Background: Congenital hereditary endothelial dystrophy (CHED) is characterized by blindness at birth or in early infancy resulting from bilateral corneal opacification, and is linked to mutation in the Slc4a11 gene. A Slc4a11 knockout (KO) mouse, generated by gene deletion (Vithana et al. Nat Genet 2006), was acquired in order to study this disease. To confirm the phenotype of this Slc4a11 KO mouse model as a function of age, using the wild type (WT) mouse as a control.

Methods: Genotyping was performed by PCR (REDExtract-N-AmpTM Tissue PCR Kit, Sigma-Aldrich, Oakville, ON). Slc4a11 WT and KO mice populations aged from 5 to 50 weeks were studied (n=5 animals per age group; 5-year age intervals). Slit lamp examination, anterior segment-ocular coherence tomography (OCT930SR; Thorlabs, Inc., Newton, NJ), corneal endothelial cell staining, and scanning (SEM) and transmission (TEM) electron microscopy were used to assess the morphological and cellular differences between the two groups. The expression of basolateral membrane transporter NaBC1 within the corneal endothelium was also assessed using immunohistochemistry.

Results: Diffuse and progressive corneal opacification was observed at the slit lamp in the Slc4a11 KO mice, starting at 10 weeks. The central corneal thickness (CCT) also increased progressively as a function of time. In comparison, Slc4a11 WT corneas remained clear over the entire study period. Early TEM results showed vacuole degeneration of the corneal endothelium in the 15-week KO mouse, which was not seen in the same age WT mouse.

Conclusions: The corneal phenotype of this Slc4a11 KO mouse is representative of the clinical manifestations of CHED in human subjects, confirming the usefulness of this model for studying pathophysiology and therapeutic alternatives for Slc4a11-associated corneal dystrophies.

Abstract: Since the 21st century, the development of corneal tissue engineering technology has been developing rapidly. With the progress of biomaterials, cell culture and tissue engineering technology, tissue engineering cornea has gained great development in both basic scientific research and clinical application. In particular, tissue engineered corneal scaffolds are the core components of tissue engineered corneas. It is the focus of current research on tissue engineering cornea to search for scaffolds with good biocompatibility, high safety and good biomechanical properties. In this paper, the recent research progress of tissue engineering corneal materials is reviewed.

Background: To evaluate the association between corneal central endothelial cell count (CECC) with reactivity for hepatitis B virus (HBV), hepatitis C virus (HCV), human immunodeficiency virus (HIV), human T-lymphotropic virus-1 (HTLV1), and syphilis from an eye bank database.

Methods: Eye bank data included 19,159 donors and 38,318 corneas screened for HBV, HCV, HIV, HTLV1, and syphilis from July 2007–May 2015. Linear and binary mixed effects models were used to determine the adjusted marginal effect a positive viral screening test had on CECC and morphology, respectively. The models were adjusted for age, race, gender, lens status, and death to preservation. Eyes with missing data were excluded from the analysis. Statistical significance was defined as P values <0.05.

Results: A total of 18,097 donors and 35,136 corneas were included in the final analysis. Average CECC for eyes with negative viral screening was 2,597±436 while the average CECC for eyes screening positive for syphilis, HBV, HCV, HIV, and HTLV1 were 2,638±392 (P=0.073), 2,569±419 (P=0.815), 2,603±363 (P=0.207), 2,615±360 (P=0.733), and 2,625±436 (P=0.362) respectively.

Conclusions: The presence of HBV, HCV, HIV, HTLV1, and syphilis display no association with a statistically significant difference in CECC when compared to normal non-diseased donors.

Abstract: In this review, recent studies regarding riboflavin-ultraviolet A (UVA) collagen cross-linking for the treatment of acanthamoeba keratitis (AK) were reviewed. English written studies about acanthamoeba, keratitis, riboflavin and collagen cross-linking were retrieved from PubMed search engine (www.ncbi.nlm.nih.gov/pubmed). Although there were significant numbers of cases reporting the effectiveness of riboflavin-UVA collagen cross-linking in AK, experimental studies (in vivo and in vitro) failed to verify amoebicidal or cysticidal effect of riboflavin-UVA collagen cross-linking. In conclusion, the efficacy of riboflavin-UVA collagen cross-linking for the treatment of AK is still debatable. It is necessary to conduct a prospective case-control study for clear guidance for clinicians.