry. results. NFAT5 was induced and translocated to the nucleus under conditions of hyperosmolar stress. It was inhibited by SB239063, a p38 MAPK inhibitor. Among the inflammatory cytokines induced in hyperosmolar stress conditions, IL-1β and TNF-α levels were significantly reduced after inhibition of NFAT5. Of interest, even after 48 hours of hyperosmolar stress, 45% of HLECs survived. HLEC apoptosis increased markedly as a result of NFAT5 suppression. Moreover, most of the HLECs underwent cell death on dual inhibition of NF-κB and NFAT5. conclusions. NFAT5 is induced and translocates to the nucleus in HLECs undergoing hyperosmolar stress through activation of p38. IL-1 β and TNF-α are induced via NFAT5 activation. Our data collectively indicate that NFAT5 may be an important gene regulator and survival factor in hyperosmolar stressed HLECs.

To describe the pathoanatomy of diabetic macular edema in optical coherence tomography and its correlation with fluorescein angiography patterns. Sixty eyes of 56 patients were analyzed. Diabetic macular edema was classified into typical focal leakage (from microaneurysm), typical diffuse leakage (the capillary plexus), or combined/questionable leakage using fluorescein angiography and retinal thickness profiles. The leakage and pooling patterns in fluorescein angiography were matched to the corresponding optical coherence tomography images and analyzed. Focal leakage shows swelling predominantly in the outer plexiform layer (OPL). Deeply located microaneurysms directly leak into the loose fiber portion of OPL (Henle layer) through the “fluid conductivity barrier” (synaptic portion of OPL). Diffuse leakage caused swelling predominantly in the inner nuclear layer and secondarily in the OPL. The deep capillary plexus is located between the two “fluid barriers” (inner plexiform layer and OPL); thus, diffuse leakage is primarily related with swelling in the inner nuclear layer. In the combined/questionable leakage, partial sections consisting of inner nuclear layer swelling and much larger areas of OPL/outer nuclear layer swelling are noticed. Based on the concept of the fluid conductivity barrier, we revealed a correlation between the intraretinal location of the leakage source and where the fluid accumulated within the retinal layers.