The aim was to compare the outcomes acquired from the OSA-Vet® device with conventional quantitative and qualitative tear tests and between groups within each test, in brachycephalic dogs both healthy and those diagnosed with keratoconjunctivitis sicca. The dogs were divided into four groups: healthy dogs (HD), with mild KCS (MIKCS); moderate KCS (MOKCS); severe KCS (SKCS). All patients underwent ocular surface diagnostic examination in the following order, with a 10-minute interval between tests: non-invasive tear film breakup time (TBUTNI - OSA-Vet®), tear meniscus height (TMH-OSA-Vet®), meniscometry (I-Tear® test), Schirmer Tear Test-1 (STT-1), and tear film breakup time (TBUT). Kruskal-Wallis H tests were performed to establish the difference between the groups and Spearman´s correlation coefficient test to assess the correlation between tests. And an analysis of variance (ANOVA) followed by Tukey-Kramer post-hoc test was performed for TMH. Results with (p <.05) were considered statistically significant. The correlation of conventional tests in relation to those obtained by OSA-Vet® proved to be low, except between TBUTNI (OSA-Vet®) and TBUT in MOKCS, with a strong correlation (r =.925). In the comparison between TBUTNI (OSA-Vet®) and TBUT in MIKCS the correlation was moderate (r =.547) as well as STT-1 and I-Tear® test in MOKCS (r =.416). In the comparison between groups, the main result observed was a significant difference between all the KCS groups and HD, in the TBUT and TBUTNI (OSA-Vet®) test. The OSA-Vet® and conventional tests are useful for evaluating the ocular surface of brachycephalic dogs. However, the OSA-Vet® does not correlate well with conventional standardized tests.

PURPOSE. We sought to define the role of Wwtr1 in murine ocular structure and function and determine the role of mechanotransduction in Fuchs' endothelial corneal dystrophy (FECD), with emphasis on interactions between corneal endothelial cells (CEnCs) and Descemet's membrane (DM).METHODS. A Wwtr1 deficient mouse colony was established, and advanced ocular imaging, atomic force microscope (AFM), and histology/immunofluorescence were performed. Corneal endothelial wound healing was assessed using cryoinjury and phototherapeutic keratectomy in Wwtr1 deficient mice. Expression of WWTR1/TAZ was determined in the corneal endothelium from normal and FECD-affected patients; WWTR1 was screened for coding sequence variants in this FECD cohort.RESULTS. Mice deficient in Wwtr1 had reduced CEnC density, abnormal CEnC morphology, softer DM, and thinner corneas versus wildtype controls by 2 months of age. Additionally, CEnCs had altered expression and localization of Na/K-ATPase and ZO-1. Further, Wwtr1 deficient mice had impaired CEnC wound healing. The WWTR1 transcript was highly expressed in healthy human CEnCs comparable to other genes implicated in FECD pathogenesis. Although WWTR1 mRNA expression was comparable between healthy and FECD-affected patients, WWTR1/TAZ protein concentrations were higher and localized to the nucleus surrounding guttae. No genetic associations were found in WWTR1 and FECD in a patient cohort compared to controls.CONCLUSIONS. There are common phenotypic abnormalities seen between Wwtr1 deficient and FECD-affected patients, suggesting that Wwtr1 deficient mice could function as a murine model of late-onset FECD. Despite the lack of a genetic association between FECD and WWTR1, aberrant WWTR1/TAZ protein subcellular localization and degradation may play critical roles in the pathogenesis of FECD.

Graphene-based nanomaterials (GBNs) are widely used due to their chemical and physical properties for multiple commercial and environmental applications. From an occupational health perspective, there is concern regarding the effects of inhalation on the respiratory system, and many studies have been conducted to study inhalation impacts on lung. Similar to the respiratory system, the eyes may also be exposed to GBNs and thus impacted. In this study, immortalized human corneal epithelial (hTCEpi) cells and rabbit corneal fibroblasts (RCFs) were used to investigate the toxicity of eight types of GBN: graphene oxide (GO; 400 nm), GO (1 μm), partially reduced graphene oxide (PRGO; 400 nm), reduced graphene oxide (RGO; 400 nm), RGO (2 μm), graphene (110 nm), graphene (140 nm), and graphene (1 μm). We next examined the effects of these GBNs on hTCEpi cell migration. We also determined whether the expression of α-smooth muscle actin (αSMA), a myofibroblast marker, is altered by the GBNs using RCFs. We found that RGO (400 nm) and RGO (2 μm) were highly toxic to hTCEPi cells and RCFs meanwhile, PRGO (400 nm) was toxic only to hTCEpi cells. In addition, PRGO (400 nm), RGO (400 nm), and RGO (2 μm) inhibited hTCEpi cell migration and significantly increased αSMA mRNA expression. Further study in vivo is required to determine if RGO nanomaterials delay corneal epithelial healing and induce scar formation.