Pathology in Practice.

In collaboration with the American College of Veterinary Pathologists.

Clear and Single Binocular Vision in Near 3D Displays.

SIGNIFICANCE: Accommodation/convergence mismatch induced by 3D displays can cause discomfort symptoms such as those induced by accommodation/convergence mismatch in clinical vergence testing. We found that the limits of clear and single vision during vergence tests are very different between 3D and clinical tests. Clinical vergences should not be used as substitutes for measures of vergences in 3D displays. PURPOSE: The purposes of this study were to determine whether the limits of clear and single binocular vision derived from phoropter prism vergence tests match the limits measured in a 3D display and to determine whether vergence mode, smooth versus jump, affected those limits in the 3D display. METHODS: We tested the phoropter prism vergence limits of clear and single vision at 40 cm in 47 binocular young adults. In separate sessions, we tested, in a 3D display, the analogous 40-cm vergence limits for smooth vergence and jump vergence. The 3D fixation target was a Maltese cross whose visual angle changed congruently with target disparity. RESULTS: Our mean phoropter vergence blur and break values were similar to those reported in previous studies. The mean smooth divergence limit was less in the 3D display (9.8Δ) than in the phoropter (12.8Δ). Most smooth convergence limits were much larger in the 3D display than in the phoropter, reaching the 35Δ limit of the 3D display without blur or diplopia in 24 subjects. Mean jump vergence limits were significantly smaller than smooth vergence limits in the 3D display. CONCLUSIONS: The limits of clear and single binocular vision derived from phoropter vergence tests were not a good approximation of the analogous limits in our 3D display.

Inhibition of tubulin polymerization by hypochlorous acid and chloramines.

Protein thiol oxidation and modification by nitric oxide and glutathione are emerging as common mechanisms to regulate protein function and to modify protein structure. Also, thiol oxidation is a probable outcome of cellular oxidative stress and is linked to degenerative disease progression. We assessed the effect of the oxidants hypochlorous acid and chloramines on the cytoskeletal protein tubulin. Total cysteine oxidation by the oxidants was monitored by labeling tubulin with the thiol-selective reagent 5-iodoacetamidofluorescein; by reaction with Ellman's reagent, 5,5'-dithiobis(2-nitrobenzoic acid); and by detecting interchain tubulin disulfides by Western blot under nonreducing conditions. Whereas HOCl induced both cysteine and methionine oxidation of tubulin, chloramines were predominantly cysteine oxidants. Cysteine oxidation of tubulin, rather than methionine oxidation, was associated with loss of microtubule polymerization activity, and treatment of oxidized tubulin with disulfide reducing agents restored a considerable portion of the polymerization activity that was lost after oxidation. By comparing the reactivity of hypochlorous acid and chloramines with the previously characterized oxidants, peroxynitrite and the nitroxyl donor Angeli's salt, we have identified tubulin thiol oxidation, not methionine oxidation or tyrosine nitration, as a common outcome responsible for decreased polymerization activity.