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Biomedical subjects

Kensaku Miyake

Publications and source records attributed to Kensaku Miyake.

7 recordsLinked to original sources
PubMed2003

Human lens epithelial cell damage and stimulation of their secretion of chemical mediators by benzalkonium chloride rather than latanoprost and timolol.

OBJECTIVE: To investigate the effects of latanoprost, timolol maleate, and benzalkonium chloride on cell damage and induction of the secretion of chemical mediators of stress and wound healing by human lens epithelial cells in culture. METHODS: Cells from a human lens epithelial cell line (SRA01/04) were cultured in Dulbecco minimum essential medium supplemented with 5% fetal bovine serum. The amounts of latanoprost (50 micro g/mL), timolol maleate (5 mg/mL), or benzalkonium chloride (200 micro g/mL) used in eyedrops, and x10 to x1000 dilutions thereof, were added to the medium. After 7 days' culture, cell morphological changes were assessed using phase-contrast microscopy, and cell-free culture supernatants were collected for prostaglandin E2 (PGE2), interleukin 1alpha (IL-1alpha), and interleukin 6 (IL-6) iodine I 125 radioimmunoassay, enzyme-linked immunosorbent assay, and chemiluminescent enzyme immunoassay, respectively. RESULTS: All cells that were cultured with the concentrations of latanoprost, timolol, or benzalkonium chloride used in eyedrops detached from the culture dish and died within 3 days. At a x10 dilution of latanoprost or timolol or a x100 dilution of benzalkonium chloride, no proliferation or elongation of the cells was observed. Secretions of PGE2, IL-1alpha, and IL-6 at x10 dilutions of latanoprost or timolol were 3 to 77 times higher than in controls, whereas they were 190 to 305 times higher at a x180 dilution of benzalkonium chloride. The amounts of these soluble mediators in culture supernatants depended on the dose of latanoprost, timolol, or benzalkonium chloride added. CONCLUSION: Our results indicate that benzalkonium chloride, used as the preservative in eyedrops containing latanoprost or timolol, is the agent most damaging to lens epithelial cells and most strongly stimulates the expression of soluble chemical mediators in these cells.

Antihypertensive Agents↗
PubMed2003

Reduced oscillatory potentials of the full-field electroretinogram of eyes with aphakic or pseudophakic cystoid macular edema.

PURPOSE: To report reduced oscillatory potentials (OPs) in the full-field electroretinogram (ERG) of eyes with aphakic or pseudophakic cystoid macular edema (CME). DESIGN: Observational case series. METHODS: Bright white flash full-field ERGs were recorded from 19 eyes of 19 patients (ages, 53-84 years) with aphakic or pseudophakic CME. Seven of the cases had uncomplicated phacoemulsification (PE) with implantation of a posterior chamber intraocular lens (PC-IOL) and 6 had posterior capsular rupture during phacoemulsification and aspiration with implantation of a PC-IOL. Four additional patients had uncomplicated intracapsular cataract extraction (ICCE), and 2 had secondary anterior chamber intraocular lens after ICCE. Their fellow eyes without CME served as controls. Cystoid macular edema was diagnosed as clinically significant by slit-lamp examination and by fluorescein angiography. The grading for severity of CME was based on the fluorescein angiography. The visual acuity ranged from 20/200 to 20/16. RESULTS: There were no significant differences in the mean amplitudes and implicit times of the a-waves and b-waves between the affected eyes and the fellow eyes. The mean summed amplitude of the OPs was significantly reduced in the affected eyes (P =.0003, Wilcoxon signed rank test). This decrease was strongly correlated with visual acuity (r =.779, P <.0001). The mean implicit time of the first OP was significantly delayed in the affected eyes (P =.0089, Wilcoxon signed rank test). CONCLUSIONS: Because the peripheral retina contributes more significantly to full-field ERGs than the macula, the reduced OP amplitudes of the full-field ERGs in eyes with aphakic or pseudophakic CME suggest a functional impairment not only in the macula but also throughout the retina.

Aged↗
PubMed2003

Morphologic and angiographic assessment of the macula after macular translocation surgery with 360 degrees retinotomy.

PURPOSE: To compare the optical coherence tomographic assessment of retinal thickness and the fluorescein angiographic appearance after macular translocation surgery for subfoveal choroidal neovascularization. DESIGN: Retrospective, noncomparative, interventional case series. PARTICIPANTS: Twenty-three consecutive eyes. INTERVENTION AND TESTING: Optical coherence tomography and fluorescein angiography were performed before and 6 to 15 months (mean +/- standard error [SE], 10.4+/-0.7) after macular translocation surgery with a 360 degrees retinotomy in 23 patients, ages 48 to 79 years, with age-related macular degeneration (12 eyes), polypoidal choroidal vasculopathy (2 eyes), and high myopia (9 eyes). The diameter of the choroidal neovascularizations ranged from 0.3 to 2.6 disc diameters (mean +/- SE, 1.2+/-0.2), and the angle of rotation of the retina ranged from 11 degrees to 45 degrees (mean +/- SE, 29.1+/-2.1 degrees ). RESULTS: The preoperative best-corrected visual acuity ranged from hand motions to 20/100, and the postoperative best-corrected visual acuity ranged from 20/667 to 20/25. Optical coherence tomography demonstrated a concave foveal configuration after surgery in all 23 eyes, with a mean foveal thickness of 150+/-11 micro m (mean +/- SE). Fluorescein angiography showed various degrees of fluorescein leakage with a pattern similar to cystoid macular edema in 16 of 23 eyes (70%). CONCLUSIONS: The newly located macula after macular translocation surgery with a 360 degrees retinotomy had cystoid macular edema on fluorescein angiography and normal macular configuration with normal thickness in optical coherence tomography.

Aged↗
PubMed2003

Localized liquefied after-cataract.

We report 2 cases with a new type of after-cataract. In both, a milky white substance accumulated in a semicircular, closed chamber formed by the intraocular lens optic and the posterior lens capsule. Unlike in previous reports, the closed chamber did not cover the entire capsule but was based on residual lens remnants in the equatorial region of the lens capsule.

Aged↗
PubMed2003

ESCRS Binkhorst lecture 2002: Pseudophakic preservative maculopathy.

Many antiglaucoma eyedrops are reported to cause cystoid macular edema (CME) in aphakia and pseudophakia. We review 4 clinical and laboratory studies that compare the incidence of CME in early postoperative pseudophakia in eyes that received preserved latanoprost and timolol, nonpreserved timolol, and the preserved and nonpreserved vehicle for these drugs and looked at the morphological damage to cells and the changes in the indicators of cytokine and prostaglandin (PG) synthesis caused by latanoprost and timolol and the preservative benzalkonium chloride. Based on the findings of these studies, which indicate that the preservative causes increased synthesis of PGs and other substances and intensified postoperative inflammation, the term pseudophakic preservative maculopathy is proposed for CME caused by antiglaucoma eyedrops.

Aqueous Humor↗
PubMed2002

Prostaglandins and cystoid macular edema.

This review discusses the roles and interactions of prostaglandins and other possible chemical mediators in cystoid macular edema. Prostaglandins have been studied as a potential causative factor of cystoid macular edema following cataract/intraocular lens surgery. The authors' hypothesis and data with regard to the mechanisms of postoperative cystoid macular edema and other inflammatory conditions are presented. The effects of nonsteroidal anti-inflammatory drugs, which are antagonists of prostaglandin biosynthesis, on postoperative inflammatory conditions including cystoid macular edema are also reviewed. Lastly, a mechanism for the induction of cystoid macular edema by anti-glaucoma eyedrops, including prostaglandin analogs is proposed. The results from two clinical trials recently conducted by the authors suggest that the preservative rather than the active ingredient is the causative factor.

Anti-Inflammatory Agents, Non-Steroidal↗