29719651 2018 05 02

2008-2010 13 2 2018 Apr-Jun J Ophthalmic Vis Res Combined Tenonplasty and Scleral Graft for Refractory Pseudomonas Scleritis Following Pterygium Removal with Mitomycin C Application. 200-202 10.4103/jovr.jovr_122_16 To report a surgical approach combining scleral patch graft and tenonplasty for successful management of refractory Pseudomonas scleritis following pterygium removal with mitomycin C application. A 75-year-old diabetic woman with a history of prior pterygium excision and mitomycin C application developed infectious necrotizing scleritis caused by Pseudomonas aeruginosa. Owing to progression of scleritis despite medical management, the patient underwent surgery. Intraoperatively, extensive scleral ischemia was noted. Therefore, debridement of the necrotic tissue, scleral graft, tenonplasty to bring blood vessels to the ischemic sclera, and amniotic membrane transplantation were performed. Postoperatively, no signs of ischemia or recurrence of infection were observed. During 6 months of follow-up, the patient achieved complete restoration of the globe integrity with a non-inflamed ocular surface. Through restoration of blood supply to the ischemic sclera, tenonplasty is an effective adjunctive procedure in addition to conventional scleral patch graft for the treatment of refractory Pseudomonas scleritis associated with ischemia. Siatiri Heidar H Department of Ophthalmology, Farabi Eye Hospital, Tehran University of Medical Sciences, Tehran, Iran. Mirzaee-Rad Nima N Department of Ophthalmology, Farabi Eye Hospital, Tehran University of Medical Sciences, Tehran, Iran. Aggarwal Shruti S Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Kheirkhah Ahmad A Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. eng Journal Article

Iran J Ophthalmic Vis Res 101497643 2008-322X Infectious Scleritis Mitomycin C Pseudomonas Aeruginosa Pterygium Excision Tenonplasty There are no conflicts of interest. 2018 5 3 6 0 2018 5 3 6 0 2018 5 3 6 1 ppublish 29719651 10.4103/jovr.jovr_122_16 JOVR-13-200 PMC5905316 29710246 2018 04 30

2168-6173 2018 Apr 19 JAMA Ophthalmol Blurry Vision and Eye Pain After Pterygium Surgery. 10.1001/jamaophthalmol.2017.6054 Moussa Kareem K Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts. Shantha Jessica J Department of Ophthalmology, Emory Eye Center, Emory University School of Medicine, Atlanta, Georgia. Schallhorn Julie M JM Department of Ophthalmology and the Francis I. Proctor Foundation, University of California, San Francisco. eng Journal Article 2018 04 19

United States JAMA Ophthalmol 101589539 2168-6165 2018 5 1 6 0 2018 5 2 6 0 2018 5 2 6 0 aheadofprint 29710246 2677665 10.1001/jamaophthalmol.2017.6054 29702100 2018 04 27

1096-0007 2018 Apr 24 Exp. Eye Res. Signaling pathways activated by resolvin E1 to stimulate mucin secretion and increase intracellular Ca²⁺ in cultured rat conjunctival goblet cells. S0014-4835(18)30006-X 10.1016/j.exer.2018.04.015 Glycoconjugate mucin secretion from conjunctival goblet cells is tightly regulated by nerves and specialized pro-resolving mediators (SPMs) to maintain ocular surface health. Here we investigated the actions of the SPM resolvin E1 (RvE1) on cultured rat conjunctival goblet cell glycoconjugate secretion and intracellular [Ca²⁺] ([Ca²⁺]_i) and the signaling pathways used by RvE1. Goblet cells were cultured from rat conjunctiva in RPMI medium. The amount of RvE1-stimulated glycoconjugate mucin secretion was determined using an enzyme-linked lectin assay with Ulex Europaeus Agglutinin 1 lectin. Cultured goblet cells were also incubated with the Ca²⁺ indicator dye fura 2/AM and [Ca²⁺]_i was measured. Cultured goblet cells were incubated with inhibitors to phospholipase (PL-) C, D, and A2 signaling pathways. RvE1 stimulated glycoconjugate secretion in a concentration dependent manner and was inhibited with the Ca²⁺ chelator BAPTA. The Ca²⁺_i response was also increased in a concentration manner when stimulated by RvE1. Inhibition of PLC, PLD, and PLA2, but not Ca²⁺/calmodulin-dependent kinase blocked RvE1-stimulated increase in [Ca²⁺]_i and glycoconjugate secretion. We conclude that under normal, physiological conditions RvE1 stimulates multiple pathways to increase glycoconjugate secretion and [Ca²⁺]_i. RvE1 could be an important regulator of goblet cell glycoconjugate mucin secretion to maintain ocular surface health. Copyright © 2018. Published by Elsevier Ltd. Lippestad Marit M Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA; Faculty of Medicine, University of Oslo, Oslo, Norway; Department of Medical Biochemistry, Oslo University Hospital, Oslo, Norway. Hodges Robin R RR Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Utheim Tor P TP Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA; Department of Medical Biochemistry, Oslo University Hospital, Oslo, Norway; Department of Plastic and Reconstructive Surgery, University of Oslo, Oslo, Norway. Serhan Charles N CN Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. Dartt Darlene A DA Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA; Department of Plastic and Reconstructive Surgery, University of Oslo, Oslo, Norway. Electronic address: Darlene_dartt@meei.harvard.edu. eng Journal Article 2018 04 24

England Exp Eye Res 0370707 0014-4835 Allergy Conjunctiva Goblet cells Inflammation Pro-resolving mediators 2018 01 04 2018 04 18 2018 04 23 2018 4 28 6 0 2018 4 28 6 0 2018 4 28 6 0 aheadofprint 29702100 S0014-4835(18)30006-X 10.1016/j.exer.2018.04.015 29699986 2018 04 27

1468-2079 2018 Apr 26 Br J Ophthalmol Resting nailfold capillary blood flow in primary open-angle glaucoma. bjophthalmol-2018-311846 10.1136/bjophthalmol-2018-311846 An altered haemodynamic profile for various ocular posterior segment capillary beds has been documented in primary open-angle glaucoma (POAG). POAG may also involve abnormal non-ocular blood flow, and the nailfold capillaries, which are not affected by elevated intraocular pressure (IOP), are readily assessable. We measured resting nailfold capillary blood flow in 67 POAG and 63 control subjects using video capillaroscopy. Masked readers tracked blood column voids between consecutive, registered image sequence frames, measured vessel diameter and calculated blood flow. We used multiple logistic regression to investigate the relation between nailfold capillary blood flow and POAG. In secondary analyses, we stratified cases by maximum IOP and concurrent topical beta-blocker use. Mean (±SD) blood flow in picolitres per second was 26.8±17.6 for POAG cases and 50.1±24.2 for controls (p<0.0001). After adjustment for demographic and clinical factors including blood pressure and pulse, every picolitre per second increase in resting nailfold blood flow was associated with a 6% (95% CI 0.92 to 0.96) reduced odds of POAG (p<0.0001). Similar relations between nailfold capillary blood flow and POAG were found for cases stratified by maximum known IOP and for cases stratified by concurrent topical beta-blocker use. Reduced resting nailfold capillary blood flow is present in POAG independent of covariates such as blood pressure, pulse and IOP. © Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted. Cousins Clara C CC http://orcid.org/0000-0002-7874-0581 Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, USA. Chou Jonathan C JC Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, USA. Greenstein Scott H SH Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, USA. Brauner Stacey C SC Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, USA. Shen Lucy Q LQ Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, USA. Turalba Angela V AV Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, USA. Houlihan Patricia P Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, USA. Ritch Robert R Einhorn Clinical Research Center, New York Eye and Ear Infirmary of Mount Sinai, New York, USA. Wiggs Janey L JL Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, USA. Knepper Paul A PA Department of Ophthalmology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA. Pasquale Louis R LR Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, USA louis_pasquale@meei.harvard.edu. Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA. eng Journal Article 2018 04 26

England Br J Ophthalmol 0421041 0007-1161 blood flow capillaries nailfold video capillaroscopy primary open-angle glaucoma 2018 01 01 2018 04 04 2018 4 28 6 0 2018 4 28 6 0 2018 4 28 6 0 aheadofprint 29699986 bjophthalmol-2018-311846 10.1136/bjophthalmol-2018-311846 29694386 2018 04 25

1932-6203 13 4 2018 PLoS ONE Attenuation of choroidal neovascularization by dietary intake of ω-3 long-chain polyunsaturated fatty acids and lutein in mice. e0196037 10.1371/journal.pone.0196037 Dietary ω-3 long-chain polyunsaturated fatty acids (LCPUFAs) and lutein each protect against age-related macular degeneration (AMD). We here examined the effects of ω-3 LCPUFAs and lutein supplementation in a mouse model of AMD. Mice were assigned to four groups: (1) a control group fed an ω-3 LCPUFA-free diet, (2) a lutein group fed an ω-3 LCPUFA-free diet with oral administration of lutein, (3) an ω-3 group fed an ω-3 LCPUFA-supplemented diet, and (4) an ω-3 + lutein group fed an ω-3 LCPUFA-supplemented diet with oral administration of lutein. Mice were fed the defined diets beginning 2 weeks before, and received lutein with an oral gavage needle beginning 1 week before, induction of choroidal neovascularization (CNV) by laser photocoagulation. The area of CNV measured in choroidal flat-mount preparations was significantly reduced in mice fed ω-3 LCPUFAs or lutein compared with those in the control group, and it was reduced in an additive manner in those receiving both ω-3 LCPUFAs and lutein. The concentrations of various inflammatory mediators in the retina or choroid were reduced in mice fed ω-3 LCPUFAs or lutein, but no additive effect was apparent. The generation of reactive oxygen species (ROS) in chorioretinal lesions revealed by dihydroethidium staining as well as the expression of NADPH oxidase 4 (Nox4) in the retina revealed by immunohistofluorescence and immunoblot analyses were attenuated by ω-3 LCPUFAs and lutein in a synergistic manner. Our results thus show that dietary intake of ω-3 LCPUFAs and lutein attenuated CNV in an additive manner and in association with suppression of inflammatory mediator production, ROS generation, and Nox4 expression. Dietary supplementation with both ω-3 LCPUFAs and lutein warrants further study as a means to protect against AMD. Yanai Ryoji R http://orcid.org/0000-0002-0265-9760 Department of Ophthalmology, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi, Japan. Chen Shang S Department of Ophthalmology, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi, Japan. Uchi Sho-Hei SH Department of Ophthalmology, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi, Japan. Nanri Tomoaki T Santen Pharmaceutical Co. Ltd., Osaka, Japan. Connor Kip M KM Angiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Cambridge, Massachusetts, United States of America. Kimura Kazuhiro K Department of Ophthalmology, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi, Japan. eng Journal Article 2018 04 25

United States PLoS One 101285081 1932-6203 2017 11 27 2018 04 05 2018 4 26 6 0 2018 4 26 6 0 2018 4 26 6 0 epublish 29694386 10.1371/journal.pone.0196037 PONE-D-17-41780 29686476 2018 04 26

1051-8215 28 4 2018 Apr IEEE Trans Circuits Syst Video Technol A Compact VLSI System for Bio-Inspired Visual Motion Estimation. 1021-1036 10.1109/TCSVT.2016.2630848 This paper proposes a bio-inspired visual motion estimation algorithm based on motion energy, along with its compact very-large-scale integration (VLSI) architecture using low-cost embedded systems. The algorithm mimics motion perception functions of retina, V1, and MT neurons in a primate visual system. It involves operations of ternary edge extraction, spatiotemporal filtering, motion energy extraction, and velocity integration. Moreover, we propose the concept of confidence map to indicate the reliability of estimation results on each probing location. Our algorithm involves only additions and multiplications during runtime, which is suitable for low-cost hardware implementation. The proposed VLSI architecture employs multiple (frame, pixel, and operation) levels of pipeline and massively parallel processing arrays to boost the system performance. The array unit circuits are optimized to minimize hardware resource consumption. We have prototyped the proposed architecture on a low-cost field-programmable gate array platform (Zynq 7020) running at 53-MHz clock frequency. It achieved 30-frame/s real-time performance for velocity estimation on 160 × 120 probing locations. A comprehensive evaluation experiment showed that the estimated velocity by our prototype has relatively small errors (average endpoint error < 0.5 pixel and angular error < 10°) for most motion cases. Shi Cong C Department of Ophthalmology, Harvard Medical School, Schepens Eye Research Institute, Massachusetts Eye and Ear, Boston, MA 02114 USA. Luo Gang G Department of Ophthalmology, Harvard Medical School, Schepens Eye Research Institute, Massachusetts Eye and Ear, Boston, MA 02114 USA. eng R01 AG041974 AG NIA NIH HHS United States Journal Article 2016 11 18

United States IEEE Trans Circuits Syst Video Technol 101210563 1051-8215 PLoS One. 2013;8(1):e54678 23358555 Nat Commun. 2015 Aug 04;6:7900 26238697 IEEE Trans Pattern Anal Mach Intell. 2014 Apr;36(4):784-96 26353200 IEEE Trans Pattern Anal Mach Intell. 2005 Aug;27(8):1279-91 16119266 Nat Neurosci. 2001 May;4(5):461-2 11319551 J Opt Soc Am A. 1985 Feb;2(2):284-99 3973762 IEEE Trans Image Process. 2006 Nov;15(11):3417-30 17076401 Nat Neurosci. 2001 May;4(5):526-32 11319562 Proc R Soc Lond B Biol Sci. 1990 Mar 22;239(1295):129-61 1970435 IEEE Trans Image Process. 2000;9(2):287-90 18255398 IEEE Trans Image Process. 2014 Aug;23(8):3281-93 24968405 J Vis. 2012 Aug 01;12(8):null 22854102 Invest Ophthalmol Vis Sci. 2015 Apr;56(4):2571-9 25788655 IEEE Trans Image Process. 2012 Feb;21(2):481-93 21791410 IEEE Trans Inf Technol Biomed. 2012 Sep;16(5):859-68 22717523 Neuron. 2011 Sep 22;71(6):974-94 21943597 Vision Res. 1998 Mar;38(5):743-61 9604103 Bio-inspired motion estimation motion energy multiple levels of pipeline optical flow spatiotemporal filtering very-large-scale integration (VLSI) architecture 2019 04 01 2018 4 25 6 0 2018 4 25 6 0 2018 4 25 6 1 ppublish 29686476 10.1109/TCSVT.2016.2630848 PMC5909735 NIHMS958008 29679529 2018 04 21

1941-2444 2018 Apr 21 JPEN J Parenter Enteral Nutr Influence of Human Milk and Parenteral Lipid Emulsions on Serum Fatty Acid Profiles in Extremely Preterm Infants. 10.1002/jpen.1172 Infants born prematurely are at risk of a deficiency in ω-6 and ω-3 long-chain polyunsaturated fatty acids (LC-PUFAs) arachidonic acid (AA) and docosahexaenoic acid (DHA). We investigated how fatty acids from breast milk and parenteral lipid emulsions shape serum LC-PUFA profiles in extremely preterm infants during early perinatal life. Ninety infants born < 28 weeks gestational age were randomized to receive parenteral lipids with or without the ω-3 LC-PUFAs eicosapentaenoic acid (EPA) and DHA (SMOFlipid: Fresenius Kabi, Uppsala, Sweden, or Clinoleic: Baxter Medical AB, Kista, Sweden, respectively). The fatty acid composition of infant serum phospholipids was determined from birth to postmenstrual age 40 weeks, and in mother's milk total lipids on postnatal day 7. Enteral and parenteral intake of LC-PUFAs was correlated with levels in infant serum. Infants administered parenteral ω-3 LC-PUFAs received 4.4 and 19.3 times more DHA and EPA, respectively, over the first 2 weeks of life. Parenteral EPA but not DHA correlated with levels in infant serum. We found linear relationships between dietary EPA and DHA and infant serum levels in the Clinoleic (Baxter Medical AB) group. The volume of administered SMOFlipid (Fresenius Kabi) was inversely correlated with serum AA, whereas Clinoleic (Baxter Medical AB) inversely correlated with serum EPA and DHA. There appears to be no or low correlation between the amount of DHA administered parenterally and levels measured in serum. Whether this observation reflects serum phospholipid fraction only or truly represents the amount of accreted DHA needs to be investigated. None of the parenteral lipid emulsions satisfactorily maintained high levels of both ω-6 and ω-3 LC-PUFAs in infant serum. © 2018 The Authors. Journal of Parenteral and Enteral Nutrition published by American Society for Parenteral and Enteral Nutrition. Nilsson Anders K AK Section for Ophthalmology, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Löfqvist Chatarina C Section for Ophthalmology, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Najm Svetlana S Department of Paediatrics, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Hellgren Gunnel G Section for Ophthalmology, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Sävman Karin K Department of Paediatrics, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Andersson Mats X MX Department of Biology and Environmental Sciences, The Faculty of Science, University of Gothenburg, Gothenburg. Smith Lois E H LEH Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA. Hellström Ann A Section for Ophthalmology, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. eng Journal Article 2018 04 21

United States JPEN J Parenter Enteral Nutr 7804134 0148-6071 arachidonic acid docosahexaenoic acid (DHA) extremely preterm human milk long-chain polyunsaturated fatty acids (LC-PUFA) parenteral nutrition 2018 01 12 2018 03 19 2018 4 22 6 0 2018 4 22 6 0 2018 4 22 6 0 aheadofprint 29679529 10.1002/jpen.1172 29678964 2018 04 29

2044-6055 8 4 2018 Apr 20 BMJ Open Technology-enabled examinations of cardiac rhythm, optic nerve, oral health, tympanic membrane, gait and coordination evaluated jointly with routine health screenings: an observational study at the 2015 Kumbh Mela in India. e018774 10.1136/bmjopen-2017-018774 Technology-enabled non-invasive diagnostic screening (TES) using smartphones and other point-of-care medical devices was evaluated in conjunction with conventional routine health screenings for the primary care screening of patients. Dental conditions, cardiac ECG arrhythmias, tympanic membrane disorders, blood oxygenation levels, optic nerve disorders and neurological fitness were evaluated using FDA-approved advanced smartphone powered technologies. Routine health screenings were also conducted. A novel remote web platform was developed to allow expert physicians to examine TES data and compare efficacy with routine health screenings. The study was conducted at a primary care centre during the 2015 Kumbh Mela in Maharashtra, India. 494 consenting 18-90 years old adults attending the 2015 Kumbh Mela were tested. TES and routine health screenings identified unique clinical conditions in distinct patients. Intraoral fluorescent imaging classified 63.3% of the population with dental caries and periodontal diseases. An association between poor oral health and cardiovascular illnesses was also identified. Tympanic membrane imaging detected eardrum abnormalities in 13.0% of the population, several with a medical history of hearing difficulties. Gait and coordination issues were discovered in eight subjects and one subject had arrhythmia. Cross-correlations were observed between low oxygen saturation and low body mass index (BMI) with smokers (p=0.0087 and p=0.0122, respectively), and high BMI was associated with elevated blood pressure in middle-aged subjects. TES synergistically identified clinically significant abnormalities in several subjects who otherwise presented as normal in routine health screenings. Physicians validated TES findings and used routine health screening data and medical history responses for comprehensive diagnoses for at-risk patients. TES identified high prevalence of oral diseases, hypertension, obesity and ophthalmic conditions among the middle-aged and elderly Indian population, calling for public health interventions. © Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted. Shah Pratik P Media Lab, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA. Yauney Gregory G Media Lab, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA. Gupta Otkrist O Media Lab, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA. Patalano Ii Vincent V Department of Ophthalmology, Cambridge Health Alliance, Cambridge, Massachusetts, USA. Department of Opthalmology, Harvard Medical School, Boston, Massachusetts, USA. Mohit Mrinal M Media Lab, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA. Merchant Rikin R Department of Prosthodontics, Karmaveer Bhausaheb Hiray Dental College and Hospital, Nashik, Maharashtra, India. Subramanian S V SV Department of Social and Behavioral Sciences, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA. eng Journal Article 2018 04 20

England BMJ Open 101552874 2044-6055 Clin Oral Investig. 2016 Jan;20(1):151-9 25914048 Am J Surg. 1998 Aug;176(2):153-7 9737622 Circulation. 2005 Feb 8;111(5):697-716 15699287 Am Fam Physician. 2010 Jul 1;82(1):61-8 20590073 Am Fam Physician. 2009 Jun 15;79(12):1051 19530634 IEEE J Transl Eng Health Med. 2015 Mar 05;3:2800110 27170902 Trans Am Ophthalmol Soc. 2002;100:181-5; discussion 185-6 12545692 PLoS Curr. 2015 Apr 13;7:null 25932345 Sci Rep. 2015 Aug 25;5:13368 26303238 Can J Neurol Sci. 2004 Nov;31(4):484-9 15595252 Sci Transl Med. 2010 Jan 27;2(16):16cm4 20371472 Am J Emerg Med. 2015 Aug;33(8):1089-92 25979304 Scientifica (Cairo). 2012;2012:432892 24278694 Obes Res. 1998 Sep;6 Suppl 2:51S-209S 9813653 J Glaucoma. 2010 Aug;19(6):391-7 20711029 J Electrocardiol. 2015 Mar-Apr;48(2):249-59 25601407 Lancet. 2010 Nov 20;376(9754):1785-97 21074253 Ophthalmic Res. 2014;52(4):206-11 25402747 Pediatr Dent. 2008 Jul-Aug;30(4):329-33 18767513 Indian J Community Med. 2011 Dec;36(Suppl 1):S84-5 22628920 Lancet. 2010 Nov 27;376(9755):1861-8 21074258 Indian J Endocrinol Metab. 2016 Jul-Aug;20(4):429-31 27366706 J Ophthalmol. 2015;2015:823139 26137320 Conf Proc IEEE Eng Med Biol Soc. 2012;2012:1964-7 23366301 Med Devices (Auckl). 2014 Jul 08;7:231-9 25031547 Telemed J E Health. 2003 Winter;9(4):325-30 14980089 Int Dent J. 2016 Jun;66(3):169-77 26825051 AIDS. 2016 Jan 2;30(1):159-61 26731762 PLoS One. 2008 Apr 30;3(4):e2075 18446199 Front Neurol. 2013 May 10;4:50 23717299 Neurol India. 2014 Nov-Dec;62(6):588-98 25591669 Conf Proc IEEE Eng Med Biol Soc. 2016 Aug;2016:1870-1873 28268691 BMJ. 1993 Mar 13;306(6879):688-91 8471920 Int J Chron Obstruct Pulmon Dis. 2014 Oct 21;9:1225-33 25364242 Int J Pediatr Otorhinolaryngol. 2005 Jun;69(6):739-44 15885325 J Int Soc Prev Community Dent. 2011 Jul;1(2):37-44 24478952 glaucoma primary care telemedicine Competing interests: None declared. 2018 4 22 6 0 2018 4 22 6 0 2018 4 22 6 0 epublish 29678964 bmjopen-2017-018774 10.1136/bmjopen-2017-018774 PMC5914894 29677365 2018 04 20

1552-5783 59 5 2018 Apr 01 Invest. Ophthalmol. Vis. Sci. Age-Related Changes to Human Tear Composition. 2024-2031 10.1167/iovs.17-23358 We characterize age-associated alterations in the expression of inflammatory mediators and tissue remodeling factors in human tears. A total of 75 consecutive volunteers (32 male/44 female; 19-93 years) underwent clinical assessment of ocular surface status, ocular surface disease index (OSDI) grading and tear sampling. The volunteers were categorized into three groups: young (18-40 years), middle-aged (41-60 years), and old (>60 years). Total protein profiles and chip-based protein array evaluations were conducted to investigate the expression of 60 potential candidates, including pro-/anti-inflammatory mediators and tissue remodeling factors. Appropriate validations were performed using conventional assays. Multiple comparisons for regression between potential candidates and age were performed, as well as statistical analyses among the three age groups. Nonpooled samples were used for quantifications. Pearson analysis of chip-arrays identified 9 of 60 potential candidates. Specifically, IL-8, IL-6, and regulated on activation, normal T cell expressed and secreted (RANTES; P < 0.0083) protein as well as matrix metalloproteinase (MMP)-1, IL-3, and TNF-α (P < 0.05) correlated positively with aging. MIP-3β showed an opposite tendency. Western blot and ELISA analysis corroborated the array data. OSDI grading did not correlate with aging. Dynamic changes to tear protein profiles occur with aging. Our study identifies the expression of IL-8, IL-6, RANTES, MMP-1, and MIP-3β as increasing with age. These select inflammatory and matrix remodeling factors may be relevant to the development of novel diagnostic tools and therapeutics in the context of age-related ocular surface disease. Micera Alessandra A Research Laboratories in Ophthalmology, IRCCS-G.B. Bietti Foundation, Rome, Italy. Di Zazzo Antonio A Ophthalmology Complex Operative Unit, University Campus Bio-Medico, Rome, Italy. Esposito Graziana G Research Laboratories in Ophthalmology, IRCCS-G.B. Bietti Foundation, Rome, Italy. Longo Rosa R Ophthalmology Complex Operative Unit, University Campus Bio-Medico, Rome, Italy. Foulsham William W Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Maryland, United States. Sacco Roberto R Neuropsychiatry Research Unit, University Campus Bio-Medico, Rome, Italy. Sgrulletta Roberto R Ophthalmology Complex Operative Unit, University Campus Bio-Medico, Rome, Italy. Bonini Stefano S Ophthalmology Complex Operative Unit, University Campus Bio-Medico, Rome, Italy. eng Journal Article

United States Invest Ophthalmol Vis Sci 7703701 0146-0404 2018 4 21 6 0 2018 4 21 6 0 2018 4 21 6 0 ppublish 29677365 2679096 10.1167/iovs.17-23358 29677003 2018 04 20

1536-4798 2018 Apr 19 Cornea Identification of a Novel TCF4 Isoform in the Human Corneal Endothelium. 10.1097/ICO.0000000000001521 Alternative splice isoforms of TCF4, a gene implicated in Fuchs corneal dystrophy, have been identified in multiple human tissues outside of the eye. The aim of this study was to identify the transcriptional profile of TCF4 in the corneal endothelium. We extracted RNA from the donor corneal endothelium and performed rapid amplification of cDNA ends. We tested the expression pattern of 1 newly identified isoform (7b) in a panel of cDNA derived from multiple human tissues and included cDNA from corneal endothelial (CE) and retinal pigment epithelial cell lines. To further delineate differential expression of TCF4 splice variants that span CTG18.1, we analyzed expression of 6 alternative splice isoforms that are transcribed from either exon 2 or 3 in RNA extracted from the corneal endothelium of 3 normal donors and a CE cell line. We identified 11 different isoforms in control CE tissue, including 1 isoform (7b) not reported previously. This isoform is enriched specifically in the corneal endothelium and placenta compared with other tissues in a panel of human cDNA. We demonstrate the complex expression profile of TCF4 in the human corneal endothelium and reveal expression of alternative splice variants of TCF4. Eghrari Allen O AO The Wilmer Eye Institute, Department of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, MD. Vasanth Shivakumar S The Wilmer Eye Institute, Department of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, MD. Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston MA. Gapsis Briana C BC The Wilmer Eye Institute, Department of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, MD. Bison Henry H The Wilmer Eye Institute, Department of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, MD. Jurkunas Ula U Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston MA. Riazuddin S Amer SA The Wilmer Eye Institute, Department of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, MD. Gottsch John D JD The Wilmer Eye Institute, Department of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, MD. eng Journal Article 2018 04 19

United States Cornea 8216186 0277-3740 2018 4 21 6 0 2018 4 21 6 0 2018 4 21 6 0 aheadofprint 29677003 10.1097/ICO.0000000000001521 29675394 2018 04 22

2222-3959 11 4 2018 Int J Ophthalmol Cryopreserved limbal lamellar keratoplasty for peripheral corneal and limbal reconstruction. 699-702 10.18240/ijo.2018.04.27 This study aimed to evaluate the outcomes and described the recovery process of cryopreserved limbal lamellar keratoplasty (CLLK) for peripheral corneal and limbal diseases. Thirteen eyes of 12 patients with a mean age of 41±23.9y were included. The average follow-up was 12.1±5.6mo. Stable ocular surface was achieved in all eyes at last follow-up. Epithelialization originated from both recipient and graft in 9 eyes. We conclude that CLLK compensates for the shortage of donor corneas and cryopreserved limbal grafts provide epithelialization sources in ocular surface reconstruction. Xie Hua-Tao HT Department of Ophthalmology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. Li Jing J Department of Ophthalmology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. Liu Yang Y Schepens Eye Research Institute, Massachusetts Eye and Ear, Harvard Medical School, Boston 02114, USA. Jiang Dong-Ling DL Department of Ophthalmology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. Shen Rui-Fen RF Department of Ophthalmology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. Zhang Ming-Chang MC Department of Ophthalmology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. eng Journal Article 2018 04 18

China Int J Ophthalmol 101553860 2222-3959 Clin Ophthalmol. 2013;7:607-14 23576860 Cornea. 2006 May;25(4):377-82 16670472 Graefes Arch Clin Exp Ophthalmol. 2012 Dec;250(12):1795-801 22573412 Am J Ophthalmol. 2011 Nov;152(5):762-70.e3 21803324 J Zhejiang Univ Sci B. 2014 Dec;15(12):1055-63 25471835 Ophthalmology. 2005 Mar;112(3):425-30 15745769 Lancet. 2010 Sep 25;376(9746):1033-4 20870080 Int J Ophthalmol. 2013 Apr 18;6(2):251-2 23638432 Curr Opin Ophthalmol. 2017 Jul;28(4):377-381 28379858 Cornea. 2014 Jan;33(1):27-31 24240486 JAMA Ophthalmol. 2016 Feb;134(2):167-73 26633035 Transplant Proc. 2007 Oct;39(8):2609-11 17954190 Cornea. 2016 Apr;35(4):506-9 26890659 Exp Eye Res. 2004 Mar;78(3):433-46 15106923 Graefes Arch Clin Exp Ophthalmol. 2014 Jun;252(6):963-8 24796771 cryopreserve epithelialization lamellar keratoplasty limbus neovascularization ocular surface peripheral corneal and limbal diseases stem cells 2017 05 15 2017 08 28 2018 4 21 6 0 2018 4 21 6 0 2018 4 21 6 1 epublish 29675394 10.18240/ijo.2018.04.27 ijo-11-04-699 PMC5902380 29666122 2018 04 18

1468-2079 2018 Apr 17 Br J Ophthalmol Iontophoretic delivery of dexamethasone phosphate for non-infectious, non-necrotising anterior scleritis, dose-finding clinical trial. bjophthalmol-2017-311610 10.1136/bjophthalmol-2017-311610 Currently available treatment options for non-infectious scleritis, including non-steroidal anti-inflammatory drugs, systemic corticosteroids and immunosuppressive therapies, have both efficacy and side effect limitations. Iontophoretic delivery of corticosteroids has been demonstrated to be effective for anterior uveitis and represents a potential new approach to scleritis therapy. We hypothesised that iontophoretic delivery would provide effective and precise medication delivery to the sclera, while limiting systemic exposure and side effects. This first-in-human randomised, double-masked, dose-escalating study of iontophoretic administration of dexamethasone phosphate for scleritis suggests the treatment to be well tolerated and safe (within the limitations of the 18 patients sample size). There was a suggestion of efficacy in the lowest (1.2 mA/min at 0.4 mA) dose group (corresponding to the superficial location of scleritis compared with anterior uveitis), with 5/7 eyes meeting the primary efficacy outcome within 28 days. Our results suggest iontophoretic delivery of corticosteroids is a promising potential treatment for scleritis, with favourable safety and preliminary efficacy results in this phase 1 trial. NCT01059955. © Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted. O'Neil Erin C EC Department of Ophthalmology, Scheie Eye Institute, Philadelphia, Pennsylvania, USA. Huang Jiayan J Department of Ophthalmology, Center for Preventive Ophthalmology and Biostatistics, Philadelphia, Pennsylvania, USA. Suhler Eric B EB Department of Ophthalmology, Oregon Health and Sciences University, Portland, Oregon, USA. Dunn James P JP Jr Mid-Atlantic Retina, Wills Eye Hospital, Philadelphia, Pennsylvania, USA. Wilmer Eye Institute, Johns Hopkins University, Baltimore, Maryland, USA. Perez Victor L VL Bascom Palmer Eye Institute, University of Miami, Miami, Florida, USA. Gritz David C DC Wilmer Eye Institute, Johns Hopkins University, Baltimore, Maryland, USA. McWilliams Kathy K Department of Ophthalmology, Center for Preventive Ophthalmology and Biostatistics, Philadelphia, Pennsylvania, USA. Peskin Ellen E Department of Ophthalmology, Center for Preventive Ophthalmology and Biostatistics, Philadelphia, Pennsylvania, USA. Ying Gui-Shuang GS Department of Ophthalmology, Center for Preventive Ophthalmology and Biostatistics, Philadelphia, Pennsylvania, USA. Department of Biostatistics and Epidemiology, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Bunya Vatinee Y VY Department of Ophthalmology, Scheie Eye Institute, Philadelphia, Pennsylvania, USA. Maguire Maureen G MG Department of Ophthalmology, Center for Preventive Ophthalmology and Biostatistics, Philadelphia, Pennsylvania, USA. Department of Biostatistics and Epidemiology, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Kempen John H JH http://orcid.org/0000-0002-2967-4792 Bascom Palmer Eye Institute, University of Miami, Miami, Florida, USA kempenjh@yahoo.com. Department of Ophthalmology, Massachusetts Eye and Ear, Boston, Massachusetts, USA. Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Discovery Eye Center, MyungSung Christian Medical Center, Addis Ababa, Ethiopia. eng ClinicalTrials.gov NCT01059955 Journal Article 2018 04 17

England Br J Ophthalmol 0421041 0007-1161 Clinical Trial Drugs Sclera and Episclera Treatment other 2017 11 13 2018 03 20 2018 03 22 2018 4 19 6 0 2018 4 19 6 0 2018 4 19 6 0 aheadofprint 29666122 bjophthalmol-2017-311610 10.1136/bjophthalmol-2017-311610 29659833 2018 04 16

1460-2083 2018 Apr 05 Hum. Mol. Genet. Ift172 conditional knockout mice exhibit rapid retinal degeneration and protein trafficking defects. 10.1093/hmg/ddy109 Intraflagellar transport (IFT) is a bidirectional transport process that occurs along primary cilia and specialized sensory cilia, such as photoreceptor outer-segments. Genes coding for various IFT components are associated with ciliopathies. Mutations in IFT172 lead to diseases ranging from isolated retinal degeneration to severe syndromic ciliopathies. In this study, we created a mouse model of IFT172-associated retinal degeneration to investigate the ocular disease mechanism. We found that depletion of IFT172 in rod photoreceptors leads to a rapid degeneration of the retina, with severely reduced electroretinography responses by one month and complete outer-nuclear layer degeneration by two months. We investigated molecular mechanisms of degeneration and show that IFT172 protein reduction leads to mislocalization of specific photoreceptor outer-segment proteins (RHO, RP1, IFT139), aberrant light-driven translocation of alpha transducin and altered localization of glioma-associated oncogene family member 1 (GLI1). This mouse model exhibits key features of the retinal phenotype observed in patients with IFT172-associated blindness and can be used for in vivo testing of ciliopathy therapies. Gupta Priya R PR Ocular Genomics Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, 02114, USA. Weill Cornell Medical College, New York, New York, 10021, USA. Pendse Nachiket N Ocular Genomics Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, 02114, USA. Greenwald Scott H SH Ocular Genomics Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, 02114, USA. Leon Mihoko M Ocular Genomics Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, 02114, USA. Liu Qin Q Ocular Genomics Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, 02114, USA. Pierce Eric A EA Ocular Genomics Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, 02114, USA. Bujakowska Kinga M KM Ocular Genomics Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, 02114, USA. eng Journal Article 2018 04 05

England Hum Mol Genet 9208958 0964-6906 2017 11 17 2018 03 26 2018 4 17 6 0 2018 4 17 6 0 2018 4 17 6 0 aheadofprint 29659833 4961539 10.1093/hmg/ddy109 29659558 2018 04 16

2073-4425 9 4 2018 Apr 16 Genes (Basel) Special Issue Introduction: Inherited Retinal Disease: Novel Candidate Genes, Genotype-Phenotype Correlations, and Inheritance Models. E215 10.3390/genes9040215 Inherited retinal diseases (IRDs) are genetically and clinically heterogeneous disorders.[...]. Cremers Frans P M FPM Department of Human Genetics and Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands. Frans.Cremers@radboudumc.nl. Boon Camiel J F CJF Department of Ophthalmology, Leiden University Medical Center, P.O. Box 9600, 2300 RC Leiden, The Netherlands. C.J.F.Boon@lumc.nl. Academic Medical Center, Department of Ophthalmology, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. C.J.F.Boon@lumc.nl. Bujakowska Kinga K Ocular Genomics Institute, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA 02114, USA. Kinga_Bujakowska@MEEI.HARVARD.EDU. Zeitz Christina C 0000-0002-3510-1712 Sorbonne Université, INSERM, CNRS, Institut de la Vision, Department of Genetics, 17 rue Moreau, 75012 Paris, France. christina.zeitz@inserm.fr. eng Editorial 2018 04 16

Switzerland Genes (Basel) 101551097 2073-4425 The authors declare no conflict of interest. 2018 04 05 2018 04 13 2018 4 17 6 0 2018 4 17 6 0 2018 4 17 6 1 epublish 29659558 genes9040215 10.3390/genes9040215 29649829 2018 04 17

1661-7819 114 1 2018 Apr 12 Neonatology Relation of Retinopathy of Prematurity to Brain Volumes at Term Equivalent Age and Developmental Outcome at 2 Years of Corrected Age in Very Preterm Infants. 46-52 10.1159/000487847 Retinopathy of prematurity (ROP) is a major complication of preterm birth and has been associated with later visual and nonvisual impairments. To evaluate relationships between any stage of ROP, brain volumes, and developmental outcomes. This study included 52 very preterm infants (gestational age [mean ± SD]: 26.4 ± 1.9 weeks). Total brain, gray matter, unmyelinated white matter (UWMV), and cerebellar volumes were estimated in 51 out of 52 infants by magnetic resonance imaging at term-equivalent age. Bayley Scales of Infant Development were used to assess developmental outcomes in 49 out of 52 infants at a mean corrected age of 24.6 months. Nineteen out of 52 infants developed any stage of ROP. Infants with ROP had a lower median (IQR) UWMV (173 [156-181] vs. 204 [186-216] mL, p < 0.001) and cerebellar volume (18.3 [16.5-20] vs. 22.3 [20.3-24.7] mL, p < 0.001) than infants without ROP. They also had a lower median (IQR) mental developmental index (72 [56-83] vs. 100 [88-104], p < 0.001) and a lower psychomotor developmental index (80 [60-85] vs. 92 [81-103], p = 0.002). Brain volumes and developmental outcomes did not differ among infants with different stages of ROP. Any stage of ROP in preterm infants was associated with a reduced brain volume and an impaired developmental outcome. These results suggest that common pathways may lead to impaired neural and neurovascular development in the brain and retina and that all stages of ROP may be considered in future studies on ROP and development. © 2018 S. Karger AG, Basel. Sveinsdóttir Kristbjörg K Division of Pediatrics, Department of Clinical Sciences, Skåne University Hospital, Lund University, Lund, Sweden. Ley David D Division of Pediatrics, Department of Clinical Sciences, Skåne University Hospital, Lund University, Lund, Sweden. Hövel Holger H Division of Pediatrics, Department of Clinical Sciences, Central Hospital Kristianstad, Lund, Sweden. Fellman Vineta V Division of Pediatrics, Department of Clinical Sciences, Skåne University Hospital, Lund University, Lund, Sweden. Children's Hospital, University of Helsinki, Helsinki, Finland. Hüppi Petra S PS Division of Development and Growth, Department of Pediatrics, University Hospital of Geneva, Geneva, Switzerland. Smith Lois E H LEH Department of Opthalmology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA. Hellström Ann A Sahlgrenska Center for Pediatric Ophthalmology Research, Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden. Hansen Pupp Ingrid I Division of Pediatrics, Department of Clinical Sciences, Skåne University Hospital, Lund University, Lund, Sweden. eng R01 EY017017 EY NEI NIH HHS United States R24 EY024864 EY NEI NIH HHS United States Journal Article 2018 04 12

Switzerland Neonatology 101286577 1661-7800 Brain volume Developmental outcome Magnetic resonance imaging Mental developmental index Preterm birth Psychomotor developmental index Retinopathy of prematurity 2017 11 26 2018 02 17 2018 4 13 6 0 2018 4 13 6 0 2018 4 13 6 0 aheadofprint 29649829 000487847 10.1159/000487847 29633588 2018 04 10

2162-0989 2018 Apr 09 Asia Pac J Ophthalmol (Phila) Familial Exudative Vitreoretinopathy: Pathophysiology, Diagnosis, and Management. 10.22608/APO.201855 Familial exudative vitreoretinopathy (FEVR) is a heritable vitreoretinopathy characterized by anomalous retinal vascular development. The principal feature of the disease is an avascular peripheral retina. This in turn can cause further pathological changes including neovascularization, exudation, hemorrhage, and retinal detachment. The biological basis of the disease is thought to be from defects in the Wnt signaling pathway. Many gene mutations have been implicated, and these can be inherited in an autosomal dominant (most common), autosomal recessive, and X-linked recessive fashion. Examination with wide-field fluorescein angiography is essential and can identify the disease in its earlier stages, enabling timely treatment, in addition to helping identify asymptomatic family members. The current treatment paradigm involves laser photocoagulation of the avascular peripheral retina for neovascular sequelae and vitreoretinal surgery for progressive retinal detachment. Further studies are underway to better characterize this complex vitreoretinopathy. Copyright 2018 Asia-Pacific Academy of Ophthalmology. Tauqeer Zujaja Z Retina Service, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts. Yonekawa Yoshihiro Y Retina Service, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts. Pediatric Retina Surgery, Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts. eng Journal Article 2018 04 09

China Asia Pac J Ophthalmol (Phila) 101583622 2162-0989 FEVR familial exudative vitreoretinopathy 2018 4 11 6 0 2018 4 11 6 0 2018 4 11 6 0 aheadofprint 29633588 10.22608/APO.201855 29631901 2018 04 10

1549-4713 2018 Apr 06 Ophthalmology Contact Lens Correction of Aphakia in Children: A Report by the American Academy of Ophthalmology. S0161-6420(18)30675-4 10.1016/j.ophtha.2018.03.014 To review the published literature to assess the visual outcomes and adverse events associated with the 2 most commonly used contact lenses for treating aphakia in children: silicone elastomer (SE) and rigid gas permeable (RGP). Literature searches were last conducted in January 2018 in the PubMed, Cochrane Library, and ClinicalTrials.gov databases with no date or language restrictions. These combined searches yielded 167 citations, 27 of which were reviewed in full text. Of these, 10 articles were deemed appropriate for inclusion in this assessment and subsequently assigned a level of evidence rating by the panel methodologist. The literature search identified 4 level II studies and 6 level III studies. There were insufficient data to compare visual outcomes for eyes treated using SE lenses versus RGP lenses. Silicone elastomer lenses have the advantage that they can be worn on an extended-wear basis, but they were associated with more adverse events than RGP lenses. These adverse events included microbial keratitis, corneal infiltrates, corneal edema, corneal scars, lenses adhering to the cornea, superficial punctate keratopathy, lid swelling, and conjunctival hyperemia. The lens replacement rate was approximately 50% higher for RGP lenses in the only study that directly compared SE and RGP lenses. Limited evidence was found in the literature on this topic. Silicone elastomer and RGP contact lenses were found to be effective for treating aphakia in children. Silicone elastomer lenses are easier to fit and may be worn on an extended-wear basis. Rigid gas permeable lenses must be removed every night and require a more customized fit, but they are associated with fewer adverse events. The choice of which lens a practitioner prescribes should be based on the particular needs of each patient. Copyright © 2018 American Academy of Ophthalmology. Published by Elsevier Inc. All rights reserved. Lambert Scott R SR Department of Ophthalmology, Stanford University School of Medicine, Palo Alto, California. Kraker Raymond T RT Jaeb Center for Health Research, Tampa, Florida. Pineles Stacy L SL Jules Stein Eye Institute, Los Angeles, California. Hutchinson Amy K AK Department of Ophthalmology, Emory University School of Medicine, Atlanta, Georgia. Wilson Lorri B LB Casey Eye Institute, Oregon Health & Science University, Portland, Oregon. Galvin Jennifer A JA Eye Surgery Associates, LLC, Department of Ophthalmology and Visual Science, Yale School of Medicine, New Haven, Connecticut. VanderVeen Deborah K DK Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts. eng Journal Article 2018 04 06

United States Ophthalmology 7802443 0161-6420 2018 03 08 2018 03 08 2018 03 09 2018 4 11 6 0 2018 4 11 6 0 2018 4 11 6 0 aheadofprint 29631901 S0161-6420(18)30675-4 10.1016/j.ophtha.2018.03.014 29630857 2018 04 21

1525-2191 2018 Apr 06 Am. J. Pathol. The Role of Microglia and Peripheral Monocytes in Retinal Damage Following Corneal Chemical Injury. S0002-9440(17)31228-2 10.1016/j.ajpath.2018.03.005 Eyes that have suffered alkali burn to the surface are excessively susceptible to subsequent severe glaucoma and retinal ganglion cell loss, despite maximal efforts to prevent or slow down the disease. Recently, we have shown in mice and rabbits, that such retinal damage is neither mediated by the alkali itself reaching the retina nor by intraocular pressure elevation. Rather, it is caused by the up-regulation of tumor necrosis factor alpha (TNF-α) that rapidly diffuses posteriorly, causing retinal ganglion cell apoptosis and CD45⁺ cell activation. Here, we investigated the involvement of peripheral blood monocytes and microglia in retinal damage. Using CX3CR1^+/EGFP::CCR2^+/RFP reporter mice and bone marrow chimeras, we show that peripheral CX3CR1⁺CD45^hiCD11b⁺MHC-II⁺ monocyte infiltrate into the retina from the optic nerve at 24 hours after the burn and release further TNF-α. A secondary source of peripheral monocyte response originates from a rare population of 'patrolling' myeloid CCR2⁺ cells of the retina that differentiate into CX3CR1⁺ macrophages within hours after the injury. As a result, CX3CR1⁺CD45^loCD11b⁺ microglia become reactive at 7 days, causing further TNF-α release. Prompt TNF-α inhibition after corneal burn suppresses monocyte infiltration and microglia activation, and protects the retina. This study may prove relevant to other injuries of the central nervous system. Copyright © 2018. Published by Elsevier Inc. Paschalis Eleftherios I EI Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA; Massachusetts Eye and Ear / Schepens Eye Research Institute, Boston Keratoprosthesis Laboratory, Harvard Medical School, Boston, MA; Disruptive Technology Laboratory, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA. Electronic address: eleftherios_paschalis@meei.harvard.edu. Lei Fengyang F Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA; Massachusetts Eye and Ear / Schepens Eye Research Institute, Boston Keratoprosthesis Laboratory, Harvard Medical School, Boston, MA; Disruptive Technology Laboratory, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA. Zhou Chengxin C Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA; Massachusetts Eye and Ear / Schepens Eye Research Institute, Boston Keratoprosthesis Laboratory, Harvard Medical School, Boston, MA; Disruptive Technology Laboratory, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA. Kapoulea Vassiliki V Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA; Massachusetts Eye and Ear / Schepens Eye Research Institute, Boston Keratoprosthesis Laboratory, Harvard Medical School, Boston, MA; Disruptive Technology Laboratory, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA. Thanos Aristomenis A Angiogenesis Laboratory, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA. Dana Reza R Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA. Vavvas Demetrios D Angiogenesis Laboratory, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA. Chodosh James J Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA; Disruptive Technology Laboratory, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA. Dohlman Claes H CH Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA; Massachusetts Eye and Ear / Schepens Eye Research Institute, Boston Keratoprosthesis Laboratory, Harvard Medical School, Boston, MA. eng P30 EY003790 EY NEI NIH HHS United States Journal Article 2018 04 06

United States Am J Pathol 0370502 0002-9440 2017 12 25 2018 03 04 2018 03 26 2018 4 10 6 0 2018 4 10 6 0 2018 4 10 6 0 aheadofprint 29630857 S0002-9440(17)31228-2 10.1016/j.ajpath.2018.03.005 29627826 2018 04 08

1423-0259 2018 Apr 06 Ophthalmic Res. Meibomian Gland Dysfunction in Primary and Secondary Sjögren Syndrome. 10.1159/000487487 We hypothesized that women with primary (pSS) and secondary Sjögren syndrome (sSS; with systemic lupus erythematosus [SLE] or rheumatoid arthritis [RA]) have meibomian gland dysfunction (MGD). We sought to test our hypothesis. Subjects with pSS, sSS + SLE, sSS + RA, and non-SS-related MGD were recruited from the Sjögren's Syndrome Foundation or outpatient clinics at Tufts University School of Dental Medicine or Brigham and Women's Hospital. The control population was recruited from the Greater Boston area. After providing written informed consent, the subjects underwent an eye examination and/or completed two questionnaires that assess symptoms of dry eye disease (DED). Our results demonstrate that pSS and sSS patients have MGD. These subjects had meibomian gland orifice metaplasia, an increased number of occluded meibomian gland orifices, and a reduced quality of meibomian gland secretions. Further, patients with pSS, sSS + SLE, sSS + RA, and MGD had significant alterations in their tear film, lid margin, cornea, and conjunctiva. Symptoms of DED were increased ∼10-fold in all pSS, sSS, and MGD groups relative to controls. Our findings support our hypothesis and show that individuals with pSS, sSS + SLE, and sSS + RA have MGD. In addition, our study indicates that patients with pSS and sSS have both aqueous-deficient and evaporative DED. © 2018 S. Karger AG, Basel. Sullivan David A DA Schepens Eye Research Institute, Boston, Massachusetts, USA. Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Massachusetts Eye and Ear, Boston, Massachusetts, USA. Dana Reza R Schepens Eye Research Institute, Boston, Massachusetts, USA. Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Massachusetts Eye and Ear, Boston, Massachusetts, USA. Sullivan Rose M RM Schepens Eye Research Institute, Boston, Massachusetts, USA. Krenzer Kathleen L KL Schepens Eye Research Institute, Boston, Massachusetts, USA. Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Sahin Afsun A Schepens Eye Research Institute, Boston, Massachusetts, USA. Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Koç University Medical School, Istanbul, Turkey. Arica Beril B Schepens Eye Research Institute, Boston, Massachusetts, USA. Liu Yang Y Schepens Eye Research Institute, Boston, Massachusetts, USA. Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Massachusetts Eye and Ear, Boston, Massachusetts, USA. Kam Wendy R WR Schepens Eye Research Institute, Boston, Massachusetts, USA. Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Massachusetts Eye and Ear, Boston, Massachusetts, USA. Papas Athena S AS Tufts University School of Dental Medicine, Boston, Massachusetts, USA. Cermak Jennifer M JM Schepens Eye Research Institute, Boston, Massachusetts, USA. Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. eng Journal Article 2018 04 06

Switzerland Ophthalmic Res 0267442 0030-3747 Lacrimal gland Meibomian gland Primary Sjögren syndrome Rheumatoid arthritis Secondary Sjögren syndrome Systemic lupus erythematosus Tear film 2017 10 18 2018 02 07 2018 4 9 6 0 2018 4 9 6 0 2018 4 9 6 0 aheadofprint 29627826 000487487 10.1159/000487487 29627599 2018 04 08

1937-5913 2018 Apr 05 Ocul Surf Improving the practicality and safety of artificial corneas: Pre-assembly and gamma-rays sterilization of the boston keratoprosthesis. S1542-0124(18)30044-2 10.1016/j.jtos.2018.04.002 To make the Boston keratoprosthesis (B-KPro), together with its carrier corneal graft, more easily procured, transported and stored, as well as less expensive, easier for the surgeon to implant and safer for the patient, it is proposed that the B-KPro-graft combination be pre-assembled by an expert technician, followed by sterilization with gamma ray irradiation (GI) allowing long-term storage at room temperature. For this to be possible, it must be shown that the B-KPro itself (not only the graft) remains unharmed by the irradiation. Polymethyl methacrylate (PMMA) discs and B-KPros were submitted to either ethylene oxide sterilization or different doses of GI. Cell biocompatibility, mechanical strength and optical quality were evaluated. The feasibility of assembling the B-KPro to a corneal graft, and gamma-radiate afterwards, was also assessed. There were no differences in cell biocompatibility between the samples. The optical evaluation showed high levels of transparency for all the groups. The absorbance of ultraviolet was higher for the groups treated with GI. The mechanical evaluation by nanoindentation showed no alterations of the PMMA discs after GI. The flexure test revealed a similar mechanical behavior. Technically, pre-assembly and GI of the B-KPro revealed no problems. Sterilization of B-KPro using GI has no detrimental influence on the device. The pre-assembly of B-KPro to a donor cornea, followed by gamma sterilization, emerges as an efficient and safe procedure. Copyright © 2018. Published by Elsevier Inc. Gonzalez-Andrades Miguel M Massachusetts Eye and Ear and Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Electronic address: miguel_gonzalez@meei.harvard.edu. Sharifi Roholah R Massachusetts Eye and Ear and Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Islam Mohammad-Mirazul MM Massachusetts Eye and Ear and Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Divoux Thibaut T Centre de Recherche Paul Pascal, CNRS UMR, 5031, Pessac, France; MultiScale Material Science for Energy and Environment, UMI 3466, CNRS-MIT, Cambridge, MA, United States. Haist Michael M Institute of Concrete Structures and Building Materials, Karlsruhe Institute of Technology, Karlsruhe, Germany; Massachusetts Institute of Technology, Civil and Environmental Engineering Department, Cambridge, MA, United States. Paschalis Eleftherios E Massachusetts Eye and Ear and Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Gelfand Larisa L Massachusetts Eye and Ear and Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Mamodaly Shamina S Massachusetts Eye and Ear and Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Di Cecilia Luca L Massachusetts Eye and Ear and Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Cruzat Andrea A Massachusetts Eye and Ear and Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Ulm Franz-Josef FJ Massachusetts Institute of Technology, Civil and Environmental Engineering Department, Cambridge, MA, United States. Chodosh James J Massachusetts Eye and Ear and Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Delori Francois F Massachusetts Eye and Ear and Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Dohlman Claes H CH Massachusetts Eye and Ear and Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. eng Journal Article 2018 04 05

United States Ocul Surf 101156063 1542-0124 Artificial corneas Boston keratoprosthesis Gamma radiation Gamma rays Preassembly Sterilization 2018 02 12 2018 04 03 2018 04 04 2018 4 9 6 0 2018 4 9 6 0 2018 4 9 6 0 aheadofprint 29627599 S1542-0124(18)30044-2 10.1016/j.jtos.2018.04.002 29626663 2018 04 30

1528-3933 2018 Apr 04 J AAPOS A case of Graves' ophthalmopathy associated with pembrolizumab (Keytruda) therapy. S1091-8531(18)30039-9 10.1016/j.jaapos.2018.01.006 We present the first reported case of Graves' orbitopathy induced by pembrolizumab, a new FDA-approved drug used for the treatment of multiple refractory solid tumors and classic Hodgkin lymphoma. Pembrolizumab elicits T-lymphocyte proliferation; we suspect that thyroid eye disease may result in some cases. Copyright © 2018. Published by Elsevier Inc. Park Ella S Y ESY Yonsei University College of Medicine, Seoul, South Korea. Rabinowits Guilherme G Medical Oncology Department, Dana-Farber Cancer Institute and Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts. Hamnvik Ole-Petter R OR Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts. Dagi Linda R LR Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts. Electronic address: Linda.Dagi@childrens.harvard.edu. eng Journal Article 2018 04 04

United States J AAPOS 9710011 1091-8531 2017 10 22 2018 01 17 2018 01 18 2018 4 8 6 0 2018 4 8 6 0 2018 4 8 6 0 aheadofprint 29626663 S1091-8531(18)30039-9 10.1016/j.jaapos.2018.01.006 29621510 2018 04 05

1879-1891 2018 Apr 02 Am. J. Ophthalmol. Peripheral Changes Associated with Delayed Dark Adaptation in Age-related Macular Degeneration. S0002-9394(18)30150-8 10.1016/j.ajo.2018.03.035 To study the association between peripheral changes in Age-related Macular Degeneration (AMD) and dark adaptation (DA). Prospective, cross-sectional study. We recruited patients with AMD and a control group (> 50 years) without any vitreoretinal disease. Ultra-widefield (UWF) pseudocolor and fundus autofluorescence (FAF) (Optos Inc, MA) were obtained, and were assessed by two graders for the presence of several peripheral changes in perimacular, mid- and far-peripheral zones. All participants were also imaged with 7 field color fundus photographs used for AMD staging (AREDS system). Both eyes of study participants were tested with the AdaptDx® (MacuLogix, PA) DA extended protocol (20 minutes). Multilevel, mixed-effect models (accounting for correlated outcomes between 2 eyes) were used for analyses. We included 128 eyes (n= 72 patients), 75% with AMD and the remainder controls. The presence of reticular pigmentary changes in the mid- (ß= 4.3, p=0.012) and far- peripheral zones (ß= 8.4, p<0.001) was associated with delayed rod-intercept times (RITs), even after adjusting for confounding factors. The presence, number and extent of peripheral classic drusen did not show a similar association (p ≥ 0.148). The presence of a mottled decreased FAF pattern in the mid-peripheral zone was also associated with prolonged RITs (β= 4.4, p= 0.031). Our results suggest an association between DA and the presence of peripheral reticular pigmentary changes, as well as the presence of a peripheral mottled decreased FAF pattern. This provides new insights on the clinical significance of peripheral changes in AMD, and their contribution to impairments on DA. Copyright © 2018. Published by Elsevier Inc. Laíns Inês I Retina Service, Massachusetts Eye and Ear, Harvard Ophthalmology AMD Center of Excellence, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Park Dong Ho DH Retina Service, Massachusetts Eye and Ear, Harvard Ophthalmology AMD Center of Excellence, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Mukai Ryo R Retina Service, Massachusetts Eye and Ear, Harvard Ophthalmology AMD Center of Excellence, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Silverman Rebecca R Retina Service, Massachusetts Eye and Ear, Harvard Ophthalmology AMD Center of Excellence, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Oellers Patrick P Retina Service, Massachusetts Eye and Ear, Harvard Ophthalmology AMD Center of Excellence, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Mach Steven S Retina Service, Massachusetts Eye and Ear, Harvard Ophthalmology AMD Center of Excellence, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Kim Ivana K IK Retina Service, Massachusetts Eye and Ear, Harvard Ophthalmology AMD Center of Excellence, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Vavvas Demetrios G DG Retina Service, Massachusetts Eye and Ear, Harvard Ophthalmology AMD Center of Excellence, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Miller Joan W JW Retina Service, Massachusetts Eye and Ear, Harvard Ophthalmology AMD Center of Excellence, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Miller John B JB Retina Service, Massachusetts Eye and Ear, Harvard Ophthalmology AMD Center of Excellence, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Husain Deeba D Retina Service, Massachusetts Eye and Ear, Harvard Ophthalmology AMD Center of Excellence, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Electronic address: Deeba_Husain@meei.harvard.edu. eng Journal Article 2018 04 02

United States Am J Ophthalmol 0370500 0002-9394 2018 01 10 2018 03 14 2018 03 22 2018 4 6 6 0 2018 4 6 6 0 2018 4 6 6 0 aheadofprint 29621510 S0002-9394(18)30150-8 10.1016/j.ajo.2018.03.035 29621365 2018 04 05

2168-6173 2018 Apr 05 JAMA Ophthalmol Association of Hypovitaminosis D With Increased Risk of Uveitis in a Large Health Care Claims Database. 10.1001/jamaophthalmol.2018.0642 Understanding the role of vitamin D-which regulates inflammatory responses-in noninfectious uveitis (an inflammatory disease) may provide insight into treatment and prevention of this disease. To investigate whether there is an association between hypovitaminosis D and incident noninfectious uveitis. In a retrospective case-control study, data from a health care claims database containing deidentified medical claims from a large private insurer were used to identify 558 adults enrolled from January 1, 2000, to December 31, 2016, who received a diagnosis of noninfectious uveitis from an eye care clinician (with receipt of a confirmatory diagnosis within 120 days of the initial diagnosis) and who had a vitamin D level measured within 1 year before the first diagnosis. Exclusion criteria included having systemic disease or receiving medication known to lower vitamin D levels, having undergone intraocular surgery, and having infectious uveitis. Each case patient was matched with 5 controls on the basis of age, sex, race/ethnicity, and index date (2790 controls). The controls had vitamin D level determined either within 1 year before or within 6 months after receiving an eye examination with normal findings. Multiple logistic regression models were used to examine the association between hypovitaminosis D and noninfectious uveitis. The primary, prespecified analysis assessed the association of noninfectious uveitis with hypovitaminosis D (vitamin D level ≤20 ng/mL). The 558 cases and 2790 controls were matched on age, and each group had a mean (SD) age of 58.9 (14.7) years. Among the cohort of 3348 patients, 2526 (75.4%) were female, and the racial/ethnic distribution in the matched samples was 2022 (60.4%) white, 552 (16.5%) black, 402 (12.0%) Hispanic, 162 (4.8%) Asian, and 210 (6.3%) unknown. Patients with normal vitamin D levels had 21% lower odds of having noninfectious uveitis than patients with low vitamin D levels (odds ratio [OR], 0.79; 95% CI, 0.62-0.99; P = .04). In a race-stratified analysis, an association between vitamin D and uveitis was found in black patients (OR, 0.49; 95% CI, 0.30-0.80; P = .004) and was qualitatively similar but nonsignificant in white patients (OR, 0.87; 95% CI, 0.62-1.21; P = .40) and Hispanic patients (OR, 0.60; 95% CI, 0.33-1.10; P = .10). This and other reports have found an association between hypovitaminosis D and noninfectious uveitis. However, these studies cannot establish a causal relationship. Prospective studies are warranted to evaluate whether hypovitaminosis D causes increased risk of uveitis and the role of vitamin D supplementation in prevention and treatment of uveitis. Sobrin Lucia L Department of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston. Stanwyck Lynn K LK Department of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston. Pan Wei W Department of Ophthalmology, Scheie Eye Institute, University of Pennsylvania, Philadelphia. Hubbard Rebecca A RA Department of Biostatistics, Epidemiology & Informatics, University of Pennsylvania, Philadelphia. Kempen John H JH Department of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston. Discovery Eye Center, MyungSung Christian Medical Center, MyungSung Medical School, Addis Ababa, Ethiopia. VanderBeek Brian L BL Department of Ophthalmology, Scheie Eye Institute, University of Pennsylvania, Philadelphia. eng Journal Article 2018 04 05

United States JAMA Ophthalmol 101589539 2168-6165 2018 4 6 6 0 2018 4 6 6 0 2018 4 6 6 0 aheadofprint 29621365 2677067 10.1001/jamaophthalmol.2018.0642 29620729 2018 04 10

1476-4687 556 7699 2018 Apr 04 Nature Lens regeneration in children. E2-E3 10.1038/nature26149 Vavvas Demetrios G DG Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, USA. Dryja Thaddeus P TP Ocular Pathology Service, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Wilson M Edward ME Albert Florens Storm Eye Institute, Medical University of South Carolina, Charleston, South Carolina, USA. Olsen Timothy W TW Department of Ophthalmology, Mayo Clinic, Rochester, Minnesota, USA. Shah Ankoor A Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Department of Ophthalmology, Boston Children's Hospital, Boston, Massachusetts, USA. Jurkunas Ula U Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, USA. Pineda Roberto R Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, USA. Poulaki Vasiliki V Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Department of Ophthalmology, Veterans Affairs Hospital, Boston University, Boston, Massachusetts, USA. Palioura Sotiria S Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami, Miami, Florida, USA. Veldman Peter P Department of Ophthalmology, University of Chicago, Chicago, Illinois, USA. Moreno-Montañés Javier J Department of Ophthalmology, University of Navarra, Pamplona, Spain. Pinazo-Duran Maria D MD Ophthalmic Research Unit "Santiago Grisolía" and Cellular and Molecular Ophthalmobiology Group at the Department of Ophthalmology, University of Valencia, Valencia, Spain. Pastor José Carlos JC Department of Ophthalmology, Hospital Clinico Universitario and IOBA (Eye Institute) University of Valladolid, Valladolid, Spain. Tsilimbaris Miltiadis M Department of Ophthalmology, University of Crete, Crete, Greece. Rhee Douglas D Department of Ophthalmology, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA. Colby Kathryn K Department of Ophthalmology, University of Chicago, Chicago, Illinois, USA. Hunter David G DG Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Department of Ophthalmology, Boston Children's Hospital, Boston, Massachusetts, USA. Thanos Solon S Institute of Experimental Ophthalmology, Westfalian Wilhelms-University of Münster, Albert-Schweitzer Campus 1, D15, 48149 Münster, Germany. Sakamoto Taiji T Department of Ophthalmology, Kagoshima University, Kagoshima, Japan. Pasquale Louis R LR Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, USA. Miller Joan W JW Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, USA. VanderVeen Deborah D Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Department of Ophthalmology, Boston Children's Hospital, Boston, Massachusetts, USA. Lambert Scott R SR Department of Ophthalmology, Stanford University School of Medicine, Stanford, California, USA. eng Journal Article

England Nature 0410462 0028-0836 Nature. 2018 Apr 4;556(7699):E3-E4 29620731 Differentiation. 1981;19(3):134-53 7030840 J AAPOS. 2012 Dec;16(6):554-7 23237753 Nature. 2016 Mar 17;531(7594):323-8 26958831 Am J Ophthalmol. 1998 Apr;125(4):429-35 9559727 Indian J Ophthalmol. 2014 Dec;62(12 ):1132-5 25579356 Development. 2014 Dec;141(23 ):4432-47 25406393 Invest Ophthalmol. 1963 Aug;2:344-54 14090724 J AAPOS. 2006 Feb;10(1):30-6 16527677 J Theor Biol. 2015 Jul 7;376:15-31 25816743 Arch Ophthalmol. 1961 Jul;66:103-7 13711263 Arch Ophthalmol. 1960 Jan;63:58-65 14399723 Exp Eye Res. 2010 Jun;90(6):643-54 20171212 Sci Rep. 2016 Jun 23;6:28564 27334676 2016 04 13 2018 01 23 2018 4 6 6 0 2018 4 6 6 0 2018 4 6 6 0 ppublish 29620729 nature26149 10.1038/nature26149 29616680 2018 04 18

1643-3750 24 2018 Apr 04 Med. Sci. Monit. Comparison of T Helper Cell Patterns in Primary Open-Angle Glaucoma and Normal-Pressure Glaucoma. 1988-1996 BACKGROUND HSP60-related immunological activities are found in normal-pressure glaucoma (NPG) patients, in whom an elevated intraocular pressure (IOP) found in primary open-angle glaucoma (POAG) is not observed. HSP60 was found in POAG and NPG patients, while anti-HSP60 level was mainly found to be higher in NPG patients. The purpose of this study was to compare the percentages of Th cells and levels of related cytokines, attempting to provide evidence to explain this discrepancy. MATERIAL AND METHODS Blood samples from POAG, NPG, and normal control (NC) groups were collected and peripheral blood monocytes were isolated and cultured with or without the stimulation of HSP60. Flow cytometry and enzyme-linked immunosorbent assay were used to assess the percentages of Th1, Th2, Th17, and Treg cells, as well as HSP60 antibody levels and related cytokine levels, before and after culture. RESULTS Significantly higher titers of anti-HSP60 were observed only in NPG patients. Comparable Th1 and Th2 cell frequencies, IL-4 level, and IFN-γ level were found in POAG and NPG patients, while higher Treg cell frequency was only found in POAG patients. After culturing with HSP60, increased Th2 frequencies and decreased Th1 frequencies were observed in the POAG, NPG, and NC groups, while increased Treg frequency was only identified in the POAG and NC groups. CONCLUSIONS Different Th cell patterns were observed among POAG, NPG, and NC groups. Lack of induction of Treg cells and imbalance of the pro-inflammatory and anti-inflammatory response patterns of Th cells exist in some NPG patients. Guo Chunyu C Department of Ophthalmology, Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China (mainland). Wu Ningbo N Shanghai Institute of Immunology, Shanghai JiaoTong University School of Medicine, Shanghai, China (mainland). Niu Xiaoyin X Shanghai Institute of Immunology, Shanghai JiaoTong University School of Medicine, Shanghai, China (mainland). Wu Yue Y Department of Ophthalmology, Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China (mainland). Chen Dongfeng D Department of Ophthalmology, Schepens Eye Research Institute, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA, USA. VA Boston Healthcare System, Boston, MA, USA. Guo Wenyi W Department of Ophthalmology, Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China (mainland). eng Journal Article 2018 04 04

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1552-5783 59 5 2018 Apr 01 Invest. Ophthalmol. Vis. Sci. Mast Cells Initiate the Recruitment of Neutrophils Following Ocular Surface Injury. 1732-1740 10.1167/iovs.17-23398 The purpose of this study was to investigate the contribution of mast cells to early neutrophil recruitment during ocular inflammation. In a murine model of corneal injury, the epithelium and anterior stroma were removed using a handheld motor brush. Cromolyn sodium (2% in PBS) eye drops were administered topically for mast cell inhibition. In vitro, bone marrow-derived mast cells were cultured alone or with corneal tissue. The frequencies of CD45+ inflammatory cells, CD11b+Ly6G+ neutrophils, and ckit+FcεR1+ mast cells in the cornea were assessed by flow cytometry. mRNA expression of CXCL2 was evaluated by real-time PCR and protein expression by ELISA. β-Hexosaminidase assays were performed to gauge mast cell activation. Neutrophil infiltration of the cornea was observed within 1 hour of injury, with neutrophil frequencies increasing over subsequent hours. Concurrent expansion of mast cell frequencies at the cornea were observed, with mast cell activation (assessed by β-hexosaminidase levels) peaking at 6 hours after injury. Evaluation of CXCL2 mRNA and protein expression levels demonstrated augmented expression by injured corneal tissue relative to naïve corneal tissue. Mast cells were observed to constitutively express CXCL2, with significantly higher expression of CXCL2 protein compared with naïve corneal tissue. Culture with harvested injured corneas further amplified CXCL2 expression by mast cells. In vivo, mast cell inhibition was observed to decrease CXCL2 expression, limit early neutrophil infiltration, and reduce inflammatory cytokine expression by the cornea. Our data suggest that mast cell activation after corneal injury amplifies their secretion of CXCL2 and promotes the initiation of early neutrophil recruitment. Sahu Srikant K SK Schepens Eye Research Institute, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, United States. L.V. Prasad Eye Institute, Bhubaneswar, Odisha, India. Mittal Sharad K SK Schepens Eye Research Institute, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, United States. Foulsham William W Schepens Eye Research Institute, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, United States. Li Mingshun M Schepens Eye Research Institute, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, United States. Department of Ophthalmology, Beijing Hospital, National Center of Gerontology, Beijing, P.R. China. Sangwan Virender S VS L.V. Prasad Eye Institute, Bhubaneswar, Odisha, India. L.V. Prasad Eye Institute, Hyderabad, India. Chauhan Sunil K SK Schepens Eye Research Institute, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, United States. eng P30 EY003790 EY NEI NIH HHS United States Journal Article

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1476-4687 556 7699 2018 04 05 Nature A new class of synthetic retinoid antibiotics effective against bacterial persisters. 103-107 10.1038/nature26157 A challenge in the treatment of Staphylococcus aureus infections is the high prevalence of methicillin-resistant S. aureus (MRSA) strains and the formation of non-growing, dormant 'persister' subpopulations that exhibit high levels of tolerance to antibiotics and have a role in chronic or recurrent infections. As conventional antibiotics are not effective in the treatment of infections caused by such bacteria, novel antibacterial therapeutics are urgently required. Here we used a Caenorhabditis elegans-MRSA infection screen to identify two synthetic retinoids, CD437 and CD1530, which kill both growing and persister MRSA cells by disrupting lipid bilayers. CD437 and CD1530 exhibit high killing rates, synergism with gentamicin, and a low probability of resistance selection. All-atom molecular dynamics simulations demonstrated that the ability of retinoids to penetrate and embed in lipid bilayers correlates with their bactericidal ability. An analogue of CD437 was found to retain anti-persister activity and show an improved cytotoxicity profile. Both CD437 and this analogue, alone or in combination with gentamicin, exhibit considerable efficacy in a mouse model of chronic MRSA infection. With further development and optimization, synthetic retinoids have the potential to become a new class of antimicrobials for the treatment of Gram-positive bacterial infections that are currently difficult to cure. Kim Wooseong W Division of Infectious Diseases, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, Rhode Island 02903, USA. Zhu Wenpeng W School of Engineering, Brown University, Providence, Rhode Island 02903, USA. Hendricks Gabriel Lambert GL Division of Infectious Diseases, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, Rhode Island 02903, USA. Van Tyne Daria D Department of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts 02114, USA. Department of Microbiology and Immunobiology, Harvard Medical School, Massachusetts 02115, USA. Steele Andrew D AD Department of Chemistry, Emory University, Atlanta, Georgia 30322, USA. Emory Antibiotic Resistance Center, Emory University, Atlanta, Georgia 30322, USA. Keohane Colleen E CE Department of Chemistry, Emory University, Atlanta, Georgia 30322, USA. Emory Antibiotic Resistance Center, Emory University, Atlanta, Georgia 30322, USA. Fricke Nico N School of Engineering, Brown University, Providence, Rhode Island 02903, USA. Conery Annie L AL Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA. Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA. Shen Steven S Division of Infectious Diseases, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, Rhode Island 02903, USA. Pan Wen W Division of Infectious Diseases, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, Rhode Island 02903, USA. Lee Kiho K Division of Infectious Diseases, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, Rhode Island 02903, USA. Rajamuthiah Rajmohan R Division of Infectious Diseases, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, Rhode Island 02903, USA. Fuchs Beth Burgwyn BB Division of Infectious Diseases, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, Rhode Island 02903, USA. Vlahovska Petia M PM Department of Engineering Sciences and Applied Mathematics, Northwestern University, Evanston, Illinois 60208, USA. Wuest William M WM Department of Chemistry, Emory University, Atlanta, Georgia 30322, USA. Emory Antibiotic Resistance Center, Emory University, Atlanta, Georgia 30322, USA. Gilmore Michael S MS Department of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts 02114, USA. Department of Microbiology and Immunobiology, Harvard Medical School, Massachusetts 02115, USA. Gao Huajian H School of Engineering, Brown University, Providence, Rhode Island 02903, USA. Ausubel Frederick M FM Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA. Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA. Mylonakis Eleftherios E Division of Infectious Diseases, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, Rhode Island 02903, USA. eng P01 AI083214 AI NIAID NIH HHS United States R35 GM119426 GM NIGMS NIH HHS United States K99 EY028222 EY NEI NIH HHS United States Journal Article Research Support, Non-U.S. Gov't Research Support, N.I.H., Extramural Research Support, U.S. Gov't, Non-P.H.S. 2018 03 28

England Nature 0410462 0028-0836 Blood. 2000 Apr 15;95(8):2672-82 10753850 Chem Rev. 2014 Jan 8;114(1):1-125 24266866 Nature. 2013 Nov 21;503(7476):365-70 24226776 Antimicrob Agents Chemother. 2000 Aug;44(8):2086-92 10898680 Circulation. 2015 Oct 13;132(15):1435-86 26373316 J Adolesc Health. 2008 Nov;43(5):421-4 18848668 Mol Cancer Ther. 2008 Sep;7(9):2941-54 18790775 J Cell Biol. 1996 Dec;135(6 Pt 2):1889-98 8991099 Nat Rev Microbiol. 2011 Jan;9(1):62-75 21164535 Infect Immun. 2012 Jan;80(1):74-81 21986630 Cancer Chemother Pharmacol. 1998;42(5):429-32 9771960 Antimicrob Agents Chemother. 2011 Dec;55(12):5452-8 21947404 J Phys Chem B. 2011 Nov 17;115(45):13381-8 21970408 Lancet. 2004 Jul 24-30;364(9431):369-79 15276398 Antimicrob Agents Chemother. 2007 Aug;51(8):2679-89 17502406 Nature. 2011 May 12;473(7346):216-20 21562562 Int J Cancer. 2016 Mar 15;138(6):1528-37 26453552 J Chromatogr B Analyt Technol Biomed Life Sci. 2009 Oct 1;877(27):3118-26 19695967 Nat Rev Drug Discov. 2007 Oct;6(10):793-810 17906642 Proc Natl Acad Sci U S A. 2014 Jun 17;111(24):8907-12 24927566 Nat Chem Biol. 2016 Jul;12 (7):511-5 27182663 PLoS One. 2014 Feb 19;9(2):e89189 24586584 Microbiol Mol Biol Rev. 2010 Sep;74(3):417-33 20805405 Biochemistry. 2014 Aug 26;53(33):5384-92 25093761 PLoS Genet. 2010 Sep 16;6(9):e1001119 20862359 PLoS One. 2011;6(7):e21323 21765893 Chem Biol. 2013 Sep 19;20(9):1168-78 23972939 Clin Infect Dis. 2009 Mar 15;48(6):713-21 19207079 2016 08 31 2018 02 26 2018 3 29 6 0 2018 3 29 6 0 2018 3 29 6 0 ppublish 29590091 nature26157 10.1038/nature26157 29523772 2018 04 20

1470-8752 46 2 2018 Apr 17 Biochem. Soc. Trans. Glycosylation pathways at the ocular surface. 343-350 10.1042/BST20170408 Glycosylation is a major form of enzymatic modification of organic molecules responsible for multiple biological processes in an organism. The biosynthesis of glycans is controlled by a series of glycosyltransferases, glycosidases and glycan-modifying enzymes that collectively assemble and process monosaccharide moieties into a diverse array of structures. Many studies have provided insight into various pathways of glycosylation at the ocular surface, such as those related to the biosynthesis of mucin-type O-glycans and N-glycans on proteins, but many others still remain largely unknown. This review provides an overview of the different classes of glycans described at the ocular surface focusing on their biosynthetic pathways and biological relevance. A precise understanding of these pathways under physiological and pathological conditions could help identify biomarkers and novel targets for therapeutic intervention. © 2018 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society. Rodriguez Benavente Maria C MC Schepens Eye Research Institute of Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, U.S.A. Argüeso Pablo P Schepens Eye Research Institute of Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, U.S.A. pablo_argueso@meei.harvard.edu. eng R01 EY024031 EY NEI NIH HHS United States R01 EY026147 EY NEI NIH HHS United States P30 EY003790 EY NEI NIH HHS United States Journal Article Review 2018 03 09

England Biochem Soc Trans 7506897 0300-5127 biosynthetic pathways glycosylation ocular surface 2018 01 03 2018 01 23 2018 01 30 2018 3 11 6 0 2018 3 11 6 0 2018 3 11 6 0 ppublish 29523772 BST20170408 10.1042/BST20170408 29476686 2018 04 20

2168-6173 136 4 2018 Apr 01 JAMA Ophthalmol The SCORE2 Comparison of Treat-and-Extend vs Monthly Anti-Vascular Endothelial Growth Factor Dosing: Short-term Similarities and Longer-term Questions. 346-347 10.1001/jamaophthalmol.2017.6855 Sun Jennifer K JK Beetham Eye Institute, Joslin Diabetes Center, Boston, Massachusetts. Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts. CME Editor. eng Journal Article

United States JAMA Ophthalmol 101589539 2168-6165 2018 2 25 6 0 2018 2 25 6 0 2018 2 25 6 0 ppublish 29476686 2673601 10.1001/jamaophthalmol.2017.6855 29452408 2018 04 04

1460-2083 27 8 2018 Apr 15 Hum. Mol. Genet. Genome-wide association study identifies seven novel susceptibility loci for primary open-angle glaucoma. 1486-1496 10.1093/hmg/ddy053 Primary open-angle glaucoma (POAG) is the leading cause of irreversible blindness worldwide for which 15 disease-associated loci had been discovered. Among them, only 5 loci have been associated with POAG in Asians. We carried out a genome-wide association study and a replication study that included a total of 7378 POAG cases and 36 385 controls from a Japanese population. After combining the genome-wide association study and the two replication sets, we identified 11 POAG-associated loci, including 4 known (CDKN2B-AS1, ABCA1, SIX6 and AFAP1) and 7 novel loci (FNDC3B, ANKRD55-MAP3K1, LMX1B, LHPP, HMGA2, MEIS2 and LOXL1) at a genome-wide significance level (P < 5.0×10-8), bringing the total number of POAG-susceptibility loci to 22. The 7 novel variants were subsequently evaluated in a multiethnic population comprising non-Japanese East Asians (1008 cases, 591 controls), Europeans (5008 cases, 35 472 controls) and Africans (2341 cases, 2037 controls). The candidate genes located within the new loci were related to ocular development (LMX1B, HMGA2 and MAP3K1) and glaucoma-related phenotypes (FNDC3B, LMX1B and LOXL1). Pathway analysis suggested epidermal growth factor receptor signaling might be involved in POAG pathogenesis. Genetic correlation analysis revealed the relationships between POAG and systemic diseases, including type 2 diabetes and cardiovascular diseases. These results improve our understanding of the genetic factors that affect the risk of developing POAG and provide new insight into the genetic architecture of POAG in Asians. Shiga Yukihiro Y Laboratory for Statistical Analysis, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan. Department of Ophthalmology, Tohoku University Graduate School of Medicine, Miyagi, Japan. Akiyama Masato M Laboratory for Statistical Analysis, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan. Nishiguchi Koji M KM Department of Ophthalmology, Tohoku University Graduate School of Medicine, Miyagi, Japan. Department of Advanced Ophthalmic Medicine, Tohoku University Graduate School of Medicine, Miyagi, Japan. Sato Kota K Department of Ophthalmology, Tohoku University Graduate School of Medicine, Miyagi, Japan. Department of Ophthalmic Imaging and Information Analytics, Tohoku University Graduate School of Medicine, Miyagi, Japan. Shimozawa Nobuhiro N Tsukuba Primate Research Center, National Institutes of Biomedical Innovation, Health and Nutrition, Ibaraki, Japan. Takahashi Atsushi A Laboratory for Statistical Analysis, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan. Omics Research Center, National Cerebral and Cardiovascular Center, Osaka, Japan. Momozawa Yukihide Y Laboratory for Genotyping Development, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan. Hirata Makoto M Institute of Medical Science, The University of Tokyo, Tokyo, Japan. Matsuda Koichi K Graduate School of Frontier Sciences, The University of Tokyo, Tokyo, Japan. Yamaji Taiki T Division of Epidemiology, Center for Public Health Sciences, National Cancer Center, Tokyo, Japan. Iwasaki Motoki M Division of Epidemiology, Center for Public Health Sciences, National Cancer Center, Tokyo, Japan. Tsugane Shoichiro S Center for Public Health Sciences, National Cancer Center, Tokyo, Japan. Oze Isao I Division of Molecular and Clinical Epidemiology, Aichi Cancer Center Research Institute, Nagoya, Japan. Mikami Haruo H Cancer Prevention Center, Chiba Cancer Center Research Institute, Chiba, Japan. Naito Mariko M Department of Preventive Medicine, Nagoya University Graduate School of Medicine, Nagoya, Japan. Wakai Kenji K Department of Preventive Medicine, Nagoya University Graduate School of Medicine, Nagoya, Japan. Yoshikawa Munemitsu M Department of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan. Miyake Masahiro M Department of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan. Yamashiro Kenji K Department of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan. Department of Ophthalmology, Otsu Red-Cross Hospital, Otsu, Japan. Japan Glaucoma Society Omics Group (JGS-OG) Kashiwagi Kenji K Department of Ophthalmology, Faculty of Medicine, University of Yamanashi, Yamanashi, Japan. Iwata Takeshi T Division of Molecular and Cellular Biology, National Institute of Sensory Organs, Tokyo Medical Center, National Hospital Organization, Tokyo, Japan. Mabuchi Fumihiko F Department of Ophthalmology, Faculty of Medicine, University of Yamanashi, Yamanashi, Japan. Takamoto Mitsuko M Department of Ophthalmology, University of Tokyo, Tokyo, Japan. Ozaki Mineo M Ozaki Eye Hospital, Hyuga, Miyazaki, Japan. Department of Ophthalmology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan. Kawase Kazuhide K Department of Ophthalmology, Gifu University Graduate School of Medicine, Gifu, Japan. Aihara Makoto M Department of Ophthalmology, University of Tokyo, Tokyo, Japan. Araie Makoto M Kanto Central Hospital of the Mutual Aid Association of Public School Teachers, Tokyo, Japan. Yamamoto Tetsuya T Department of Ophthalmology, Gifu University Graduate School of Medicine, Gifu, Japan. Kiuchi Yoshiaki Y Department of Ophthalmology and Visual Sciences, Hiroshima University, Hiroshima, Japan. Nakamura Makoto M Division of Ophthalmology, Department of Surgery, Kobe University Graduate School of Medicine, Kobe, Japan. Ikeda Yasuhiro Y Department of Ophthalmology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Sonoda Koh-Hei KH Department of Ophthalmology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Ishibashi Tatsuro T Department of Ophthalmology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Nitta Koji K Fukuiken Saiseikai Hospital, Fukui, Japan. Iwase Aiko A Tajimi Iwase Eye Clinic, Tajimi, Japan. Shirato Shiroaki S Yotsuya Shirato Eye Clinic, Tokyo, Japan. Oka Yoshitaka Y Oka Eye Clinic, Fukuoka, Japan. Satoh Mamoru M Iwate Tohoku Medical Megabank Organization, Iwate Medical University, Iwate, Japan. Sasaki Makoto M Iwate Tohoku Medical Megabank Organization, Iwate Medical University, Iwate, Japan. Fuse Nobuo N Department of Integrative Genomics, Tohoku Medical Megabank Organization, Miyagi, Japan. Suzuki Yoichi Y Department of Education and Training, Tohoku Medical Megabank Organization, Miyagi, Japan. Cheng Ching-Yu CY Singapore Eye Research Institute, Singapore National Eye Centre, Singapore. Ophthalmology and Visual Sciences Academic Clinical Program (Eye ACP), Duke-NUS Medical School, Singapore. Department of Ophthalmology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore. Khor Chiea Chuen CC Genome Institute of Singapore, Singapore. Baskaran Mani M Singapore Eye Research Institute, Singapore National Eye Centre, Singapore. Ophthalmology and Visual Sciences Academic Clinical Program (Eye ACP), Duke-NUS Medical School, Singapore. Perera Shamira S Singapore Eye Research Institute, Singapore National Eye Centre, Singapore. Aung Tin T Singapore Eye Research Institute, Singapore National Eye Centre, Singapore. Ophthalmology and Visual Sciences Academic Clinical Program (Eye ACP), Duke-NUS Medical School, Singapore. Department of Ophthalmology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore. Vithana Eranga N EN Singapore Eye Research Institute, Singapore National Eye Centre, Singapore. Cooke Bailey Jessica N JN Department of Population and Quantitative Health Sciences, Institute for Computational Biology, Case Western Reserve University School of Medicine, Cleveland, OH, USA. Kang Jae H JH Channing Division of Network Medicine, Brigham and Women's Hospital, Boston, MA, USA. Pasquale Louis R LR Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Haines Jonathan L JL Department of Population and Quantitative Health Sciences, Institute for Computational Biology, Case Western Reserve University School of Medicine, Cleveland, OH, USA. NEIGHBORHOOD Consortium Wiggs Janey L JL Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Burdon Kathryn P KP Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia. Department of Ophthalmology, Flinders University, Adelaide, SA, Australia. Gharahkhani Puya P QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia. Hewitt Alex W AW Centre for Eye Research Australia, University of Melbourne, Melbourne, VIC, Australia. Department of Ophthalmology, Royal Victorian Eye and Ear Hospital, Melbourne, VIC, Australia. Mackey David A DA Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia. Centre for Ophthalmology and Visual Science, Lions Eye Institute, University of Western Australia, Perth, WA, Australia. MacGregor Stuart S QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia. Craig Jamie E JE Department of Ophthalmology, Flinders University, Adelaide, SA, Australia. Allingham R Rand RR Department of Ophthalmology, Duke University, Durham, NC, USA. Hauser Micheal M Duke University Medical Center, Durham, NC, USA. Ashaye Adeyinka A Department of Ophthalmology, College of Medicine, University of Ibadan, Ibadan, Nigeria. Budenz Donald L DL Department of Ophthalmology, University of North Carolina at Chapel Hill, USA. Akafo Stephan S University of Ghana School of Medicine and Dentistry, Ghana. Williams Susan E I SEI Division of Ophthalmology, Department of Neurosciences, University of the Witwatersrand, South Africa. Kamatani Yoichiro Y Laboratory for Statistical Analysis, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan. Center for Genomic Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan. Nakazawa Toru T Department of Ophthalmology, Tohoku University Graduate School of Medicine, Miyagi, Japan. Department of Advanced Ophthalmic Medicine, Tohoku University Graduate School of Medicine, Miyagi, Japan. Department of Ophthalmic Imaging and Information Analytics, Tohoku University Graduate School of Medicine, Miyagi, Japan. Kubo Michiaki M Laboratory for Genotyping Development, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan. eng R21 EY028671 EY NEI NIH HHS United States Journal Article

England Hum Mol Genet 9208958 0964-6906 2017 12 02 2018 01 17 2018 2 17 6 0 2018 2 17 6 0 2018 2 17 6 0 ppublish 29452408 4857230 10.1093/hmg/ddy053 29421330 2018 04 29

1096-0007 169 2018 Apr Exp. Eye Res. Genomic loci modulating retinal ganglion cell death following elevated IOP in the mouse. 61-67 S0014-4835(17)30660-7 10.1016/j.exer.2017.12.013 The present study was designed to identify genomic loci modulating the susceptibility of retinal ganglion cells (RGC) to elevated intraocular pressure (IOP) in the BXD recombinant inbred mouse strain set. IOP was elevated by injecting magnetic microspheres into the anterior chamber and blocking the trabecular meshwork using a handheld magnet to impede drainage. The IOP was then measured over the next 21 days. Only animals with IOP greater than 25 mmHg for two consecutive days or an IOP above 30 mmHg on a single day after microsphere-injection were used in this study. On day 21, mice were sacrificed and the optic nerve was processed for histology. Axons were counted for both the injected and the control eye in 49 BXD strains, totaling 181 normal counts and 191 counts associated with elevated IOP. The axon loss for each strain was calculated and the data were entered into genenetwork.org. The average number of normal axons in the optic nerve across all strains was 54,788 ± 16% (SD), which dropped to 49,545 ± 20% in animals with artificially elevated IOP. Interval mapping demonstrated a relatively similar genome-wide map for both conditions with a suggestive Quantitative Trait Locus (QTL) on proximal Chromosome 3. When the relative axon loss was used to generate a genome-wide interval map, we identified one significant QTL (p < 0.05) on Chromosome 18 between 53.6 and 57 Mb. Within this region, the best candidate gene for modulating axon loss was Aldh7a1. Immunohistochemistry demonstrated ALDH7A1 expression in mouse RGCs. ALDH7A1 variants were not significantly associated with glaucoma in the NEIGHBORHOOD GWAS dataset, but this enzyme was identified as part of the butanoate pathway previously associated with glaucoma risk. Our results suggest that genomic background influences susceptibility to RGC degeneration and death in an inducible glaucoma model. Copyright © 2018 The Authors. Published by Elsevier Ltd.. All rights reserved. Struebing Felix L FL Department of Ophthalmology, Emory University, 1365B Clifton Road NE, Atlanta, GA, 30322, USA. King Rebecca R Department of Ophthalmology, Emory University, 1365B Clifton Road NE, Atlanta, GA, 30322, USA. Li Ying Y Department of Ophthalmology, Emory University, 1365B Clifton Road NE, Atlanta, GA, 30322, USA. Cooke Bailey Jessica N JN Department of Population and Quantitative Health Sciences, Case Western Reserve University School of Medicine, USA. NEIGHBORHOOD consortium Wiggs Janey L JL Department of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, USA. Geisert Eldon E EE Department of Ophthalmology, Emory University, 1365B Clifton Road NE, Atlanta, GA, 30322, USA. Electronic address: egeiser@emory.edu. eng R01 EY017841 EY NEI NIH HHS United States Journal Article 2018 02 03

England Exp Eye Res 0370707 0014-4835 Butanoate pathway GeneNetwork Glaucoma model QTL mapping Systems genetics 2017 09 13 2017 11 13 2017 12 28 2018 2 9 6 0 2018 2 9 6 0 2018 2 9 6 0 ppublish 29421330 S0014-4835(17)30660-7 10.1016/j.exer.2017.12.013 29409963 2018 04 06

1937-5913 16 2 2018 Apr Ocul Surf Web-based longitudinal remote assessment of dry eye symptoms. 249-253 S1542-0124(17)30338-5 10.1016/j.jtos.2018.01.002 To investigate the feasibility of remote assessment and follow-up of dry eye symptoms using electronic versions of two validated questionnaires. We conducted a prospective study of consecutive patients with dry eye disease (DED). Patients were enrolled during a clinical visit and were explained how to respond electronic versions of the Ocular surface Disease Index (OSDI) and the Symptom Assessment in Dry Eye (SANDE) questionnaires using a computer in the presence of investigators. A secure link to both questionnaires was sent to each patient every 2 weeks in order to respond and submit their symptoms over a 3-month period. We analyzed the number of patients who responded to both questionnaires, the recurrence, and the symptoms scores reported. A total of 1121 questionnaires were collected; 103 patients (85%) reported their symptoms at least once during the 3-month study duration. The majority of participants who completed the study (71.6%) responded remotely at least once per month during the 3-month duration of the study. The mean OSDI and SANDE scores from the total of remote evaluations were 34.9 ± 21.9 (range 0-97.5) and 50.3 ± 24.9 (range 0-100), respectively. There was a statistically significant correlation between the total scores collected with the two questionnaires (R = 0.67, P < 0.001). Patients are motivated to report DED symptoms while away from the clinic. Distance-based evaluation of DED symptoms is both feasible and convenient, and can be implemented to follow symptoms in large populations with chronic dry eye. Copyright © 2018 Elsevier Inc. All rights reserved. Amparo Francisco F Cornea Service, Massachusetts Eye & Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Dana Reza R Cornea Service, Massachusetts Eye & Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Electronic address: reza_dana@meei.harvard.edu. eng Journal Article 2018 02 02

United States Ocul Surf 101156063 1542-0124 Dry eye symptoms Electronic questionnaire Remote assessment 2017 11 30 2018 01 24 2018 01 30 2018 2 8 6 0 2018 2 8 6 0 2018 2 8 6 0 ppublish 29409963 S1542-0124(17)30338-5 10.1016/j.jtos.2018.01.002 29396036 2018 03 27

1879-1891 188 2018 Apr Am. J. Ophthalmol. Progress Toward Precisely Diagnosing Autoimmune Retinopathy. xiv-xv S0002-9394(18)30003-5 10.1016/j.ajo.2018.01.002 Sobrin Lucia L Department of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts. Electronic address: Lucia_sobrin@meei.harvard.edu. eng Editorial 2018 02 01

United States Am J Ophthalmol 0370500 0002-9394 2017 12 11 2017 12 27 2018 01 01 2018 2 6 6 0 2018 2 6 6 0 2018 2 4 6 0 ppublish 29396036 S0002-9394(18)30003-5 10.1016/j.ajo.2018.01.002 29393489 2018 03 29

1791-3004 17 4 2018 Apr Mol Med Rep Lysyl oxidase inhibition via β-aminoproprionitrile hampers human umbilical vein endothelial cell angiogenesis and migration in vitro. 5029-5036 10.3892/mmr.2018.8508 Lysyl oxidase (LOX) is an enzyme that oxidizes lysine residues in collagens and elastin. It stabilizes or remodels the extracellular matrix and basement membrane of blood vessels. Current oncology studies have revealed that LOX is upregulated in invasive cancer cells and bolstered cell movement, and LOX was observed to promote the angiogenesis and migration of endothelial cells. In the present study, angiogenesis and migration were examined in human umbilical vein endothelial cells (HUVECs). Following cell treatment with 0.1-0.4 mM β-aminoproprionitrile (BAPN), a specific inhibitor of LOX, angiogenesis was analyzed with a fibrin gel in vitro angiogenesis assay kit and migration was examined via a Boyden Chamber assay. Angiogenesis-associated gene expression was investigated with a microarray assay and confirmed with reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The results showed that HUVEC angiogenesis substantially increased in the presence of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF) and phorbol 12-myristate 13-acetate (PMA). In addition, LOX inhibition blocked the angiogenesis stimulated by VEGF bFGF and PMA, and the inhibition of LOX reduced the migration of HUVECs. Furthermore, the microarray and RT-qPCR revealed that BAPN downregulated myeloid progenitor inhibitory factor 1, and western blot analysis demonstrated that BAPN decreased the phosphorylation of MAPK and Akt, suggesting that the specific inhibitor of LOX, BAPN, may serve as an alternative strategy for preventing angiogenesis. Shi Lin L Department of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China. Zhang Ning N Department of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China. Liu Hetao H Department of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China. Zhao Lei L Department of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China. Liu Jing J Department of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China. Wan Juan J Department of Rheumatology and Immunology, The General Hospital of Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China. Wu Wenyi W Schepens Eye Research Institute of Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USA. Lei Hetian H Schepens Eye Research Institute of Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USA. Liu Rongqing R Department of Rheumatology and Immunology, The General Hospital of Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China. Han Mei M Department of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China. eng Journal Article 2018 01 26

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1536-4798 37 4 2018 Apr Cornea Descemetorhexis Without Endothelial Keratoplasty (DWEK): Proposal for Nomenclature Standardization. e20-e21 10.1097/ICO.0000000000001528 Kaufman Aaron R AR Boston University School of Medicine, Boston, MA. Nosé Ricardo M RM Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA. Pineda Roberto R 2nd Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA. eng Journal Article

United States Cornea 8216186 0277-3740 2018 2 1 6 0 2018 2 1 6 0 2018 2 1 6 0 ppublish 29384812 10.1097/ICO.0000000000001528 29343568 2018 04 17 2018 04 25

1098-5514 92 7 2018 04 01 J. Virol. An Alternate Route for Adeno-associated Virus (AAV) Entry Independent of AAV Receptor. e02213-17 10.1128/JVI.02213-17 Determinants and mechanisms of cell attachment and entry steer adeno-associated virus (AAV) in its utility as a gene therapy vector. Thus far, a systematic assessment of how diverse AAV serotypes engage their proteinaceous receptor AAVR (KIAA0319L) to establish transduction has been lacking, despite potential implications for cell and tissue tropism. Here, a large set of human and simian AAVs as well as in silico-reconstructed ancestral AAV capsids were interrogated for AAVR usage. We identified a distinct AAV capsid lineage comprised of AAV4 and AAVrh32.33 that can bind and transduce cells in the absence of AAVR, independent of the multiplicity of infection. Virus overlay assays and rescue experiments in nonpermissive cells demonstrate that these AAVs are unable to bind to or use the AAVR protein for entry. Further evidence for a distinct entry pathway was observed in vivo, as AAVR knockout mice were equally as permissive to transduction by AAVrh32.33 as wild-type mice upon systemic injection. We interestingly observe that some AAV capsids undergo a low level of transduction in the absence of AAVR, both in vitro and in vivo, suggesting that some capsids may have a multimodal entry pathway. In aggregate, our results demonstrate that AAVR usage is conserved among all primate AAVs except for those of the AAV4 lineage, and a non-AAVR pathway may be available to other serotypes. This work furthers our understanding of the entry of AAV, a vector system of broad utility in gene therapy.IMPORTANCE Adeno-associated virus (AAV) is a nonpathogenic virus that is used as a vehicle for gene delivery. Here, we have identified several situations in which transduction is retained in both cell lines and a mouse model in the absence of a previously defined entry receptor, AAVR. Defining the molecular determinants of the infectious pathway of this highly relevant viral vector system can help refine future applications and therapies with this vector. Copyright © 2018 American Society for Microbiology. Dudek Amanda M AM Grousbeck Gene Therapy Center, Schepens Eye Research Institute and Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, USA. Harvard Ph.D. Program in Virology, Division of Medical Sciences, Harvard University, Boston, Massachusetts, USA. Ocular Genomics Institute, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Pillay Sirika S Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California, USA. Puschnik Andreas S AS Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California, USA. Nagamine Claude M CM Department of Comparative Medicine, Stanford University School of Medicine, Stanford, California, USA. Cheng Fang F Department of Microbiology, Molecular Genetics and Immunology, University of Kansas Medical Center, Kansas City, Kansas, USA. Qiu Jianming J Department of Microbiology, Molecular Genetics and Immunology, University of Kansas Medical Center, Kansas City, Kansas, USA. Carette Jan E JE Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California, USA. Vandenberghe Luk H LH 0000-0002-3508-4924 Grousbeck Gene Therapy Center, Schepens Eye Research Institute and Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, USA Luk_Vandenberghe@MEEI.harvard.edu. Harvard Ph.D. Program in Virology, Division of Medical Sciences, Harvard University, Boston, Massachusetts, USA. Ocular Genomics Institute, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. The Broad Institute of Harvard and MIT, Cambridge, Massachusetts, USA. eng P30 EY003790 EY NEI NIH HHS United States Journal Article Research Support, N.I.H., Extramural 2018 03 14

United States J Virol 0113724 0022-538X 0 KIAA0319L protein, mouse 0 Receptors, Cell Surface IM Animals Capsid metabolism Cell Line Dependovirus genetics metabolism Genetic Vectors Mice Mice, Knockout Receptors, Cell Surface genetics metabolism Transduction, Genetic Virus Internalization AAV adeno-associated virus attachment gene therapy vector viral entry viral gene transfer virus virus receptor 2018 01 02 2018 01 03 2018 1 19 6 0 2018 4 18 6 0 2018 1 19 6 0 epublish 29343568 JVI.02213-17 10.1128/JVI.02213-17 29341971 2018 03 02

1536-4798 37 4 2018 Apr Cornea Atopy in Patients With Ocular Cicatricial Pemphigoid. 436-441 10.1097/ICO.0000000000001477 To evaluate the presence of atopy in patients with ocular cicatricial pemphigoid (OCP). Patient encounters between August 2005 and November 2016 at the Massachusetts Eye Research and Surgery Institute (MERSI) were searched to identify those with biopsy-proven OCP who had concurrent evidence of atopy. There were 230 patients with biopsy-proven OCP. Thirty-three of them were found to have clinical symptoms of atopy (asthma, hay fever, and eczema) and of these, 23 had evidence of atopy in their conjunctival biopsy specimens. All patients were administered immunomodulatory therapy for treatment of their OCP with 20 patients requiring additional antiallergy treatment to control residual atopic ocular symptoms. Among patients who used antiallergy medications, 80% showed improvement in residual symptoms. Rituximab and/or intravenous immunoglobulin is a preferred OCP medication for patients with OCP with some evidence of atopy. Clinicians should consider the coexistence of atopy in patients with OCP, especially in those with persistent symptoms after initiation of immunomodulatory therapy. Ebrahimiadib Nazanin N Massachusetts Eye Research and Surgery Institution (MERSI), Waltham, MA. Ocular Immunology and Uveitis Foundation, Weston, MA. Hernandez Mikhail M Massachusetts Eye Research and Surgery Institution (MERSI), Waltham, MA. Ocular Immunology and Uveitis Foundation, Weston, MA. Modjtahedi Bobeck S BS Massachusetts Eye Research and Surgery Institution (MERSI), Waltham, MA. Ocular Immunology and Uveitis Foundation, Weston, MA. Roohipoor C Ramak CR Massachusetts Eye Research and Surgery Institution (MERSI), Waltham, MA. Ocular Immunology and Uveitis Foundation, Weston, MA. Foster C Stephen CS Massachusetts Eye Research and Surgery Institution (MERSI), Waltham, MA. Ocular Immunology and Uveitis Foundation, Weston, MA. Department of Ophthalmology, Harvard Medical School, Boston, MA. eng Journal Article

United States Cornea 8216186 0277-3740 2018 1 18 6 0 2018 1 18 6 0 2018 1 18 6 0 ppublish 29341971 10.1097/ICO.0000000000001477 29305292 2018 04 08

1937-5913 16 2 2018 Apr Ocul Surf Corneal nerve regeneration after herpes simplex keratitis: A longitudinal in vivo confocal microscopy study. 218-225 S1542-0124(17)30306-3 10.1016/j.jtos.2017.12.001 To evaluate the long-term alterations of corneal nerves in patients with herpes simplex virus (HSV) keratitis using in vivo confocal microscopy (IVCM). Prospective, longitudinal, cross sectional. This study included 16 patients with a history of HSV keratitis and 15 age-matched normal controls. Slit-scanning IVCM was performed in all subjects at baseline and then after a mean follow-up of 37.3 ± 1.7 months in the patient group. Corneal subbasal nerve density and corneal sensation were compared between groups at baseline and follow-up. At baseline, the mean subbasal nerve density was significantly lower in both affected eyes (1.4 ± 0.6 mm/mm²) and contralateral unaffected eyes (6.4 ± 0.7 mm/mm²) compared with the controls (14.1 ± 1.6 mm/mm²; all P < .001). At the end of follow-up, the mean nerve density in affected eyes increased to 2.8 ± 0.7 mm/mm² (P = .006), with no significant change in contralateral unaffected eyes (6.5 ± 1.0 mm/mm², P = .72). However, both eyes had lower nerve density than controls (all P < .001). Corneal sensation was significantly lower in affected eyes (2.6 ± 0.6 cm) than in the control group (6.0 ± 0.0, P < .001) and showed no significant change at the end of follow-up (2.5 ± 0.6 cm, P = .80). Corneal sensation in contralateral unaffected eyes was not different in comparison with controls at both baseline and follow up (all p > .05). Our results demonstrate that although corneal nerve regeneration occurs in patients with HSV keratitis, this change is not clinically significant and does not results in changes of corneal sensation. Therefore, these patients need to be followed closely for complications of neurotrophic keratopathy and might benefit from neuro-regenerative therapies. Copyright © 2018 Elsevier Inc. All rights reserved. Moein Hamid-Reza HR Ocular Surface Imaging Center, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA; Center for Translational Ocular Immunology, Department of Ophthalmology, Tufts Medical Center, Tufts University School of Medicine, Boston, MA, USA. Kheirkhah Ahmad A Ocular Surface Imaging Center, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA; Cornea and Refractive Surgery Service, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Muller Rodrigo T RT Ocular Surface Imaging Center, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA; Cornea and Refractive Surgery Service, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Cruzat Andrea C AC Ocular Surface Imaging Center, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA; Cornea and Refractive Surgery Service, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Pavan-Langston Deborah D Cornea and Refractive Surgery Service, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Hamrah Pedram P Ocular Surface Imaging Center, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA; Cornea and Refractive Surgery Service, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA; Cornea Service, New England Eye Center, Department of Ophthalmology, Tufts Medical Center, Tufts University School of Medicine, Boston, MA, USA; Center for Translational Ocular Immunology, Department of Ophthalmology, Tufts Medical Center, Tufts University School of Medicine, Boston, MA, USA. Electronic address: pedram.hamrah@tufts.edu. eng K08 EY020575 EY NEI NIH HHS United States R01 EY022695 EY NEI NIH HHS United States R21 EY025393 EY NEI NIH HHS United States Journal Article 2018 01 03

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1532-2238 39 2018 Apr Growth Horm. IGF Res. Increased postnatal concentrations of pro-inflammatory cytokines are associated with reduced IGF-I levels and retinopathy of prematurity. 19-24 S1096-6374(17)30107-7 10.1016/j.ghir.2017.11.006 Retinopathy of prematurity (ROP) is a multifactorial disease linked to low insulin-like growth factor (IGF)-I levels and perhaps to postnatal inflammation. Here, we investigated the longitudinal postnatal serum concentrations of pro-inflammatory cytokines interleukin (IL)-6 and tumor necrosis factor (TNF)-α in relation to IGF-I levels and ROP. The study cohort included 52 infants born before 31 gestational weeks. The infants were screened for ROP and classified as non-ROP (n=33), non-proliferative ROP (stages 1 and 2; n=10), or proliferative ROP (stage 3, all treated for ROP; n=9). Blood samples were collected at birth, 24h after birth, and then weekly until at least 36weeks postmenstrual age (PMA) (i.e., up to 13weeks after birth). Circulating levels of IL-6 and TNF-α were evaluated in relation to circulating IGF-I levels and ROP. IL-6 levels negatively correlated with IGF-I levels between 5 and 8weeks after birth, (p<0.01 to p<0.05). At birth, the IL-6 and TNF-α levels were similar independent of later ROP. Twenty-four hours after birth, both IL-6 and TNF-α levels had increased in infants later treated for ROP (p<0.05). Postnatal, infants treated for ROP had higher IL-6 levels than infants without ROP. The pro-inflammatory response is associated with low IGF-I levels and the development of ROP. Copyright © 2017 The Authors. Published by Elsevier Ltd.. All rights reserved. Hellgren Gunnel G Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; Department of Pediatrics, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Electronic address: gunnel.hellgren@gu.se. Löfqvist Chatarina C Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Hansen-Pupp Ingrid I Department of Clinical Sciences, Lund University, Lund, Sweden; Skåne University Hospital, Sweden. Gram Magnus M Department of Clinical Sciences, Lund University, Lund, Sweden; Skåne University Hospital, Sweden. Smith Lois E LE Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, USA. Ley David D Department of Clinical Sciences, Lund University, Lund, Sweden; Skåne University Hospital, Sweden. Hellström Ann A Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. eng R01 EY017017 EY NEI NIH HHS United States U54 HD090255 HD NICHD NIH HHS United States Journal Article 2017 11 27

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1471-4981 39 4 2018 Apr Trends Immunol. When Clarity Is Crucial: Regulating Ocular Surface Immunity. 288-301 S1471-4906(17)30229-6 10.1016/j.it.2017.11.007 The ocular surface is a unique mucosal immune compartment in which anatomical, physiological, and immunological features act in concert to foster a particularly tolerant microenvironment. These mechanisms are vital to the functional competence of the eye, a fact underscored by the devastating toll of excessive inflammation at the cornea - blindness. Recent data have elucidated the contributions of specific anatomical components, immune cells, and soluble immunoregulatory factors in promoting homeostasis at the ocular surface. We highlight research trends at this distinctive mucosal barrier and identify crucial gaps in our current knowledge. Copyright © 2017 Elsevier Ltd. All rights reserved. Foulsham William W Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA; University College London (UCL) Institute of Ophthalmology, University College London, London, UK. Coco Giulia G Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Amouzegar Afsaneh A Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Chauhan Sunil K SK Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Electronic address: sunil_chauhan@meei.harvard.edu. Dana Reza R Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Electronic address: reza_dana@meei.harvard.edu. eng R01 EY012963 EY NEI NIH HHS United States R01 EY020889 EY NEI NIH HHS United States R01 EY024602 EY NEI NIH HHS United States Journal Article Review 2017 12 14

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1545-5017 65 4 2018 Apr Pediatr Blood Cancer AML presenting with a preleukemic episode and acquired heterochromia in a child with macrosomia. 10.1002/pbc.26899 Yang Youyang Y http://orcid.org/0000-0003-3447-1401 Department of Pediatrics, Massachusetts General Hospital for Children, Boston, Massachusetts. Department of Pediatrics, Harvard Medical School, Boston, Massachusetts. Kazlas Melanie M Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts. Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts. Sharma Medha M Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts. Friedmann Alison A Department of Pediatrics, Massachusetts General Hospital for Children, Boston, Massachusetts. Department of Pediatrics, Harvard Medical School, Boston, Massachusetts. eng Letter 2017 11 22

United States Pediatr Blood Cancer 101186624 1545-5009 AML heterochromia macrosomia overgrowth preleukemia pseudohypopyon 2017 06 30 2017 10 23 2017 10 24 2017 11 23 6 0 2017 11 23 6 0 2017 11 23 6 0 ppublish 29165874 10.1002/pbc.26899 29130354 2018 04 25

1557-7422 29 4 2018 Apr Hum. Gene Ther. Delivery of Adeno-Associated Virus Vectors in Adult Mammalian Inner-Ear Cell Subtypes Without Auditory Dysfunction. 492-506 10.1089/hum.2017.120 Hearing loss, including genetic hearing loss, is one of the most common forms of sensory deficits in humans with limited options of treatment. Adeno-associated virus (AAV)-mediated gene transfer has been shown to recover auditory functions effectively in mouse models of genetic deafness when delivered at neonatal stages. However, the mouse cochlea is still developing at those time points, whereas in humans, the newborn inner ears are already fully mature. For effective gene therapy to treat genetic deafness, it is necessary to determine whether AAV-mediated therapy can be equally effective in the fully mature mouse inner ear without causing damage to the inner ear. This study tested several AAV serotypes by canalostomy in adult mice. It is shown that most AAVs transduce the sensory inner hair cells efficiently, but are less efficient at transducing outer hair cells. A subset of AAVs also transduces non-sensory cochlear cell types. Neither the surgical procedure of canalostomy nor the AAV serotypes damage hair cells or impair normal hearing. The studies indicate that canalostomy can be a viable route for safe and efficient gene delivery, and they expand the repertoire of AAVs to target diverse cell types in the adult inner ear. Tao Yong Y 1 Department of Otolaryngology and Program in Neuroscience, Harvard Medical School and Eaton Peabody Laboratory, Massachusetts Eye and Ear Infirmary , Boston, Massachusetts. 2 Department of Otorhinolaryngology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan, China . Huang Mingqian M 1 Department of Otolaryngology and Program in Neuroscience, Harvard Medical School and Eaton Peabody Laboratory, Massachusetts Eye and Ear Infirmary , Boston, Massachusetts. Shu Yilai Y 1 Department of Otolaryngology and Program in Neuroscience, Harvard Medical School and Eaton Peabody Laboratory, Massachusetts Eye and Ear Infirmary , Boston, Massachusetts. 3 Department of Otolaryngology-Head and Neck Surgery, Eye and ENT Hospital, Shanghai Medical College, Fudan University , Shanghai, China . Ruprecht Adam A 1 Department of Otolaryngology and Program in Neuroscience, Harvard Medical School and Eaton Peabody Laboratory, Massachusetts Eye and Ear Infirmary , Boston, Massachusetts. Wang Hongyang H 1 Department of Otolaryngology and Program in Neuroscience, Harvard Medical School and Eaton Peabody Laboratory, Massachusetts Eye and Ear Infirmary , Boston, Massachusetts. 4 Chinese PLA Institute of Otolaryngology, Chinese PLA General Hospital, Medical School of Chinese PLA , Beijing, China . Tang Yong Y 1 Department of Otolaryngology and Program in Neuroscience, Harvard Medical School and Eaton Peabody Laboratory, Massachusetts Eye and Ear Infirmary , Boston, Massachusetts. 5 Department of Ear, Nose and Throat, People's Hospital of Jilin Province , Changchun, China . Vandenberghe Luk H LH 6 Grousbeck Gene Therapy Center, Schepens Eye Research Institute and Massachusetts Eye and Ear Infirmary , Boston, Massachusetts. 7 Ocular Genomics Institute, Department of Ophthalmology, Harvard Medical School , Boston, Massachusetts. Wang Qiuju Q 4 Chinese PLA Institute of Otolaryngology, Chinese PLA General Hospital, Medical School of Chinese PLA , Beijing, China . Gao Guangping G 8 Horae Gene Therapy Center and Department of Microbiology and Physiological Systems, University of Massachusetts Medical School , Worcester, Massachusetts. 9 State Key Laboratory of Biotherapy, West China Hospital, Sichuan University , Chengdu, China . Kong Wei-Jia WJ 2 Department of Otorhinolaryngology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan, China . Chen Zheng-Yi ZY 1 Department of Otolaryngology and Program in Neuroscience, Harvard Medical School and Eaton Peabody Laboratory, Massachusetts Eye and Ear Infirmary , Boston, Massachusetts. eng Journal Article 2018 01 22

United States Hum Gene Ther 9008950 1043-0342 Hum Gene Ther. 2016 Sep;27(9):687-99 27342665 Gene Ther. 2009 Aug;16(8):990-7 19458651 Science. 2014 May 9;344(6184):1241062 24812404 Hum Gene Ther. 2008 Apr;19(4):384-90 18439125 Hum Gene Ther. 2015 Aug;26(8):525-37 26222377 Mol Ther. 2006 Sep;14(3):328-35 16765094 Lancet. 2009 Nov 7;374(9701):1597-605 19854499 Exp Mol Med. 2007 Apr 30;39(2):170-5 17464178 J Clin Invest. 2011 Jun;121(6):2160-8 21606598 Hear Res. 2013 Sep;303:20-9 23347917 Adv Otorhinolaryngol. 2009;66:37-51 19494571 Ann N Y Acad Sci. 1991;630:16-31 1952587 Mol Ther. 2001 Jun;3(6):958-63 11407910 Hum Gene Ther. 2011 May;22(5):523-9 21443427 Nat Med. 2005 Mar;11(3):271-6 15711559 Sci China Life Sci. 2015 Sep;58(9):829-38 26432548 Otol Neurotol. 2007 Dec;28(8):1100-8 18043435 Cell Rep. 2015 Aug 11;12(6):1056-68 26235624 Nat Rev Drug Discov. 2015 May;14(5):346-65 25792261 Proc Natl Acad Sci U S A. 2003 May 13;100(10):6081-6 12716974 N Engl J Med. 2011 Dec 22;365(25):2357-65 22149959 Mol Ther. 2000 Oct;2(4):368-73 11020352 J Neurosci. 2013 Sep 18;33(38):15086-94 24048839 Hear Res. 2013 Mar;297:99-105 23265411 Mol Ther. 2005 Oct;12(4):725-33 16169458 Hum Gene Ther. 2016 Feb;27(2):134-47 26751519 Gene Ther. 1996 Jul;3(7):588-92 8818645 Sci Transl Med. 2015 Jul 8;7(295):295ra108 26157030 J Neurosci. 1998 May 1;18(9):3327-35 9547240 Anat Embryol (Berl). 1995 Feb;191(2):101-18 7726389 Hum Gene Ther. 1994 Jul;5(7):793-801 7981305 Hear Res. 2005 Apr;202(1-2):63-73 15811700 Gene Ther. 2011 Jun;18(6):569-78 21209625 EMBO Mol Med. 2015 Jun 17;7(8):1077-86 26084842 Am J Hum Genet. 1997 Apr;60(4):758-64 9106521 Mol Ther. 2017 Mar 1;25(3):780-791 28254438 Hum Gene Ther. 2000 Oct 10;11(15):2059-66 11044908 Neural Plast. 2016;2016:9409846 28116172 Mol Ther. 2001 Dec;4(6):575-85 11735342 Neuron. 2012 Jul 26;75(2):283-93 22841313 Anat Rec (Hoboken). 2012 Nov;295(11):1830-6 23044932 J Pediatr. 1986 Jul;109(1):158-71 3522833 Sci Rep. 2017 Apr 03;7:45524 28367981 N Engl J Med. 2006 May 18;354(20):2151-64 16707752 Hear Res. 1999 Oct;136(1-2):124-30 10511631 Nat Biotechnol. 2017 Mar;35(3):280-284 28165475 Lancet. 2016 Aug 13;388(10045):661-72 27375040 Nat Biotechnol. 2017 Mar;35(3):264-272 28165476 Hum Gene Ther. 2012 Aug;23(8):796-807 22734691 AAV adult mouse hair cells hearing inner ear 2019 04 01 2017 11 14 6 0 2017 11 14 6 0 2017 11 14 6 0 ppublish 29130354 10.1089/hum.2017.120 PMC5909114 28944477 2018 03 25

1531-4995 128 4 2018 Apr Laryngoscope Long-term impact of endoscopic orbital decompression on sinonasal-specific quality of life. 785-788 10.1002/lary.26812 Endoscopic orbital decompression (EOD) is the workhorse surgical intervention for severe thyroid eye disease in Graves disease. Although EOD is a safe and effective procedure, the objective of this study is to determine the impact of orbital decompression on long-term sinonasal-pecific quality of life. Retrospective study of 27 patients who underwent EOD by a single surgeon. The primary endpoint was change in preoperative 22-item Sinonasal Outcomes Test (SNOT-22) score at a minimum of 1 year. The secondary endpoint was to determine whether the performance of septoplasty for surgical access in patients without nasal obstruction impacted domain 1 (i.e., rhinologic domain) and total SNOT-22 scores. The mean follow-up was 25.7 ± 11.4 months. Domain 1 scores significantly increased at the first postoperative visit (P ≤ 0.01) and returned to baseline values between 1 and 3 months. At 1 year, significant improvements in both total score and domain 4 and 5 (psychological and sleep dysfunction, respectively) scores were seen (P < 0.01 for all scores). Septoplasty was not associated with a significant change in SNOT-22 score at 1 year (P = 0.48). Endoscopic orbital decompression is associated at 1 year with a significant improvement in sinonasal-specific quality of life, which is driven by the psychological and sleep dysfunction domains. Adjunctive septoplasty has no significant impact on SNOT-22 scores. 4. Laryngoscope, 128:785-788, 2018. © 2017 The American Laryngological, Rhinological and Otological Society, Inc. Mueller Sarina K SK http://orcid.org/0000-0001-5790-0841 Department of Otolaryngology, University of Erlangen-Nuremberg, Erlangen, Germany. Department of Otolaryngology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts, U.S.A. Miyake Marcel M MM Department of Otolaryngology, Santa Casa de Sao Paulo School of Medical Sciences, Sao Paulo, Brazil. Department of Otolaryngology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts, U.S.A. Lefebvre Daniel R DR Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts, U.S.A. Freitag Suzanne K SK Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts, U.S.A. Bleier Benjamin S BS Department of Otolaryngology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts, U.S.A. eng Journal Article 2017 09 25

United States Laryngoscope 8607378 0023-852X Endoscopy Graves disease orbit paranasal sinus quality of life surgical decompression 2017 06 28 2017 9 26 6 0 2017 9 26 6 0 2017 9 26 6 0 ppublish 28944477 10.1002/lary.26812 28786234 2018 03 25

1531-4995 128 4 2018 Apr Laryngoscope Endoscopic DCR using bipedicled interlacing mucosal flaps. 794-797 10.1002/lary.26730 Obstruction of the nasolacrimal duct is a relatively common condition that affects patients of all ages, races, and sexes. The surgical gold standard for complete nasolacrimal duct obstruction and dacryocystitis is dacryocystorhinostomy (DCR). The purpose of this study was to describe a novel, bipedicled interlacing mucosal sparing flap technique for endoscopic DCR (eDCR). A posteriorly based mucosal flap over the fundus is combined with a novel, anteriorly based mucosal flap over the intraosseus portion of the nasolacrimal duct (NLD). This exposes a wide area of the maxillary bone, allowing for exposure and identification of the NLD/sac complex in a safer, more inferior position. The interlacing mucosal flaps may be replaced at the conclusion of the procedure, thereby minimizing bone exposure and maintaining excellent long-term patency. The authors have utilized this technique in 55 procedures with 100% positive identification of the NLD and lacrimal sac, 0% complication rate, 100% anatomical patency rate, and 96.4% success rate after a minimal follow-up of 6 months. The bipedicled interlacing flap technique for eDCR provides for safe and reproducible identification of the NLD and lacrimal sac while minimizing bone exposure and restenosis rate. The bipedicled interlacing flap technique for eDCR provides for safe and reproducible identification of the NLD and lacrimal sac while minimizing bone exposure and restenosis rate. NA. Laryngoscope, 128:794-797, 2018. © 2017 The American Laryngological, Rhinological and Otological Society, Inc. Mueller Sarina K SK http://orcid.org/0000-0001-5790-0841 Department of Otolaryngology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, U.S.A. Department of Otolaryngology, University of Erlangen-Nuremberg, Erlangen, Germany. Freitag Suzanne K SK Department of Ophthalmology Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, U.S.A. Lefebvre Daniel R DR Department of Ophthalmology Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, U.S.A. Bleier Benjamin S BS Department of Otolaryngology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, U.S.A. eng Journal Article 2017 08 08

United States Laryngoscope 8607378 0023-852X Allergy/Rhinology Basic Science Clinical 2017 04 17 2017 05 09 2017 8 9 6 0 2017 8 9 6 0 2017 8 9 6 0 ppublish 28786234 10.1002/lary.26730