Incidence of Retinal Lesions before and after Refractive Surgery and Preoperative Prophylactic Laser Treatment

Purpose : We investigated the incidence of retinal lesions before and after surgery and the percentage of preoperative prophylactic laser treatment in patients who underwent corneal refractive surgery or phakic intraocular lens implantation (pIOLi). Methods : The medical records of patients who underwent refractive surgery from January 2005 to June 2013 were reviewed retrospectively. We investigated the incidence and type of retinal lesions identified during the preoperative examination. Additionally, the percentage of preoperative prophylactic laser treatment and the incidence of postoperative newly developed retinal lesions were analyzed. Results : A total of 894 eyes of 466 subjects (laser in situ keratomileusis [LASIK] 225 eyes, 117 subjects; laser-assisted subepithelial keratectomy [LASEK] or photorefractive keratectomy [PRK] 450 eyes, 231 subjects; pIOLi 219 eyes, 121 subjects) were enrolled in the present study. Retinal lesions were found in 268 eyes (29.98%) and of those, 144 eyes (16.11%) received prophylactic laser treatment. Postoperative newly developed retinal lesions were detected in 8 cases (LASEK or PRK, 5 cases; pIOLi, 3 cases) during the follow-up period. There was a significant correlation between preoperative spherical equivalent and the presence of retinal lesions. Conclusions : The patient population of refractive surgery is largely myopic and thus particularly vulnerable to retinal lesions. Additionally, a considerable number of patients required preoperative prophylactic laser treatment. Therefore, both surgeons and patients should be aware of the risks of developing postoperative retinal lesions.ope

T 세포에서 NADPH oxidase 2 의 면역조절 역할

학위논문(박사) - 한국과학기술원 : 의과학대학원, 2018.2,[vii, 72 p. :]Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is a professional reactive oxygen species (ROS) generating enzyme. NADPH oxidase 2 (Nox2) initially identified in phagocytes is responsible for the production of ROS that kills engulfed pathogens. Chronic granulomatous disease (CGD) is a rare hereditary disorder caused by mutations in a component of NADPH complex. Therefore, CGD patients are prone to be severely susceptible to life-threatening infections from bacteria and fungi. However, paradoxically, CGD patients also suffer from autoimmune diseases caused by excessive immune reactions. Despite the co-existence of these contradictory symptoms, the molecular mechanisms are still unclear and controversial. In this study, we uncovered Nox2 deficiency in T cells promotes in vitro T cell proliferation and type 1 help T cell (Th1) and Th17 cell-mediated immune responses in a T cell-intrinsic manner. Furthermore, using Th1 and Th17-mediated disease model, experimental autoimmune encephalomyelitis (EAE), we clarified Nox2 deficiency enhances Th1/Th17-mediated inflammation through augmented mitochondrial reactive oxygen species (ROS). These are due to increased mitochondrial respiration capacity and mitochondrial biogenesis induced by lack of Nox2. We revealed increased mitochondrial ROS diminishes tyrosine phosphatase SHP-1 activity and this attenuated SHP1 activity by mitochondrial ROS promotes Th1/Th17 immune responses through JAK/STAT signaling. Collectively, we show enhanced T cell proliferation and Th1/Th17 differentiation in Nox2 deficient CD4+ T cells via regulation of mitochondrial ROS and exaggerated EAE phenotypes through increased Th1/Th17-mediated inflammation. Therefore, our data indicate mitochondrial ROS-induced by a Nox2 deficiency in T cells is crucial for the Th1/Th17 inflammatory program.한국과학기술원 :의과학대학원