Disease relevance of Corneal Diseases

• Mice in which the IL-4 gene was disrupted failed to develop corneal disease, demonstrating that IL-4 is essential in the immunopathogenesis of O. volvulus-mediated stromal keratitis [1].
• The heterotypic gD2 vaccine was as efficacious as the homotypic gD1 vaccine against recurrent corneal disease, whereas the homotypic vaccine was much more efficacious than the heterotypic vaccine against recurrent HSV-1 shedding [2].
• Effect of famciclovir on herpes simplex virus type 1 corneal disease and establishment of latency in rabbits [3].
• Herpetic keratitis remains a prominent cause of recurrent or chronic and blinding corneal disease; areas of particular difficulty are indolent ulceration, herpetic keratouveitis, keratoplasty and problems associated with steroid therapy [4].
• Keratoconus is a corneal disease that has increased gelatinase A activity [5].

High impact information on Corneal Diseases

• The evolution of the corneal disease during treatment and follow-up was evaluated by slit-lamp examination, photography, fluorescein-dye testing, and tests of corneal sensitivity and best corrected visual acuity [6].
• Treatment decreased corneal disease severity and reduced significantly the number of B7-positive cells as well as the recruitment and activation of CD4(+) T cells in the cornea [7].
• A combination of subconjunctival and i.p. administration of IL-1beta polyclonal Ab significantly reduced corneal disease [8].
• Systemic neutralization of IL-2 after the onset of corneal disease resulted in a rapid regression of inflammation and complete resolution in 50% of the treated mice [9].
• CONCLUSIONS: Bacterial toxins, and especially alpha-toxin, can mediate corneal disease in mice [10].

Chemical compound and disease context of Corneal Diseases

• Altered antigenicity of keratan sulfate proteoglycan in selected corneal diseases [11].
• The severity of the herpes virus-induced corneal disease, assessed by biomicroscopic examination and by counting the number of corneal lesions as well as by determining the virus titers, was significantly less in vitamin A deficient animals than in controls [12].
• Chronic oral administration of acyclovir or bromovinyl deoxyuridine to rabbits did not prevent recurrence of virus shedding or clinical corneal disease, nor did it alter the clinical course of recurrences of ocular herpetic disease or result in the appearance of resistant virus in tears [13].
• These findings, together with similar previous reports concerning diclofenac sodium and ketorolac, suggest that careful observation is required when using topical NSAIDs in the treatment of corneal disease [14].
• This demonstration that vitamin A is present in the tears as retinol establishes the rationale for treatment of corneal disease with topical vitamin A [15].

Biological context of Corneal Diseases

• RESULTS: For the cytotoxic strain, mutation of either exoU or exoT alone had little effect on virulence, whereas simultaneous mutation of both exoT and exoU or of exsA resulted in a significantly reduced capacity to cause corneal disease [16].
• Beside oncology, new therapeutic applications of SS analogs could be presumed among others in ophthalmology; it concerns the treatment of progressive Graves-Basedow ophtalmopathy, diabetic retinopathy, glaucoma and corneal diseases connected with corneal vascularization [17].

Anatomical context of Corneal Diseases

• Local administration of IL-10 also dramatically reduced the number of T cells and neutrophils migrating into the cornea and suppressed the severity of corneal disease [18].
• CONCLUSIONS: Polymerase chain reaction evidence shows that HSV DNA is present in a substantial percentage of ICE syndrome corneal specimens and that HSV-DNA is absent in normal corneas and in corneas from patients with three other chronic corneal diseases [19].
• Occasional lymphocytes were seen within the endothelium in one case but were also observed in one case of an inherited corneal disease, posterior polymorphous dystrophy, suggesting that they might be normal "passenger" cells migrating in the endothelial monolayer [20].

Gene context of Corneal Diseases

• The absence of TFF peptide production in the healthy cornea indicates that TFF3 secretion is induced in different corneal diseases by yet unknown stimuli [21].
• We conclude that local IL-10 administration can suppress chemokine synthesis, thereby ameliorating corneal disease [18].
• CONCLUSIONS: Taken together, the above findings show that NGF plays an important role in corneal physiopathology and suggest that this neurotrophin may exert therapeutic action in wide-spectrum corneal diseases [22].
• Using candidate genes in the 5q22-q32 interval, we investigated the possibility that mutations in the SPARC or LOX genes cause these corneal diseases [23].
• Gelsolin, cytokeratin 3, and cytokeratin 12 have previously been described to be involved in other corneal diseases [24].

Analytical, diagnostic and therapeutic context of Corneal Diseases

• The corneal disease in both eyes responded swiftly to topical fibronectin, topical nonpreserved tears, vitamin A ointment, and therapeutic soft contact lenses [25].
• MATERIALS AND METHODS: In this retrospective study all small animal patients were identified that presented to the Royal Veterinary College, University of London over a 2-year period, in which corneal disease was managed by the application of butyl 2-cyanoacrylate [26].

References