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Purpose: To investigate whether pigment epithelium-derived factor (PEDF) or vascular endothelial growth factor (VEGF) influences macular edema in patients with central retinal vein occlusion (CRVO). Materials and Methods: In 27 patients who had CRVO with macular edema and 21 patients with nonischemic ocular diseases (control group), retinal ischemia was evaluated by measuring the area of capillary nonperfusion on fluorescein angiography and macular edema was examined by optical coherence tomography. Vitreous fluid samples were obtained during pars plana vitrectomy. Results: The vitreous level of VEGF was significantly higher in the CRVO patients than in the controls (median: 366 vs. 15.6 pg/ml, P < 0.0001), while the vitreous level of PEDF was significantly lower in the patients than in the controls (median: 17.5 vs. 28.4 ng/ml, P == 0.0298). Vitreous levels of VEGF were significantly higher in CRVO patients with retinal ischemia than in those without ischemia ( P < 0.0001), while PEDF levels did not show a significant difference. Vitreous levels of VEGF and PEDF were related to the retinal thickness at the central fovea ( P == 0.0059 and P == 0.0308, respectively). Conclusions: VEGF and PEDF may independently influence retinal vascular permeability in CRVO patients with macular edema. [ABSTRACT FROM AUTHOR]

Diabetic retinopathy, a cause of blindness, is often associated with the upregulation of vascular endothelial growth factor (VEGF) in the retina. Recently, leukocyte adhesion (leukostasis) is claimed for the occlusion of retinal capillary vascularity, which ultimately assists in the progression of diabetic retinopathy. In addition, intercellular adhesion molecule-1 (ICAM-1), a representative factor for leukostasis, is increased in diabetic retina. Endothelin (ET)-1, a potent vasoconstrictor peptide, is closely linked to the pathogenesis of diabetic retinopathy. Different therapeutic interventions concerning VEGF have already been proposed to prevent diabetic retinopathy. However, no study has yet reported concerning the effects of ET-1 receptor antagonist on the upregulated VEGF and ICAM-1 in morphologically intact diabetic retina. The current study investigated the effect of ETA receptor antagonist (TA-0201; 1 mg kg-1 day-1) on the expressions of VEGF and ICAM-1 in rat diabetic retina. Diabetes was induced by intraperitoneal injection of streptozotocin (70 mg/kg) in Sprague-Dawley rats, whereas control rats (Cont) received only citrate buffer. After 1 week, the streptozotocin-administered rats were randomly divided into two groups: ETA receptor antagonist-treated group (DM+TA-0201) and saline-treated group (DM+vehicle). After the treatment for 4 weeks, the retina was removed from the eyeball. In DM+vehicle group, the VEGF expression of retina was significantly increased (33.5 pg/mg) in comparison with that in the Cont group (25.1 pg/mg), and the upregulation of VEGF was reversed in DM+TA-0201 group (26.9 pg/mg), a phenomenon consistent with the change in VEGF mRNA levels. The expression of retinal ICAM-1 was increased in DM+vehicle group (55.1 pg/mg) compared with Cont group (43.8 pg/mg), and ET antagonism completely blocked this increase (43.8 pg/mg). Moreover, an increased leukostasis by 3.3-fold in DM+vehicle retina was returned to the control level by ET antagonism. In the current study, there was no obvious retinal morphological alteration from both the hematoxylin and eosin staining and the FITC-dextran angiography. Thus, ETA receptor antagonist might be useful in preventing the progression of diabetic retinopathy, as evidenced by suppressing the increase in VEGF and ICAM-1 levels as well as leukostasis in morphologically intact diabetic retina. [ABSTRACT FROM AUTHOR]

Thin plant-supporting poles penetrated the orbits of two patients. In one case (a 66-year-old female), the pole penetrated into the skull and reached the dorsal pons, producing a transient one-and-a-half syndrome. The lesion was confirmed by MRI. In the other (a 55-year-old female), the pole damaged the optic nerve at the orbital apex, leading to permanent monocular blindness. [ABSTRACT FROM AUTHOR]

: PurposeTo determine the appropriate correction of predicted intraocular lens (IOL) power for sulcus fixation and to prospectively assess the validity of the obtained correction value in patients having sulcus fixation.: SettingDepartment of Ophthalmology, Saiseikai Kurihashi Hospital, Saitama, Japan.: MethodsThe postoperative refraction, virtual in-the-bag IOL power for the same postoperative refraction, predicted refraction with an increase in in-the-bag IOL power by 0.50 to 2.00 diopters (D), and effective lens position (ELP) in 30 eyes with a normal axial length after sulcus fixation were retrospectively evaluated. The results were confirmed prospectively in 16 other eyes requiring sulcus fixation.: ResultsA significant myopic shift (mean 0.78 D ± 0.47 [SD]) from the predicted refraction occurred after sulcus fixation (P<.0001). The mean virtual IOL power was 1.11 ± 0.67 D higher than that of the actual sulcus-fixated IOL. The difference between the predicted refraction and the refraction after sulcus fixation was less when the difference in IOL power was 1.00 D. The ELP of the IOLs was 0.75 mm shorter using A-mode measurement and 0.62 mm shorter using back calculation from the theoretical formula with sulcus fixation than with in-the-bag fixation. In the prospective study, there was a small refractive error (mean −0.06 ± 0.19 D) when the planned IOL power was reduced by 1.00 D for sulcus fixation.: ConclusionFor sulcus fixation in eyes with a normal axial length, the IOL power should be 1.00 D less than the power for in-the-bag fixation. [Copyright &y& Elsevier]