Body Mass Index Is Associated With Orbital Pulley Degeneration Syndrome, Including Sagging Eye Syndrome.

Purpose: Sagging eye syndrome (SES), esotropia with high myopia including heavy eye syndrome, and age-related esotropia (ARE)-collectively termed orbital pulley degeneration syndrome (OPDS)-are characterized by strabismus with orbital pulley lateral rectus-superior rectus band impairment. Herein, we examined body mass index (BMI) in OPDS to determine SES-associated anthropometric characteristics.

Design: Retrospective cohort study.

Anatomical Changes in the Anterior Chamber Volume After Descemet Membrane Endothelial Keratoplasty.

Purpose: To evaluate changes in the anterior chamber of eyes that have undergone Descemet membrane endothelial keratoplasty (DMEK) and to identify factors that affect these changes.

Methods: This retrospective study included 25 pseudophakic eyes of 25 patients who underwent DMEK. We determined the preoperative and postoperative values of the best spectacle-corrected visual acuity, spherical equivalent (SE), anterior chamber volume (ACV), anterior chamber depth (ACD), central corneal thickness (CCT), and scleral spur angle (SSA) evaluated using anterior segment optical coherence tomography and iris damage score and iris posterior synechiae score.

Endogenous reactive oxygen species cause astrocyte defects and neuronal dysfunctions in the hippocampus: a new model for aging brain.

The etiology of astrocyte dysfunction is not well understood even though neuronal defects have been extensively studied in a variety of neuronal degenerative diseases. Astrocyte defects could be triggered by the oxidative stress that occurs during physiological aging. Here, we provide evidence that intracellular or mitochondrial reactive oxygen species (ROS) at physiological levels can cause hippocampal (neuronal) dysfunctions.

Genetically induced oxidative stress in mice causes thrombocytosis, splenomegaly and placental angiodysplasia that leads to recurrent abortion.

Historical data in the 1950s suggests that 7%, 11%, 33%, and 87% of couples were infertile by ages 30, 35, 40 and 45, respectively. Up to 22.3% of infertile couples have unexplained infertility.

Topical dorzolamide for macular edema in the early phase after vitrectomy and epiretinal membrane removal.

Background: The purpose of this study was to evaluate prospectively the efficacy of a topical carbonic anhydrase inhibitor in macular edema after vitrectomy.

Methods: Forty patients were included, all of whom had undergone vitrectomy combined with phacoemulsification and intraocular lens implantation for epiretinal membrane. Twenty eyes from 40 patients received topical 2% dorzolamide three times a day.

Model animals for the study of oxidative stress from complex II.

Mitochondria play a role of energy production and produce intracellular reactive oxygen species (ROS), especially superoxide anion (O2(-)) as a byproduct of energy metabolism at the same time. O2(-) is converted from oxygen and is overproduced by excessive electron leakage from the mitochondrial respiratory chain. It is well known that mitochondrial complexes I and III in the electron transport system are the major endogenous ROS sources.

Oxidative stress induced inflammation initiates functional decline of tear production.

Oxidative damage and inflammation are proposed to be involved in an age-related functional decline of exocrine glands. However, the molecular mechanism of how oxidative stress affects the secretory function of exocrine glands is unclear. We developed a novel mev-1 conditional transgenic mouse model (Tet-mev-1) using a modified tetracycline system (Tet-On/Off system).

Mitochondrial superoxide anion overproduction in Tet-mev-1 transgenic mice accelerates age-dependent corneal cell dysfunctions.

Purpose: The Tet-mev-1 mouse expressing a mitochondrial complex-II mutated SDHC(V69E) gene controlled by a tetracycline (Tet)-On/Off system can overproduce O(2)(·-) and is a versatile whole-animal model for studying mitochondrial oxidative stress. Here we report a series of age-dependent variations in corneal epithelium, endothelium, and parenchymal cells of the Tet-mev-1 mice relative to wild-type C57BL/6j mice.

Methods: Measurements of (1) mitochondrial electron transport enzyme activities; (2) O(2)(·-) production; (3) carbonylated protein, and 8-hydroxydeoxyguanosine (8-OHdG) levels as markers of oxidative stress; (4) pathologic analyses under optical and electron microscopy; (5) hematoxylin-eosin or toluidine-blue staining; and (6) immunohistochemistry with an anti-β-catenin antibody were performed in the eye, especially the cornea.

Expression of PCNA, ICAM-1, and vimentin in lens epithelial cells of cataract patients with and without type 2 diabetes.

Objective: In order to explore the pathological feature in the progression of cataract with type 2 diabetes, we compared the expression of proliferating cell nuclear antigen (PCNA), intercellular adhesion molecule-1 (ICAM-1), and vimentin in lens epithelial cells (LECs) of cataract patients with and without type 2 diabetes.

Methods: The indirect immunoperoxidase technique was performed on anterior capsules obtained from 25 patients with type 2 diabetes (DM group) and 25 patients without diabetes (control group). Immunohistochemical difference in the expression of PCNA, ICAM-1, and vimentin in LECs between the 2 groups was investigated.

A case of recurrence of congenital ocular toxoplasmosis with frosted branch angiitis (ocular toxoplasmosis with frosted branch angiitis).

Purpose: To describe a case of recurrence of congenital ocular toxoplasmosis with frosted branch angiitis.

Case Report: A 24-year-old woman presented with hyperemia in her right eye. Medical history included epilepsy at age 14 and mild mental retardation.

The role of mitochondrial superoxide anion (O2(-)) on physiological aging in C57BL/6J mice.

Much attention has been focused on the mitochondrial superoxide anion (O2(-)), which is also a critical free radial produced by ionizing radiation. The specific role of the mitochondrial O2(-) on physiological aging in mammals is still unclear despite wide-spread evidence that oxidative stress is involved in aging and age-related diseases. The major endogenous source of O2(-) is generated as a byproduct of energy metabolism from mitochondria.