Our side by side comparison of the rabbit and the human meibum demonstrated their vast differences. Thus, the rabbit seems to be a poor animal model of the human tear film, at least when studying its biochemistry and biophysics.

Hyperglycemia leads to corneal DC infiltration, and obesity aggravates this immune response. The direct contact between DCs and the SNP can be assumed to be a trigger of nerve fiber damage and thus a contributing factor to polyneuropathy in diabetic corneas.

IOP values measured with the TonoVet demonstrated species specific deviation from the manometric measurements. These differences should be considered when interpreting IOP values. Using the regression formulae presented, corrected IOP values could be calculated in a clinical setting.

The aim of this study was to evaluate the lipidome of meibomian gland secretions in canines (cMGS) – a common pet and laboratory animal – and to compare it with that of human MGS (hMGS), to determine whether canines could be used as a valid experimental animal model in studies of the biochemistry and physiology of the human ocular surface in general, and of the Meibomian glands in particular. The MGS of both species were evaluated using HPLC in combination with atmospheric pressure chemical ionization ion trap mass spectrometry. The main lipid classes found in cMGS were very long chain cholesteryl esters, wax esters, (O-acyl)-omega-hydroxy fatty acids (OAHFA), and cholesteryl esters of OAHFA. The lipidomes of cMGS and hMGS were found to be qualitatively similar, which implies similar biosynthetic and biodegradation pathways in canines and humans. However, some quantitative differences between the two were observed.

Intraocular pressure (IOP) was measured with the TonoVet rebound tonometer in 10 raptor species, and possible factors affecting IOP were investigated. A complete ophthalmic examination was performed, and IOP was assessed in 2 positions, upright and dorsal recumbency, in 237 birds belonging to the families Accipitridae, Falconidae, Strigidae, and Tytonidae. Mean IOP values of healthy eyes were calculated for each species, and differences between families, species, age, sex, left and right eye, as well as the 2 body positions were evaluated. Physiologic fluctuations of IOP were assessed by measuring IOP serially for 5 days at the same time of day in 15 birds of 3 species. Results showed IOP values varied by family and species, with the following mean IOP values (mm Hg +/- SD) determined: white-tailed sea eagle (Haliaeetus albicilla), 26.9 +/- 5.8; red kite (Milvus milvus), 13.0 +/- 5.5; northern goshawk (Accipiter gentilis), 18.3 +/- 3.8; Eurasian sparrowhawk (Accipiter nisus), 15.5 +/- 2.5; common buzzard (Buteo buteo), 26.9 +/- 7.0; common kestrel (Falco tinnunculus), 9.8 +/- 2.5; peregrine falcon, (Falco peregrinus), 12.7 +/- 5.8; tawny owl (Strix aluco), 9.4 +/- 4.1; long-eared owl (Asio otus), 7.8 +/- 3.2; and barn owl (Tyto alba), 10.8 +/- 3.8. No significant differences were found between sexes or between left and right eyes. In goshawks, common buzzards, and common kestrels, mean IOP was significantly lower in juvenile birds than it was in adult birds. Mean IOP differed significantly by body position in tawny owls (P = .01) and common buzzards (P = .04). By measuring IOP over several days, mean physiologic variations of +/- 2 mm Hg were detected. Differences in IOP between species and age groups should be considered when interpreting tonometric results. Physiologic fluctuations of IOP may occur and should not be misinterpreted. These results show that rebound tonometry is a useful diagnostic tool in measuring IOP in birds of prey because it provides rapid results and is well tolerated by birds.

Because of the small amount of tears, the PRT test is recommended for tear measurements in chinchillas. The IOP in chinchillas seems to be quiet is low in comparison to other rodents.

A dominantly inherited syndrome associated with hypopigmentation, heterochromia irides, colobomatous eyes and bilateral hearing loss has been ascertained in Fleckvieh cattle (German White Fleckvieh syndrome). This syndrome has been mapped to bovine chromosome (BTA) 22 using a genome-wide association study with the bovine high density single nucleotide polymorphism array. An R210I missense mutation has been identified within microphthalmia-associated transcription factor (MITF) as responsible for this syndrome. The mutation is located in the highly conserved basic region of the protein and causes a negative-dominant effect. SOX10 and PAX3 promoter binding site mutations in MITF could be ruled out as causative for the German White Fleckvieh syndrome. Molecular characterization of this newly detected bovine syndrome means a large animal model is now available for the Tietz syndrome in humans.

During forebrain development, LRP2 promotes morphogen signaling as an auxiliary SHH receptor. However, in the developing retina, LRP2 assumes the opposing function, mediating endocytic clearance of SHH and antagonizing morphogen action. LRP2-mediated clearance prevents spread of SHH activity from the central retina into the retinal margin to protect quiescent progenitor cells in this niche from mitogenic stimuli. Loss of LRP2 in mice increases the sensitivity of the retinal margin for SHH, causing expansion of the retinal progenitor cell pool and hyperproliferation of this tissue. Our findings document the ability of LRP2 to act, in a context-dependent manner, as activator or inhibitor of the SHH pathway. Our current findings uncovered LRP2 activity as the molecular mechanism imposing quiescence of the retinal margin in the mammalian eye and suggest SHH-induced proliferation of the retinal margin as cause of the large eye phenotype observed in mouse models and patients with LRP2 defects.