Purpose: To test in a 'real world' diabetic eye-screening programme, a computer-based personal risk evaluation for progression to sight-threatening diabetic retinopathy. Screening intervals were individualized, and clinical outcomes, safety and cost-effectiveness documented. Methods: The RETINARISK algorithm was used in an ophthalmology clinic in Norway. The diabetes cohort was divided on voluntary basis into two groups: one with variable screening intervals based on their personal risk profile and the other group with conventional fixed interval diabetic eye screening. Compliance, clinical outcomes, safety and health economics were evaluated. A total of 843 diabetic patients participated in the program 2014-2019. A total of 63 had type 1 and 780 type 2 diabetes. A total of 671 patients had no diabetic retinopathy at baseline and 171 had retinopathy. Results: A total of 444 (53%) diabetic patients were included in the personal risk profile program and 399 in the fixed interval group. The RETINARISK algorithm calculated 563 screening intervals for the variable interval group, which was 23 AE 16 months (mean AE SD), compared to 14 AE 5 months for the group with fixed screening intervals. Due to selection bias, the two groups could not be directly compared. We did not experience any delay in detecting diabetic retinal changes when using the personal risk profile program. Conclusion: The RETINARISK algorithm was safe and effective in a diabetic screening program in an ophthalmology clinic over 5 years. The use of the program reduces the mean frequency of screening visits and liberates valuable time in ophthalmic practice to be used on high-risk diabetic patients or other patient groups.
ABSTRACT. The induction of DNA photoproducts in rat corneal epithelium was studied after in vivo exposure to different doses of ultraviolet B light at 297 nm. Affinity-purified antibodies with a major specificity against UV-induced (6-4) photoproducts were used. The results indicate a dose dependent formation of (6-4) photoproducts. Even a minimal erythema dose (25 mJ/cm2) produced (6-4) photoproducts, demonstrating that DNA damage occurs in corneal tissue following exposure to biologically relevant doses of UVB light.
ABSTRACT.Purpose: To study the influence of a previous erosion in the fellow eye on the proliferative response during healing of a central corneal erosion.
ABSTRACT.Purpose: To determine whether apoptosis contributes to regeneration of the corneal epithelium following erosion and following ultraviolet irradiation. Methods: Central corneal erosions were made on one eye of 16 rats. One eye of another set of 16 rats was exposed to UVB irradiation. The rats were killed at time intervals varying from 12 hours to 7 days after treatment. Enucleated eyes were fixed in buffered formaldehyde and evaluated by terminal deoxynucleotidyl transferase-mediated deoxyuridinetriphosphate (dUTP) nick-end labelling (TUNEL) and morphology. The total number of cells and the number of TUNEL positive cells were counted in perpendicular sections using light microscopy. Results: Following central erosion the total epithelial cell number was restored by day 3. During the first 5 days, TUNEL positive cells were observed only in small numbers, but an increase occurred by days 6 and 7. After UVB, an increase in TU-NEL positive cells was noted for at least 3 days, and by day 7 there was a small increase of TUNEL positive cells. This differed from the results seen in control animals.
Conclusions:The present study indicates that after injury, apoptosis occurs in two distinct phases. There is an initial early phase of apoptosis which subsides at about the time the cell mass is being restored and after damaged cells have been removed. A later phase of apoptosis occurs suggests it has a homeostatic role which contributes to the regulation of the cell population.
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