The results show that in the dark-adapted retina, arrestin1 and -4 interact with enolase1. The SPR data show that the interaction between arrestin1 and enolase1 was direct, not requiring a third element to form the complex. Arrestin1 slowed the catalytic activity of enolase1, suggesting that light-driven translocation of arrestin1 may modulate the metabolic activity of photoreceptors.
Exposure of corneas to a DE after PRK with previous mechanical epithelial scraping increases epithelial turnover and is associated with a higher number of reflective structures in the stroma. Additionally increased nerve beading, nerve sprouts and tortuosity of sub-basal nerves were observed in the DE group, possibly directed to repair the alterations observed at the epithelial level.
PURPOSE-To evaluate the healing response at the flap interface in corneas with LASIK ectasia that required penetrating keratoplasty (PK).
METHODS-Corneasof five patients who developed corneal ectasia after LASIK (range: 2.5 to 5 years postoperative) were collected after corneal transplant surgery. The corneas were bisected and processed for conventional histologic analysis and immunofluorescence.RESULTS-Light microscopy showed a hypocellular fibrotic scar at the wound margin compared with the adjacent corneal stroma in all eyes. All corneas had positive staining for alpha-smooth muscle actin (SMA), a myofibroblast marker. In one eye, alpha-SMA cells were located in the fibrotic scar region in the area of the semicircular ring of haze along the margin of the LASIK flap corresponding to an area of epithelial ingrowth. In all other eyes, alpha-SMA positive cells were fewer and mainly located in the superficial stroma under the epithelial wound margin surface. Type III collagen was minimal or absent in the central zone and wound margin of all corneas except for the cornea with epithelial ingrowth present in the hypercellular fibrotic scar region. Chondroitin sulfate was stronger in the periphery of the flap wound coinciding with a higher presence of alpha-SMA-positive cells in that region. Positive staining for matrix metalloproteinase 9 (MMP-9) in the paracentral wound margin scar was seen.CONCLUSIONS-A wound-healing process characterized by absence of significant fibrosis and myofibroblasts at the wound edge in the flap interface was noted in all keratectatic eyes. However, changes in the composition of collagen and the presence of MMP-9 at the wound edge several years after LASIK indicates active wound remodeling that may explain the ongoing loss of tissue and tendency of the cornea to bulge.Ectasia after LASIK is a devastating complication of lamellar corneal surgery that results in a progressive deformation and thinning of the cornea associated with severe visual impairment. 1 Multiple risk factors have been implicated in the development of corneal ectasia. 2 Among them are abnormal or suspicious topography suggestive of pre-existing forme fruste keratoconus and an excessive resection of corneal tissue that makes the cornea mechanically unstable. However, in some cases none of these risk factors are identified. Additionally, this complication is seldom seen in deep lamellar keratoplasty. In such cases, the residual stromal bed thickness is usually no more than 10% to 20% of the corneal thickness (50 to 100 μm).We recently suggested that an increase in the amount of myofibroblasts induced by sutures at the edge of the flap in rabbit eyes may reduce the amount of steepening when intraocular pressure (IOP) is artificially increased up to 25 mmHg. 3 We postulated that corneal ectasia may be related to the clinically observed lack of corneal wound-healing response at the edge of the flap, which allows the cornea to bulge.Evaluations of the results and complications of LASIK surgery focus mainly on clinical o...
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