PURPOSE: To evaluate the long-term outcome of myopic photorefractive keratectomy (PRK). METHODS: This prospective study included 31 patients (49 eyes) who underwent PRK between 1991 and 1993. A Summit UV200 excimer laser was used. Patients were divided into two groups-low myopia: preoperative Ͻ6.00 diopters (D) (range: Ϫ1.50 to Ϫ5.75 D) (n=19); and high myopia: preoperative у6.00 D (range: Ϫ6.00 to Ϫ13.00 D) (n=12). Long-term postoperative follow-up was every 2 years up to 14 years. Refraction, visual acuity, corneal status, and intraocular pressure (IOP) were evaluated. At 14 years, corneal topography and endothelial cell count were performed. RESULTS: At last follow-up, manifest refraction spherical equivalent (MRSE) for the low myopia group was Ϫ0.17Ϯ0.8, uncorrected visual acuity (UCVA) logMAR was Ϫ0.06Ϯ0.55, and best spectacle-corrected visual acuity (BSCVA) logMAR was 0.00Ϯ1.00. The high myopia group had a fi nal MRSE of Ϫ0.67Ϯ1.4, UCVA log-MAR Ϫ0.11Ϯ0.55, and BSCVA logMAR Ϫ0.03Ϯ1.00. At 14 years, BSCVA for most eyes was at least equal to preoperative BSCVA. In both groups, haze increased between 3 and 6 months, then declined in the fi rst year. A temporary increase of IOP was seen in 4 eyes. Complications were minor haze (2 eyes), transient anisocoria (9 eyes), and intraepithelial hemosiderin deposits (4 eyes). No abnormalities in endothelial cell count or morphology, astigmatism, or ectasia were noted. Three patients reported night vision disturbance, but the majority of patients were satisfi ed with the outcome based on subjective questionnaire (low myopia group: 84%; high myopia group: 75%).
Background: To verify the accuracy of applanation tonometry through disposable latex caps used to prevent transmission of infectious diseases. Methods: Tonometry was performed in 80 patients. Each patient underwent two intraocular pressure (IOP) measurements with and without the latex. In group A patients tonometry was performed first without the cap; in group B tonometry was performed first with the cap. Each group was also divided into patients with IOP, ≥20 mm Hg (A1; B1) and patients with IOP <20 mm Hg (A2; B2). Results: The mean difference of tonometry readings was equal to –0.36 ± 1.62 mm Hg in group A, –0.03 ± 1.77 mm Hg in group A1, –0.61 ± 1.45 mm Hg in group A2, 0.23 ± 1.44 in group B, 0.64 ± 1.41 mm Hg in group B1, 0.05 ± 1.42 in group B2. A statistically significant correlation was found in group A, in group A2, B, B1 and B2; a less significant correlation was found in group A1. Conclusions: The use of the latex caps does not alter the reliability of tonometry readings as long as the cap is applied tightly. Measurement variation in our study is comparable to published data on applanation tonometry.
The effects of fasting and ischemic preconditioning (IP) on heart function of Langendorff-perfused rat hearts exposed to 25 min global ischemia plus 30 min reperfusion (RP), were correlated with lactate release and tissue-levels of long-chain acyl carnitine (LCCa) and CoA (LCCoA). IP was achieved by a 3 min ischemia plus a 5 min reperfusion cycle. Creatine kinase leakage was measured to assess the extent of cardiac injury. Fasting reduced the ischemic-induced contracture, improved RP recovery of mechanical function, reduced lactate release and increased the end-ischemia LCCoA and LCCa levels. Both in the fed and the fasted rat hearts IP delayed the pacemaker depression, reduced the amplitude of ischemic contracture and improved the RP recovery of contraction. However, IP reduced creatine kinase and lactate release only in the fed rat hearts. IP had no effects on tissue LCCa and LCCoA in both groups. These data suggest that: 1) beneficial effects of fasting may be ascribed, at least in part, to a reduced lactate production which may attenuate ischemic myocyte acidification and to the accumulation of fatty acyl esters which would favour citric acid cycle replenishment during RP. 2) beneficial effects of IP could be in part explained by the reduction of lactate production in the fed group although data obtained with the fasted rat heart indicate that another mechanisms must also be involved in the effects of IP. 3) accumulation of LCCoA and LCCa is not involved in the noxious effects of ischemia as well as in the protection effected by IP.
The investigation aimed to assess the effects of hypoxic preconditioning in right ventricle strips of fed and 24-h fasted rats, which display a fast fatty acid catabolism, and to ascertain whether these effects are associated with changes in the tissue levels of long-chain acylCoA and acyl carnitine and glycolytic activity. Strips were mounted isometrically in Krebs-bicarbonate solution with 10 mM dextrose and paced at 1 Hz. Strips were exposed to 30 min hypoxia and 60 min reoxygenation with or without a previous preconditioning cycle of 5 min hypoxia followed by a 10 min reoxygenation. During hypoxia the fasted rat strips underwent a greater contracture with respect to the fed group. Preconditioning reduced the contracture strength and accelerated the post-hypoxic recovery only in the fasted rat strips. Hypoxia evoked an increase in the acylCoA and acyl carnitine tissue-contents of the strips which reached higher levels in the fasted than in the fed rat groups. Preconditioning had no effects on the content of these metabolites. During hypoxia lactate output was lower in the fasted than in the fed rat strips and preconditioning abolished this decrease. These data suggest that the protective effects of hypoxic preconditioning occur in the heart tissue predisposed to the oxidation of fatty acid and can not be ascribed to changes in the accumulation of acylCoA and acyl carnitine but could be due, at least in part, to an activation of glycolysis.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.