29771751 2018 05 17

1752-2978 2018 May 15 Curr Opin Endocrinol Diabetes Obes Utility of optical coherence tomography in the evaluation of sellar and parasellar mass lesions. 10.1097/MED.0000000000000415 Anterior visual pathway compression is a common feature of sellar region masses. We review the visual pathway neuroanatomy pertaining to sellar and parasellar lesions and describe recent advances in optical coherence tomography (OCT) imaging that have provided a novel quantitative perspective in the evaluation and management of such patients. Ultrastructural measurements of optic nerve integrity using OCT, namely peripapillary retinal nerve fiber layer (pRNFL) and the ganglion cell and inner plexiform layer (GCIPL) thicknesses, have been shown to correlate with visual acuity and visual field deficits on perimetry in patients with compressive sellar region masses. In some cases, OCT can visualize early signs of anterior visual pathway involvement in the absence of clinically evident visual field loss or optic disc pallor. OCT is particularly useful when assessing patients who demonstrate less reliable visual field testing. Furthermore, there is growing awareness that pRNFL and GCIPL thinning preoperatively correlate with worse visual recovery following chiasmal decompression, highlighting the prognostic utility of OCT in this patient population. OCT provides a complimentary, yet critical, role in quantitatively assessing ultrastructural retinal injury in patients with sellar and parasellar lesions compressing the anterior visual pathway and should be incorporated into routine evaluation. Al-Louzi Omar O Department of Neurology, Brigham and Women's Hospital. Department of Neurology, Massachusetts General Hospital. Prasad Sashank S Department of Neurology, Brigham and Women's Hospital. Mallery Robert M RM Department of Neurology, Brigham and Women's Hospital. Department of Ophthalmology, Mass Eye and Ear, Harvard Medical School, Boston, Massachusetts, USA. eng Journal Article 2018 05 15

England Curr Opin Endocrinol Diabetes Obes 101308636 1752-296X 2018 5 18 6 0 2018 5 18 6 0 2018 5 18 6 0 aheadofprint 29771751 10.1097/MED.0000000000000415 29763694 2018 05 15

1937-5913 2018 May 12 Ocul Surf Corneal fluorescein staining and ocular symptoms but not Schirmer test are useful as indicators of response to treatment in chronic ocular GVHD. S1542-0124(18)30040-5 10.1016/j.jtos.2018.05.002 To evaluate long-term ocular surface clinical signs and symptoms response to therapy in patients with chronic ocular GVHD. Retrospective review and data modeling. We reviewed the records of post-bone marrow transplantation patients who were newly diagnosed with ocular GVHD and initiated therapy, and analyzed changes in symptoms (Ocular Surface Disease Index [OSDI]; Symptom Assessment in Dry Eye [SANDE]) and signs (corneal fluorescein staining [CFS]; Schirmer test). We used a LOESS technique to fit a model in function of data variations and obtain a predictive value of the scores progression over time. The records of 123 patients who were followed-up for over 2 years (up to 62 months) were reviewed. The median baseline scores recorded were: OSDI 52 units, SANDE 62.2 units, CFS 2.0 Oxford units, and Schirmer 4 mm. After six months of follow up, scores improved for OSDI (-18.6 units, p = 0.007), SANDE (23.7 units, p = 0.01), and CFS (-0.7 Oxford units, p < 0.001). Data analysis showed that after a 2-year follow up the three parameters continued to improve: OSDI -13.67 units (27% reduction), SANDE -17.55 units (28%), CFS -1.1 units (54%), but Schirmer test scores progressively worsened -1.2 mm (22%). In patients with ocular GVHD symptoms and corneal fluorescein staining improved after initiation of treatment, meanwhile Schirmer scores declined progressively. This indicates that appropriate treatment in chronic ocular GVHD can lead to mid- and long-term improvements in symptoms and corneal epitheliopathy; however, sustained reduction in Schirmer test scores suggests chronic tear production impairment. Copyright © 2018. Published by Elsevier Inc. Amparo Francisco F Cornea Service, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Shikari Hasanain H Cornea Service, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Saboo Ujwala U Cornea Service, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Dana Reza R Cornea Service, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Electronic address: reza_dana@meei.harvard.edu. eng Journal Article 2018 05 12

United States Ocul Surf 101156063 1542-0124 Corneal fluorescein staining Graft-vs-host disease Ocular GVHD Schirmer test 2018 02 06 2018 05 08 2018 05 11 2018 5 16 6 0 2018 5 16 6 0 2018 5 16 6 0 aheadofprint 29763694 S1542-0124(18)30040-5 10.1016/j.jtos.2018.05.002 29545417 2018 04 25

1468-2079 102 5 2018 May Br J Ophthalmol Prevalence and causes of vision loss in high-income countries and in Eastern and Central Europe in 2015: magnitude, temporal trends and projections. 575-585 10.1136/bjophthalmol-2017-311258 Within a surveillance of the prevalence and causes of vision impairment in high-income regions and Central/Eastern Europe, we update figures through 2015 and forecast expected values in 2020. Based on a systematic review of medical literature, prevalence of blindness, moderate and severe vision impairment (MSVI), mild vision impairment and presbyopia was estimated for 1990, 2010, 2015, and 2020. Age-standardised prevalence of blindness and MSVI for all ages decreased from 1990 to 2015 from 0.26% (0.10-0.46) to 0.15% (0.06-0.26) and from 1.74% (0.76-2.94) to 1.27% (0.55-2.17), respectively. In 2015, the number of individuals affected by blindness, MSVI and mild vision impairment ranged from 70 000, 630 000 and 610 000, respectively, in Australasia to 980 000, 7.46 million and 7.25 million, respectively, in North America and 1.16 million, 9.61 million and 9.47 million, respectively, in Western Europe. In 2015, cataract was the most common cause for blindness, followed by age-related macular degeneration (AMD), glaucoma, uncorrected refractive error, diabetic retinopathy and cornea-related disorders, with declining burden from cataract and AMD over time. Uncorrected refractive error was the leading cause of MSVI. While continuing to advance control of cataract and AMD as the leading causes of blindness remains a high priority, overcoming barriers to uptake of refractive error services would address approximately half of the MSVI burden. New data on burden of presbyopia identify this entity as an important public health problem in this population. Additional research on better treatments, better implementation with existing tools and ongoing surveillance of the problem is needed. © 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. Bourne Rupert R A RRA http://orcid.org/0000-0002-8169-1645 Vision & Eye Research Unit, Anglia Ruskin University, Cambridge, UK. Jonas Jost B JB http://orcid.org/0000-0003-2972-5227 Department of Ophthalmology, Universitätsmedizin, Mannheim, Germany. Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany. Bron Alain M AM http://orcid.org/0000-0002-7265-931X INRA, UMR1324 Centre des Sciences du Goût et de l'Alimentation, Dijon, France. CNRS, UMR6265 Centre des Sciences du Goût et de l'Alimentation, Dijon, France. Centre des Sciences du Goût et de l'Alimentation, Université Bourgogne Franche-Comté, Dijon, France. Ophthalmology Department, Dijon University Hospital, Dijon, France. Cicinelli Maria Vittoria MV San Raffaele Scientific Institute, Milan, Italy. Das Aditi A Health Education Yorkshire and the Humber, Leeds, UK. Flaxman Seth R SR Department of Mathematics and Data Science Institute, Imperial College London, London, UK. Department of Statistics, University of Oxford, Oxford, UK. Friedman David S DS Dana Center for Preventive Ophthalmology, Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Keeffe Jill E JE LV Prasad Eye Institute, Hyderabad, India. Kempen John H JH Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, USA. Discovery Eye Center, Addis Ababa, Ethiopia. Myungsung Christian Medical Center and Medical School, Addis Ababa, Ethiopia. Leasher Janet J http://orcid.org/0000-0002-8779-5162 Nova Southeastern University, Davie, Florida, USA. Limburg Hans H Health Information Services, Grootebroek, The Netherlands. Naidoo Kovin K African Vision Research Institute, University of Kwazulu-Natal, Brien Holden Vision Institute, Durban, South Africa. Pesudovs Konrad K NHMRC Centre for Clinical Eye Research, Flinders University, Adelaide, South Australia, Australia. Peto Tunde T School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, Belfast, UK. Saadine Jinan J Centers for Disease Control and Prevention, Atlanta, Georgia, USA. Silvester Alexander J AJ St Pauls Eye Unit, Royal Liverpool University Hospital, Liverpool, UK. Tahhan Nina N Brien Holden Vision Institute, Sydney, New South Wales, Australia. School of Optometry and Vision Science, University of New South Wales, Sydney, New South Wales, Australia. Taylor Hugh R HR Melbourne School of Population Health, University of Melbourne, Melbourne, Victoria, Australia. Varma Rohit R Department of Ophthalmology, Keck School of Medicine of USC, Los Angeles, California, USA. Wong Tien Y TY Singapore Eye Research Institute, Duke-NUS Graduate Medical School, National University of Singapore, Singapore. Resnikoff Serge S http://orcid.org/0000-0002-5866-4446 Brien Holden Vision Institute, Sydney, New South Wales, Australia. School of Optometry and Vision Science, University of New South Wales, Sydney, New South Wales, Australia. Vision Loss Expert Group of the Global Burden of Disease Study eng Journal Article 2018 03 15

England Br J Ophthalmol 0421041 0007-1161 Br J Ophthalmol. 2014 May;98(5):629-38 24665132 Am J Ophthalmol. 1997 Mar;123(3):328-37 9063242 Ophthalmic Epidemiol. 2013 Jun;20(3):123-30 23713914 Ophthalmic Epidemiol. 2013;20(1):33-9 23350553 N Engl J Med. 2006 Oct 5;355(14 ):1432-44 17021319 Am J Ophthalmol. 2012 Jul;154(1):107-116.e1 22534109 Diabetes Care. 2013 May;36(5):e69 23613609 Ophthalmology. 2013 Dec;120(12):2377-84 23850093 Health Technol Assess. 2007 Oct;11(41):iii-iv, ix-x, 1-190 17927922 N Engl J Med. 2011 May 19;364(20):1897-908 21526923 Lancet Glob Health. 2013 Dec;1(6):e339-49 25104599 Lancet Glob Health. 2017 Sep;5(9):e888-e897 28779882 N Engl J Med. 2006 Oct 5;355(14):1419-31 17021318 Ophthalmology. 2014 Jan;121(1):134-41 24823760 Ophthalmology. 2014 Jan;121(1):417-22 23993359 Lancet Glob Health. 2017 Dec;5(12 ):e1221-e1234 29032195 Invest Ophthalmol Vis Sci. 2000 Oct;41(11):3309-21 11006219 epidemiology glaucoma public health Competing interests: JBJ: consultant for Mundipharma (Cambridge, UK), patent holder with Biocompatibles UK (Farnham, Surrey, UK) (Title: Treatment of eye diseases using encapsulated cells encoding and secreting neuroprotective factor and/or anti-angiogenic factor; patent no 20120263794) and patent application with University of Heidelberg (Heidelberg, Germany) (Title: Agents for use in the therapeutic or prophylactic treatment of myopia or hyperopia; Europäische Patentanmeldung 15 000 771.4). AMB: consultant for Allergan, Bausch + Lomb, Carl Zeiss Meditec, Théa and VISUfarma. Research grants from Horus. JHK: consultant for Gilead and Santen. SR: consultant for Brien Holden Vision Institute. 2017 08 30 2018 02 12 2018 02 24 2018 3 17 6 0 2018 3 17 6 0 2018 3 17 6 0 ppublish 29545417 bjophthalmol-2017-311258 10.1136/bjophthalmol-2017-311258 PMC5909755 29484533 2018 05 12

1943-393X 80 4 2018 May Atten Percept Psychophys The Spatial Musical Association of Response Codes does not depend on a normal visual experience: A study with early blind individuals. 813-821 10.3758/s13414-018-1495-x Converging evidence suggests that the perception of auditory pitch exhibits a characteristic spatial organization. This pitch-space association can be demonstrated experimentally by the Spatial Musical Association of Response Codes (SMARC) effect. This is characterized by faster response times when a low-positioned key is pressed in response to a low-pitched tone, and a high-positioned key is pressed in response to a high-pitched tone. To investigate whether the development of this pitch-space association is mediated by normal visual experience, we tested a group of early blind individuals on a task that required them to discriminate the timbre of different instrument sounds with varying pitch. Results revealed a comparable pattern in the SMARC effect in both blind participants and sighted controls, suggesting that the lack of prior visual experience does not prevent the development of an association between pitch height and vertical space. Cattaneo Zaira Z Department of Psychology, University of Milano-Bicocca, Milano, Italy. zaira.cattaneo@unimib.it. Brain Connectivity Center, IRCCS Mondino Foundation, Pavia, Italy. zaira.cattaneo@unimib.it. Lega Carlotta C Department of Psychology, University of Milano-Bicocca, Milano, Italy. Rinaldi Luca L Department of Psychology, University of Milano-Bicocca, Milano, Italy. Fantino Micaela M Department of Brain and Behavioural Sciences, University of Pavia, Pavia, Italy. Ferrari Chiara C Department of Psychology, University of Milano-Bicocca, Milano, Italy. Merabet Lotfi B LB The Laboratory for Visual Neuroplasticity, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, USA. Vecchi Tomaso T Brain Connectivity Center, IRCCS Mondino Foundation, Pavia, Italy. Department of Brain and Behavioural Sciences, University of Pavia, Pavia, Italy. eng Journal Article

United States Atten Percept Psychophys 101495384 1943-3921 Audition Multisensory processing Spatial cognition 2018 2 28 6 0 2018 2 28 6 0 2018 2 28 6 0 ppublish 29484533 10.3758/s13414-018-1495-x 10.3758/s13414-018-1495-x 29763693 2018 06 08

1937-5913 2018 May 12 Ocul Surf Influence of lipopolysaccharide on proinflammatory gene expression in human corneal, conjunctival and meibomian gland epithelial cells. S1542-0124(18)30055-7 10.1016/j.jtos.2018.05.003 Lipopolysaccharide (LPS), a bacterial endotoxin, is known to stimulate leuokotriene B4 (LTB4) secretion by human corneal (HCECs), conjunctival (HConjECs) and meibomian gland (HMGECs) epithelial cells. We hypothesize that this LTB4 effect represents an overall induction of proinflammatory gene expression in these cells. Our objective was to test this hypothesis. Immortalized HCECs, HConjECs and HMGECs were cultured in the presence or absence of LPS (15 μg/ml) and ligand binding protein (LBP; 150 ng/ml). Cells were then processed for RNA isolation and the analysis of gene expression by using Illumina BeadChips, background subtraction, cubic spline normalization and GeneSifter software. Our findings show that LPS induces a striking increase in proinflammatory gene expression in HCECs and HConjECs. These cellular reactions are associated with a significant up-regulation of genes associated with inflammatory and immune responses (e.g. IL-1β, IL-8, and tumor necrosis factor), including those related to chemokine and Toll-like receptor signaling pathways, cytokine-cytokine receptor interactions, and chemotaxis. In contrast, with the exception of Toll-like signaling and associated innate immunity pathways, almost no proinflammatory ontologies were upregulated by LPS in HMGECs. Our results support our hypothesis that LPS stimulates proinflammatory gene expression in HCECs and HConjECs. However, our findings also show that LPS does not elicit such proinflammatory responses in HMGECs. Copyright © 2018. Published by Elsevier Inc. Chen Di D Schepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA; Department of Ophthalmology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China. Electronic address: di_chen@meei.harvard.edu. Sahin Afsun A Schepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA; Department of Ophthalmology, Koc University Medical School, Istanbul, Turkey. Kam Wendy R WR Schepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Liu Yang Y Schepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Darabad Raheleh Rahimi RR Schepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA; Department of Clinical Anesthesia, Indiana University School of Medicine, Indianapolis, IN, USA. Sullivan David A DA Schepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. eng R01 EY005612 EY NEI NIH HHS United States Journal Article 2018 05 12

United States Ocul Surf 101156063 1542-0124 Gene expression Inflammation Lipopolysaccharide Ocular surface epithelial cells 2018 02 23 2018 04 13 2018 05 11 2018 5 16 6 0 2018 5 16 6 0 2018 5 16 6 0 aheadofprint 29763693 S1542-0124(18)30055-7 10.1016/j.jtos.2018.05.003 29342033 2018 05 08

1537-2677 34 3 2018 May/Jun Ophthalmic Plast Reconstr Surg Meningoencephalocele and Cerebrospinal Fluid Leak Complicating Orbital Decompression. e79-e81 10.1097/IOP.0000000000001055 A 51-year-old man who had undergone right orbital decompression 5 months earlier developed a meningoencephalocele extending in the right sphenoid sinus through a skull base defect of the right ethmoid, sphenoid, and frontal bones. The authors report the third case to their knowledge of meningoencephalocele with cerebrospinal fluid leak after orbital decompression and discuss its management and measures that can be taken to prevent this rare but serious complication. Cohen Liza M LM Department of Ophthalmology, Ophthalmic Plastic Surgery. Jiménez Pérez Juan C JC Department of Ophthalmology, Ophthalmic Plastic Surgery. Holbrook Eric H EH Division of Rhinology, Department of Otolaryngology. Curry William T WT Department of Neurosurgery, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts, U.S.A. Yoon Michael K MK Department of Ophthalmology, Ophthalmic Plastic Surgery. eng Journal Article

United States Ophthalmic Plast Reconstr Surg 8508431 0740-9303 2018 1 18 6 0 2018 1 18 6 0 2018 1 18 6 0 ppublish 29342033 10.1097/IOP.0000000000001055 29683986 2018 05 03

1538-9235 95 5 2018 May Optom Vis Sci People with Hemianopia Report Difficulty with TV, Computer, Cinema Use, and Photography. 428-434 10.1097/OPX.0000000000001215 Our survey found that participants with hemianopia report more difficulties watching video in various formats, including television (TV), on computers, and in a movie theater, compared with participants with normal vision (NV). These reported difficulties were not as marked as those reported by people with central vision loss. The aim of this study was to survey the viewing experience (e.g., frequency, difficulty) of viewing video on TV, computers and portable visual display devices, and at the cinema of people with hemianopia and NV. This information may guide vision rehabilitation. We administered a cross-sectional survey to investigate the viewing habits of people with hemianopia (n = 91) or NV (n = 192). The survey, consisting of 22 items, was administered either in person or in a telephone interview. Descriptive statistics are reported. There were five major differences between the hemianopia and NV groups. Many participants with hemianopia reported (1) at least "some" difficulty watching TV (39/82); (2) at least "some" difficulty watching video on a computer (16/62); (3) never attending the cinema (30/87); (4) at least some difficulty watching movies in the cinema (20/56), among those who did attend the cinema; and (5) never taking photographs (24/80). Some people with hemianopia reported methods that they used to help them watch video, including video playback and head turn. Although people with hemianopia report more difficulty with viewing video on TV and at the cinema, we are not aware of any rehabilitation methods specifically designed to assist people with hemianopia to watch video. The results of this survey may guide future vision rehabilitation. Costela Francisco M FM Schepens Eye Research Institute, Massachusetts Eye and Ear, Boston, Massachusetts. Sheldon Sarah S SS Schepens Eye Research Institute, Massachusetts Eye and Ear, Boston, Massachusetts. Walker Bethany B Schepens Eye Research Institute, Massachusetts Eye and Ear, Boston, Massachusetts. Woods Russell L RL Schepens Eye Research Institute, Massachusetts Eye and Ear, Boston, Massachusetts. Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts *Francisco_costela@meei.harvard.edu. eng P30 EY003790 EY NEI NIH HHS United States R01 EY019100 EY NEI NIH HHS United States Journal Article

United States Optom Vis Sci 8904931 1040-5488 Ann Neurol. 1981 Jun;9(6):537-44 7259115 J Rehabil Res Dev. 2002 May-Jun;39(3):385-94 12173758 Neurology. 2006 Mar 28;66(6):906-10 16567710 J Med Internet Res. 2013 May 20;15(5):e100 23689038 Ophthalmic Physiol Opt. 2011 May;31(3):258-74 21410501 Top Stroke Rehabil. 2009 Nov-Dec;16(6):445-53 20139047 Cochrane Database Syst Rev. 2011 Oct 05;(10):CD008388 21975779 Invest Ophthalmol Vis Sci. 2009 Nov;50(11):5137-47 19608541 Restor Neurol Neurosci. 1992 Jan 1;4(4):245-54 21551879 Neurosci Lett. 2001 Jun 29;306(3):189-92 11406327 PLoS One. 2014 Apr 02;9(4):e93251 24695546 Invest Ophthalmol Vis Sci. 2009 Feb;50(2):577-85 18936138 Br J Ophthalmol. 1997 Apr;81(4):324-8 9215064 NeuroRehabilitation. 2012;31(1):19-30 22523012 Age Ageing. 2009 Mar;38(2):188-93 19029069 JAMA Ophthalmol. 2014 Feb;132(2):214-22 24201760 PLoS One. 2015 Aug 14;10(8):e0134459 26275160 J Neuroophthalmol. 2005 Jun;25(2):136-42 15937440 J Clin Neurosci. 2007 Aug;14(8):754-6 17270447 Neurology. 2009 Jan 27;72(4):324-31 19171828 Graefes Arch Clin Exp Ophthalmol. 2007 Dec;245(12):1749-58 17653566 Vital Health Stat 10. 2012 Jan;(252):1-207 22834228 Optom Vis Sci. 2002 Jan;79(1):31-8 11828896 Invest Ophthalmol Vis Sci. 2009 Jun;50(6):2765-76 19117930 Neurorehabil Neural Repair. 2009 Mar-Apr;23(3):246-55 19240199 Am J Occup Ther. 2009 Sep-Oct;63(5):626-33 19785262 J Vis. 2016 Jul 1;16(9):11 27472498 Health Qual Life Outcomes. 2010 Mar 26;8:33 20346125 Stroke. 2002 Oct;33(10):2417-20 12364731 Br J Ophthalmol. 2005 Jan;89(1):30-5 15615742 2019 05 01 2018 4 24 6 0 2018 4 24 6 0 2018 4 24 6 0 ppublish 29683986 10.1097/OPX.0000000000001215 PMC5930067 NIHMS950804 29887215 2018 06 11

1537-6605 2018 May 30 Am. J. Hum. Genet. Recessive MYF5 Mutations Cause External Ophthalmoplegia, Rib, and Vertebral Anomalies. S0002-9297(18)30164-2 10.1016/j.ajhg.2018.05.003 MYF5 is member of the Myc-like basic helix-loop-helix transcription factor family and, in cooperation with other myogenic regulatory factors MYOD and MYF5, is a key regulator of early stages of myogenesis. Here, we report three consanguineous families with biallelic homozygous loss-of-function mutations in MYF5 who define a clinical disorder characterized by congenital ophthalmoplegia with scoliosis and vertebral and rib anomalies. The clinical phenotype overlaps strikingly with that reported in several Myf5 knockout mouse models. Affected members of two families share a haploidentical region that contains a homozygous 10 bp frameshift mutation in exon 1 of MYF5 (c.23_32delAGTTCTCACC [p.Gln8Leufs^∗86]) predicted to undergo nonsense-mediated decay. Affected members of the third family harbor a homozygous missense change in exon 1 of MYF5 (c.283C>T [p.Arg95Cys]). Using in vitro assays, we show that this missense mutation acts as a loss-of-function allele by impairing MYF5 DNA binding and nuclear localization. We performed whole-genome sequencing in one affected individual with the frameshift mutation and did not identify additional rare variants in the haploidentical region that might account for differences in severity among the families. These data support the direct role of MYF5 in rib, spine, and extraocular muscle formation in humans. Copyright © 2018 American Society of Human Genetics. Published by Elsevier Inc. All rights reserved. Di Gioia Silvio Alessandro SA Department of Neurology, Boston Children's Hospital, Boston, MA 02115, USA; F.M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, MA 02115, USA; Department of Neurology, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of M.I.T. and Harvard, Cambridge, MA 02142, USA. Shaaban Sherin S Department of Neurology, Boston Children's Hospital, Boston, MA 02115, USA; F.M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, MA 02115, USA; Department of Neurology, Harvard Medical School, Boston, MA 02115, USA. Tüysüz Beyhan B Istanbul University, Cerrahpasa Medical School, Department of Pediatric Genetics, Istanbul, Turkey. Elcioglu Nursel H NH Department of Pediatric Genetics, Marmara University Medical School, Istanbul, Turkey; Eastern Mediterranean University Medical School, Cyprus, Mersin 10, Turkey. Chan Wai-Man WM Department of Neurology, Boston Children's Hospital, Boston, MA 02115, USA; F.M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, MA 02115, USA; Broad Institute of M.I.T. and Harvard, Cambridge, MA 02142, USA; Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA. Robson Caroline D CD Department of Radiology, Boston Children's Hospital, Boston, MA 02115, USA; Department of Radiology, Harvard Medical School, Boston, MA 02115, USA. Ecklund Kirsten K Department of Radiology, Boston Children's Hospital, Boston, MA 02115, USA; Department of Radiology, Harvard Medical School, Boston, MA 02115, USA. Gilette Nicole M NM Department of Neurology, Boston Children's Hospital, Boston, MA 02115, USA; F.M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, MA 02115, USA. Hamzaoglu Azmi A Istanbul Spine Center at Florence Nightingale Hospital, Abide-i Hurriyet Cad. No:166, Sisli, 34381, Istanbul, Turkey. Tayfun Gulsen Akay GA Department of Pediatric Genetics, Marmara University Medical School, Istanbul, Turkey. Traboulsi Elias I EI Cole Eye Institute, Cleveland Clinic, Cleveland, OH 44195, USA. Engle Elizabeth C EC Department of Neurology, Boston Children's Hospital, Boston, MA 02115, USA; F.M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, MA 02115, USA; Department of Neurology, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of M.I.T. and Harvard, Cambridge, MA 02142, USA; Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA; Department Ophthalmology, Boston Children's Hospital, Boston, MA 02115, USA; Department of Ophthalmology, Harvard Medical School, Boston, MA 02115, USA. Electronic address: elizabeth.engle@childrens.harvard.edu. eng Journal Article 2018 05 30

United States Am J Hum Genet 0370475 0002-9297 MYF5 exome sequencing extraocular muscle genome sequencing human genetics myogenesis ophthalmaplegia rib anomalies scoliosis vertebral anomalies 2017 11 06 2018 05 04 2018 6 12 6 0 2018 6 12 6 0 2018 6 12 6 0 aheadofprint 29887215 S0002-9297(18)30164-2 10.1016/j.ajhg.2018.05.003 29930992 2018 06 25

2474-1264 2 3 2018 May-Jun J Vitreoretin Dis Imaging the Deep Choroidal Vasculature Using Spectral Domain and Swept Source Optical Coherence Tomography Angiography. 146-154 10.1177/2474126418771805 To evaluate the deeper choroidal vasculature in eyes with various ocular disorders using spectral domain (SD) optical coherence tomography angiography (OCTA) and swept source (SS) OCTA. Patients underwent OCTA imaging with either SD-OCTA (Zeiss Cirrus Angioplex or Optovue AngioVue) or SS-OCTA (Topcon Triton). Retinal pigment epithelium (RPE) integrity, structural visualization of deep choroidal vessels on en face imaging, and OCTA of deep choroidal blood flow signal were analyzed. Choroidal blood flow was deemed present if deeper choroidal vessels appeared bright after appropriate segmentation. Structural visualization of choroidal vessels was feasible in all eyes by en face imaging. In both SD-OCTA and SS-OCTA, choroidal blood flow signal was present in all eyes with overlying RPE atrophy (100% of eyes with RPE atrophy, 28.6% of all imaged eyes, P < .001). While choroidal vessels can be visualized anatomically in all eyes by en face imaging, choroidal blood flow detection in deep choroidal vessel is largely restricted to areas with overlying RPE atrophy. Intact RPE acts as a barrier for reliable detection of choroidal flow using current OCTA technology, inhibiting evaluation of flow in deeper choroidal vessels in most eyes. Diaz J Daniel JD Retina Service, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Wang Jay C JC Retina Service, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Oellers Patrick P Retina Service, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Lains Inês I Retina Service, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Sobrin Lucia L Retina Service, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Husain Deeba D Retina Service, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Miller Joan W JW Retina Service, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Vavvas Demetrios G DG Retina Service, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Miller John B JB Retina Service, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. eng R01 EY025362 EY NEI NIH HHS United States R13 EY027184 EY NEI NIH HHS United States R21 EY023079 EY NEI NIH HHS United States Journal Article 2018 04 16

United States J Vitreoretin Dis 101700301 2474-1264 Ophthalmic Surg Lasers Imaging Retina. 2014 Sep-Oct;45(5):382-9 25230403 Ophthalmic Surg Lasers Imaging Retina. 2017 Aug 1;48(8):638-646 28810039 Ophthalmic Surg Lasers Imaging Retina. 2016 Jan;47(1):20-6 26731205 Retin Cases Brief Rep. 2017 Jan 13;:null 28092315 Retina. 2015 Nov;35(11):2163-80 26428607 Proc Natl Acad Sci U S A. 2013 Aug 27;110(35):14354-9 23918361 Am J Ophthalmol. 2016 Oct;170:58-67 27496785 Lasers Surg Med. 2011 Apr;43(4):339-43 21500229 Invest Ophthalmol Vis Sci. 2012 Apr 30;53(4):2337-48 22410568 Retina. 2017 Mar;37(3):460-465 27541926 Ophthalmology. 2016 Sep;123(9):1879-86 27448830 Proc Natl Acad Sci U S A. 2015 May 5;112(18):E2395-402 25897021 Stat Med. 1998 Jun 15;17(11):1261-91 9670414 choroid optical coherence tomography angiography retinal pigment epithelium Declaration of Conflicting Interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article. 2018 6 23 6 0 2018 6 23 6 0 2018 6 23 6 1 ppublish 29930992 10.1177/2474126418771805 PMC6007996 NIHMS974009 29341332 2018 04 29

1549-4918 36 5 2018 May Stem Cells Cornea-Derived Mesenchymal Stromal Cells Therapeutically Modulate Macrophage Immunophenotype and Angiogenic Function. 775-784 10.1002/stem.2781 Macrophages are crucial drivers of inflammatory corneal neovascularization and thus are potential targets for immunomodulatory therapies. We hypothesized that therapeutic use of cornea-derived mesenchymal stromal cells (cMSCs) may alter the function of macrophages. We found that cMSCs can modulate the phenotype and angiogenic function of macrophages. In vitro, cMSCs induce apoptosis of macrophages while preferentially promoting a distinct CD14^hi CD16^hi CD163^hi CD206^hi immunophenotype that has significantly reduced angiogenic effects based on in vitro angiogenesis assays. In vivo, application of cMSCs to murine corneas after injury leads to reduced macrophage infiltration and higher expression of CD206 in macrophages. Macrophages cocultured ("educated") by cMSCs express significantly higher levels of anti-angiogenic and anti-inflammatory factors compared with control macrophages. In vivo, injured corneas treated with cMSC-educated macrophages demonstrate significantly less neovascularization compared with corneas treated with control macrophages. Knocking down the expression of pigment epithelial derived factor (PEDF) in cMSCs significantly abrogates its modulating effects on macrophages, as shown by the reduced rate of apoptosis, decreased expression of sFLT-1/PEDF, and increased expression of vascular endothelial growth factor-A in the cocultured macrophages. Similarly, cMSCs isolated from PEDF knockout mice are less effective compared with wild-type cMSCs at inhibiting macrophage infiltration when applied to wild-type corneas after injury. Overall, these results demonstrate that cMSCs therapeutically suppress the angiogenic capacity of macrophages and highlight the role of cMSC secreted PEDF in the modulation of macrophage phenotype and function. Stem Cells 2018;36:775-784. © AlphaMed Press 2018. Eslani Medi M Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, Illinois, USA. Putra Ilham I Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, Illinois, USA. Shen Xiang X Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, Illinois, USA. Hamouie Judy J Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, Illinois, USA. Tadepalli Asha A Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, Illinois, USA. Anwar Khandaker N KN Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, Illinois, USA. Kink John A JA Department of Medicine and University of Wisconsin Carbone Cancer Center, University of Wisconsin-Madison, School of Medicine and Public Health, Madison, Wisconsin, USA. Ghassemi Samaneh S Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, Illinois, USA. Agnihotri Gaurav G Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, Illinois, USA. Reshetylo Sofiya S Department of Medicine and University of Wisconsin Carbone Cancer Center, University of Wisconsin-Madison, School of Medicine and Public Health, Madison, Wisconsin, USA. Mashaghi Alireza A Faculty of Mathematics and Natural Sciences, Leiden Academic Centre for Drug Research, Leiden University, Leiden, The Netherlands. Dana Reza R Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Hematti Peiman P Department of Medicine and University of Wisconsin Carbone Cancer Center, University of Wisconsin-Madison, School of Medicine and Public Health, Madison, Wisconsin, USA. Djalilian Ali R AR http://orcid.org/0000-0002-1489-0724 Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, Illinois, USA. eng K12 EY021475 EY NEI NIH HHS United States P30 CA014520 CA NCI NIH HHS United States P30 EY001792 EY NEI NIH HHS United States R01 EY024349 EY NEI NIH HHS United States Journal Article 2018 01 27

United States Stem Cells 9304532 1066-5099 Trends Mol Med. 2002 Jul;8(7):330-4 12114112 J Immunol. 2012 Oct 1;189(7):3508-20 22942426 Sci Signal. 2016 Aug 30;9(443):ra86 27577261 Nat Commun. 2015 Oct 07;6:8472 26442449 Invest Ophthalmol Vis Sci. 2017 Oct 1;58(12 ):5507-5517 29075761 J Biol Chem. 2006 Feb 10;281(6):3604-13 16339148 JCI Insight. 2016;1(7):null 27294203 Invest Ophthalmol Vis Sci. 2006 Sep;47(9):3912-8 16936104 J Clin Invest. 2012 Mar;122(3):787-95 22378047 Stem Cells. 2011 Oct;29(10):1572-9 21837654 Invest Ophthalmol Vis Sci. 2009 Jul;50(7):3151-8 19255161 Stem Cells. 2010 Aug;28(8):1446-55 20597105 Cytotherapy. 2012 Sep;14(8):925-35 22571381 Blood. 2005 Feb 15;105(4):1815-22 15494428 Am J Physiol Renal Physiol. 2004 Feb;286(2):F356-62 14570698 J Immunol. 2013 May 15;190(10):5237-46 23596310 Proc Natl Acad Sci U S A. 2016 Jan 5;113(1):158-63 26699483 Proc Natl Acad Sci U S A. 2010 Sep 28;107(39):16875-80 20837529 Prog Retin Eye Res. 2013 Jul;35:82-101 23542232 J Vis Exp. 2010 Jan 28;(35):null 20110936 Cytotherapy. 2017 Jan;19(1):1-8 27769637 Stem Cells. 2016 Aug;34(8):2210-23 27059413 Immunity. 2016 Mar 15;44(3):450-462 26982353 Exp Eye Res. 2016 Apr;145:88-92 26607808 Stem Cells. 2013 Oct;31(10):2042-6 23681848 J Clin Invest. 2007 Nov;117(11):3421-6 17975672 BMC Ophthalmol. 2015 Dec 17;15 Suppl 1:155 26818606 Transl Res. 2016 Nov;177:127-142 27469269 Nat Protoc. 2011 Jun;6(6):817-26 21637201 Ocul Surf. 2012 Apr;10(2):67-83 22482468 Physiol Rev. 2016 Jul;96(3):1127-68 27335447 Am J Ophthalmol. 2012 Dec;154(6):940-948.e1 22967868 Stem Cells. 2006 Feb;24(2):315-21 16109757 Transfus Med Rev. 2016 Jan;30(1):37-43 26689863 Expert Rev Clin Immunol. 2013 Feb;9(2):175-84 23390948 Front Immunol. 2015 Nov 03;6:560 26579133 Proc Natl Acad Sci U S A. 2010 Aug 3;107(31):13724-9 20643923 Science. 2016 Sep 9;353(6304): 27492475 Graefes Arch Clin Exp Ophthalmol. 2009 Oct;247(10):1375-82 19415316 PLoS One. 2009 Aug 21;4(8):e6712 19696933 Transplant Proc. 1999 May;31(3):1472-5 10330973 Biochim Biophys Acta. 2016 Oct;1860(10 ):2148-56 27233452 Sci Transl Med. 2013 Mar 20;5(177):177fs9 23515074 Proc Natl Acad Sci U S A. 2014 Nov 25;111(47):16766-71 25385603 Trans Am Ophthalmol Soc. 2006;104:264-302 17471348 Biol Blood Marrow Transplant. 2017 Jun;23 (6):897-905 28257800 Stem Cells. 2008 Apr;26(4):1047-55 18192235 Cornea. 2016 Nov;35 Suppl 1:S9-S19 27631350 Stem Cell Res Ther. 2016 Mar 09;7:37 26960535 Invest Ophthalmol Vis Sci. 2015 Dec;56(13):8199-206 26720472 Curr Stem Cell Res Ther. 2010 Jun;5(2):103-10 19941460 Biomaterials. 2014 May;35(15):4477-88 24589361 Am J Physiol Heart Circ Physiol. 2015 Sep;309(5):H812-26 26163443 Stem Cells. 2017 Jun;35(6):1603-1613 28233380 Immunity. 2014 Jul 17;41(1):14-20 25035950 Transplantation. 1999 Jun 27;67(12):1503-8 10401754 Arch Ophthalmol. 2009 Apr;127(4):381-9 19365012 Ocul Surf. 2016 Apr;14 (2):121-34 26804815 Mol Ther. 2012 Jan;20(1):14-20 22008910 Am J Pathol. 2015 Aug;185(8):2324-35 26079814 Exp Hematol. 2009 Dec;37(12):1445-53 19772890 Invest Ophthalmol Vis Sci. 2004 Apr;45(4):1117-24 15037577 J Clin Invest. 2004 Apr;113(7):1040-50 15057311 Proc Natl Acad Sci U S A. 2006 Jul 25;103(30):11405-10 16849433 PLoS One. 2014 Mar 06;9(3):e89375 24603711 Invest Ophthalmol Vis Sci. 2012 May 31;53(6):3145-53 22511631 Trends Immunol. 2004 Dec;25(12):677-86 15530839 Stem Cells. 2017 Apr;35(4):851-858 28294454 F1000Res. 2017 Apr 20;6: 28491279 Curr Mol Med. 2013 Jun;13(5):856-67 23642066 Nature. 2006 Oct 26;443(7114):993-7 17051153 Stem Cell Reports. 2017 Apr 11;8(4):961-976 28330617 Ann Biomed Eng. 2015 Mar;43(3):616-27 25331098 Sci Transl Med. 2014 Dec 10;6(266):266ra172 25504883 Front Med. 2011 Dec;5(4):333-5 22198744 Blood. 2011 Jul 14;118(2):330-8 21551236 Angiogenesis Cornea Inflammation Macrophages Mesenchymal stromal cells Pigment epithelial derived factor 2017 07 09 2018 01 02 2018 01 08 2019 05 01 2018 1 18 6 0 2018 1 18 6 0 2018 1 18 6 0 ppublish 29341332 10.1002/stem.2781 PMC5918156 NIHMS934865 29847655 2018 06 02

1552-5783 59 6 2018 May 01 Invest. Ophthalmol. Vis. Sci. Family-Based Genome-Wide Association Study of South Indian Pedigrees Supports WNT7B as a Central Corneal Thickness Locus. 2495-2502 10.1167/iovs.17-23536 To identify genetic risk factors contributing to central corneal thickness (CCT) in individuals from South India, a population with a high prevalence of ocular disorders. One hundred ninety-five individuals from 15 large South Indian pedigrees were genotyped using the Omni2.5 bead array. Family-based association for CCT was conducted using the score test in MERLIN. Genome-wide association study (GWAS) identified strongest association for single nucleotide polymorphisms (SNPs) in the first intron of WNT7B and CCT (top SNP rs9330813; β = -0.57, 95% confidence interval [CI]: -0.78 to -0.36; P = 1.7 × 10-7). We further investigated rs9330813 in a Latino cohort and four independent European cohorts. A meta-analysis of these data sets demonstrated statistically significant association between rs9330813 and CCT (β = -3.94, 95% CI: -5.23 to -2.66; P = 1.7 × 10-9). WNT7B SNPs located in the same genomic region that includes rs9330813 have previously been associated with CCT in Latinos but with other ocular quantitative traits related to myopia (corneal curvature and axial length) in a Japanese population (rs10453441 and rs200329677). To evaluate the specificity of the observed WNT7B association with CCT in the South Indian families, we completed an ocular phenome-wide association study (PheWAS) for the top WNT7B SNPs using 45 ocular traits measured in these same families including corneal curvature and axial length. The ocular PheWAS results indicate that in the South Indian families WNT7B SNPs are primarily associated with CCT. The results indicate robust evidence for association between WNT7B SNPs and CCT in South Indian pedigrees, and suggest that WNT7B SNPs can have population-specific effects on ocular quantitative traits. Fan Bao Jian BJ Department of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, United States. Chen Xueli X Department of Ophthalmology & Visual Science, Eye & Ear Nose Throat Hospital, Shanghai Medical College, Fudan University, Shanghai, China. Sondhi Nisha N Department of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, United States. Sharmila P Ferdinamarie PF SNONGC Department of Genetics and Molecular Biology, Vision Research Foundation, Sankara Nethralaya, Chennai, India. Soumittra Nagasamy N SNONGC Department of Genetics and Molecular Biology, Vision Research Foundation, Sankara Nethralaya, Chennai, India. Sripriya Sarangapani S SNONGC Department of Genetics and Molecular Biology, Vision Research Foundation, Sankara Nethralaya, Chennai, India. Sacikala Srinivasan S SNONGC Department of Genetics and Molecular Biology, Vision Research Foundation, Sankara Nethralaya, Chennai, India. Asokan Rashima R Medical Research Foundation, Sankara Nethralaya, Chennai, India. Friedman David S DS The Dana Center for Preventive Ophthalmology, Johns Hopkins Medical School, Wilmer Eye Institute, Baltimore, Maryland, United States. Pasquale Louis R LR Department of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, United States. Channing Division of Network Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States. Gao X Raymond XR Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, Illinois, United States. Vijaya Lingam L Medical Research Foundation, Sankara Nethralaya, Chennai, India. Cooke Bailey Jessica J Department of Epidemiology and Biostatistics, Institute for Computational Biology, Case Western Reserve University School of Medicine, Cleveland, Ohio, United States. Vitart Veronique V MRC Human Genetics Unit, Institute for Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, United Kingdom. MacGregor Stuart S QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia. Hammond Christopher J CJ Department of Twin Research and Genetic Epidemiology, King's College London, London, United Kingdom. Khor Chiea Chuen CC Division of Human Genetics, Genome Institute of Singapore, Singapore. Haines Jonathan L JL Department of Epidemiology and Biostatistics, Institute for Computational Biology, Case Western Reserve University School of Medicine, Cleveland, Ohio, United States. George Ronnie R Medical Research Foundation, Sankara Nethralaya, Chennai, India. Wiggs Janey L JL Department of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, United States. Mexican American Glaucoma Genetic Study; International Glaucoma Genetics Consortium; and NEIGHBORHOOD Consortium eng P30 EY001792 EY NEI NIH HHS United States R01 EY027129 EY NEI NIH HHS United States R21 EY018149 EY NEI NIH HHS United States R01 EY022651 EY NEI NIH HHS United States P30 EY014104 EY NEI NIH HHS United States Journal Article

United States Invest Ophthalmol Vis Sci 7703701 0146-0404 Invest Ophthalmol Vis Sci. 2010 Jul;51(7):3509-14 20237253 Hum Mol Genet. 2010 Nov 1;19(21):4304-11 20719862 Bioinformatics. 2008 Dec 15;24(24):2938-9 18974171 Nat Genet. 2013 Feb;45(2):155-63 23291589 Annu Rev Genomics Hum Genet. 2016 Aug 31;17 :353-73 27147087 Nat Genet. 2010 Jul;42(7):565-9 20562875 Eur J Ophthalmol. 2007 Jul-Aug;17 (4):545-9 17671929 Ophthalmology. 2012 Nov;119(11):2245-53 22796305 Genome Res. 2013 Dec;23(12):2066-77 24002784 Bioinformatics. 2003 Jan;19(1):149-50 12499305 Invest Ophthalmol Vis Sci. 2013 Apr 01;54(4):2435-43 23493294 Br J Ophthalmol. 2010 Aug;94(8):971-6 19556215 Hum Genet. 2012 Nov;131(11):1783-93 22814818 Ophthalmology. 2014 Oct;121(10):2013-22 24950592 J Glaucoma. 2006 Apr;15(2):91-7 16633220 Ophthalmology. 2014 Jul;121(7):1370-6 24650554 Invest Ophthalmol Vis Sci. 2014 Aug 05;55(9):5629-35 25097247 Nat Biotechnol. 2013 Dec;31(12):1102-10 24270849 PLoS One. 2015 Mar 23;10(3):e0119703 25798827 Arch Ophthalmol. 2002 Jun;120(6):714-20; discussion 829-30 12049575 PLoS One. 2011;6(8):e22103 21853026 BMJ. 2003 Sep 6;327(7414):557-60 12958120 Indian J Ophthalmol. 2014 Apr;62(4):477-81 23619490 Br J Ophthalmol. 2015 May;99(5):604-8 25388449 PLoS Genet. 2010 May 13;6(5):e1000947 20485516 Lancet Glob Health. 2013 Dec;1(6):e339-49 25104599 Hum Mol Genet. 2011 Feb 15;20(4):649-58 21098505 Invest Ophthalmol Vis Sci. 2013 Dec 11;54(13):8062-8 24168998 Nat Genet. 2002 Jan;30(1):97-101 11731797 Hum Mol Genet. 2015 Sep 1;24(17):5060-8 26049155 Am J Ophthalmol. 2004 Feb;137(2):348-50 14962429 Nat Genet. 2017 Sep;49(9):1392-1397 28714974 Ophthalmology. 2003 Aug;110(8):1491-8 12917162 Nat Genet. 2016 Feb;48(2):189-94 26752265 Am J Hum Genet. 2007 Sep;81(3):559-75 17701901 Ann Hum Genet. 2009 Sep;73(Pt 5):527-31 19604226 Nucleic Acids Res. 2015 Oct 15;43(18):8694-712 26338778 Am J Hum Genet. 2007 Nov;81(5):913-26 17924335 Nat Commun. 2015 Mar 31;6:6689 25823570 Bioinformatics. 2010 Nov 15;26(22):2867-73 20926424 Invest Ophthalmol Vis Sci. 2005 Apr;46(4):1269-74 15790889 Hum Mol Genet. 2016 Nov 15;25(22):5035-5045 28171582 Stem Cell Reports. 2016 May 10;6(5):652-659 27167156 Cell Mol Life Sci. 2015 Nov;72(21):4157-72 26306936 Invest Ophthalmol Vis Sci. 2014 Aug 07;55(9):5545-50 25103268 Invest Ophthalmol Vis Sci. 2011 Jul 01;52(7):4734-41 21357396 2018 5 31 6 0 2018 5 31 6 0 2018 5 31 6 0 ppublish 29847655 2682365 10.1167/iovs.17-23536 PMC5961220 29487115 2018 05 25 2018 05 25

1939-327X 67 5 2018 05 Diabetes Fibroblast Growth Factor 21 Protects Photoreceptor Function in Type 1 Diabetic Mice. 974-985 10.2337/db17-0830 Retinal neuronal abnormalities occur before vascular changes in diabetic retinopathy. Accumulating experimental evidence suggests that neurons control vascular pathology in diabetic and other neovascular retinal diseases. Therefore, normalizing neuronal activity in diabetes may prevent vascular pathology. We investigated whether fibroblast growth factor 21 (FGF21) prevented retinal neuronal dysfunction in insulin-deficient diabetic mice. We found that in diabetic neural retina, photoreceptor rather than inner retinal function was most affected and administration of the long-acting FGF21 analog PF-05231023 restored the retinal neuronal functional deficits detected by electroretinography. PF-05231023 administration protected against diabetes-induced disorganization of photoreceptor segments seen in retinal cross section with immunohistochemistry and attenuated the reduction in the thickness of photoreceptor segments measured by optical coherence tomography. PF-05231023, independent of its downstream metabolic modulator adiponectin, reduced inflammatory marker interleukin-1β (IL-1β) mRNA levels. PF-05231023 activated the AKT-nuclear factor erythroid 2-related factor 2 pathway and reduced IL-1β expression in stressed photoreceptors. PF-05231023 administration did not change retinal expression of vascular endothelial growth factor A, suggesting a novel therapeutic approach for the prevention of early diabetic retinopathy by protecting photoreceptor function in diabetes. © 2018 by the American Diabetes Association. Fu Zhongjie Z Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA. Wang Zhongxiao Z Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA. Liu Chi-Hsiu CH Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA. Gong Yan Y Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA. Cakir Bertan B Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA. Liegl Raffael R Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA. Sun Ye Y Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA. Meng Steven S SS Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA. Burnim Samuel B SB Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA. Arellano Ivana I Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA. Moran Elizabeth E Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA. Duran Rubi R Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA. Poblete Alexander A Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA. Cho Steve S SS Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA. Talukdar Saswata S Merck Research Laboratories, Boston, MA. Akula James D JD Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA. Hellström Ann A Section for Ophthalmology, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Göteborg, Sweden. Smith Lois E H LEH 0000-0001-7644-6410 Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA lois.smith@childrens.harvard.edu. eng R01 EY017017 EY NEI NIH HHS United States R24 EY024864 EY NEI NIH HHS United States Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't 2018 02 27

United States Diabetes 0372763 0012-1797 0 Antibodies, Monoclonal, Humanized 0 IL1B protein, mouse 0 Interleukin-1beta 0 NF-E2-Related Factor 2 0 Nfe2l2 protein, mouse 0 PF-05231023 0 Vascular Endothelial Growth Factor A 0 fibroblast growth factor 21 0 vascular endothelial growth factor A, mouse 62031-54-3 Fibroblast Growth Factors EC 2.7.11.1 Proto-Oncogene Proteins c-akt AIM IM Toxicol Appl Pharmacol. 2004 Nov 15;201(1):21-31 15519605 Endocrine. 2015 Apr;48(3):848-55 25194937 Vision Res. 2001 Apr;41(8):1091-101 11301082 PLoS One. 2012;7(5):e36949 22615852 Oxid Med Cell Longev. 2016;2016:7469326 27818722 Invest Ophthalmol Vis Sci. 2008 Dec;49(12):5581-92 19037001 Invest Ophthalmol Vis Sci. 2016 Aug 1;57(10 ):4272-81 27548901 Invest Ophthalmol Vis Sci. 2016 Aug 1;57(10 ):4264-71 27548900 Nat Med. 2016 Apr;22(4):439-45 26974308 Curr Diab Rep. 2013 Aug;13(4):481-7 23649947 Nat Med. 2013 Sep;19(9):1147-52 23933984 Vis Neurosci. 1995 Sep-Oct;12(5):837-50 8924408 Int Immunopharmacol. 2016 Sep;38:144-52 27276443 Nat Commun. 2016 May 23;7:11624 27211851 Indian J Ophthalmol. 2012 Sep-Oct;60(5):428-31 22944754 Mol Vis. 2008;14:2499-508 19112532 Cell. 2012 Feb 3;148(3):556-67 22304921 Cell Metab. 2012 Sep 5;16(3):387-93 22958921 BMC Gastroenterol. 2013 Apr 17;13:67 23590285 FASEB J. 2004 Sep;18(12):1450-2 15231732 Cell Metab. 2013 May 7;17(5):790-7 23663742 Vis Neurosci. 2004 Jul-Aug;21(4):533-43 15579219 Free Radic Biol Med. 2016 Apr;93:94-109 26849944 Eye Brain. 2010;2:99-116 23226947 Circ Res. 2009 May 8;104(9):1058-65 19342600 Sci Transl Med. 2012 Nov 28;4(162):162ra153 23197570 Toxicol Lett. 2013 May 10;219(1):65-76 23499715 Biochim Biophys Acta. 2016 Aug;1862(8):1392-400 27155572 Trends Endocrinol Metab. 2015 Jan;26(1):22-9 25476453 J Clin Invest. 2015 Apr;125(4):1433-45 25798616 Invest Ophthalmol Vis Sci. 2008 Apr;49(4):1671-8 18385090 Prog Retin Eye Res. 2017 Jan;56:32-57 27671171 World Allergy Organ J. 2012 Jan;5(1):9-19 23268465 Rev Endocr Metab Disord. 2008 Dec;9(4):315-27 18654858 Cell Metab. 2016 Feb 9;23 (2):344-9 26724861 J Biol Chem. 1994 Feb 11;269(6):4613-9 8308033 Invest Ophthalmol Vis Sci. 2006 Jun;47(6):2732-8 16723493 Biochim Biophys Acta. 2015 Nov;1852(11):2474-83 26248057 J Diabetes Res. 2013;2013:106594 24286086 Endocr Relat Cancer. 2012 May 24;19(3):423-34 22499437 Invest Ophthalmol Vis Sci. 2007 Dec;48(12):5788-97 18055833 J Physiol. 1992 Apr;449:719-58 1326052 Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10368-73 11526242 Invest Ophthalmol Vis Sci. 2007 Sep;48(9):4351-9 17724227 Peptides. 2007 Dec;28(12):2382-6 17996984 Am J Clin Nutr. 2015 Apr;101(4):879-88 25833984 J Biol Chem. 2015 Aug 28;290(35):21568-79 26139608 PLoS One. 2013 Dec 09;8(12):e82275 24349242 Cell Rep. 2017 Feb 14;18(7):1606-1613 28199833 Vision Res. 1978;18(7):793-800 676087 Invest Ophthalmol Vis Sci. 2004 Nov;45(11):4161-6 15505070 J Diabetes Res. 2015;2015:319692 26075282 Doc Ophthalmol. 2009 Feb;118(1):55-61 18483822 Diabetes. 2014 Dec;63(12):4057-63 25008183 J Clin Endocrinol Metab. 2012 Jan;97(1):E54-8 22013098 J Immunol. 1994 Jul 15;153(2):712-23 8021507 Ophthalmologica. 2017;237(1):1-10 28152535 Prog Retin Eye Res. 2013 May;34:19-48 23416119 Mol Metab. 2014 Oct 08;4(1):51-7 25685689 Curr Biol. 2008 Dec 23;18(24):1917-21 19084410 Vis Neurosci. 1992 Feb;8(2):107-26 1558823 Cell Metab. 2016 Mar 8;23 (3):427-40 26959184 Proc Natl Acad Sci U S A. 2013 Oct 8;110(41):16586-91 24067647 Vis Neurosci. 2002 Jul-Aug;19(4):395-407 12511073 J Diabetes Investig. 2015 Jul;6(4):371-80 26221514 Cell Metab. 2013 May 7;17(5):779-89 23663741 Invest Ophthalmol Vis Sci. 2015 Aug;56(9):5407-16 26284544 Eye (Lond). 2014 May;28(5):510-20 24525867 Animals Antibodies, Monoclonal, Humanized pharmacology Diabetes Mellitus, Experimental complications metabolism pathology Diabetes Mellitus, Type 1 complications metabolism pathology Diabetic Retinopathy etiology metabolism pathology Disease Models, Animal Electroretinography Fibroblast Growth Factors pharmacology Interleukin-1beta drug effects genetics metabolism Male Mice NF-E2-Related Factor 2 drug effects genetics metabolism Photoreceptor Cells, Vertebrate drug effects metabolism pathology Proto-Oncogene Proteins c-akt drug effects metabolism Retinal Neurons drug effects metabolism pathology Tomography, Optical Coherence Vascular Endothelial Growth Factor A drug effects metabolism 2017 07 14 2018 02 07 2019 05 01 2018 3 1 6 0 2018 5 26 6 0 2018 3 1 6 0 ppublish 29487115 db17-0830 10.2337/db17-0830 PMC5909994 29781807 2018 05 21

1741-2552 2018 May 21 J Neural Eng Word recognition: Re-thinking prosthetic vision evaluation. 10.1088/1741-2552/aac663 Evaluations of vision prostheses and sensory substitution devices have frequently relied on repeated training and testing with the same small set of items. These multiple forced-choice tasks have been shown to produce above chance performance in blind patients, but it is unclear if the observed performance represents restoration of vision that transfers to novel, untrained items. Here, we tested the generalizability of the forced-choice paradigm on the discrimination of low-resolution word images. Extensive visual training was conducted with the same 10 words used in previous BrainPort tongue stimulating studies. The performance on these 10 words and an additional 50 words was measured before and after the training session. The results revealed minimal performance improvement with the untrained words, demonstrating instead pattern discrimination limited mostly to the trained words. These findings highlight the need to reconsider current evaluation practices, in particular, the use of forced-choice paradigms with a few highly trained items. While appropriate for measuring the performance thresholds in acuity or contrast sensitivity of a functioning visual system, performance on such tasks cannot be taken to indicate restored spatial pattern vision. © 2018 IOP Publishing Ltd. Han Shui'Er S 0000-0002-2521-1416 School of Psychology, University of Sydney - Mallett Street Campus, Griffith Taylor Building (A19), The University of Sydney, Camperdown, New South Wales, 2050, AUSTRALIA. Qiu Cheng C Department of Psychology, University of Pennsylvania School of Arts and Sciences, Philadelphia, Pennsylvania, UNITED STATES. Lee Kassandra R KR Department of Ophthalmology, Schepens Eye Research Institute, Boston, Massachusetts, UNITED STATES. Jung JaeHyun J Schepens Eye Research Institute, Boston, Massachusetts, UNITED STATES. Peli Eli E Schepens Eye Research Institute, Boston, Massachusetts, UNITED STATES. eng Journal Article 2018 05 21

England J Neural Eng 101217933 1741-2552 Object recognition Pattern discrimination Prosthetic vision evaluation Vision rehabilitation 2018 5 22 6 0 2018 5 22 6 0 2018 5 22 6 0 aheadofprint 29781807 10.1088/1741-2552/aac663 29452108 2018 05 02

1096-0007 170 2018 May Exp. Eye Res. Effect of brimonidine, an α2 adrenergic agonist, on human meibomian gland epithelial cells. 20-28 S0014-4835(18)30014-9 10.1016/j.exer.2018.02.009 We recently discovered that the anti-glaucoma pharmaceuticals timolol, a β adrenergic antagonist, and pilocarpine, a cholinergic compound, negatively influence the morphology, proliferative capacity and survival of human meibomian gland epithelial cells (HMGECs). We hypothesize that another class of anti-glaucoma drugs, the α2 adrenergic agonists, also acts directly on HMGECs to affect their structure and function. We tested this hypothesis. Immortalized (i) HMGECs were cultured with brimonidine, as well as clonidine (α2 agonist), phenylephrine (α1 agonist), RX821002 (inverse α2 agonist) and MK912 (neutral α2 agonist) for up to 7 days. Cells were counted with a hemocytometer, and evaluated for morphology, signaling pathway activity, protein biomarker expression, and the accumulation of neutral lipids, phospholipids and lysosomes. Our findings demonstrate that brimondine treatment induces a dose-dependent decrease in Akt signaling and proliferation of iHMGECs. In contrast, brimonidine also promotes a dose-dependent differentiation of iHMGECs, including an increase in neutral lipid, phospholipid and lysosome levels. These effects were paralleled by an inhibition of p38 signaling, and duplicated by cellular exposure to clonidine, but not phenylephrine. Brimonidine also enhanced the cellular content of sterol regulatory binding protein-1, a master regulator of lipid synthesis. Of particular interest, the putative α2 antagonists, RX821002 and MK912, did not interfere with brimonidine action, but rather stimulated IHMGEC differentiation. Our results support our hypothesis and demonstrate that α2 adrenergic agonists act directly on iHMGECs. However, these compounds do not elicit an overall negative effect. Rather, the α2 agonists promote the differentiation of iHMGECs. Copyright © 2018 Elsevier Ltd. All rights reserved. Han Xi X Schepens Eye Research Institute, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA, USA; Department of Ophthalmology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Liu Yang Y Schepens Eye Research Institute, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA, USA. Kam Wendy R WR Schepens Eye Research Institute, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA, USA. Sullivan David A DA Schepens Eye Research Institute, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA, USA. Electronic address: david.sullivan@schepens.harvard.edu. eng R21 EY028653 EY NEI NIH HHS United States Journal Article 2018 02 13

England Exp Eye Res 0370707 0014-4835 J Ophthalmol. 2012;2012:285851 23050121 Drugs Aging. 2011 Apr 1;28(4):267-82 21428462 Oftalmologia. 1999;47(2):35-40 10641099 Mol Aspects Med. 2006 Oct-Dec;27(5-6):495-502 16973206 Mol Pharmacol. 2012 Jul;82(1):115-24 22511543 J Biol Chem. 2007 Feb 16;282(7):4975-82 17172644 Ocul Surf. 2017 Jul;15(3):511-538 28736341 Exp Biol Med (Maywood). 2001 Oct;226(9):825-30 11568304 J Biol Chem. 1989 Dec 5;264(34):20526-31 2584229 Cornea. 2017 Oct;36(10 ):1249-1255 28825921 J Glaucoma. 2014 Jan;23 (1):56-60 22828007 Biol Pharm Bull. 2016;39(8):1319-24 27476940 Arch Ophthalmol. 1997 Jul;115(7):847-52 9230823 Urology. 1988 Dec;32(6 Suppl):16-20 2462300 J Biomol Screen. 2014 Jan;19(1):66-76 24003057 J Biol Chem. 1991 Apr 5;266(10):6365-9 1706716 Invest Ophthalmol Vis Sci. 2016 Jun 1;57(7):3268-75 27327582 Pharmacol Toxicol. 1995 Jun;76(6):353-64 7479575 Cornea. 2017 Jun;36(6):719-724 28476050 J Glaucoma. 2004 Apr;13(2):168-73 15097265 Eur J Cell Biol. 2001 Jul;80(7):466-78 11499789 J Allergy Clin Immunol. 2001 Nov;108(5):671-80 11692087 J Ophthalmol. 2014;2014:460483 25009742 Cornea. 2016 Aug;35(8):1112-6 27055218 PLoS One. 2009 Jun 05;4(6):e5806 19503797 Ocul Surf. 2017 Jul;15(3):276-283 28736335 Semin Oncol. 1997 Feb;24(1 Suppl 1):S1-71-S1-80 9045319 Autophagy. 2016;12 (1):1-222 26799652 J Ophthalmol. 2017;2017:4586763 29057117 Invest Ophthalmol Vis Sci. 2000 Mar;41(3):870-6 10711706 Ophthal Plast Reconstr Surg. 2016 Mar-Apr;32(2):102-5 25719374 Invest Ophthalmol Vis Sci. 2010 Aug;51(8):3993-4005 20335607 J Clin Invest. 2002 May;109(9):1125-31 11994399 Eur J Pharmacol. 2000 Jun 16;398(2):185-91 10854829 Ophthalmology. 2006 Aug;113(8):1333-9 16877072 J Lipid Res. 2005 Apr;46(4):697-705 15627654 Drug Metab Dispos. 2002 Apr;30(4):421-9 11901096 Ophthal Plast Reconstr Surg. 2011 Sep-Oct;27(5):e128-9 21178796 J Invest Dermatol. 2017 Mar;137(3):587-594 27771328 Br J Ophthalmol. 2013 Mar;97(3):343-9 23269683 Trends Pharmacol Sci. 1997 Jun;18(6):211-9 9227000 Cornea. 2012 Nov;31(11):1229-34 22406943 ChemMedChem. 2012 Nov;7(11):1925-34 22945602 Proc Natl Acad Sci U S A. 2013 Jan 2;110(1):E79-88 23236157 Toxicology. 2014 Jun 5;320:1-5 24613571 Methods Mol Biol. 2008;445:77-88 18425443 CNS Drug Rev. 2002 Summer;8(2):177-92 12177687 Surv Ophthalmol. 1996 Nov;41 Suppl 1:S39-47 8970248 Invest Ophthalmol Vis Sci. 2011 Mar 30;52(4):1938-78 21450915 Drugs. 1991 Mar;41(3):326-44 1711441 Biochimie. 2004 Nov;86(11):839-48 15589694 Invest Ophthalmol Vis Sci. 2014 May 27;55(6):3866-77 24867579 J Glaucoma. 2016 Sep;25(9):770-4 27513901 Biochim Biophys Acta. 2012 Feb;1822(2):161-7 22137887 Arzneimittelforschung. 2007;57(2):92-100 17396619 Endocr Rev. 1999 Jun;20(3):418-34 10368777 Toxicol Pathol. 1997 Jan-Feb;25(1):53-60 9061852 Brimonidine Dry eye disease Meibomian gland dysfunction Phospholipidosis α2 adrenergic agonist α2 adrenergic antagonist 2018 01 09 2018 02 09 2018 02 12 2019 05 01 2018 2 17 6 0 2018 2 17 6 0 2018 2 17 6 0 ppublish 29452108 S0014-4835(18)30014-9 10.1016/j.exer.2018.02.009 PMC5924632 NIHMS945351 28742610 2018 05 15

1536-3724 28 3 2018 May Clin J Sport Med Near Point of Convergence and Gait Deficits in Adolescents After Sport-Related Concussion. 262-267 10.1097/JSM.0000000000000439 To prospectively examine gait characteristics of participants acutely after concussion with and without receded near point of convergence (NPC), compared with healthy controls. Cross-sectional study. Sports-medicine clinic. Patients examined after concussion (n = 33; mean ± SD = 7.2 ± 3.1 days) and a group of uninjured athletes (n = 31) completed a Postconcussion Symptom Scale, underwent NPC testing, and single/dual-task gait assessments. Near point of convergence was defined as the patient-reported diplopia distance when a fixation target moved toward the nose. Receded NPC was defined as a distance >5 cm from the tip of the nose. Spatiotemporal gait characteristics in single-task and dual-task conditions were evaluated with analysis of variance; correlations were calculated between NPC and gait measures. Eighteen of 33 (55%) patients with concussion presented with receded NPC. Those with receded NPC exhibited slower gait speed (single-task = 1.06 ± 0.14 m/s vs 1.19 ± 0.15 m/s; dual-task = 0.80 ± 0.13 m/s vs 0.94 ± 0.13 m/s; P = 0.003) and shorter stride lengths (single-task = 1.11 ± 0.10 m vs 1.24 ± 0.11 m; dual-task = 0.97 ± 0.11 m vs 1.09 ± 0.11 m; P = 0.001) than healthy controls. Near point of convergence was moderately correlated with dual-task average walking speed for the normal NPC group (ρ = -0.56; P = 0.05). Postconcussion Symptom Scale scores did not significantly differ between groups (27 ± 18 vs 28 ± 16). After concussion, adolescents with receded NPC exhibited significant gait-related deficits compared with healthy controls, whereas those with normal NPC did not. Vergence and gross motor system dysfunction may be associated after concussion. Gait and vergence measures may contribute useful information to postconcussion evaluations. Howell David R DR The Micheli Center for Sports Injury Prevention, Waltham, Massachusetts. Division of Sports Medicine, Department of Orthopaedics, Boston Children's Hospital, Boston, Massachusetts. Brain Injury Center, Boston Children's Hospital, Boston, Massachusetts. OʼBrien Michael J MJ The Micheli Center for Sports Injury Prevention, Waltham, Massachusetts. Division of Sports Medicine, Department of Orthopaedics, Boston Children's Hospital, Boston, Massachusetts. Brain Injury Center, Boston Children's Hospital, Boston, Massachusetts. Department of Orthopaedic Surgery, Harvard Medical School, Boston, Massachusetts. Raghuram Aparna A Brain Injury Center, Boston Children's Hospital, Boston, Massachusetts. Department of Ophthalmology, Boston Children's Hospital, Boston, Massachusetts. Shah Ankoor S AS Brain Injury Center, Boston Children's Hospital, Boston, Massachusetts. Department of Ophthalmology, Boston Children's Hospital, Boston, Massachusetts. Meehan William P WP 3rd The Micheli Center for Sports Injury Prevention, Waltham, Massachusetts. Division of Sports Medicine, Department of Orthopaedics, Boston Children's Hospital, Boston, Massachusetts. Brain Injury Center, Boston Children's Hospital, Boston, Massachusetts. Department of Orthopaedic Surgery, Harvard Medical School, Boston, Massachusetts. Pediatrics, Harvard Medical School, Boston, Massachusetts. eng Journal Article

United States Clin J Sport Med 9103300 1050-642X 2017 7 26 6 0 2017 7 26 6 0 2017 7 26 6 0 ppublish 28742610 10.1097/JSM.0000000000000439 29728574 2018 06 12

2045-2322 8 1 2018 May 04 Sci Rep Pathological conversion of regulatory T cells is associated with loss of allotolerance. 7059 10.1038/s41598-018-25384-x CD4⁺CD25⁺Foxp3⁺ Regulatory T cells (Tregs) play a critical role in immune tolerance. The plasticity and functional adaptability of Tregs in an inflammatory microenvironment has been demonstrated in autoimmunity. Here, using a double transgenic mouse model that permits Foxp3 lineage tracing, we investigated the phenotypic plasticity of Foxp3⁺ Tregs in a well-characterized murine model of corneal transplantation. In order to subvert the normal immune privilege of the cornea and foster an inflammatory milieu, host mice were exposed to desiccating stress prior to transplantation. Treg frequencies and function were decreased following desiccating stress, and this corresponded to decreased graft survival. A fraction of Tregs converted to IL-17⁺ or IFNγ⁺ 'exFoxp3' T cells that were phenotypically indistinguishable from effector Th17 or Th1 cells, respectively. We investigated how Foxp3 expression is modulated in different Treg subsets, demonstrating that neuropilin-1^- peripherally-derived Tregs are particularly susceptible to conversion to IL-17⁺/IFNγ⁺ exFoxp3 cells in response to cues from their microenvironment. Finally, we show that IL-6 and IL-23 are implicated in the conversion of Tregs to exFoxp3 cells. This report demonstrates that the pathological conversion of Tregs contributes to the loss of corneal immune privilege. Hua Jing J Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Inomata Takenori T http://orcid.org/0000-0003-3435-1055 Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Chen Yihe Y Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Foulsham William W http://orcid.org/0000-0002-7088-605X Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Stevenson William W Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Shiang Tina T Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Bluestone Jeffrey A JA Diabetes Center, University of California San Francisco, San Francisco, CA, USA. Dana Reza R Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Reza_Dana@meei.harvard.edu. eng R01 EY012963 EY NEI NIH HHS United States Journal Article 2018 05 04

England Sci Rep 101563288 2045-2322 Nature. 2008 May 8;453(7192):236-40 18368049 Immunity. 2012 Feb 24;36(2):262-75 22326580 Nat Rev Immunol. 2009 Feb;9(2):83-9 19114986 Invest Ophthalmol Vis Sci. 2012 Jun 14;53(7):3584-91 22577075 Invest Ophthalmol Vis Sci. 2010 Jun;51(6):3083-91 20130281 J Immunol. 2014 Sep 15;193(6):2699-708 25092890 Eur J Immunol. 2007 Jan;37(1):43-53 17171761 Immunol Rev. 2014 May;259(1):173-91 24712466 Nature. 2014 Sep 25;513(7519):564-568 25043027 Nat Immunol. 2003 Apr;4(4):330-6 12612578 J Exp Med. 2011 Sep 26;208(10 ):2055-67 21893603 Transplantation. 2016 Mar;100(3):525-32 26881788 Nat Med. 2014 Jan;20(1):62-8 24362934 Front Immunol. 2013 Aug 07;4:232 23966994 Cornea. 2017 Apr;36(4):491-496 28060028 J Biol Methods. 2015;2(3):null 26550579 PLoS One. 2017 Apr 5;12 (4):e0173301 28379971 Immunol Rev. 2014 May;259(1):88-102 24712461 Immunity. 2013 Nov 14;39(5):949-62 24238343 J Exp Med. 1996 Aug 1;184(2):387-96 8760792 Science. 2003 Feb 14;299(5609):1033-6 12532024 Nat Immunol. 2005 Apr;6(4):345-52 15785760 J Immunol. 2007 Sep 15;179(6):3672-9 17785803 Immunity. 2009 Jun 19;30(6):899-911 19464196 Nat Immunol. 2009 Sep;10(9):1000-7 19633673 Immunity. 2008 Apr;28(4):559-70 18400195 Front Immunol. 2014 Feb 11;5:46 24575095 Eur J Immunol. 2009 Apr;39(4):948-55 19291701 Sci Transl Med. 2015 Nov 25;7(315 ):315ra189 26606968 Diabetes Care. 2012 Sep;35(9):1817-20 22723342 CLAO J. 1995 Oct;21(4):221-32 8565190 Immunol Today. 1995 Feb;16(2):61-7 7888068 J Exp Med. 2008 Sep 1;205(9):1983-91 18725525 Transplantation. 1992 Oct;54(4):694-704 1412761 Sci Rep. 2016 Dec 23;6:39924 28008995 Cell Mol Immunol. 2015 Sep;12(5):525-32 25942597 Eur J Immunol. 2010 Jul;40(7):1830-5 20583029 Cell. 2008 May 30;133(5):775-87 18510923 Mol Med. 2016 Nov 22;22:null 27878210 J Immunol. 2011 Apr 1;186(7):3918-26 21368230 Nature. 2007 Feb 15;445(7129):766-70 17220876 Immunity. 2008 Jul 18;29(1):44-56 18585065 Nat Rev Immunol. 2016 Mar;16(3):149-63 26875830 J Exp Med. 2012 Sep 24;209(10):1723-42, S1 22966001 J Immunol. 2017 Aug 15;199(4):1342-1352 28710254 J Immunol. 2009 Jan 1;182(1):148-53 19109145 J Immunol. 2004 Oct 1;173(7):4464-9 15383577 Annu Rev Immunol. 2012;30:733-58 22224762 J Immunol. 2001 Aug 15;167(4):1891-9 11489968 Cornea. 2018 Jan;37(1):95-101 29023237 Exp Eye Res. 2007 May;84(5):973-7 17397831 Nat Med. 2011 Jun;17(6):673-5 21540856 Am J Transplant. 2007 Jun;7(6):1457-63 17511675 Ocul Surf. 2007 Apr;5(2):75-92 17508116 Clin Sci (Lond). 2012 Jun;122(11):487-511 22324470 2018 01 05 2018 04 11 2018 5 6 6 0 2018 5 8 6 0 2018 5 8 6 0 epublish 29728574 10.1038/s41598-018-25384-x 10.1038/s41598-018-25384-x PMC5935752 29760442 2018 06 15

2041-1723 9 1 2018 May 14 Nat Commun Cross-ancestry genome-wide association analysis of corneal thickness strengthens link between complex and Mendelian eye diseases. 1864 10.1038/s41467-018-03646-6 Central corneal thickness (CCT) is a highly heritable trait associated with complex eye diseases such as keratoconus and glaucoma. We perform a genome-wide association meta-analysis of CCT and identify 19 novel regions. In addition to adding support for known connective tissue-related pathways, pathway analyses uncover previously unreported gene sets. Remarkably, >20% of the CCT-loci are near or within Mendelian disorder genes. These included FBN1, ADAMTS2 and TGFB2 which associate with connective tissue disorders (Marfan, Ehlers-Danlos and Loeys-Dietz syndromes), and the LUM-DCN-KERA gene complex involved in myopia, corneal dystrophies and cornea plana. Using index CCT-increasing variants, we find a significant inverse correlation in effect sizes between CCT and keratoconus (r = -0.62, P = 5.30 × 10^-5) but not between CCT and primary open-angle glaucoma (r = -0.17, P = 0.2). Our findings provide evidence for shared genetic influences between CCT and keratoconus, and implicate candidate genes acting in collagen and extracellular matrix regulation. Iglesias Adriana I AI http://orcid.org/0000-0001-5532-764X Department of Ophthalmology, Erasmus Medical Center, 3000 CA, Rotterdam, The Netherlands. Department of Epidemiology, Erasmus Medical Center, 3000 CA, Rotterdam, The Netherlands. Department of Clinical Genetics, Erasmus Medical Center, 3000 CA, Rotterdam, The Netherlands. Mishra Aniket A University of Bordeaux, Bordeaux Population Health Research Center, INSERM UMR 1219, F-33000, Bordeaux, France. Vitart Veronique V Institute of Genetics and Molecular Medicine, Medical Research Council Human Genetics Unit, University of Edinburgh, EH42XU, Edinburgh, UK. Bykhovskaya Yelena Y Regenerative Medicine Institute and Department of Surgery, Cedars-Sinai Medical Center, CA 90048, Los Angeles, CA, USA. Cornea Genetic Eye Institute, CA 90048, Los Angeles, CA, USA. Höhn René R Department of Ophthalmology, University Medical Center Mainz, 55131, Mainz, Germany. Department of Ophthalmology, Inselspital, University Hospital Bern, University of Bern, Bern, CH-3010, Switzerland. Springelkamp Henriët H Department of Ophthalmology, Erasmus Medical Center, 3000 CA, Rotterdam, The Netherlands. Cuellar-Partida Gabriel G Statistical Genetics, QIMR Berghofer Medical Research Institute, QLD 4029, Brisbane, Australia. Gharahkhani Puya P http://orcid.org/0000-0002-4203-5952 Statistical Genetics, QIMR Berghofer Medical Research Institute, QLD 4029, Brisbane, Australia. Bailey Jessica N Cooke JNC http://orcid.org/0000-0002-4001-8702 Department of Population and Quantitative Health Sciences, Case Western Reserve University, OH 44106, Cleveland, OH, USA. Institute for Computational Biology, Case Western Reserve University, Cleveland, OH, 44106, USA. Willoughby Colin E CE Biomedical Sciences Research Institute, Ulster University, BT52 1SA, Belfast, Northern Ireland, UK. Royal Victoria Hospital, Belfast Health and Social Care Trust, BT12 6BA, Belfast, Northern Ireland, UK. Li Xiaohui X http://orcid.org/0000-0002-5037-3572 Institute for Translational Genomics and Population Sciences and Department of Pediatrics, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA 90509, CA, USA. Division of Genomic Outcomes, Departments of Pediatrics and Medicine, Harbor-UCLA Medical Center, Torrance, CA 90502, CA, USA. Yazar Seyhan S Institute of Genetics and Molecular Medicine, Medical Research Council Human Genetics Unit, University of Edinburgh, EH42XU, Edinburgh, UK. Centre for Ophthalmology and Visual Science, University of Western Australia, Lions Eye Institute, WA 6009, Perth, WA, Australia. Nag Abhishek A Department of Twin Research and Genetic Epidemiology, King's College London, WC2R 2LS, London, UK. Khawaja Anthony P AP http://orcid.org/0000-0001-6802-8585 Department of Public Health and Primary Care, Institute of Public Health, University of Cambridge School of Clinical Medicine, CB2 0SR, Cambridge, UK. NIHR Biomedical Research Centre, Moorfields Eye Hospital NHS Foundation Trust and UCL Institute of Ophthalmology, EC1V 9EL, London, UK. Polašek Ozren O Faculty of Medicine, University of Split, HR-21000, Split, Croatia. Siscovick David D Departments of Medicine and Epidemiology and Cardiovascular Health Research Unit, University of Washington, WA 98101, Washington, USA. The New York Academy of Medicine, NY 10029, New York, NY, USA. Mitchell Paul P Centre for Vision Research, Department of Ophthalmology and Westmead Institute for Medical Research, University of Sydney, NSW 2145, Sydney, NSW, Australia. Tham Yih Chung YC Singapore Eye Research Institute, Singapore National Eye Centre, 168751, Singapore, Singapore. Haines Jonathan L JL http://orcid.org/0000-0002-4351-4728 Department of Population and Quantitative Health Sciences, Case Western Reserve University, OH 44106, Cleveland, OH, USA. Institute for Computational Biology, Case Western Reserve University, Cleveland, OH, 44106, USA. Kearns Lisa S LS Centre for Eye Research Australia, University of Melbourne, Royal Victorian Eye and Ear Hospital, VIC 3002, East Melbourne, Australia. Hayward Caroline C http://orcid.org/0000-0002-9405-9550 Institute of Genetics and Molecular Medicine, Medical Research Council Human Genetics Unit, University of Edinburgh, EH42XU, Edinburgh, UK. Shi Yuan Y Singapore Eye Research Institute, Singapore National Eye Centre, 168751, Singapore, Singapore. van Leeuwen Elisabeth M EM Department of Ophthalmology, Erasmus Medical Center, 3000 CA, Rotterdam, The Netherlands. Taylor Kent D KD Institute for Translational Genomics and Population Sciences and Department of Pediatrics, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA 90509, CA, USA. Division of Genomic Outcomes, Departments of Pediatrics and Medicine, Harbor-UCLA Medical Center, Torrance, CA 90502, CA, USA. Blue Mountains Eye Study—GWAS group Bonnemaijer Pieter P http://orcid.org/0000-0001-5154-6765 Department of Ophthalmology, Erasmus Medical Center, 3000 CA, Rotterdam, The Netherlands. Rotter Jerome I JI Institute for Translational Genomics and Population Sciences and Department of Pediatrics, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA 90509, CA, USA. Division of Genomic Outcomes, Departments of Pediatrics and Medicine, Harbor-UCLA Medical Center, Torrance, CA 90502, CA, USA. Martin Nicholas G NG Department of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, QLD 4029, Brisbane, Australia. Zeller Tanja T Department of General and Interventional Cardiology, University Heart Center Hamburg, 20251, Hamburg, Germany. German Center for Cardiovascular Research (DZHK), Partner Site Hamburg/Kiel/Lübeck, 20246, Hamburg, Germany. Mills Richard A RA Department of Ophthalmology, Flinders University, SA 5042, Adelaide, Australia. Staffieri Sandra E SE http://orcid.org/0000-0003-3131-9359 Centre for Eye Research Australia, University of Melbourne, Royal Victorian Eye and Ear Hospital, VIC 3002, East Melbourne, Australia. Jonas Jost B JB http://orcid.org/0000-0003-2972-5227 Department of Ophthalmology, Medical Faculty Mannheim of the Ruprecht-Karls-University of Heidelberg, 68167, Mannheim, Germany. Schmidtmann Irene I Institute for Medical Biostatistics, Epidemiology and Informatics, University Medical Center Mainz, 55131, Mainz, Germany. Boutin Thibaud T Institute of Genetics and Molecular Medicine, Medical Research Council Human Genetics Unit, University of Edinburgh, EH42XU, Edinburgh, UK. Kang Jae H JH http://orcid.org/0000-0003-4812-0557 Channing Division of Network Medicine, Brigham and Women's Hospital, Boston, MA 02115, MA, USA. Lucas Sionne E M SEM Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS 7005, TAS, Australia. Wong Tien Yin TY Singapore Eye Research Institute, Singapore National Eye Centre, 168751, Singapore, Singapore. Ophthalmology & Visual Sciences Academic Clinical Program (Eye ACP), Duke-NUS Medical School, 169857, Singapore, Singapore. Department of Ophthalmology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, 117549, Singapore. Beutel Manfred E ME Department of Psychosomatic Medicine and Psychotherapy, University Medical Center Mainz, Mainz, 55131, Germany. Wilson James F JF http://orcid.org/0000-0001-5751-9178 Institute of Genetics and Molecular Medicine, Medical Research Council Human Genetics Unit, University of Edinburgh, EH42XU, Edinburgh, UK. Centre for Global Health Research, Usher Institute for Population Health Sciences and Informatics, University of Edinburgh, EH16 4UX, Edinburgh, UK. NEIGHBORHOOD Consortium Wellcome Trust Case Control Consortium 2 (WTCCC2) Uitterlinden André G AG Department of Epidemiology, Erasmus Medical Center, 3000 CA, Rotterdam, The Netherlands. Department of Internal Medicine, Erasmus Medical Center, 3000 CA, Rotterdam, The Netherlands. Netherlands Consortium for Healthy Ageing, Netherlands Genomics Initiative, 2593 HW, The Hague, The Netherlands. Vithana Eranga N EN Singapore Eye Research Institute, Singapore National Eye Centre, 168751, Singapore, Singapore. Foster Paul J PJ http://orcid.org/0000-0002-4755-177X NIHR Biomedical Research Centre, Moorfields Eye Hospital NHS Foundation Trust and UCL Institute of Ophthalmology, EC1V 9EL, London, UK. Hysi Pirro G PG http://orcid.org/0000-0001-5752-2510 Department of Twin Research and Genetic Epidemiology, King's College London, WC2R 2LS, London, UK. Hewitt Alex W AW http://orcid.org/0000-0002-5123-5999 Centre for Eye Research Australia, University of Melbourne, Royal Victorian Eye and Ear Hospital, VIC 3002, East Melbourne, Australia. School of Medicine, Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS 7005, TAS, Australia. Khor Chiea Chuen CC http://orcid.org/0000-0002-1128-4729 Genome Institute of Singapore, 60 Biopolis Street, Singapore, 138672, Singapore. Pasquale Louis R LR http://orcid.org/0000-0002-5835-3496 Channing Division of Network Medicine, Brigham and Women's Hospital, Boston, MA 02115, MA, USA. Department of Ophthalmology, Harvard Medical School and Massachusetts Eye and Ear Infirmary, Boston, MA 02114, MA, USA. Montgomery Grant W GW http://orcid.org/0000-0002-4140-8139 Department of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, QLD 4029, Brisbane, Australia. Institute for Molecular Bioscience, University of Queensland, QLD 4067, Brisbane, Australia. Klaver Caroline C W CCW http://orcid.org/0000-0002-2355-5258 Department of Ophthalmology, Erasmus Medical Center, 3000 CA, Rotterdam, The Netherlands. Department of Epidemiology, Erasmus Medical Center, 3000 CA, Rotterdam, The Netherlands. Department of Ophthalmology, Radboud University Medical Center, 6525 GA, Nijmegen, The Netherlands. Aung Tin T Singapore Eye Research Institute, Singapore National Eye Centre, 168751, Singapore, Singapore. Ophthalmology & Visual Sciences Academic Clinical Program (Eye ACP), Duke-NUS Medical School, 169857, Singapore, Singapore. Department of Ophthalmology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, 117549, Singapore. Pfeiffer Norbert N Department of Ophthalmology, University Medical Center Mainz, 55131, Mainz, Germany. Mackey David A DA Centre for Ophthalmology and Visual Science, University of Western Australia, Lions Eye Institute, WA 6009, Perth, WA, Australia. Hammond Christopher J CJ http://orcid.org/0000-0002-3227-2620 Department of Twin Research and Genetic Epidemiology, King's College London, WC2R 2LS, London, UK. Cheng Ching-Yu CY Singapore Eye Research Institute, Singapore National Eye Centre, 168751, Singapore, Singapore. Ophthalmology & Visual Sciences Academic Clinical Program (Eye ACP), Duke-NUS Medical School, 169857, Singapore, Singapore. Department of Ophthalmology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, 117549, Singapore. Craig Jamie E JE Department of Ophthalmology, Flinders University, SA 5042, Adelaide, Australia. Rabinowitz Yaron S YS Regenerative Medicine Institute and Department of Surgery, Cedars-Sinai Medical Center, CA 90048, Los Angeles, CA, USA. Cornea Genetic Eye Institute, CA 90048, Los Angeles, CA, USA. Wiggs Janey L JL http://orcid.org/0000-0003-1890-3278 Department of Ophthalmology, Harvard Medical School and Massachusetts Eye and Ear Infirmary, Boston, MA 02114, MA, USA. Burdon Kathryn P KP http://orcid.org/0000-0001-8217-1249 Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS 7005, TAS, Australia. van Duijn Cornelia M CM Department of Epidemiology, Erasmus Medical Center, 3000 CA, Rotterdam, The Netherlands. MacGregor Stuart S http://orcid.org/0000-0001-6731-8142 Statistical Genetics, QIMR Berghofer Medical Research Institute, QLD 4029, Brisbane, Australia. Stuart.MacGregor@qimrberghofer.edu.au. eng R01 EY023242 EY NEI NIH HHS United States UL1 TR001881 TR NCATS NIH HHS United States Journal Article 2018 05 14

England Nat Commun 101528555 2041-1723 Cornea. 2011 Dec;30(12):1473-7 21993463 Nat Genet. 2013 Feb;45(2):155-63 23291589 Biochem J. 1991 Dec 1;280 ( Pt 2):411-4 1747115 Cell. 2015 Aug 27;162(5):1051-65 26300125 Ophthalmology. 2004 Nov;111(11):2126-32 15522381 Invest Ophthalmol Vis Sci. 2008 Oct;49(10):4303-7 18502994 Exp Eye Res. 2008 Sep;87(3):214-25 18582462 Bioinformatics. 2007 May 15;23(10):1294-6 17384015 J Cell Biol. 1998 Jun 1;141(5):1277-86 9606218 Nat Genet. 2000 May;25(1):91-5 10802664 Genome Res. 2012 Sep;22(9):1748-59 22955986 Hum Mol Genet. 2012 Jan 15;21(2):437-45 21984434 Invest Ophthalmol Vis Sci. 2013 May 07;54(5):3297-308 23599329 Nat Commun. 2015 Jan 19;6:5890 25597830 Br J Ophthalmol. 2006 Mar;90(3):262-7 16488940 Am J Ophthalmol. 2008 Jun;145(6):997-1001 18378212 Eye (Lond). 2000 Aug;14 ( Pt 4):625-8 11040911 Nucleic Acids Res. 2010 Jan;38(Database issue):D492-6 19854944 J Biol Chem. 2000 Jan 28;275(4):2607-12 10644720 Hum Genet. 2010 Jan;127(1):33-44 19714363 Ophthalmology. 1995 Oct;102(10):1450-60 9097791 Nucleic Acids Res. 2012 Jan;40(Database issue):D930-4 22064851 Invest Ophthalmol Vis Sci. 2013 Apr 01;54(4):2435-43 23493294 Arch Ophthalmol. 2004 Jan;122(1):17-21 14718289 Br J Ophthalmol. 2010 Aug;94(8):971-6 19556215 Dev Biol. 2001 Dec 15;240(2):419-32 11784073 Hum Genet. 2012 Nov;131(11):1783-93 22814818 Cont Lens Anterior Eye. 2015 Jun;38(3):199-205 25707930 J Biol Chem. 2010 Sep 3;285(36):28141-55 20551313 Hum Mol Genet. 2017 Jan 15;26(2):438-453 28073927 Arch Ophthalmol. 2002 Jun;120(6):714-20; discussion 829-30 12049575 J Invest Dermatol. 2004 Oct;123(4):656-63 15373769 Am J Hum Genet. 2013 Oct 3;93(4):758-64 24094747 Am J Hum Genet. 2011 Jun 10;88(6):767-777 21664999 Nat Commun. 2016 Mar 29;7:11008 27020472 BMC Cancer. 2011 Dec 30;11:529 22208948 Twin Res Hum Genet. 2015 Feb;18(1):86-91 25518859 Bioinformatics. 2010 Sep 1;26(17):2190-1 20616382 Cell. 1997 May 30;89(5):765-71 9182764 Invest Ophthalmol Vis Sci. 2002 Jun;43(6):1757-64 12036976 Surv Ophthalmol. 2015 Sep-Oct;60(5):459-80 26077628 Surv Ophthalmol. 1998 Jan-Feb;42(4):297-319 9493273 Biochem J. 2001 Apr 15;355(Pt 2):271-8 11284712 Nat Genet. 2003 Mar;33(3):331-2 12610545 Eye (Lond). 2010 Jun;24(6):1093-101 20010793 Genet Epidemiol. 2006 Sep;30(6):471-84 16685720 Am J Hum Genet. 2010 Jul 9;87(1):139-45 20598278 J Biol Chem. 2003 Jun 13;278(24):21672-7 12665512 Hum Mol Genet. 2011 Feb 15;20(4):649-58 21098505 Nat Genet. 2013 Jun;45(6):580-5 23715323 Invest Ophthalmol Vis Sci. 2013 Dec 11;54(13):8062-8 24168998 Nat Genet. 2002 Jan;30(1):97-101 11731797 Invest Ophthalmol Vis Sci. 2017 Apr 1;58(4):2106-2116 28395026 Science. 2009 Sep 4;325(5945):1246-50 19644074 Hum Mol Genet. 2015 Sep 1;24(17):5060-8 26049155 Exp Eye Res. 2013 Jun;111:105-11 23500522 Ophthalmic Genet. 2004 Jun;25(2):147-52 15370545 Invest Ophthalmol Vis Sci. 2009 Sep;50(9):4087-90 19420341 Genome Res. 2012 Sep;22(9):1790-7 22955989 Proc Natl Acad Sci U S A. 2003 Sep 30;100(20):11484-9 14500911 Nat Genet. 2012 Mar 18;44(4):369-75, S1-3 22426310 Am J Hum Genet. 2011 Jan 7;88(1):76-82 21167468 J Glaucoma. 2014 Jan;23(1):1-4 22668983 Nucleic Acids Res. 2015 Jan;43(Database issue):D670-81 25428374 Invest Ophthalmol Vis Sci. 2005 Feb;46(2):420-6 15671264 Nucleic Acids Res. 2015 Jan;43(Database issue):D789-98 25428349 Invest Ophthalmol Vis Sci. 2005 Oct;46(10 ):3718-22 16186354 Am J Hum Genet. 1999 Aug;65(2):308-17 10417273 Wang Jie Jin JJ Rochtchina Elena E Attia John J Scott Rodney R Holliday Elizabeth G EG Wong Tien Yin TY Baird Paul N PN Xie Jing J Inouye Michael M Viswanathan Ananth A Sim Xueling X Allingham R Rand RR Brilliant Murray H MH Budenz Donald L DL Christen William G WG Fingert John J Friedman David S DS Gaasterland Douglas D Gaasterland Terry T Hauser Michael A MA Kraft Peter P Lee Richard K RK Lichter Paul R PR Liu Yutao Y Loomis Stephanie J SJ Moroi Sayoko E SE Pericak-Vance Margaret A MA Realini Anthony A Richards Julia E JE Schuman Joel S JS Scott William K WK Singh Kuldev K Sit Arthur J AJ Vollrath Douglas D Weinreb Robert N RN Wollstein Gadi G Zack Donald J DJ Zhang Kang K Donnelly Peter P Barroso Ines I Blackwell Jenefer M JM Bramon Elvira E Brown Matthew A MA Casas Juan P JP Corvin Aiden A Deloukas Panos P Duncanson Audrey A Jankowski Janusz J Markus Hugh S HS Mathew Christopher G CG Palmer Colin N A CNA Plomin Robert R Rautanen Anna A Sawcer Stephen J SJ Trembath Richard C RC Wood Nicholas W NW Spencer Chris C A CCA Band Gavin G Bellenguez Céline C Freeman Colin C Hellenthal Garrett G Giannoulatou Eleni E Pirinen Matti M Pearson Richard R Strange Amy A Su Zhan Z Vukcevic Damjan D Langford Cordelia C Hunt Sarah E SE Edkins Sarah S Gwilliam Rhian R Blackburn Hannah H Bumpstead Suzannah J SJ Dronov Serge S Gillman Matthew M Gray Emma E Hammond Naomi N Jayakumar Alagurevathi A McCann Owen T OT Liddle Jennifer J Potter Simon C SC Ravindrarajah Radhi R Ricketts Michelle M Waller Matthew M Weston Paul P Widaa Sara S Whittaker Pamela P 2017 06 24 2018 03 02 2018 5 16 6 0 2018 5 16 6 0 2018 5 16 6 0 epublish 29760442 10.1038/s41467-018-03646-6 10.1038/s41467-018-03646-6 PMC5951816 29728636 2018 06 27

2045-2322 8 1 2018 May 04 Sci Rep Propyl-5-hydroxy-3-methyl-1-phenyl-1H-pyrazole-4-carbodithioate (HMPC): a new bacteriostatic agent against methicillin-resistant Staphylococcus aureus. 7062 10.1038/s41598-018-25571-w The emergence of Staphylococcus aureus strains resistant to 'last resort' antibiotics compels the development of new antimicrobials against this important human pathogen. We found that propyl 5-hydroxy-3-methyl-1-phenyl-1H-pyrazole-4-carbodithioate (HMPC) shows bacteriostatic activity against S. aureus (MIC = 4 μg/ml) and rescues Caenorhabditis elegans from S. aureus infection. Whole-genome sequencing of S. aureus mutants resistant to the compound, along with screening of a S. aureus promoter-lux reporter array, were used to explore possible mechanisms of action. All mutants resistant to HMPC acquired missense mutations at distinct codon positions in the global transcriptional regulator mgrA, followed by secondary mutations in the phosphatidylglycerol lysyltransferase fmtC/mprF. The S. aureus promoter-lux array treated with HMPC displayed a luminescence profile that was unique but showed similarity to DNA-damaging agents and/or DNA replication inhibitors. Overall, HMPC is a new anti-staphylococcal compound that appears to act via an unknown mechanism linked to the global transcriptional regulator MgrA. Johnston Tatiana T Department of Infectious Disease, Rhode Island Hospital, Alpert Medical School of Brown University, Providence, Rhode Island, USA. Van Tyne Daria D Department of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, USA. Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts, USA. Chen Roy F RF Department of Infectious Disease, Rhode Island Hospital, Alpert Medical School of Brown University, Providence, Rhode Island, USA. Fawzi Nicolas L NL http://orcid.org/0000-0001-5483-0577 Department of Molecular Pharmacology, Physiology, and Biotechnology, Brown University, Providence, Rhode Island, USA. Kwon Bumsup B Department of Neurology, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, RI, 02903, USA. Kelso Michael J MJ http://orcid.org/0000-0001-7809-6637 School of Chemistry and Illawarra Health and Medical Research Institute, University of Wollongong, Wollongong, NSW 2522, Australia. Gilmore Michael S MS Department of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, USA. Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts, USA. Mylonakis Eleftherios E Department of Infectious Disease, Rhode Island Hospital, Alpert Medical School of Brown University, Providence, Rhode Island, USA. emylonakis@lifespan.org. eng P01 AI083214 AI NIAID NIH HHS United States Journal Article 2018 05 04

England Sci Rep 101563288 2045-2322 J Antimicrob Chemother. 2009 Jul;64(1):37-45 19457930 ACS Chem Biol. 2009 Jul 17;4(7):527-33 19572548 Antimicrob Agents Chemother. 2005 Jan;49(1):161-9 15616291 Plasmid. 2009 May;61(3):182-7 19399993 Antimicrob Agents Chemother. 2012 Jul;56(7):3492-7 22491694 J Bacteriol. 2003 Jul;185(13):3703-10 12813062 Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10892-7 11535834 Curr Protoc Chem Biol. 2014 Mar 14;6(1):25-37 24652621 Antimicrob Agents Chemother. 2008 Apr;52(4):1209-14 18250188 Infect Control Hosp Epidemiol. 2010 Nov;31 Suppl 1:S7-10 20929376 J Bacteriol. 2006 Mar;188(5):1899-910 16484201 Essays Biochem. 2017 Mar 3;61(1):71-79 28258231 Clin Infect Dis. 1998 May;26(5):1179-81 9597249 BMC Microbiol. 2015 Oct 24;15:232 26498754 Chem Biol. 2011 Aug 26;18(8):1032-41 21867918 Infect Immun. 2005 Mar;73(3):1423-31 15731040 J Bacteriol. 2003 May;185(10):3127-38 12730173 Science. 2004 Sep 10;305(5690):1629-31 15308764 Open Microbiol J. 2013;7:59-71 23569469 PLoS One. 2014 Nov 19;9(11):e112963 25409509 Nat Protoc. 2008;3(2):163-75 18274517 Antimicrob Agents Chemother. 2004 Dec;48(12):4800-7 15561859 N Engl J Med. 2003 Apr 3;348(14):1342-7 12672861 Microbiology. 2004 Jan;150(Pt 1):45-51 14702396 Nat Rev Microbiol. 2016 Mar;14(3):150-62 26806595 Biol Open. 2014 Jun 27;3(7):644-55 24972867 Science. 1995 Jun 30;268(5219):1899-902 7604262 Microbiol Mol Biol Rev. 2015 Mar;79(1):101-16 25652543 J Antibiot (Tokyo). 2010 Aug;63(8):492-8 20606700 Int J Biochem Cell Biol. 2008;40(3):355-61 18083623 FEMS Microbiol Lett. 1992 Jul 1;73(1-2):133-8 1521761 Curr Microbiol. 2011 May;62(5):1363-7 21234755 FEMS Immunol Med Microbiol. 2004 Jan 15;40(1):1-9 14734180 PLoS One. 2014 Sep 16;9(9):e107426 25226591 Lancet. 2002 May 25;359(9320):1819-27 12044378 Int J Antimicrob Agents. 2003 Sep;22(3):250-3 13678829 Cancer Res. 2015 Sep 1;75(17):3568-82 26100670 Nat Chem Biol. 2006 Nov;2(11):591-5 16980961 J Bacteriol. 2005 Apr;187(7):2395-405 15774883 Antimicrob Agents Chemother. 2011 Jul;55(7):3345-56 21502617 PLoS Pathog. 2016 May 04;12 (5):e1005604 27144398 Nature. 2015 Jan 22;517(7535):455-9 25561178 J Vis Exp. 2013 Mar 09;(73):e50166 23524982 PLoS One. 2014 Apr 09;9(4):e93913 24718609 FEMS Microbiol Lett. 2001 Sep 11;203(1):49-54 11557139 Curr Opin Pharmacol. 2013 Oct;13(5):769-74 23993686 BMC Microbiol. 2010 Mar 04;10:68 20202188 N Engl J Med. 2014 Apr 17;370(16):1524-31 24738669 FEMS Microbiol Rev. 2004 May;28(2):183-200 15109784 PLoS One. 2014 Feb 19;9(2):e89189 24586584 Clin Infect Dis. 2009 Jan 1;48(1):1-12 19035777 J Bacteriol. 2011 May;193(9):2332-5 21378186 Biochim Biophys Acta. 2017 Nov;1862(11):1310-1318 27940309 Expert Rev Vaccines. 2016 Nov;15(11):1373-1392 27118628 Mol Microbiol. 2003 Jun;48(6):1451-66 12791130 Appl Microbiol Biotechnol. 2015 Nov;99(21):9161-76 26252968 Int J Med Microbiol. 2015 Feb;305(2):196-202 25595024 N Engl J Med. 1998 Aug 20;339(8):520-32 9709046 2018 01 24 2018 04 20 2018 5 6 6 0 2018 5 8 6 0 2018 5 8 6 0 epublish 29728636 10.1038/s41598-018-25571-w 10.1038/s41598-018-25571-w PMC5935714 29175509 2018 05 29

1873-1635 64 2018 May Prog Retin Eye Res Retinal energy demands control vascular supply of the retina in development and disease: The role of neuronal lipid and glucose metabolism. 131-156 S1350-9462(17)30074-5 10.1016/j.preteyeres.2017.11.002 Joyal Jean-Sébastien JS Department of Pediatrics, Pharmacology and Ophthalmology, CHU Sainte-Justine Research Center, Université de Montréal, Montreal, Qc, Canada; Department of Pharmacology and Therapeutics, McGill University, Montreal, Qc, Canada. Electronic address: js.joyal@umontreal.ca. Gantner Marin L ML The Lowy Medical Research Institute, La Jolla, United States. Smith Lois E H LEH Department of Ophthalmology, Harvard Medical School, Boston Children's Hospital, 300 Longwood Avenue, Boston MA 02115, United States. Electronic address: lois.smith@childrens.harvard.edu. eng P30 HD018655 HD NICHD NIH HHS United States R01 EY017017 EY NEI NIH HHS United States R24 EY024864 EY NEI NIH HHS United States U54 HD090255 HD NICHD NIH HHS United States Journal Article Review 2017 11 22

England Prog Retin Eye Res 9431859 1350-9462 Annu Rev Pharmacol Toxicol. 2009;49:123-50 18834304 J Biol Chem. 2014 Jul 25;289(30):20570-82 24898254 Br J Ophthalmol. 2013 Jan;97(1):66-9 23093617 Eye (Lond). 2006 Dec;20(12):1408-10 16456588 Am J Pathol. 2010 Jun;176(6):3085-97 20395434 Epilepsia. 2008 Nov;49 Suppl 8:46-9 19049586 Invest Ophthalmol Vis Sci. 1997 Mar;38(3):652-7 9071219 Brain Res. 2012 Jan 13;1432:74-83 22137657 Novartis Found Symp. 2006;272:15-25; discussion 25-36 16686427 Am J Ophthalmol. 1952 May;35(5 2):126-33 14923766 J Clin Invest. 2011 Jul;121(7):2625-40 21670500 Am J Physiol Cell Physiol. 2001 Jun;280(6):C1367-74 11350731 J Neurosci Res. 2015 Jul;93(7):1079-92 25801286 Arch Ophthalmol. 2003 Apr;121(4):547-57 12695252 J Clin Invest. 2007 Oct;117(10):2920-8 17909628 Exp Dermatol. 2006 Dec;15(12):1005-15 17083367 Invest Ophthalmol Vis Sci. 1995 Jun;36(7):1259-70 7775103 J Neurosci. 1995 Jul;15(7 Pt 2):5179-91 7623144 Biochem J. 1975 Mar;146(3):527-35 1147907 Biochim Biophys Acta. 1973 Nov 30;330(1):76-9 4543474 Methods. 2010 Apr;50(4):282-8 20064613 Biol Chem. 2006 Oct-Nov;387(10-11):1337-46 17081104 Acta Ophthalmol Scand. 1997 Feb;75(1):101-3 9088414 J Cell Biol. 2006 Jun 5;173(5):719-31 16735577 Nat Med. 2016 Apr;22(4):439-45 26974308 Prog Retin Eye Res. 2003 Jan;22(1):1-29 12597922 Science. 1999 Mar 5;283(5407):1482-8 10066162 PLoS One. 2015 Jul 10;10(7):e0132643 26161975 Cytokine Growth Factor Rev. 2005 Aug-Oct;16(4-5):535-48 15979925 Novartis Found Symp. 2007;287:60-3; discussion 63-9 18074631 Br J Pharmacol. 2006 Jul;148(5):619-28 16702987 Am J Clin Nutr. 2000 Jan;71(1 Suppl):228S-31S 10617976 Exp Eye Res. 1990 Aug;51(2):167-76 2167231 Arch Ophthalmol. 1996 Oct;114(10 ):1219-28 8859081 Invest Ophthalmol Vis Sci. 2010 Nov;51(11):6009-17 20538989 Eye (Lond). 2010 Mar;24(3):408-15 20075975 Trends Cell Biol. 1998 Sep;8(9):353-8 9728396 Invest Ophthalmol Vis Sci. 2006 Sep;47(9):4072-6 16936126 Circ J. 2015;79(5):934-41 25787231 Trends Neurosci. 2013 Oct;36(10):587-97 23968694 Mol Vis. 2003 Mar 11;9:60-73 12632036 Cell Tissue Res. 2005 Nov;322(2):207-15 16044321 Clin Pharmacol Ther. 2012 Jul;92(1):29-39 22669289 J Lipid Res. 2010 Nov;51(11):3217-29 20688753 Lancet. 2013 Oct 26;382(9902):1445-57 23782686 Invest Ophthalmol Vis Sci. 2009 Mar;50(3):1329-35 18952918 J Clin Invest. 2009 Mar;119(3):611-23 19188685 Invest Ophthalmol Vis Sci. 2010 Jan;51(1):79-88 19696174 Invest Ophthalmol Vis Sci. 2008 Oct;49(10):4613-9 18566456 Ophthalmic Genet. 2012 Dec;33(4):249-52 22686558 Proc Natl Acad Sci U S A. 2014 Oct 28;111(43):15579-84 25313047 Arch Ophthalmol. 1964 Dec;72:792-5 14205438 J Clin Invest. 2012 Nov;122(11):4213-7 23093773 Prog Retin Eye Res. 2016 Mar;51:156-86 26297071 Nat Neurosci. 2009 Jan;12(1):44-52 19060896 J Lipid Res. 2003 Dec;44(12):2221-33 13130128 Invest Ophthalmol Vis Sci. 2011 Aug 01;52(9):6089-95 21051730 J Clin Invest. 2015 Jun;125(6):2335-46 25915585 Invest Ophthalmol Vis Sci. 1989 Apr;30(4):591-9 2539341 J Clin Invest. 1983 Nov;72(5):1737-47 6138367 Biochem Soc Trans. 2009 Dec;37(Pt 6):1228-32 19909252 Nat Med. 2009 Nov;15(11):1298-306 19881493 Proc Natl Acad Sci U S A. 2005 Aug 16;102(33):11900-5 16079201 Br J Ophthalmol. 1963 Jan;47:39-44 14186858 J Pharmacol Exp Ther. 2012 Feb;340(2):483-9 22106100 J Lipid Res. 2010 Jul;51(7):1624-42 20299492 J Cell Biol. 2011 Nov 14;195(4):689-701 22084310 Br J Ophthalmol. 1959 Jan;43(1):34-9 13618528 Physiol Rev. 2009 Apr;89(2):607-48 19342615 Prog Retin Eye Res. 2016 Nov;55:52-81 27260426 Nature. 2004 May 13;429(6988):188-93 15141213 Angiogenesis. 2007;10(2):133-40 17332988 Invest Ophthalmol Vis Sci. 2007 Aug;48(8):3827-36 17652758 Nat Genet. 2008 Oct;40(10):1230-4 18806796 J Lipid Res. 2010 Apr;51(4):685-700 19828910 Sci Rep. 2016 Nov 24;6:37727 27883057 Nat Rev Cancer. 2016 Oct;16(10 ):650-62 27634448 Eur J Clin Nutr. 1998 Feb;52(2):104-9 9505154 Adv Exp Med Biol. 2010;703:105-25 20711710 Genes Dev. 1999 Feb 1;13(3):295-306 9990854 J Lipid Res. 2011 Feb;52(2):245-55 21106902 Proc Natl Acad Sci U S A. 1995 Jan 31;92(3):905-9 7846076 Arch Ophthalmol. 2005 Dec;123(12):1644-50 16344434 Mol Cell Endocrinol. 2007 Jan 15;263(1-2):173-80 17101212 Invest Ophthalmol Vis Sci. 2006 Dec;47(12 ):5553-60 17122148 Invest Ophthalmol Vis Sci. 2000 Apr;41(5):1217-28 10752963 Ophthalmic Genet. 2009 Sep;30(3):109-20 19941415 Curr Neurol Neurosci Rep. 2006 Sep;6(5):403-13 16928351 Cell. 2007 Aug 24;130(4):691-703 17719546 Vet Pathol. 2010 May;47(3):396-413 20382825 Surv Ophthalmol. 2006 May-Jun;51(3):232-58 16644365 Prog Retin Eye Res. 2008 Jul;27(4):372-90 18621565 Nat Med. 2007 Jul;13(7):868-873 17589522 Prog Retin Eye Res. 2015 Mar;45:1-29 25486088 N Engl J Med. 2012 Mar 29;366(13):1227-39 22455417 Mol Genet Metab. 2012 May;106(1):18-24 22459206 J Neurochem. 1960 May;5:253-76 13810977 Curr Opin Neurol. 2003 Feb;16(1):35-43 12544855 Am J Hum Genet. 1972 May;24(3):348-9 5063796 Nutr Diabetes. 2012 Jul 23;2:e36 23448719 J Biol Chem. 1978 Nov 25;253(22):8294-300 711753 Sci STKE. 2007 Oct 09;2007(407):cm8 17925579 Philos Trans R Soc Lond B Biol Sci. 2005 Dec 29;360(1464):2335-45 16321804 Johns Hopkins Med J. 1982 Dec;151(6):344-51 7176294 Alzheimer Dis Assoc Disord. 2007 Oct-Dec;21(4):276-91 18090434 Arch Ophthalmol. 2010 Apr;128(4):443-7 20385939 Science. 1988 Dec 9;242(4884):1427-30 3201231 Nat Protoc. 2009;4(11):1565-73 19816419 Nat Rev Neurol. 2012 Oct;8(10):545-56 22945544 Am J Pathol. 2015 Feb;185(2):581-95 25478809 Physiol Rev. 2005 Jul;85(3):845-81 15987797 Hum Mol Genet. 2015 Dec 15;24(24):6921-31 26410888 Ann N Y Acad Sci. 1982;386:138-52 6953844 Invest Ophthalmol Vis Sci. 2016 Jan 1;57(1):66-80 26780311 Dev Cell. 2009 Feb;16(2):167-79 19217420 Exp Eye Res. 1990 Aug;51(2):159-65 2387334 Prog Clin Biol Res. 1989;312:15-37 2508122 J Biol Chem. 2001 Mar 23;276(12):8934-41 11121409 Cell Metab. 2014 Mar 4;19(3):380-92 24508507 J Gen Physiol. 1981 Jun;77(6):667-92 6267165 Science. 2006 Aug 4;313(5787):640-4 16809490 Invest Ophthalmol Vis Sci. 2006 Jan;47(1):329-35 16384981 Endothelium. 2006 Mar-Apr;13(2):81-91 16728327 Pediatr Res. 1999 Jan;45(1):87-93 9890614 Blood. 2011 Jun 2;117(22):6024-35 21355092 Mol Cell. 2011 Jun 10;42(5):561-8 21658599 J Cell Biol. 2003 Jun 23;161(6):1163-77 12810700 Proc Natl Acad Sci U S A. 2007 Oct 9;104(41):16227-32 17884985 J Biol Chem. 1995 Jun 30;270(26):15747-54 7797576 Physiol Rev. 2010 Jan;90(1):207-58 20086077 Nat Commun. 2015 Mar 04;6:6228 25736573 J Inherit Metab Dis. 2010 Oct;33(5):469-77 20195903 Circ Res. 2010 Aug 20;107(4):495-500 20634487 Blood. 2012 Sep 13;120(11):2182-94 22705597 Ophthalmic Res. 2006;38(2):71-3 16352919 Acta Ophthalmol Scand. 1998 Feb;76(1):6-13 9541428 Nature. 2005 Dec 15;438(7070):960-6 16355161 J Biol Chem. 1956 Jun;220(2):879-92 13331946 Dev Cell. 2009 Feb;16(2):222-31 19217424 J Biol Chem. 1991 Jun 15;266(17 ):10711-4 1710212 Surg Neurol. 1989 Mar;31(3):177-82 2922659 Circ Res. 1999 Oct 15;85(8):699-706 10521243 Exp Eye Res. 2008 Dec;87(6):561-70 18848932 EBioMedicine. 2016 Nov;13:201-211 27720395 J Clin Invest. 2008 Feb;118(2):526-33 18219389 J Exp Med. 2011 Feb 14;208(2):313-26 21242296 Am J Ophthalmol. 1997 Jun;123(6):846-8 9535636 Mol Vis. 2016 Jul 23;22:847-85 27499608 J Child Neurol. 2009 Oct;24(10):1310-5 19332571 PLoS One. 2011 Feb 22;6(2):e16733 21364932 J Cell Sci. 2010 Nov 1;123(Pt 21):3639-44 20923839 Science. 1976 Dec 3;194(4269):1071-4 982063 Invest Ophthalmol Vis Sci. 1997 Jan;38(1):62-71 9008631 Lancet. 2012 May 5;379(9827):1728-38 22559899 Cell Mol Life Sci. 2013 May;70(10):1675-84 23475065 Invest Ophthalmol Vis Sci. 2000 Sep;41(10):3183-90 10967082 Invest Ophthalmol Vis Sci. 1992 Sep;33(10):2798-808 1526729 Pediatr Res. 2004 Nov;56(5):744-50 15347768 Neurosci Res. 2007 Aug;58(4):394-401 17583366 Mol Microbiol. 1999 Jun;32(5):1002-12 10361302 Glia. 2010 Aug;58(10 ):1177-85 20544853 Nat Med. 2014 Oct;20(10):1165-73 25216639 Biochim Biophys Acta. 2014 Aug;1837(8):1330-7 24699309 Exp Physiol. 2006 Sep;91(5):807-19 16857720 J Cell Biol. 1987 Mar;104(3):483-90 3818789 Shock. 2001 Apr;15(4):297-301 11303729 Nat Genet. 2017 Apr;49(4):559-567 28250457 J Neurosci. 1984 Oct;4(10):2445-59 6092560 Lancet. 2012 Apr 14;379(9824):1403-11 22374408 Cancer Cell. 2003 Jul;4(1):19-29 12892710 Cell. 2014 Oct 23;159(3):584-96 25417109 Invest Ophthalmol Vis Sci. 2009 Jun;50(6):2966-74 19151382 Invest Ophthalmol Vis Sci. 1997 Jan;38(1):48-55 9008629 Biochim Biophys Acta. 2009 Jul;1791(7):573-83 19230850 Nat Med. 2008 Oct;14(10):1067-76 18836459 Acta Ophthalmol (Copenh). 1975 Sep;53(4):610-9 1242281 Adv Exp Med Biol. 1979;111:169-88 371355 Retina. 2003 Jun;23(3):387-91 12824841 Prog Retin Eye Res. 2003 Nov;22(6):721-48 14575722 J Biol Chem. 2008 Jun 13;283(24):16269-73 18385136 Cell. 2005 Feb 25;120(4):483-95 15734681 Nature. 2000 Jul 13;406(6792):195-9 10910361 Development. 2008 Nov;135(21):3567-76 18832390 Pediatr Res. 2000 Oct;48(4):524-30 11004245 Nat Rev Genet. 2010 Apr;11(4):273-84 20212494 Prog Retin Eye Res. 2017 Jan;56:32-57 27671171 PLoS One. 2015 Oct 14;10 (10 ):e0139664 26466127 Resuscitation. 1997 Oct;35(2):165-70 9316202 J Clin Invest. 1977 Jul;60(1):265-70 874089 Circ Res. 2010 Oct 29;107(9):1058-70 21030723 Br J Ophthalmol. 2010 Jan;94(1):121-7 20385529 Retina. 2012 Feb;32 Suppl 1:450-60 22451954 Am J Perinatol. 2016 Sep;33(11):1067-71 27603537 Brain. 2014 Feb;137(Pt 2):335-53 24369379 J Lipids. 2011;2011:189876 21773049 Invest Ophthalmol Vis Sci. 2013 Nov 15;54(12):7567-77 24150756 J Comp Neurol. 1990 Feb 22;292(4):497-523 2324310 Dev Cell. 2009 Feb;16(2):209-21 19217423 Elife. 2016 Mar 15;5: 26978795 Invest Ophthalmol Vis Sci. 2004 Jan;45(1):7-14 14691147 Prog Retin Eye Res. 2008 Nov;27(6):596-607 18848639 Trends Endocrinol Metab. 2003 Jul;14(5):201-3 12826323 Histochem Cell Biol. 2010 Dec;134(6):565-79 21046137 Proc Natl Acad Sci U S A. 2004 Sep 21;101(38):13850-5 15365174 J Neurosci. 1992 Mar;12(3):840-53 1312136 Prog Retin Eye Res. 2015 Nov;49:67-81 26113211 Early Hum Dev. 2016 Nov;102:13-19 27650433 Clin Exp Ophthalmol. 2013 May-Jun;41(4):396-403 22957991 Cell Metab. 2010 Dec 1;12(6):662-7 21109198 J Child Neurol. 2002 Dec;17 Suppl 3:3S15-23; discussion 3S24-5 12597052 Arterioscler Thromb Vasc Biol. 2016 Sep;36(9):1919-27 27417579 Proc Nutr Soc. 1997 Jul;56(2):731-7 9264123 J Biol Chem. 2011 May 6;286(18):16229-37 21454496 Environ Mol Mutagen. 2010 Jun;51(5):417-26 20544882 Proc Natl Acad Sci U S A. 2008 Sep 2;105(35):12843-8 18728184 Exp Eye Res. 1970 Oct;10(2):339-44 4320824 Lancet. 2006 Nov 18;368(9549):1795-809 17113430 Brain Res. 1974 Nov 15;80(2):265-79 4154061 Mol Pharmacol. 2005 May;67(5):1385-7 15703375 Oncogene. 2006 Aug 7;25(34):4675-82 16892081 Invest Ophthalmol Vis Sci. 2003 Sep;44(9):3911-9 12939309 Pediatr Res. 2005 Jun;57(6):755-9 15845636 Neurobiol Aging. 2006 Jul;27(7):983-93 15979212 Prog Clin Biol Res. 1989;312:95-112 2529559 Diabet Med. 2001 Nov;18(11):883-8 11703432 PLoS One. 2012;7(2):e31243 22355348 Cell. 2015 May 7;161(4):817-32 25957687 J Biol Chem. 2016 Feb 26;291(9):4698-710 26677218 J Biol Chem. 2003 Mar 28;278(13):11303-11 12496284 Prog Retin Eye Res. 2001 Mar;20(2):175-208 11173251 Lab Invest. 2000 Apr;80(4):545-55 10780671 Invest Ophthalmol Vis Sci. 1995 Mar;36(3):579-85 7890489 Exp Eye Res. 1991 Oct;53(4):437-46 1834476 Invest Ophthalmol Vis Sci. 2008 Apr;49(4):1660-4 18385088 Cell Stem Cell. 2017 May 4;20(5):635-647.e7 28132833 Hum Mol Genet. 2001 Jan 1;10(1):63-8 11136715 Nippon Ganka Gakkai Zasshi. 1994 May;98(5):469-76 8197917 Nat Chem Biol. 2016 Jul 19;12 (8):577-8 27434766 Methods Mol Biol. 2010;652:163-76 20552428 J Clin Invest. 2010 Sep;120(9):3022-32 20811158 Adv Exp Med Biol. 2012;942:287-308 22399428 Acta Paediatr. 2012 Aug;101(8):819-26 22497252 Br J Ophthalmol. 2000 May;84(5):534-5 10781521 Am J Clin Nutr. 2015 Apr;101(4):879-88 25833984 Proc Natl Acad Sci U S A. 1989 Apr;86(8):2903-7 2523075 Am J Physiol Endocrinol Metab. 2009 Sep;297(3):E578-91 19531645 Nature. 2013 Feb 14;494(7436):243-6 23334418 Cell Metab. 2005 Apr;1(4):245-58 16054069 J Biol Chem. 1987 Jan 25;262(3):1180-6 3805016 Ophthalmology. 2017 Jun;124(6):843-850 28196731 J Biol Chem. 2003 Mar 28;278(13):11312-9 12496283 J Clin Pharmacol. 2012 Jul;52(7):1007-16 21610201 Curr Eye Res. 2005 Nov;30(11):959-68 16282130 Retina. 2003 Aug;23(4):518-22 12972764 Aging (Albany NY). 2011 Jan;3(1):44-54 21191149 Exp Eye Res. 1995 Sep;61(3):273-84 7556491 Exp Eye Res. 1961 Dec;1:128-36 13880203 Retina. 2012 May;32(5):996-1006 22266930 Biochem Soc Trans. 2009 Feb;37(Pt 1):291-4 19143649 Therapie. 1997 Sep-Oct;52(5):447-51 9501573 J Biol Chem. 1998 Mar 6;273(10):5678-84 9488698 Pediatr Res. 2002 Oct;52(4):595-600 12357056 Hippocampus. 2011 Feb;21(2):162-71 20014382 Nat Cell Biol. 2012 Aug;14(8):859-64 22750943 J Biol Chem. 2007 Nov 23;282(47):34420-8 17890782 Biophys J. 1970 May;10(5):380-412 5439318 Dev Biol. 2000 Jul 15;223(2):383-98 10882523 Nat Rev Cancer. 2005 Nov;5(11):857-66 16327764 Invest Ophthalmol Vis Sci. 2012 Nov 09;53(12):7608-17 23060142 Arch Ophthalmol. 1984 Jul;102(7):981-9 6743093 Arterioscler Thromb Vasc Biol. 2014 Mar;34(3):581-6 24458713 Acta Ophthalmol. 2011 Feb;89(1):82-90 19764912 Nat Med. 1995 Oct;1(10):1024-8 7489357 Clin Exp Ophthalmol. 2015 May-Jun;43(4):367-76 25330055 Prog Retin Eye Res. 2004 Jan;23(1):53-89 14766317 Am J Ophthalmol. 2000 Dec;130(6):803-12 11124301 Diabet Med. 2007 Jun;24(6):582-6 17490424 Mol Endocrinol. 2013 Aug;27(8):1188-97 23820899 Proc Natl Acad Sci U S A. 2006 Jul 25;103(30):11282-7 16844785 Invest Ophthalmol Vis Sci. 2006 Dec;47(12 ):5561-8 17122149 Development. 2010 May;137(9):1563-71 20388654 Prog Retin Eye Res. 2017 Nov;61:98-128 28602950 Invest Ophthalmol Vis Sci. 2000 Feb;41(2):537-45 10670486 Nat Med. 2003 Nov;9(11):1390-7 14566334 Graefes Arch Clin Exp Ophthalmol. 2017 Jul;255 (7):1287-1295 28314954 J Cell Biol. 1963 May;17 :279-88 13976534 Nat Rev Mol Cell Biol. 2004 May;5(5):343-54 15122348 J Neurol Neurosurg Psychiatry. 1997 Jul;63(1):16-22 9221962 Prog Neurobiol. 2008 Feb;84(2):105-15 18191887 Science. 2009 May 22;324(5930):1029-33 19460998 Cell. 2002 Jun 14;109(6):693-705 12086669 Nat Genet. 2008 Jul;40(7):892-6 18511946 Proc Natl Acad Sci U S A. 2001 May 8;98(10):5804-8 11331770 J Appl Physiol. 1964 Sep;19:914-8 14207744 PLoS One. 2012;7(2):e30874 22348027 J Biol Chem. 2003 Jan 17;278(3):1932-5 12409290 Am J Physiol Heart Circ Physiol. 2003 Jun;284(6):H2083-90 12560212 Retina. 2012 Feb;32(2):265-74 21968508 J Clin Invest. 2011 Jan;121(1):369-83 21135502 Can J Physiol Pharmacol. 1992;70 Suppl:S158-64 1295666 J Biol Chem. 2012 Jan 13;287(3):1642-8 22074929 Am J Ophthalmol. 2014 Nov;158(5):1071-78 25089351 Ann N Y Acad Sci. 2006 Aug;1073:208-20 17102089 J Mol Biol. 2001 Mar 30;307(3):799-813 11273702 J Lipid Res. 2004 Aug;45(8):1475-81 15145981 Oncogene. 2006 Aug 7;25(34):4777-86 16892090 Invest Ophthalmol Vis Sci. 2009 Sep;50(9):4394-401 19264893 Acta Ophthalmol Scand. 1997 Jun;75(3):227-31 9253962 Eye Brain. 2016 May 20;8:91-102 28539804 J Mol Neurosci. 2001 Apr-Jun;16(2-3):205-14; discussion 215-21 11478376 Nat Med. 1999 Dec;5(12):1390-5 10581081 J Biol Chem. 2006 Mar 31;281(13):8716-23 16410253 J Clin Invest. 2002 Dec;110(11):1615-7 12464666 Curr Biol. 2008 Dec 23;18(24):1917-21 19084410 Lipids. 1996 Mar;31 Suppl:S193-7 8729118 J Physiol. 2003 Sep 15;551(Pt 3):787-99 12876212 Curr Eye Res. 2011 Dec;36(12):1069-77 21978133 J Neurochem. 2011 May;117(4):735-46 21395585 Nat Med. 2003 Jun;9(6):781-8 12730690 J Clin Invest. 2002 Feb;109(3):327-36 11827992 Brain Res. 2010 May 12;1330:1-8 20211608 Invest Ophthalmol Vis Sci. 2011 May 18;52(6):3436-45 21357400 Angiogenesis. 2007;10(2):77-88 17322966 J Lipid Res. 2002 May;43(5):772-84 11971949 Cell Metab. 2015 Oct 6;22(4):560-75 26278049 Cell Rep. 2016 Apr 12;15(2):372-85 27050517 Biochem Pharmacol. 2014 Apr 15;88(4):584-93 24316434 Cardiovasc Res. 2000 Aug 18;47(3):489-509 10963722 Nature. 2016 Apr 7;532(7597):112-6 27027295 Invest Ophthalmol Vis Sci. 2009 Dec;50(12):5934-43 19578022 Prog Retin Eye Res. 2017 May;58:115-151 28109737 Arch Ophthalmol. 1983 Jul;101(7):1059-68 6870629 Ophthalmologica. 2006;220(1):31-6 16374046 J Pharmacol Exp Ther. 2011 Oct;339(1):228-37 21752941 PLoS One. 2010 Jul 29;5(7):e11863 20686684 Nat Med. 2003 Jun;9(6):677-84 12778166 Dev Dyn. 1998 Nov;213(3):322-33 9825867 Proc Natl Acad Sci U S A. 2012 Dec 4;109(49):20065-70 23129651 PLoS One. 2012;7(11):e50231 23166839 Nature. 2003 Mar 13;422(6928):173-6 12629551 Int Ophthalmol. 1983 Feb;6(2):101-7 6403480 Invest Ophthalmol Vis Sci. 1995 Jun;36(7):1201-14 7775098 Br J Ophthalmol. 1959 Aug;43:486-93 13829137 Vision Res. 1998 May;38(10):1455-77 9667011 Neurobiol Aging. 1986 Jan-Feb;7(1):23-9 3951656 Nature. 2005 Sep 15;437(7057):417-21 16163358 J Neurochem. 1991 Nov;57(5):1690-9 1833510 Am J Pathol. 1997 Sep;151(3):707-14 9284819 Proc Natl Acad Sci U S A. 2010 May 11;107(19):8599-604 20445106 Vis Neurosci. 2002 Jul-Aug;19(4):395-407 12511073 Invest Ophthalmol Vis Sci. 2016 Nov 1;57(14 ):6360-6366 27898981 Int J Dev Biol. 2004;48(8-9):1045-58 15558494 Invest Ophthalmol Vis Sci. 2014 Jan 21;55(1):424-39 24334447 Neuron. 1996 Dec;17(6):1117-31 8982160 Biochem J. 1986 Apr 15;235(2):607-10 3741408 Invest Ophthalmol Vis Sci. 2009 Apr;50(4):1831-7 18997086 PLoS One. 2011 Apr 29;6(4):e19456 21559389 Cell. 2010 Sep 3;142(5):687-98 20813258 Prog Lipid Res. 1983;22(2):79-131 6348799 Exp Eye Res. 2005 Jun;80(6):745-51 15939030 Expert Opin Ther Targets. 2015 Jun;19(6):717-21 25976229 J Clin Invest. 2010 Sep;120(9):3033-41 20811159 Am J Pathol. 2002 Feb;160(2):711-9 11839592 Am J Clin Nutr. 2017 Jul;106(1):16-26 28515072 Prog Retin Eye Res. 2005 Jan;24(1):87-138 15555528 J Biol Chem. 1961 Oct;236:2813-20 14466982 N Engl J Med. 1970 Mar 19;282(12):668-75 4915800 Acta Physiol Scand. 1997 May;160(1):75-81 9179314 Curr Opin Ophthalmol. 2009 Sep;20(5):369-76 19587596 Prog Retin Eye Res. 2006 May;25(3):277-95 16515881 Curr Opin Ophthalmol. 2011 Sep;22(5):325-31 21730846 Prog Retin Eye Res. 2018 Jan;62:24-37 28962928 Mol Aspects Med. 2012 Aug;33(4):295-317 22542780 Horm Metab Res. 1993 Jan;25(1):9-12 8428713 J Gen Physiol. 1986 Oct;88(4):521-42 3783124 J Gen Physiol. 1992 Feb;99(2):177-97 1613482 Subcell Biochem. 2013;69:23-44 23821141 FASEB J. 2001 May;15(7):1215-7 11344092 Endothelium. 2005 Jan-Apr;12(1-2):63-72 16036317 Exp Eye Res. 2014 Sep;126:77-84 24485945 Prog Retin Eye Res. 2018 Jan;62:77-119 28958885 Arterioscler Thromb. 1992 Mar;12 (3):369-79 1532127 AMA Arch Ophthalmol. 1958 Aug;60(2):280-9 13558799 Physiology (Bethesda). 2004 Dec;19:348-54 15546852 Mol Aspects Med. 2012 Aug;33(4):487-509 22705444 Mol Cell Proteomics. 2011 Mar;10(3):M110.002469 21173383 Nature. 2005 Jul 14;436(7048):193-200 16015319 Nature. 1964 Feb 8;201:615-6 14160652 Vascul Pharmacol. 2012 Nov-Dec;57(5-6):133-8 22609133 Prostaglandins Other Lipid Mediat. 2009 Sep;89(3-4):82-8 19460454 J AAPOS. 2008 Jun;12(3):221-2 18396079 Am J Physiol. 1996 Apr;270(4 Pt 1):E733-8 8928782 Physiology (Bethesda). 2011 Jun;26(3):192-205 21670165 J Neurosci. 1995 Jul;15(7 Pt 1):4738-47 7623107 Biochim Biophys Acta. 2010 Mar;1801(3):272-80 20064629 Br J Ophthalmol. 2010 Sep;94(9):1127-32 19666930 Mol Genet Metab. 2016 Mar;117(3):313-21 26750748 J Neurosci. 1989 Dec;9(12):4416-29 2480402 Semin Fetal Neonatal Med. 2013 Feb 18;:null 23428885 Biochemistry (Mosc). 2005 Jul;70(7):726-9 16097935 Sci Transl Med. 2011 Feb 9;3(69):69ra12 21307302 Horm Metab Res. 2005 Apr;37 Suppl 1:39-43 15918109 Elife. 2017 Jun 09;6: 28598329 Brain. 2016 Mar;139(Pt 3):e17 26657166 Neurology. 1984 Nov;34(11):1482-4 6493496 2017 08 03 2017 11 11 2017 11 15 2018 11 01 2017 11 28 6 0 2017 11 28 6 0 2017 11 28 6 0 ppublish 29175509 S1350-9462(17)30074-5 10.1016/j.preteyeres.2017.11.002 PMC5963988 NIHMS935410 29787481 2018 05 27

1530-0374 2018 May 21 Menopause Sex hormone levels and risk of primary open-angle glaucoma in postmenopausal women. 10.1097/GME.0000000000001120 We evaluated the relation of prediagnostic sex hormone levels in postmenopausal women with primary open-angle glaucoma (POAG) and intraocular pressure (IOP). Among postmenopausal participants of the Nurses' Health Study, POAG cases (n = 189; diagnosed 1990-2008) and controls (n = 189) were matched on age, fasting status, and postmenopausal hormone use at blood draw (1989-1990). Plasma concentrations of estrone sulfate, estradiol, testosterone, sex hormone binding globulin, and dehydroepiandrosterone sulfate were assessed. The primary outcome was POAG; in secondary analyses, among cases only, we evaluated maximum untreated IOP at diagnosis. Multivariable-adjusted logistic/multiple linear regression models were used to evaluate tertiles (Ts) of biomarker levels and the two outcomes, adjusting for various potential confounders. We observed no significant associations of estrone, estradiol, sex hormone binding globulin, or dehydroepiandrosterone sulfate with POAG risk or with maximum IOP at glaucoma diagnosis among cases. Suggestive significant associations were observed with highest testosterone and POAG risk (T3 vs T1 multivariable-adjusted odds ratio 1.84; 95% confidence interval 1.02, 3.33; P trend 0.10). Similarly, for maximum IOP at diagnosis among cases only (mean 8 years after blood draw), higher testosterone was significantly associated with higher IOP (multivariable-adjusted difference in IOP T3 vs T1 2.17 mm Hg; 95% confidence interval 0.34, 3.99; P trend 0.02). Overall, plasma sex hormone levels in postmenopausal women were not associated with POAG risk; however, a trend of higher testosterone levels being associated with higher POAG risk and higher IOP at diagnosis was observed and needs confirmation. Kang Jae Hee JH Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, MA. Rosner Bernard A BA Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, MA. Department of Biostatistics, Harvard T. H. Chan School of Public Health, Boston, MA. Wiggs Janey L JL Department of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston, MA. Pasquale Louis R LR Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, MA. Department of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston, MA. eng UM1 CA186107 CA NCI NIH HHS United States R01 EY015473 EY NEI NIH HHS United States R01 EY009611 EY NEI NIH HHS United States R21 EY022766 EY NEI NIH HHS United States R01 CA049449 CA NCI NIH HHS United States Journal Article 2018 05 21

United States Menopause 9433353 1072-3714 2018 5 23 6 0 2018 5 23 6 0 2018 5 23 6 0 aheadofprint 29787481 10.1097/GME.0000000000001120 29785010 2018 06 13

1546-1718 50 6 2018 Jun Nat. Genet. Genome-wide analyses identify 68 new loci associated with intraocular pressure and improve risk prediction for primary open-angle glaucoma. 778-782 10.1038/s41588-018-0126-8 Glaucoma is the leading cause of irreversible blindness globally ¹ . Despite its gravity, the disease is frequently undiagnosed in the community ² . Raised intraocular pressure (IOP) is the most important risk factor for primary open-angle glaucoma (POAG)^3,4. Here we present a meta-analysis of 139,555 European participants, which identified 112 genomic loci associated with IOP, 68 of which are novel. These loci suggest a strong role for angiopoietin-receptor tyrosine kinase signaling, lipid metabolism, mitochondrial function and developmental processes underlying risk for elevated IOP. In addition, 48 of these loci were nominally associated with glaucoma in an independent cohort, 14 of which were significant at a Bonferroni-corrected threshold. Regression-based glaucoma-prediction models had an area under the receiver operating characteristic curve (AUROC) of 0.76 in US NEIGHBORHOOD study participants and 0.74 in independent glaucoma cases from the UK Biobank. Genetic-prediction models for POAG offer an opportunity to target screening and timely therapy to individuals most at risk. Khawaja Anthony P AP http://orcid.org/0000-0001-6802-8585 NIHR Biomedical Research Centre, Moorfields Eye Hospital NHS Foundation Trust and UCL Institute of Ophthalmology, London, UK. Department of Public Health and Primary Care, Institute of Public Health, University of Cambridge School of Clinical Medicine, Cambridge, UK. Cooke Bailey Jessica N JN http://orcid.org/0000-0002-4001-8702 Department of Population and Quantitative Health Sciences, Institute for Computational Biology, Case Western Reserve University School of Medicine, Cleveland, OH, USA. Wareham Nicholas J NJ MRC Epidemiology Unit, University of Cambridge School of Clinical Medicine, Institute of Metabolic Science, Cambridge Biomedical Campus, Cambridge, UK. Scott Robert A RA MRC Epidemiology Unit, University of Cambridge School of Clinical Medicine, Institute of Metabolic Science, Cambridge Biomedical Campus, Cambridge, UK. Simcoe Mark M http://orcid.org/0000-0003-2432-0810 Department of Ophthalmology, King's College London, St. Thomas' Hospital, London, UK. Department of Twin Research & Genetic Epidemiology, King's College London, St. Thomas' Hospital, London, UK. Igo Robert P RP Jr Department of Population and Quantitative Health Sciences, Institute for Computational Biology, Case Western Reserve University School of Medicine, Cleveland, OH, USA. Song Yeunjoo E YE Department of Population and Quantitative Health Sciences, Institute for Computational Biology, Case Western Reserve University School of Medicine, Cleveland, OH, USA. Wojciechowski Robert R Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA. Johns Hopkins Wilmer Eye Institute, Baltimore, MD, USA. Cheng Ching-Yu CY Singapore Eye Research Institute, Singapore National Eye Centre, Singapore, Singapore. Department of Ophthalmology, National University of Singapore and National University Health System, Singapore, Singapore. Ophthalmology & Visual Sciences Academic Clinical Program (Eye-ACP), Duke-NUS Medical School, Singapore, Singapore. Khaw Peng T PT NIHR Biomedical Research Centre, Moorfields Eye Hospital NHS Foundation Trust and UCL Institute of Ophthalmology, London, UK. Pasquale Louis R LR http://orcid.org/0000-0002-5835-3496 Department of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston, MA, USA. Haines Jonathan L JL http://orcid.org/0000-0002-4351-4728 Department of Population and Quantitative Health Sciences, Institute for Computational Biology, Case Western Reserve University School of Medicine, Cleveland, OH, USA. Foster Paul J PJ http://orcid.org/0000-0002-4755-177X NIHR Biomedical Research Centre, Moorfields Eye Hospital NHS Foundation Trust and UCL Institute of Ophthalmology, London, UK. Division of Genetics and Epidemiology, UCL Institute of Ophthalmology, London, UK. Wiggs Janey L JL http://orcid.org/0000-0003-1890-3278 Department of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston, MA, USA. janey_wiggs@meei.harvard.edu. Hammond Chris J CJ http://orcid.org/0000-0002-3227-2620 Department of Ophthalmology, King's College London, St. Thomas' Hospital, London, UK. chris.hammond@kcl.ac.uk. Hysi Pirro G PG http://orcid.org/0000-0001-5752-2510 Department of Ophthalmology, King's College London, St. Thomas' Hospital, London, UK. pirro.hysi@kcl.ac.uk. Department of Twin Research & Genetic Epidemiology, King's College London, St. Thomas' Hospital, London, UK. pirro.hysi@kcl.ac.uk. UK Biobank Eye and Vision Consortium NEIGHBORHOOD Consortium eng R01 EY011671 EY NEI NIH HHS United States U01 HG004728 HG NHGRI NIH HHS United States U01 HG004446 HG NHGRI NIH HHS United States R21 EY028671 EY NEI NIH HHS United States UL1 TR000427 TR NCATS NIH HHS United States R01 EY011008 EY NEI NIH HHS United States P01 CA087969 CA NCI NIH HHS United States R01 HL043851 HL NHLBI NIH HHS United States P01 HL073042 HL NHLBI NIH HHS United States U01 HG004424 HG NHGRI NIH HHS United States R01 HL073389 HL NHLBI NIH HHS United States R01 EY012118 EY NEI NIH HHS United States R01 EY015543 EY NEI NIH HHS United States R56 EY011671 EY NEI NIH HHS United States U01 HG006389 HG NHGRI NIH HHS United States R01 EY008208 EY NEI NIH HHS United States R01 EY013178 EY NEI NIH HHS United States R01 EY019126 EY NEI NIH HHS United States R03 EY015682 EY NEI NIH HHS United States R01 EY022305 EY NEI NIH HHS United States P20 RR015574 RR NCRR NIH HHS United States UM1 CA186107 CA NCI NIH HHS United States R01 EY015473 EY NEI NIH HHS United States R01 CA047988 CA NCI NIH HHS United States R01 HL080467 HL NHLBI NIH HHS United States UM1 CA167552 CA NCI NIH HHS United States R01 EY009580 EY NEI NIH HHS United States Wellcome Trust United Kingdom U10 EY012118 EY NEI NIH HHS United States R01 CA049449 CA NCI NIH HHS United States R01 CA131332 CA NCI NIH HHS United States P30 EY014104 EY NEI NIH HHS United States R01 EY015872 EY NEI NIH HHS United States R01 EY009847 EY NEI NIH HHS United States R01 EY010886 EY NEI NIH HHS United States U01 CA049449 CA NCI NIH HHS United States U01 HG004608 HG NHGRI NIH HHS United States R01 EY013315 EY NEI NIH HHS United States R01 EY018660 EY NEI NIH HHS United States Journal Article 2018 05 21

United States Nat Genet 9216904 1061-4036 Am J Hum Genet. 2013 Aug 8;93(2):264-77 24144296 Br J Ophthalmol. 2012 May;96(5):614-8 22133988 Expert Opin Ther Targets. 2014 May;18(5):527-39 24579961 Biometrics. 1999 Dec;55(4):997-1004 11315092 Mol Vis. 2011;17:1929-39 21850167 Nat Genet. 2006 Aug;38(8):904-9 16862161 Hum Mutat. 2013 Sep;34(9):1195-9 23818446 Ophthalmology. 2016 Apr;123(4):771-82 26795295 Nat Genet. 2010 Jul;42(7):565-9 20562875 J Cataract Refract Surg. 2005 Jan;31(1):156-62 15721708 Nat Genet. 2015 Mar;47(3):291-5 25642630 Am J Hum Genet. 2009 May;84(5):664-71 19361779 Exp Eye Res. 2018 Feb;167:91-99 27914989 J Clin Invest. 2014 Oct;124(10 ):4320-4 25202984 J Clin Invest. 2016 Jul 1;126(7):2575-87 27270174 J Clin Invest. 2014 Sep;124(9):3975-86 25061878 Nat Genet. 2014 Oct;46(10):1115-9 25173107 Nat Genet. 2016 May;48(5):556-62 27064256 Development. 2015 Sep 1;142(17):3009-20 26253404 Br J Cancer. 1999 Jul;80 Suppl 1:95-103 10466767 Hum Mol Genet. 2017 Jan 15;26(2):438-453 28073927 Am J Hum Genet. 2011 Aug 12;89(2):334-43 21835309 Nat Commun. 2017 Dec 13;8(1):2108 29235454 Nat Genet. 2014 Oct;46(10 ):1126-1130 25173106 Nucleic Acids Res. 2012 Jan;40(1):65-74 21908408 Nat Genet. 2014 Oct;46(10 ):1120-1125 25173105 Bioinformatics. 2010 Sep 1;26(17):2190-1 20616382 PLoS Genet. 2012;8(5):e1002611 22570627 Am J Ophthalmol. 2002 Jan;133(1):19-28 11755836 Am J Ophthalmol. 2007 Oct;144(4):511-9 17893012 Nat Genet. 2015 Nov;47(11):1236-41 26414676 Int J Epidemiol. 1997;26 Suppl 1:S6-14 9126529 J Glaucoma. 2001 Jun;10(3):177-83 11442179 Nat Genet. 2013 Jun;45(6):580-5 23715323 Nat Genet. 2015 Mar;47(3):284-90 25642633 Dev Biol. 2002 Aug 15;248(2):265-80 12167403 PLoS Biol. 2014 Jul 22;12 (7):e1001912 25051267 Ophthalmology. 2005 Sep;112(9):1487-93 16039716 Nat Genet. 2016 Feb;48(2):189-94 26752265 Nucleic Acids Res. 2017 Jan 4;45(D1):D896-D901 27899670 Nat Genet. 2012 Mar 18;44(4):369-75, S1-3 22426310 Nat Genet. 2015 Sep;47(9):1091-8 26258848 Am J Hum Genet. 2011 Jan 7;88(1):76-82 21167468 J Glaucoma. 2013 Sep;22(7):517-25 22828004 Semin Ophthalmol. 2013 May;28(3):185-90 23697622 PLoS Genet. 2012;8(4):e1002654 22570617 Surv Ophthalmol. 2010 Nov-Dec;55(6):561-83 20851442 Ophthalmology. 2007 Nov;114(11):1965-72 17628686 Hum Mol Genet. 2017 Aug 1;26(R1):R21-R27 28505344 Ophthalmology. 2005 Jul;112(7):1177-85 15921747 Nucleic Acids Res. 2012 Jul;40(Web Server issue):W65-70 22544707 Int J Epidemiol. 2014 Aug;43(4):1063-72 23771720 PLoS One. 2013 Apr 09;8(4):e60950 23585864 Clin Sci (Lond). 2017 Jan 1;131(1):87-103 27941161 Lancet. 2015 Apr 4;385(9975):1295-304 25533656 BMC Bioinformatics. 2010 Mar 16;11:134 20233392 BMC Bioinformatics. 2010 May 28;11:288 20509871 BMJ Open. 2013 Mar 19;3(3):null 23516272 Invest Ophthalmol Vis Sci. 2016 Sep 1;57(11):5046-5052 27661856 PLoS Genet. 2010 Aug 12;6(8):null 20714348 2017 08 31 2018 03 27 2018 11 21 2018 5 23 6 0 2018 5 23 6 0 2018 5 23 6 0 ppublish 29785010 10.1038/s41588-018-0126-8 10.1038/s41588-018-0126-8 PMC5985943 EMS76895 29505774 2018 04 24

1879-1891 189 2018 May Am. J. Ophthalmol. Subtarsal Fibrosis Is Associated With Ocular Surface Epitheliopathy in Graft-Versus-Host Disease. 102-110 S0002-9394(18)30095-3 10.1016/j.ajo.2018.02.020 To evaluate occurrence of subtarsal fibrosis in patients with graft-vs-host disease (GVHD) and to determine its association with ocular surface epitheliopathy. Cross-sectional study. We enrolled 40 patients with moderate or severe dry eye disease, including 20 patients with chronic ocular GVHD and 20 patients without (as the control group). All patients had a comprehensive ophthalmic assessment including evaluation for subtarsal fibrosis, corneal and conjunctival staining, tear break-up time (TBUT), and Schirmer test. Furthermore, meibomian gland drop-out area and densities of epithelial and stromal immune cells were measured using meibography and in vivo confocal microscopy, respectively. Subtarsal fibrosis was not seen in any eye of the non-GVHD group. However, 16 eyes (40%) of 10 patients (50%) in the GVHD group had subtarsal fibrosis (P < .001) with an average involvement of 28.9% ± 13.7% of the tarsal area. Fibrosis was more frequent in the upper lids (35%) than in the lower lids (5%). Regression analyses showed that corneal fluorescein staining was significantly associated with the extent of fibrosis (P < .001, β = 0.14) and TBUT (P < .001, β = -0.53) but not with other clinical or imaging parameters. Conjunctival lissamine green staining also had a statistically significant association with the extent of fibrosis (P = .04, β = 0.12) but not other clinical or imaging parameters. Eyes with subtarsal fibrosis had a more severe ocular surface epitheliopathy compared with eyes without fibrosis. Subtarsal fibrosis is present in a significant percentage of patients with chronic ocular GVHD, likely contributing to the ocular surface damage in these patients. Copyright © 2018 Elsevier Inc. All rights reserved. Kheirkhah Ahmad A Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts. Coco Giulia G Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts. Satitpitakul Vannarut V Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts; Department of Ophthalmology, Faculty of Medicine, Chulalongkorn University and King Chulalongkorn Memorial Hospital, Thai Red Cross Society, Bangkok, Thailand. Dana Reza R Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts. Electronic address: Reza_Dana@meei.harvard.edu. eng Journal Article 2018 03 02

United States Am J Ophthalmol 0370500 0002-9394 2017 07 18 2017 11 24 2018 02 23 2018 3 6 6 0 2018 3 6 6 0 2018 3 6 6 0 ppublish 29505774 S0002-9394(18)30095-3 10.1016/j.ajo.2018.02.020 28472010 2018 05 08

1537-2677 34 3 2018 May/Jun Ophthalmic Plast Reconstr Surg Differences in Wait Times for Cosmetic Blepharoplasty by ASOPRS Members. 222-224 10.1097/IOP.0000000000000922 Adequate access to subspecialty care is of concern to patients and physicians alike. One measure of availability is the wait time for cosmetic procedures. The authors investigated geographical differences in wait times for cosmetic upper eyelid blepharoplasty of American Society of Ophthalmic Plastic and Reconstructive Surgery members across the country. This study surveyed all 533 American Society of Ophthalmic Plastic and Reconstructive Surgery members' practices in the United States based on the publically available contact information (www.asoprs.org). Scripted telephone calls were made requesting self-referred cosmetic upper eyelid blepharoplasty. Wait times until the first available appointment and time until the first available surgery date were collected. Of the membership, 387 (72.6% response rate) respondents offered appointments for cosmetic upper eyelid blepharoplasty. Overall, 84.2% of respondents were male. Practice breakdown was 83.4% in private practice and 16.5% in academic practice. Median wait time until the next available appointment was 14 days (mean 21.2 days, 0-205 days; p = 0.145). Private practice wait time was shorter than academic (median 14 vs. 18 days, mean 19.7 vs. 28.9 days; p =0.004). However, there was wide variability based on region. Patients seeking cosmetic upper eyelid blepharoplasty have good access to care by American Society of Ophthalmic Plastic and Reconstructive Surgery members. There are variabilities based on academic versus private practice. Further study can evaluate whether similar findings exist for medically necessary functional procedures. This information may help assess the need for additional practitioners. Knezevic Alexander A Yoon Michael K MK Ophthalmic Plastic Surgery, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts. Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, U.S.A. eng Journal Article

United States Ophthalmic Plast Reconstr Surg 8508431 0740-9303 2017 5 5 6 0 2017 5 5 6 0 2017 5 5 6 0 ppublish 28472010 10.1097/IOP.0000000000000922 29496505 2018 04 30

1096-0007 170 2018 May Exp. Eye Res. Hypoxia modulates the development of a corneal stromal matrix model. 127-137 S0014-4835(17)30736-4 10.1016/j.exer.2018.02.021 Deposition of matrix proteins during development and repair is critical to the transparency of the cornea. While many cells respond to a hypoxic state that can occur in a tumor, the cornea is exposed to hypoxia during development prior to eyelid opening and during the diurnal sleep cycle where oxygen levels can drop from 21% to 8%. In this study, we used 2 three-dimensional (3-D) models to examine how stromal cells respond to periods of acute hypoxic states. The first model, a stromal construct model, is a 3-D stroma-like construct that consists of human corneal fibroblasts (HCFs) stimulated by a stable form of ascorbate for 1, 2, and 4 weeks to self-assemble their own extracellular matrix. The second model, a corneal organ culture model, is a corneal wound-healing model, which consists of wounded adult rat corneas that were removed and placed in culture to heal. Both models were exposed to either normoxic or hypoxic conditions for varying time periods, and the expression and/or localization of matrix proteins was assessed. No significant changes were detected in Type V collagen, which is associated with Type I collagen fibrils; however, significant changes were detected in the expression of both the small leucine-rich repeating proteoglycans and the larger heparan sulfate proteoglycan, perlecan. Also, hypoxia decreased both the number of Cuprolinic blue-positive glycosaminoglycan chains along collagen fibrils and Sulfatase 1, which modulates the effect of heparan sulfate by removing the 6-O-sulfate groups. In the stromal construct model, alterations were seen in fibronectin, similar to those that occur in development and after injury. These changes in fibronectin after injury were accompanied by changes in proteoglycans. Together these findings indicate that acute hypoxic changes alter the physiology of the cornea, and these models will allow us to manipulate the conditions in the extracellular environment in order to study corneal development and trauma. Copyright © 2018 Elsevier Ltd. All rights reserved. Lee Albert A Department of Biochemistry, Boston University School of Medicine, 80 E. Concord St., Boston, MA, 02118, USA. Electronic address: rusna9632@gmail.com. Karamichos Dimitrios D Department of Ophthalmology, Schepens Eye Research Institute/Mass. Eye and Ear, Harvard Medical School, 20 Staniford Street, Boston, MA, 02114, USA. Electronic address: Dimitrios-Karamichos@ouhsc.edu. Onochie Obianamma E OE Department of Biochemistry, Boston University School of Medicine, 80 E. Concord St., Boston, MA, 02118, USA. Electronic address: onochie7@bu.edu. Hutcheon Audrey E K AEK Department of Ophthalmology, Schepens Eye Research Institute/Mass. Eye and Ear, Harvard Medical School, 20 Staniford Street, Boston, MA, 02114, USA. Electronic address: Audrey_Hutcheon@meei.harvard.edu. Rich Celeste B CB Department of Biochemistry, Boston University School of Medicine, 80 E. Concord St., Boston, MA, 02118, USA. Electronic address: cbrich@bu.edu. Zieske James D JD Department of Ophthalmology, Schepens Eye Research Institute/Mass. Eye and Ear, Harvard Medical School, 20 Staniford Street, Boston, MA, 02114, USA. Electronic address: James_Zieske@meei.harvard.edu. Trinkaus-Randall Vickery V Department of Biochemistry, Boston University School of Medicine, 80 E. Concord St., Boston, MA, 02118, USA. Electronic address: vickery@bu.edu. eng P30 EY003790 EY NEI NIH HHS United States R01 EY005665 EY NEI NIH HHS United States R01 EY006000 EY NEI NIH HHS United States U42 OD011158 OD NIH HHS United States Journal Article 2018 02 27

England Exp Eye Res 0370707 0014-4835 Invest Ophthalmol Vis Sci. 2008 Oct;49(10):4384-91 18502993 EMBO J. 2015 Sep 14;34(18):2363-82 26303906 Invest Ophthalmol Vis Sci. 1988 Sep;29(9):1413-7 3417426 J Cell Physiol. 2016 Aug;231(8):1728-36 26621030 Am J Physiol Cell Physiol. 2014 May 15;306(10):C972-85 24671101 Invest Ophthalmol Vis Sci. 2007 Sep;48(9):4050-60 17724187 Curr Eye Res. 1984 Mar;3(3):489-99 6365462 Sci Rep. 2017 Nov 23;7(1):16168 29170525 Methods. 2001 Dec;25(4):402-8 11846609 Dev Dyn. 2008 Oct;237(10):2705-15 18624285 PLoS One. 2014 Jan 21;9(1):e86260 24465995 Cancer Res. 2006 Nov 1;66(21):10238-41 17079439 Exp Eye Res. 2006 May;82(5):780-7 16364292 Invest Ophthalmol Vis Sci. 1987 Oct;28(10):1668-77 3308758 J Biol Chem. 1999 Mar 12;274(11):7111-9 10066769 Cornea. 2017 Sep;36(9):1116-1123 28644233 Invest Ophthalmol Vis Sci. 1991 Mar;32(3):603-9 2001934 CLAO J. 2002 Jan;28(1):12-27 11838985 J Tissue Eng Regen Med. 2011 Aug;5(8):e228-38 21604386 J Cell Biol. 2003 Jul 21;162(2):341-51 12860968 J Histochem Cytochem. 1990 May;38(5):675-84 2332625 J Cell Biochem. 2000 Sep 18;80(1):146-55 11029762 Matrix Biol. 2014 Sep;38:59-68 25019467 Mol Vis. 2012;18:128-38 22275804 Exp Eye Res. 2015 May;134:33-8 25797478 J Biomed Mater Res B Appl Biomater. 2010 Feb;92(2):361-5 19904816 J Ocul Pharmacol Ther. 2010 Oct;26(5):407-19 20925577 Curr Opin Cell Biol. 2008 Oct;20(5):495-501 18640274 Exp Eye Res. 2017 Nov;164:1-7 28782505 Clin Exp Optom. 2017 Sep;100(5):459-472 28771841 J Funct Biomater. 2011 Sep 01;2(3):213-29 24956304 Biochemistry. 2006 Aug 29;45(34):10319-28 16922507 Arch Biochem Biophys. 1983 Apr 15;222(2):362-9 6847191 Invest Ophthalmol Vis Sci. 1988 Jul;29(7):1116-24 2971024 Wound Repair Regen. 2003 Jan-Feb;11(1):71-8 12581429 Invest Ophthalmol Vis Sci. 2012 Mar 09;53(3):1277-84 22266517 J Ocul Pharmacol Ther. 2016 Oct;32(8):498-503 27643999 Confocal fluorescence microscopy Cornea Corneal organ culture Extracellular matrix Stroma 2017 11 03 2018 02 18 2018 02 23 2019 05 01 2018 3 3 6 0 2018 3 3 6 0 2018 3 3 6 0 ppublish 29496505 S0014-4835(17)30736-4 10.1016/j.exer.2018.02.021 PMC5924608 NIHMS948773 29742012 2018 05 09

1744-5108 2018 May 09 Orbit Simultaneous ipsilateral transconjunctival repair of upper and lower eyelid retraction in thyroid-associated ophthalmopathy. 1-6 10.1080/01676830.2018.1474237 To report a simple, highly effective technique of simultaneous transconjunctival repair of upper and lower eyelid retraction in patients with thyroid eye disease (TED). A retrospective interventional case review was conducted on 22 eyes of 19 TED patients. The lower eyelid was recessed with placement of a tarsoconjunctival spacer graft harvested from the upper eyelid. The upper eyelid was then recessed through the conjunctival incision used to harvest the tarsal graft. A temporary tarsorrhaphy was placed for 5-7 days. The postoperative outcome was assessed by measuring the margin reflex distance of the upper eyelid (MRD1), inferior scleral show (ISS), and lagophthalmos. The absolute change in MRD1 ranged from 0 to 5 mm with an average of 1.86 ± 1.34 mm. The absolute change in ISS ranged from 0 to 2 mm with an average of 1.3 ± 0.49 mm. One patient had postoperative lagophthalmos and 17 of 19 had improvement in their ocular surface exposure symptoms. None of the patients' grafts were observed to undergo absorption during the postoperative course. This technique of harvesting a free tarsoconjunctival graft from the upper eyelid as a posterior spacer for the lower while simultaneously recessing the upper eyelid through the same incision is an effective and durable method of correcting eyelid retraction in TED. Lee Nahyoung Grace NG a Ophthalmic Plastic Surgery Service, Massachusetts Eye and Ear Infirmary , Harvard Medical School , Boston , Massachusetts , USA. Habib Larissa L http://orcid.org/0000-0003-1110-9450 a Ophthalmic Plastic Surgery Service, Massachusetts Eye and Ear Infirmary , Harvard Medical School , Boston , Massachusetts , USA. Hall Jonathan J b Department of Ophthalmology , MVZ Prof. Neuhann , Munich , Germany. Freitag Suzanne K SK a Ophthalmic Plastic Surgery Service, Massachusetts Eye and Ear Infirmary , Harvard Medical School , Boston , Massachusetts , USA. eng Journal Article 2018 05 09

England Orbit 8301221 0167-6830 Eyelid recession retraction spacer graft thyroid 2018 5 10 6 0 2018 5 10 6 0 2018 5 10 6 0 aheadofprint 29742012 10.1080/01676830.2018.1474237 29243312 2018 04 18

1651-2227 107 5 2018 May Acta Paediatr. Duration of anaemia during the first week of life is an independent risk factor for retinopathy of prematurity. 759-766 10.1111/apa.14187 This study evaluated the correlation between retinopathy of prematurity (ROP), anaemia and blood transfusions in extremely preterm infants. We included 227 infants born below 28 weeks of gestation at King Edward Memorial Hospital, Perth, Australia, from 2014-2016. Birth characteristics and risk factors for ROP were retrieved, and anaemia and severe anaemia were defined as a haemoglobins of <110 g/L and <80 g/L, respectively. Logistic regression was used for the analysis. Retinopathy of prematurity treatment was needed in 11% of cases and the mean number of blood transfusions (p < 0.01), and mean number of weeks of anaemia (p < 0.001) and of severe anaemia (p < 0.05), had positive associations with ROP cases warranting treatment. In the multivariate logistic regression analysis, the best-fit model of risk factors included anaemic days during first week of life, with an odds ratio (OR) of 1.46% and 95% confidence interval (CI) of 1.16-1.83 (p < 0.05), sepsis during the first 4 weeks of life (OR 3.14, 95% CI 1.10-9.00, p < 0.05) and days of ventilation (OR 1.03, 95% CI 1.01-1.06, p < 0.05). The duration of anaemia during the first week of life was an independent risk factor for ROP warranting treatment and preventing early anaemia may decrease this risk. ©2017 Foundation Acta Paediatrica. Published by John Wiley & Sons Ltd. Lundgren Pia P Centre for Neonatal Research and Education, School of Paediatrics and Child Health, University of Western Australia, Crawley, WA, Australia. Athikarisamy Sam E SE Centre for Neonatal Research and Education, School of Paediatrics and Child Health, University of Western Australia, Crawley, WA, Australia. Department of Neonatology, Princess Margaret Hospital for Children, Perth, WA, Australia. Department of Neonatology, King Edward Memorial Hospital for Women, Perth, WA, Australia. Patole Sanjay S Department of Neonatology, Princess Margaret Hospital for Children, Perth, WA, Australia. Department of Neonatology, King Edward Memorial Hospital for Women, Perth, WA, Australia. Lam Geoffrey C GC Department of Ophthalmology, Princess Margaret Hospital for Children, Perth, WA, Australia. Centre for Ophthalmology and Visual Science, University of Western Australia, Perth, WA, Australia. Smith Lois E LE Department of Ophthalmology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA. Simmer Karen K Centre for Neonatal Research and Education, School of Paediatrics and Child Health, University of Western Australia, Crawley, WA, Australia. Department of Neonatology, Princess Margaret Hospital for Children, Perth, WA, Australia. Department of Neonatology, King Edward Memorial Hospital for Women, Perth, WA, Australia. eng R01 EY017017 EY NEI NIH HHS United States U54 HD090255 HD NICHD NIH HHS United States Journal Article 2018 01 11

Norway Acta Paediatr 9205968 0803-5253 BMC Med. 2015 Jan 27;13:16 25622597 Paediatr Child Health. 2014 Apr;19(4):213-22 24855419 J Matern Fetal Neonatal Med. 2012 May;25(5):471-7 22280305 J Perinatol. 2001 Jan-Feb;21(1):21-6 11268863 Arch Ophthalmol. 2005 Jul;123(7):991-9 16009843 J Pediatr. 2000 Feb;136(2):220-4 10657829 Pediatrics. 1999 Sep;104(3 Pt 1):514-8 10469778 Pediatrics. 1983 Aug;72 (2):159-63 6408596 Pediatrics. 2005 Jun;115(6):1685-91 15930233 J Clin Invest. 2008 Feb;118(2):526-33 18219389 Pediatrics. 2010 Apr;125(4):e736-40 20231184 Am J Perinatol. 2017 Aug;34(10 ):1020-1025 28395368 Arch Dis Child Fetal Neonatal Ed. 2004 Mar;89(2):F101-7 14977890 Proc Natl Acad Sci U S A. 1995 Nov 7;92 (23 ):10457-61 7479819 Retina. 2006 Sep;26(7 Suppl):S18-23 16946672 Pediatr Neonatol. 2017 Feb;58(1):48-56 27346390 Ophthalmology. 2009 Sep;116(9):1599-603 19371954 Helv Paediatr Acta. 1984 Oct;39(4):307-17 6549554 Acta Paediatr. 1994 May;83(5):501-5 8086727 J Perinat Neonatal Nurs. 2004 Apr-Jun;18(2):170-82; quiz 183-4 15214254 J Pediatr. 2006 Sep;149(3):301-307 16939737 Pediatrics. 2005 May;115(5):e518-25 15805336 Invest Ophthalmol Vis Sci. 2014 Apr 24;55(5):3165-70 24764065 Early Hum Dev. 2001 Apr;62(1):57-63 11245995 Arch Ophthalmol. 2003 Dec;121(12 ):1684-94 14662586 Pediatrics. 2009 Feb;123(2):e333-7 19171584 Acta Ophthalmol Scand. 1998 Apr;76(2):204-7 9591954 Br J Ophthalmol. 1954 Jul;38(7):397-432 13172417 Pediatr Neonatol. 2009 Jun;50(3):110-6 19579757 Semin Perinatol. 2009 Feb;33(1):29-34 19167579 Anaemia Blood transfusions Erythropoietin Preterm infants Retinopathy of prematurity 2017 07 27 2017 10 16 2017 12 07 2018 11 01 2017 12 16 6 0 2017 12 16 6 0 2017 12 16 6 0 ppublish 29243312 10.1111/apa.14187 PMC5902413 NIHMS935405 28872709 2018 05 18

1651-2227 107 5 2018 May Acta Paediatr. Implementing higher oxygen saturation targets reduced the impact of poor weight gain as a predictor for retinopathy of prematurity. 767-773 10.1111/apa.14049 This study evaluated poor weight gain as a risk factor for infants who required treatment for retinopathy of prematurity (ROP), by comparing those born before and after the implementation of higher oxygen saturation (SpO₂ ) targets at the Queen Silvia Children's Hospital, Gothenburg, Sweden. We compared infants born at less than 31 weeks, who were screened and, or, treated for ROP: 127 in 2011-2012 when SpO₂ targets were 88-92% and 142 in 2015-2016 when they were 91-95%. The subjects were reviewed for birth characteristics, weekly weight and ROP treatment. Data were analysed using the weight, insulin-like growth factor 1, neonatal, ROP (WINROP) prediction tool. The 2011-2012 infants who needed ROP treatment (12.6%) had significantly poorer postnatal weight gain than those who did not, but this was not seen in the treated (17.6%) and nontreated ROP groups in 2015-2016. WINROP sensitivity decreased from 87.5% in 2011-12 to 48% in 2015-2016. After the SpO₂ target range was increased from 88-92% to 91-95%, postnatal weight gain was no longer a significant risk factor and WINROP lost its ability to predict ROP requiring treatment. Risk factors clearly change as neonatal care develops. ©2017 The Authors. Acta Paediatrica published by John Wiley & Sons Ltd on behalf of Foundation Acta Paediatrica. Lundgren Pia P Section for Ophthalmology, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Hård Anna-Lena AL Section for Ophthalmology, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Wilde Åsa Å 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. Smith Lois E H LEH Department of Ophthalmology, Harvard Medical School, Boston Children's Hospital, 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 R01 EY017017 EY NEI NIH HHS United States U54 HD090255 HD NICHD NIH HHS United States Journal Article 2017 09 20

Norway Acta Paediatr 9205968 0803-5253 Acta Paediatr. 1996 Jul;85(7):843-8 8819552 Arch Ophthalmol. 2012 Jun;130(6):720-3 22801831 Pediatrics. 2009 Apr;123(4):e638-45 19289449 Pediatr Res. 2016 Sep;80(3):401-6 27081928 BMJ Open. 2016 Nov 17;6(11):e012872 27856479 Arch Ophthalmol. 2005 Jul;123(7):991-9 16009843 Dev Med Child Neurol. 1964 Jun;6:313-4 14155197 JAMA Pediatr. 2015 Apr;169(4):332-40 25664703 Pediatr Res. 2013 Dec;74 Suppl 1:35-49 24366462 Pediatrics. 2008 May;121(5):882-9 18450890 Cochrane Database Syst Rev. 2017 Apr 11;4:CD011190 28398697 N Engl J Med. 1992 Apr 16;326(16):1050-4 1549150 Trans Am Ophthalmol Soc. 2006;104:78-84 17471328 Arch Ophthalmol. 2009 May;127(5):622-7 19433710 Arch Ophthalmol. 2003 Dec;121(12 ):1684-94 14662586 J Pediatr. 1960 Oct;57:553-9 13685272 Arch Ophthalmol. 2012 Aug;130(8):992-9 22491391 PLoS One. 2013 Sep 12;8(9):e73256 24069180 Pediatrics. 2006 Oct;118(4):1574-82 17015549 Pediatrics. 2010 Jun;125(6):e1483-92 20498174 Dev Neurosci. 2016;38(5):311-330 28152539 Br J Ophthalmol. 2014 Nov;98(11):1565-9 24963022 J Pediatr. 2016 Jan;168:242-4 26548746 Pediatrics. 2007 Jun;119(6):1056-60 17545370 Arch Ophthalmol. 2006 Dec;124(12):1711-8 17159030 Oxygen saturation Poor weight gain Preterm birth retinopathy of prematurity Risk factors 2017 05 04 2017 06 27 2017 08 23 2017 9 6 6 0 2017 9 6 6 0 2017 9 6 6 0 ppublish 28872709 10.1111/apa.14049 PMC5837939 NIHMS935419 29351118 2018 05 08

1537-2677 34 3 2018 May/Jun Ophthalmic Plast Reconstr Surg Multiple Eyelid Cysts (Apocrine and Eccrine Hidrocystomas, Trichilemmal Cyst, and Hybrid Cyst) in a Patient With a Prolactinoma. e83-e85 10.1097/IOP.0000000000001069 A 53-year-old man presented with smooth-domed, variegated cysts (polycystic disease) of all 4 eyelids, worse on the left side. Some of the cysts were clear, while others were creamy-white colored. In addition, multiple, very fine vesicopapules were noted along the eyelid margins. Histopathologic examination revealed a trichilemmal cyst, several pure apocrine hidrocystomas displaying multiple chambers, a hybrid cyst, and many small eccrine cysts of the deep dermis. The apocrine lesions, including the small ones at the eyelid margins, predominated. Smooth muscle actin sometimes positively stained outer myoepithelial cells in some of the apocrine cysts, which helped to distinguish them from eccrine cysts. Most noteworthy was the fact that the patient had been diagnosed with a prolactinoma 20 years earlier. There is only 1 previous report of multiple apocrine cysts and an antecedent prolactinoma in the dermatologic literature. This syndrome should be separated from that of Schöpf-Schulz-Passarge, which manifests multiple small eyelid apocrine cysts and other ectodermal dysplasias without any association with neoplasia, and from that of focal dermal hypoplasia (Goltz-Gorlin) syndrome with apocrine cysts but again without neoplasia. Ma Lina L David G. Cogan Laboratory of Ophthalmic Pathology, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts, U.S.A. Jakobiec Frederick A FA David G. Cogan Laboratory of Ophthalmic Pathology, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts, U.S.A. Wolkow Natalie N David G. Cogan Laboratory of Ophthalmic Pathology, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts, U.S.A. Dryja Thaddeus P TP David G. Cogan Laboratory of Ophthalmic Pathology, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts, U.S.A. Borodic Gary E GE Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA and Associate Eye Physicians and Surgeons, Quincy, Massachusetts, U.S.A. eng Journal Article

United States Ophthalmic Plast Reconstr Surg 8508431 0740-9303 2018 1 20 6 0 2018 1 20 6 0 2018 1 20 6 0 ppublish 29351118 10.1097/IOP.0000000000001069 29742436 2018 06 03

2211-1247 23 6 2018 May 08 Cell Rep The Assembly-Activating Protein Promotes Stability and Interactions between AAV's Viral Proteins to Nucleate Capsid Assembly. 1817-1830 S2211-1247(18)30555-2 10.1016/j.celrep.2018.04.026 The adeno-associated virus (AAV) vector is a preferred delivery platform for in vivo gene therapy. Natural and engineered variations of the AAV capsid affect a plurality of phenotypes relevant to gene therapy, including vector production and host tropism. Fundamental to these aspects is the mechanism of AAV capsid assembly. Here, the role of the viral co-factor assembly-activating protein (AAP) was evaluated in 12 naturally occurring AAVs and 9 putative ancestral capsid intermediates. The results demonstrate increased capsid protein stability and VP-VP interactions in the presence of AAP. The capsid's dependence on AAP can be partly overcome by strengthening interactions between monomers within the assembly, as illustrated by the transfer of a minimal motif defined by a phenotype-to-phylogeny mapping method. These findings suggest that the emergence of AAP within the Dependovirus genus relaxes structural constraints on AAV assembly in favor of increasing the degrees of freedom for the capsid to evolve. Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved. Maurer Anna C AC Grousbeck Gene Therapy Center, Schepens Eye Research Institute, Massachusetts Eye and Ear, Boston, MA 02114, USA; Ocular Genomics Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USA. Pacouret Simon S Grousbeck Gene Therapy Center, Schepens Eye Research Institute, Massachusetts Eye and Ear, Boston, MA 02114, USA; Ocular Genomics Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USA; INSERM UMR 1089, University of Nantes, Nantes University Hospital, 22 Boulevard Benoni Goullin, 44200 Nantes, France. Cepeda Diaz Ana Karla AK Grousbeck Gene Therapy Center, Schepens Eye Research Institute, Massachusetts Eye and Ear, Boston, MA 02114, USA; Ocular Genomics Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USA. Blake Jessica J Grousbeck Gene Therapy Center, Schepens Eye Research Institute, Massachusetts Eye and Ear, Boston, MA 02114, USA; Ocular Genomics Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USA. Andres-Mateos Eva E Grousbeck Gene Therapy Center, Schepens Eye Research Institute, Massachusetts Eye and Ear, Boston, MA 02114, USA; Ocular Genomics Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USA. Vandenberghe Luk H LH Grousbeck Gene Therapy Center, Schepens Eye Research Institute, Massachusetts Eye and Ear, Boston, MA 02114, USA; Ocular Genomics Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USA; Harvard Stem Cell Institute, Harvard University, Cambridge, MA 02138, USA; The Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA. Electronic address: luk_vandenberghe@meei.harvard.edu. eng DP1 EY023177 EY NEI NIH HHS United States DP1 OD008267 OD NIH HHS United States P30 EY003790 EY NEI NIH HHS United States Journal Article

United States Cell Rep 101573691 J Virol. 2017 Sep 27;91(20): 28768875 J Virol. 1997 Feb;71(2):1341-52 8995658 J Virol. 2007 Nov;81(22):12260-71 17728238 J Virol. 2012 Jun;86(12):6947-58 22496238 J Virol. 2017 Jan 18;91(3): 27852862 J Virol. 2006 Jan;80(2):810-20 16378983 Cell Rep. 2015 Aug 11;12(6):1056-68 26235624 Hum Gene Ther Methods. 2013 Apr;24(2):80-93 23379478 Curr Gene Ther. 2005 Jun;5(3):285-97 15975006 J Virol. 2012 Jul;86(13):7326-33 22514350 J Virol. 2012 Sep;86(17):9163-74 22696661 Mol Ther. 2015 Dec;23 (12 ):1819-31 26388463 J Virol. 2004 Mar;78(6):3110-22 14990730 J Virol. 1995 Sep;69(9):5311-9 7636974 J Virol. 2015 Mar;89(6):3038-48 25552709 Proc Natl Acad Sci U S A. 2010 Jun 1;107(22):10220-5 20479244 J Virol. 2006 Jan;80(2):821-34 16378984 Nat Rev Genet. 2014 Jul;15(7):445-51 24840552 J Virol. 2006 Jun;80(11):5199-210 16699000 J Gen Virol. 2002 May;83(Pt 5):973-8 11961250 J Gen Virol. 1997 Jun;78 ( Pt 6):1453-62 9191943 Hum Gene Ther Methods. 2013 Apr;24(2):104-16 23442071 Gene Ther. 2009 Mar;16(3):311-9 19052631 Mol Ther. 2017 Jun 7;25(6):1375-1386 28427840 Nat Biotechnol. 2009 Jan;27(1):59-65 19098898 Virology. 2008 Nov 25;381(2):194-202 18834608 J Virol. 2004 Jun;78(12):6381-8 15163731 Nature. 2016 Feb 4;530(7588):108-12 26814968 J Virol. 2014 Apr;88(8):4132-44 24478436 J Virol. 2000 Sep;74(18):8635-47 10954565 J Virol. 2003 Oct;77(20):11072-81 14512555 Nat Biotechnol. 2017 Mar;35(3):280-284 28165475 J Virol. 2012 Dec;86(23):13038-48 23015698 J Virol. 2002 Mar;76(5):2043-53 11836382 J Virol. 2011 Dec;85(23):12686-97 21917944 AAP AAV adeno-associated virus capsid capsid assembly gene therapy manufacturing structure-function vector engineering 2017 04 24 2017 07 31 2018 04 04 2018 5 10 6 0 2018 5 10 6 0 2018 5 10 6 0 ppublish 29742436 S2211-1247(18)30555-2 10.1016/j.celrep.2018.04.026 PMC5983388 NIHMS968701 29787296 2018 06 09

1460-2202 2018 May 22 Curr. Eye Res. Short Tandem Repeat (STR) Profiles of Commonly Used Human Ocular Surface Cell Lines. 1-5 10.1080/02713683.2018.1480043 The purpose of this study is to establish the short tandem repeat (STR) profiles of several human cell lines commonly used in ocular surface research. Independently DNA was extracted from multiple passages of three human corneal epithelial cell lines, two human conjunctival epithelial cell lines and one meibomian gland cell line, from different laboratories actively involved in ocular surface research. The samples were then subjected to STR analysis on a fee-for-service basis in an academic setting and the data compared against that in available databases. The STR profiles for the human corneal epithelial cells were different among the three cell lines studied and for each line the profiles were identical across the samples provided by three laboratories. Profiles for the human conjunctival epithelial cells were different among the two cell lines studied. Profiles for the meibomian gland cell line were identical across the samples provided by three laboratories. No samples were contaminated by elements of other cell lines such as HeLa. This comprehensive study provides verification of STR profiles for commonly used human ocular surface cell lines that can now be used as a reference by others in the field to authenticate the cell lines in use in their own laboratories. McDermott Alison M AM a The Ocular Surface Institute , University of Houston College of Optometry , Houston , TX , USA. e Department of Applied Sciences , Northumbria University , Newcastle upon Tyne , UK. Baidouri Hasna H a The Ocular Surface Institute , University of Houston College of Optometry , Houston , TX , USA. Woodward Ashley M AM b Schepens Eye Research Institute of Massachusetts Eye and Ear and Department of Ophthalmology , Harvard Medical School , Boston , MA , USA. Kam Wendy R WR b Schepens Eye Research Institute of Massachusetts Eye and Ear and Department of Ophthalmology , Harvard Medical School , Boston , MA , USA. Liu Yang Y b Schepens Eye Research Institute of Massachusetts Eye and Ear and Department of Ophthalmology , Harvard Medical School , Boston , MA , USA. Chen Xiaomin X b Schepens Eye Research Institute of Massachusetts Eye and Ear and Department of Ophthalmology , Harvard Medical School , Boston , MA , USA. Ziemanski Jillian F JF c Ocular Surface Research Institute of the Clinical Eye Research Facility, School of Optometry , University of Alabama at Birmingham , Birmingham , AL , USA. Vistisen Kerry K d Department of Anatomy & Cell Biology , Wayne State University School of Medicine , Detroit , MI , USA. Hazlett Linda D LD d Department of Anatomy & Cell Biology , Wayne State University School of Medicine , Detroit , MI , USA. Nichols Kelly K KK c Ocular Surface Research Institute of the Clinical Eye Research Facility, School of Optometry , University of Alabama at Birmingham , Birmingham , AL , USA. Argüeso Pablo P b Schepens Eye Research Institute of Massachusetts Eye and Ear and Department of Ophthalmology , Harvard Medical School , Boston , MA , USA. Sullivan David A DA b Schepens Eye Research Institute of Massachusetts Eye and Ear and Department of Ophthalmology , Harvard Medical School , Boston , MA , USA. eng R01 EY024031 EY NEI NIH HHS United States R01 EY026147 EY NEI NIH HHS United States Journal Article 2018 05 22

England Curr Eye Res 8104312 0271-3683 Conjunctiva cornea epithelial meibomian short tandem repeat 2018 5 23 6 0 2018 5 23 6 0 2018 5 23 6 0 aheadofprint 29787296 10.1080/02713683.2018.1480043 29681290 2018 04 23

1549-4713 125 5 2018 May Ophthalmology Public Health Burden and Potential Interventions for Myopia. 628-630 S0161-6420(17)32071-7 10.1016/j.ophtha.2018.01.033 Modjtahedi Bobeck S BS Eye Monitoring Center, Kaiser Permanente Southern California, Baldwin Park, California; Department of Ophthalmology, Southern California Permanente Medical Group, Baldwin Park, California. Electronic address: BobModj@gmail.com. Ferris Frederick L FL 3rd National Eye Institute, National Institutes of Health, Bethesda, Maryland. Hunter David G DG Department of Ophthalmology, Harvard Medical School and the Department of Ophthalmology, Boston Children's Hospital, Boston, Massachusetts. Fong Donald S DS Eye Monitoring Center, Kaiser Permanente Southern California, Baldwin Park, California; Department of Ophthalmology, Southern California Permanente Medical Group, Baldwin Park, California; Department of Research and Evaluation, Southern California Permanente Medical Group, Pasadena, California. eng Editorial

United States Ophthalmology 7802443 0161-6420 2017 07 02 2018 01 21 2018 01 24 2018 4 24 6 0 2018 4 24 6 0 2018 4 24 6 0 ppublish 29681290 S0161-6420(17)32071-7 10.1016/j.ophtha.2018.01.033 28658180 2018 05 08

1537-2677 34 3 2018 May/Jun Ophthalmic Plast Reconstr Surg Morphometric Analysis of the Orbital Process of the Palatine Bone and its Relationship to Endoscopic Orbital Apex Surgery. 254-257 10.1097/IOP.0000000000000940 Endoscopic approaches to the orbit improve the ability to directly access apical lesions while minimizing manipulation of normal structures. Inferomedial orbital access is limited by the orbital process of the palatine bone (OPPB) which prevents dissection and retraction in the inferolateral vector. The objective of this study was to examine the morphometric characteristics of the OPPB and quantify the benefit of complete resection to surgical access. Morphometric osteologic measurements of the OPPB were performed in 59 human skulls. A radius subtended by the OPPB was calculated to generate a hemispheric dissection corridor achievable by complete resection of the OPPB. Cadaveric and live surgical dissections were then performed on 15 orbits to develop discreet endoscopic surgical landmarks which could be used to both identify the OPPB and verify complete resection. The mean(± SD) radius of the OPPB was 0.47 ± 0.28 cm. Complete OPPB resection provided an additional 0.36 ± 0.42 cm of surgical exposure within the inferomedial apex. Relative to the Caucasian (n = 27) skulls, the radii in the Asian (n = 27) and African (n = 5) skulls were significantly smaller (p < 0.001 and p = 0.02, respectively). The OPPB significantly limits surgical access to the inferomedial orbital apex during endoscopic approaches. Complete surgical resection of the OPPB improves surgical exposure facilitating retraction of the inferior rectus muscle and circumferential dissection of lesions within this space. Knowledge of the morphology and clinical relevance of this structure provides an opportunity to improve surgical exposure for relevant pathologic assessment and optimize endoscopic surgical outcomes. Mueller Sarina K SK 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. Bleier Benjamin S BS Department of Otolaryngology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, U.S.A. eng Journal Article

United States Ophthalmic Plast Reconstr Surg 8508431 0740-9303 2017 6 29 6 0 2017 6 29 6 0 2017 6 29 6 0 ppublish 28658180 10.1097/IOP.0000000000000940 28991115 2018 06 27

1526-7598 126 5 2018 May Anesth. Analg. Preventing Adverse Events in Cataract Surgery: Recommendations From a Massachusetts Expert Panel. 1537-1547 10.1213/ANE.0000000000002529 Massachusetts health care facilities reported a series of cataract surgery-related adverse events (AEs) to the state in recent years, including 5 globe perforations during eye blocks performed by 1 anesthesiologist in a single day. The Betsy Lehman Center for Patient Safety, a nonregulatory Massachusetts state agency, responded by convening an expert panel of frontline providers, patient safety experts, and patients to recommend strategies for mitigating patient harm during cataract surgery. The purpose of this article is to identify contributing factors to the cataract surgery AEs reported in Massachusetts and present the panel's recommended strategies to prevent them. Data from state-mandated serious reportable event reports were supplemented by online surveys of Massachusetts cataract surgery providers and semistructured interviews with key stakeholders and frontline staff. The panel identified 2 principal categories of contributing factors to the state's cataract surgery-related AEs: systems failures and choice of anesthesia technique. Systems failures included inadequate safety protocols (48.7% of contributing factors), communication challenges (18.4%), insufficient provider training (17.1%), and lack of standardization (15.8%). Choice of anesthesia technique involved the increased relative risk of needle-based eye blocks. The panel's surveys of Massachusetts cataract surgery providers show wide variation in anesthesia practices. While 45.5% of surgeons and 69.6% of facilities reported increased use of topical anesthesia compared to 10 years earlier, needle-based blocks were still used in 47.0% of cataract surgeries performed by surgeon respondents and 40.9% of those performed at respondent facilities. Using a modified Delphi approach, the panel recommended several strategies to prevent AEs during cataract surgery, including performing a distinct time-out with at least 2 care-team members before block administration; implementing standardized, facility-wide safety protocols, including a uniform site-marking policy; strengthening the credentialing and orientation of new, contracted and locum tenens anesthesia staff; ensuring adequate and documented training in block administration for any provider who is new to a facility, including at least 10 supervised blocks before practicing independently; using the least invasive form of anesthesia appropriate to the patient; and finally, adjusting anesthesia practices, including preferred techniques, as evidence-based best practices evolve. Future research should focus on evaluating the impact of these recommendations on patient outcomes. Nanji Karen C KC From the Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard University, Boston, Massachusetts. Roberto Sarah A SA Betsy Lehman Center for Patient Safety, Boston, Massachusetts. Morley Michael G MG Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts. Bayes Joseph J Department of Anesthesia, Massachusetts Eye & Ear, Harvard Medical School, Boston, Massachusetts. eng K08 HS024764 HS AHRQ HHS United States Journal Article

United States Anesth Analg 1310650 0003-2999 2017 10 11 6 0 2017 10 11 6 0 2017 10 10 6 0 ppublish 28991115 10.1213/ANE.0000000000002529 29766399 2018 06 21

1573-7209 2018 May 15 Angiogenesis Consensus guidelines for the use and interpretation of angiogenesis assays. 10.1007/s10456-018-9613-x The formation of new blood vessels, or angiogenesis, is a complex process that plays important roles in growth and development, tissue and organ regeneration, as well as numerous pathological conditions. Angiogenesis undergoes multiple discrete steps that can be individually evaluated and quantified by a large number of bioassays. These independent assessments hold advantages but also have limitations. This article describes in vivo, ex vivo, and in vitro bioassays that are available for the evaluation of angiogenesis and highlights critical aspects that are relevant for their execution and proper interpretation. As such, this collaborative work is the first edition of consensus guidelines on angiogenesis bioassays to serve for current and future reference. Nowak-Sliwinska Patrycja P Molecular Pharmacology Group, School of Pharmaceutical Sciences, Faculty of Sciences, University of Geneva, University of Lausanne, Rue Michel-Servet 1, CMU, 1211, Geneva 4, Switzerland. Patrycja.Nowak-Sliwinska@unige.ch. Translational Research Center in Oncohaematology, University of Geneva, Geneva, Switzerland. Patrycja.Nowak-Sliwinska@unige.ch. Alitalo Kari K Wihuri Research Institute and Translational Cancer Biology Program, University of Helsinki, Helsinki, Finland. Allen Elizabeth E Laboratory of Tumor Microenvironment and Therapeutic Resistance, Department of Oncology, VIB-Center for Cancer Biology, KU Leuven, Louvain, Belgium. Anisimov Andrey A Wihuri Research Institute and Translational Cancer Biology Program, University of Helsinki, Helsinki, Finland. Aplin Alfred C AC Department of Pathology, University of Washington, Seattle, WA, USA. Auerbach Robert R University of Wisconsin, Madison, WI, USA. Augustin Hellmut G HG European Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany. Division of Vascular Oncology and Metastasis Research, German Cancer Research Center, Heidelberg, Germany. German Cancer Consortium, Heidelberg, Germany. Bates David O DO Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham, UK. van Beijnum Judy R JR Angiogenesis Laboratory, Department of Medical Oncology, VU University Medical Center, Cancer Center Amsterdam, De Boelelaan 1117, 1081 HV, Amsterdam, The Netherlands. Bender R Hugh F RHF Department of Molecular Biology and Biochemistry, University of California, Irvine, CA, USA. Bergers Gabriele G Laboratory of Tumor Microenvironment and Therapeutic Resistance, Department of Oncology, VIB-Center for Cancer Biology, KU Leuven, Louvain, Belgium. Department of Neurological Surgery, Brain Tumor Research Center, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, USA. Bikfalvi Andreas A Angiogenesis and Tumor Microenvironment Laboratory (INSERM U1029), University Bordeaux, Pessac, France. Bischoff Joyce J Vascular Biology Program and Department of Surgery, Harvard Medical School, Boston Children's Hospital, Boston, MA, USA. Böck Barbara C BC European Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany. Division of Vascular Oncology and Metastasis Research, German Cancer Research Center, Heidelberg, Germany. German Cancer Consortium, Heidelberg, Germany. Brooks Peter C PC Center for Molecular Medicine, Maine Medical Center Research Institute, Scarborough, ME, USA. Bussolino Federico F Department of Oncology, University of Torino, Turin, Italy. Candiolo Cancer Institute-FPO-IRCCS, 10060, Candiolo, Italy. Cakir Bertan B Department of Ophthalmology, Harvard Medical School, Boston Children's Hospital, Boston, MA, USA. Carmeliet Peter P Laboratory of Angiogenesis and Vascular Metabolism, Department of Oncology and Leuven Cancer Institute (LKI), KU Leuven, Leuven, Belgium. Laboratory of Angiogenesis and Vascular Metabolism, Center for Cancer Biology, VIB, Leuven, Belgium. Castranova Daniel D Division of Developmental Biology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA. Cimpean Anca M AM Department of Microscopic Morphology/Histology, Angiogenesis Research Center, Victor Babes University of Medicine and Pharmacy, Timisoara, Romania. Cleaver Ondine O Department of Molecular Biology, Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA. Coukos George G Ludwig Institute for Cancer Research, Department of Oncology, University of Lausanne, Lausanne, Switzerland. Davis George E GE Department of Medical Pharmacology and Physiology, University of Missouri, School of Medicine and Dalton Cardiovascular Center, Columbia, MO, USA. De Palma Michele M School of Life Sciences, Swiss Federal Institute of Technology, Lausanne, Switzerland. Dimberg Anna A Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden. Dings Ruud P M RPM Department of Radiation Oncology, University of Arkansas for Medical Sciences, Little Rock, AR, USA. Djonov Valentin V Institute of Anatomy, University of Bern, Bern, Switzerland. Dudley Andrew C AC Department of Microbiology, Immunology, and Cancer Biology, University of Virginia, Charlottesville, VA, USA. Emily Couric Cancer Center, The University of Virginia, Charlottesville, VA, USA. Dufton Neil P NP Vascular Sciences, Imperial Centre for Translational and Experimental Medicine, National Heart and Lung Institute, Imperial College London, London, UK. Fendt Sarah-Maria SM Laboratory of Cellular Metabolism and Metabolic Regulation, VIB Center for Cancer Biology, Leuven, Belgium. Laboratory of Cellular Metabolism and Metabolic Regulation, Department of Oncology, KU Leuven and Leuven Cancer Institute, Leuven, Belgium. Ferrara Napoleone N University of California, San Diego, La Jolla, CA, USA. Fruttiger Marcus M Institute of Ophthalmology, University College London, London, UK. Fukumura Dai D Edwin L. Steele Laboratories, Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. Ghesquière Bart B Metabolomics Expertise Center, VIB Center for Cancer Biology, VIB, Leuven, Belgium. Department of Oncology, Metabolomics Expertise Center, KU Leuven, Leuven, Belgium. Gong Yan Y Department of Ophthalmology, Harvard Medical School, Boston Children's Hospital, Boston, MA, USA. Griffin Robert J RJ Department of Radiation Oncology, University of Arkansas for Medical Sciences, Little Rock, AR, USA. Harris Adrian L AL Molecular Oncology Laboratories, Oxford University Department of Oncology, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, UK. Hughes Christopher C W CCW Department of Molecular Biology and Biochemistry, University of California, Irvine, CA, USA. Hultgren Nan W NW Department of Molecular Biology and Biochemistry, University of California, Irvine, CA, USA. Iruela-Arispe M Luisa ML MCDB, University of California, Los Angeles, CA, USA. Irving Melita M Ludwig Institute for Cancer Research, Department of Oncology, University of Lausanne, Lausanne, Switzerland. Jain Rakesh K RK Edwin L. Steele Laboratories, Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. Kalluri Raghu R Department of Cancer Biology, Metastasis Research Center, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. Kalucka Joanna J Laboratory of Angiogenesis and Vascular Metabolism, Department of Oncology and Leuven Cancer Institute (LKI), KU Leuven, Leuven, Belgium. Laboratory of Angiogenesis and Vascular Metabolism, Center for Cancer Biology, VIB, Leuven, Belgium. Kerbel Robert S RS Department of Medical Biophysics, Biological Sciences Platform, Sunnybrook Research Institute, University of Toronto, Toronto, ON, Canada. Kitajewski Jan J Department of Physiology and Biophysics, University of Illinois, Chicago, IL, USA. Klaassen Ingeborg I Ocular Angiogenesis Group, Departments of Ophthalmology and Medical Biology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. Kleinmann Hynda K HK The George Washington University School of Medicine, Washington, DC, USA. Koolwijk Pieter P Department of Ophthalmology, University of Lausanne, Jules-Gonin Eye Hospital, Fondation Asile des Aveugles, Lausanne, Switzerland. Kuczynski Elisabeth E Department of Medical Biophysics, Biological Sciences Platform, Sunnybrook Research Institute, University of Toronto, Toronto, ON, Canada. Kwak Brenda R BR Department of Pathology and Immunology, University of Geneva, Geneva, Switzerland. Marien Koen K HistoGeneX, Antwerp, Belgium. Melero-Martin Juan M JM Department of Cardiac Surgery, Harvard Medical School, Boston Children's Hospital, Boston, MA, USA. Munn Lance L LL Edwin L. Steele Laboratories, Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. Nicosia Roberto F RF Department of Pathology, University of Washington, Seattle, WA, USA. Pathology and Laboratory Medicine Service, VA Puget Sound Health Care System, Seattle, WA, USA. Noel Agnes A Laboratory of Tumor and Developmental Biology, GIGA-Cancer, University of Liège, Liège, Belgium. Nurro Jussi J Department of Biotechnology and Molecular Medicine, University of Eastern Finland, Kuopio, Finland. Olsson Anna-Karin AK Department of Medical Biochemistry and Microbiology, Science for Life Laboratory, Uppsala Biomedical Center, Uppsala University, Uppsala, Sweden. Petrova Tatiana V TV Department of oncology UNIL-CHUV, Ludwig Institute for Cancer Research Lausanne, Lausanne, Switzerland. Pietras Kristian K Division of Translational Cancer Research, Department of Laboratory Medicine, Lund, Sweden. Pili Roberto R Genitourinary Program, Indiana University-Simon Cancer Center, Indianapolis, IN, USA. Pollard Jeffrey W JW Medical Research Council Centre for Reproductive Health, College of Medicine and Veterinary Medicine, University of Edinburgh, Edinburgh, UK. Post Mark J MJ Department of Physiology, Maastricht University, Maastricht, The Netherlands. Quax Paul H A PHA Einthoven Laboratory for Experimental Vascular Medicine, Department Surgery, LUMC, Leiden, The Netherlands. Rabinovich Gabriel A GA Laboratory of Immunopathology, Institute of Biology and Experimental Medicine, National Council of Scientific and Technical Investigations (CONICET), Buenos Aires, Argentina. Raica Marius M Department of Microscopic Morphology/Histology, Angiogenesis Research Center, Victor Babes University of Medicine and Pharmacy, Timisoara, Romania. Randi Anna M AM Vascular Sciences, Imperial Centre for Translational and Experimental Medicine, National Heart and Lung Institute, Imperial College London, London, UK. Ribatti Domenico D Department of Basic Medical Sciences, Neurosciences and Sensory Organs, University of Bari Medical School, Bari, Italy. National Cancer Institute "Giovanni Paolo II", Bari, Italy. Ruegg Curzio C Department of Oncology, Microbiology and Immunology, Faculty of Science and Medicine, University of Fribourg, Fribourg, Switzerland. Schlingemann Reinier O RO Ocular Angiogenesis Group, Departments of Ophthalmology and Medical Biology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. Department of Ophthalmology, University of Lausanne, Jules-Gonin Eye Hospital, Fondation Asile des Aveugles, Lausanne, Switzerland. Schulte-Merker Stefan S Institute of Cardiovascular Organogenesis and Regeneration, Faculty of Medicine, WWU, Münster, Germany. Smith Lois E H LEH Department of Ophthalmology, Harvard Medical School, Boston Children's Hospital, Boston, MA, USA. Song Jonathan W JW Department of Mechanical and Aerospace Engineering, The Ohio State University, Columbus, OH, USA. Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA. Stacker Steven A SA Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre and The Sir Peter MacCallum, Department of Oncology, University of Melbourne, Melbourne, VIC, Australia. Stalin Jimmy J Institute of Cardiovascular Organogenesis and Regeneration, Faculty of Medicine, WWU, Münster, Germany. Stratman Amber N AN Division of Developmental Biology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA. Van de Velde Maureen M Laboratory of Tumor and Developmental Biology, GIGA-Cancer, University of Liège, Liège, Belgium. van Hinsbergh Victor W M VWM Department of Ophthalmology, University of Lausanne, Jules-Gonin Eye Hospital, Fondation Asile des Aveugles, Lausanne, Switzerland. Vermeulen Peter B PB HistoGeneX, Antwerp, Belgium. Translational Cancer Research Unit, GZA Hospitals, Sint-Augustinus & University of Antwerp, Antwerp, Belgium. Waltenberger Johannes J Medical Faculty, University of Münster, Albert-Schweitzer-Campus 1, Münster, Germany. Weinstein Brant M BM Division of Developmental Biology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA. Xin Hong H University of California, San Diego, La Jolla, CA, USA. Yetkin-Arik Bahar B Ocular Angiogenesis Group, Departments of Ophthalmology and Medical Biology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. Yla-Herttuala Seppo S Department of Biotechnology and Molecular Medicine, University of Eastern Finland, Kuopio, Finland. Yoder Mervin C MC Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN, USA. Griffioen Arjan W AW Angiogenesis Laboratory, Department of Medical Oncology, VU University Medical Center, Cancer Center Amsterdam, De Boelelaan 1117, 1081 HV, Amsterdam, The Netherlands. aw.griffioen@vumc.nl. eng R01 CA177875 CA NCI NIH HHS United States R01 CA201537 CA NCI NIH HHS United States Journal Article Review 2018 05 15

Germany Angiogenesis 9814575 0969-6970 Angiogenesis Aortic ring Chorioallantoic membrane (CAM) Corneal angiogenesis Endothelial cell migration Hindlimb ischemia Intussusceptive angiogenesis Microfluidic Myocardial angiogenesis Plug assay Proliferation Recombinant proteins Retinal vasculature Tip cells Vascular network Vessel co-option Zebrafish 2018 5 17 6 0 2018 5 17 6 0 2018 5 17 6 0 aheadofprint 29766399 10.1007/s10456-018-9613-x 10.1007/s10456-018-9613-x 29538184 2018 04 20 2018 04 20

1531-7021 29 3 2018 May Curr Opin Ophthalmol Sutureless transscleral fixation of secondary intraocular lenses. 210-216 10.1097/ICU.0000000000000474 The surgical approach to eyes needing a secondary intraocular lens have evolved rapidly in recent years. Here, we will focus on techniques for scleral-fixation of intraocular lenses (IOLs), and will review the evidence for their safety and efficacy. Transscleral fixation of IOLs refers the placement of lens haptics within scleral tunnels to stabilize the lens in eyes that lack adequate capsular support. Various surgical techniques have been reported recently to accomplish this goal. These include the use of a trocar, microvitreoretinal blade, or hypodermic needle to create the scleral tunnels, as well as several methods for placing the haptics through the tunnels. Although long-term data is lacking, each technique has been shown to have good visual outcomes without significant side effects. Surgical approaches for the transscleral fixation of secondary IOLs provide a safe and effective technique for the management of eyes with insufficient capsular support. Nudleman Eric E Department of Ophthalmology, Shiley Eye Institute and Jacobs Retina Center, University of California San Diego, La Jolla, California. Yonekawa Yoshihiro Y Department of Ophthalmology, Mass Eye and Ear and Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts. Prenner Jonathan L JL Department of Ophthalmology, Rutgers Robert Wood Johnson Medical School. NJ Retina, New Brunswick, New Jersey, USA. eng Journal Article Review

United States Curr Opin Ophthalmol 9011108 1040-8738 IM Humans Lens Implantation, Intraocular adverse effects methods Lenses, Intraocular Postoperative Complications Sclera surgery Suture Techniques adverse effects Visual Acuity 2018 3 15 6 0 2018 4 21 6 0 2018 3 15 6 0 ppublish 29538184 10.1097/ICU.0000000000000474 29851754 2018 05 31

1537-2677 2018 May 18 Ophthalmic Plast Reconstr Surg Histopathologic Findings of Linear Scleroderma Displaying Focal Trichiasis Secondary to Tarsal Thinning. 10.1097/IOP.0000000000001140 Linear scleroderma en coup de sabre with ophthalmic findings has been previously described in the literature on numerous occasions. A 57-year-old woman presented with focal trichiasis secondary to tarsal thinning, adjacent to a linear brow and forehead deformity consistent with linear scleroderma en coup de sabre. Cases of linear scleroderma en coup de sabre involving the eyelids have been reported, most often with madarosis, ptosis, or skin atrophy; however, to the authors' knowledge, this is the first reported case of linear scleroderma associated with trichiasis and involvement of the deeper eyelid tissues, particularly the tarsus. Reshef Edith R ER Department of Ophthalmology, Ophthalmic Plastic Surgery, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, U.S.A. Wolkow Natalie N Department of Ophthalmology, Ophthalmic Plastic Surgery, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, U.S.A. David G. Cogan Laboratory of Ophthalmic Pathology, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts, U.S.A. Jakobiec Frederick A FA David G. Cogan Laboratory of Ophthalmic Pathology, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts, U.S.A. Yoon Michael K MK Department of Ophthalmology, Ophthalmic Plastic Surgery, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, U.S.A. eng Journal Article 2018 05 18

United States Ophthalmic Plast Reconstr Surg 8508431 0740-9303 2018 6 1 6 0 2018 6 1 6 0 2018 6 1 6 0 aheadofprint 29851754 10.1097/IOP.0000000000001140 29746876 2018 06 08

1873-7528 90 2018 Jul Neurosci Biobehav Rev The spatial representation of number, time, and serial order following sensory deprivation: A systematic review. 371-380 S0149-7634(17)30516-X 10.1016/j.neubiorev.2018.04.021 The spatial representation of numerical and temporal information is thought to be rooted in our multisensory experiences. Accordingly, we may expect visual or auditory deprivation to affect the way we represent numerical magnitude and time spatially. Here, we systematically review recent findings on how blind and deaf individuals represent abstract concepts such as magnitude and time (e.g., past/future, serial order of events) in a spatial format. Interestingly, available evidence suggests that sensory deprivation does not prevent the spatial "re-mapping" of abstract information, but differences compared to normally sighted and hearing individuals may emerge depending on the specific dimension considered (i.e., numerical magnitude, time as past/future, serial order). Herein we discuss how the study of sensory deprived populations may shed light on the specific, and possibly distinct, mechanisms subserving the spatial representation of these concepts. Furthermore, we pinpoint unresolved issues that need to be addressed by future studies to grasp a full understanding of the spatial representation of abstract information associated with visual and auditory deprivation. Copyright © 2018 Elsevier Ltd. All rights reserved. Rinaldi Luca L Department of Psychology, University of Milano-Bicocca, Milano, Italy; NeuroMI, Milan Center for Neuroscience, Milano, Italy. Electronic address: luca.rinaldi@unimib.it. Merabet Lotfi B LB The Laboratory for Visual Neuroplasticity, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, USA. Vecchi Tomaso T Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy; IRCCS Mondino Foundation, Pavia, Italy. Cattaneo Zaira Z Department of Psychology, University of Milano-Bicocca, Milano, Italy; IRCCS Mondino Foundation, Pavia, Italy. Electronic address: zaira.cattaneo@unimib.it. eng Journal Article Review 2018 05 07

United States Neurosci Biobehav Rev 7806090 0149-7634 Blindness Deafness Number Sensory deprivation Serial order Space Spatial representation Time 2017 07 19 2018 03 15 2018 04 27 2018 5 11 6 0 2018 5 11 6 0 2018 5 11 6 0 ppublish 29746876 S0149-7634(17)30516-X 10.1016/j.neubiorev.2018.04.021 28991108 2018 06 27

1526-7598 126 5 2018 May Anesth. Analg. Patient Harm in Cataract Surgery: A Series of Adverse Events in Massachusetts. 1548-1550 10.1213/ANE.0000000000002526 Massachusetts state agencies received reports of 37 adverse events (AEs) involving cataract surgery from 2011 to 2015. Fifteen were anesthesia related, including 5 wrong eye blocks, 3 cases of hemodynamic instability, 2 retrobulbar hematoma/hemorrhages, and 5 globe perforations resulting in permanent loss of vision. While Massachusetts' reported AEs likely underrepresent the true number of AEs that occur during cataract surgery, they do offer useful signal data to indicate the types of patient harm occurring during these procedures. Roberto Sarah A SA From the Betsy Lehman Center for Patient Safety, Boston, Massachusetts. Bayes Joseph J Department of Anesthesia, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts. Karner Paul E PE From the Betsy Lehman Center for Patient Safety, Boston, Massachusetts. Morley Michael G MG Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts. Nanji Karen C KC Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard University, Boston, Massachusetts. eng K08 HS024764 HS AHRQ HHS United States Journal Article

United States Anesth Analg 1310650 0003-2999 2017 10 11 6 0 2017 10 11 6 0 2017 10 10 6 0 ppublish 28991108 10.1213/ANE.0000000000002526 29746512 2018 05 27

1932-6203 13 5 2018 PLoS ONE Visual acuity and contrast sensitivity are two important factors affecting vision-related quality of life in advanced age-related macular degeneration. e0196481 10.1371/journal.pone.0196481 Vision loss from age-related macular degeneration (AMD) has a profound effect on vision-related quality of life (VRQoL). The pupose of this study is to identify clinical factors associated with VRQoL using the Rasch- calibrated NEI VFQ-25 scales in bilateral advanced AMD patients. We retrospectively reviewed 47 patients (mean age 83.2 years) with bilateral advanced AMD. Clinical assessment included age, gender, type of AMD, high contrast visual acuity (VA), history of medical conditions, contrast sensitivity (CS), central visual field loss, report of Charles Bonnet Syndrome, current treatment for AMD and Rasch-calibrated NEI VFQ-25 visual function and socioemotional function scales. The NEI VFQ visual function scale includes items of general vision, peripheral vision, distance vision and near vision-related activity while the socioemotional function scale includes items of vision related-social functioning, role difficulties, dependency, and mental health. Multiple regression analysis (structural regression model) was performed using fixed item parameters obtained from the one-parameter item response theory model. Multivariate analysis showed that high contrast VA and CS were two factors influencing VRQoL visual function scale (β = -0.25, 95% CI-0.37 to -0.12, p<0.001 and β = 0.35, 95% CI 0.25 to 0.46, p<0.001) and socioemontional functioning scale (β = -0.2, 95% CI -0.37 to -0.03, p = 0.023, and β = 0.3, 95% CI 0.18 to 0.43, p = 0.001). Central visual field loss was not assoicated with either VRQoL visual or socioemontional functioning scale (β = -0.08, 95% CI-0.28 to 0.12,p = 0.44 and β = -0.09, 95% CI -0.03 to 0.16, p = 0.50, respectively). In patients with vision impairment secondary to bilateral advanced AMD, high contrast VA and CS are two important factors affecting VRQoL. Roh Miin M http://orcid.org/0000-0003-3346-754X Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, United States of America. Selivanova Alexandra A Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, United States of America. Shin Hyun Joon HJ Division of Aging, Brigham and Women's Hospital, Department of Medicine, VA Boston Health care system, Harvard Medical School, Boston, Massachusetts, United States of America. Miller Joan W JW Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, United States of America. Jackson Mary Lou ML VGH/Univeristy of British Coumbia Eye Care Centre, Vancouver, British Columbia, Canada. eng Journal Article 2018 05 10

United States PLoS One 101285081 1932-6203 J Cataract Refract Surg. 2010 May;36(5):718-32 20457362 Arch Ophthalmol. 2001 Jul;119(7):1050-8 11448327 Ophthalmology. 2018 Mar;125(3):369-390 29110945 Graefes Arch Clin Exp Ophthalmol. 2003 Dec;241(12):968-74 13680248 Invest Ophthalmol Vis Sci. 2012 May 31;53(6):3201-6 22491415 Invest Ophthalmol Vis Sci. 2010 Jun;51(6):2878-84 20089878 Semin Ophthalmol. 2004 Mar-Jun;19(1-2):55-61 15590535 Ophthalmology. 2005 Jan;112(1):152-8 15629836 Pharmacoeconomics. 2008;26(1):57-73 18088159 Qual Life Res. 2007 Apr;16(3):533-43 17119846 Acta Ophthalmol. 2016 Dec;94(8):e772-e778 27225020 Trans Am Ophthalmol Soc. 2005;103:173-84; discussion 184-6 17057801 Ophthalmology. 2001 Oct;108(10):1893-900; discussion 1900-1 11581068 Ophthalmology. 2011 Jul;118(7):1395-401 21444116 Ophthalmology. 2004 May;111(5):931-9 15121371 J Cataract Refract Surg. 2001 Feb;27(2):261-6 11226793 Health Qual Life Outcomes. 2006 Dec 21;4:97 17184527 Ophthalmology. 1999 Sep;106(9):1768-79 10485549 Eur J Ophthalmol. 2007 Jan-Feb;17(1):63-8 17294384 Am J Ophthalmol. 2003 Dec;136(6):1067-78 14644217 Invest Ophthalmol Vis Sci. 2010 Feb;51(2):712-7 19797233 Am J Ophthalmol. 2005 Feb;139(2):271-9 15733988 Optom Vis Sci. 2006 Mar;83(3):178-89 16534460 Vision Res. 2013 Sep 20;90:10-4 23643905 JAMA Ophthalmol. 2014 Mar;132(3):272-7 24385141 2017 05 31 2018 04 14 2018 5 11 6 0 2018 5 11 6 0 2018 5 11 6 0 epublish 29746512 10.1371/journal.pone.0196481 PONE-D-17-20886 PMC5944956 29803500 2018 05 27

1879-1883 2018 May 18 Am. J. Surg. Advances in medical polymer technology towards the panacea of complex 3D tissue and organ manufacture. S0002-9610(18)30581-6 10.1016/j.amjsurg.2018.05.012 Singh Deepti D Department of Ophthalmology, Schepens Eye Research Institute, Harvard Medical School, Boston, MA, 02114, USA. Electronic address: Deepti_singh@meei.harvard.edu. Thomas Daniel D 3Dynamic Systems, Llynfi Enterprise Centre, Heol Ty Gwyn, United Kingdom. Electronic address: daniel.thomas@engineer.com. eng Letter 2018 05 18

United States Am J Surg 0370473 0002-9610 2018 04 19 2018 05 15 2018 5 28 6 0 2018 5 29 6 0 2018 5 29 6 0 aheadofprint 29803500 S0002-9610(18)30581-6 10.1016/j.amjsurg.2018.05.012 29761759 2018 06 15

1476-1645 2018 May 14 Am. J. Trop. Med. Hyg. Seasonal and Temporal Trends in Childhood Conjunctivitis in Burkina Faso. 10.4269/ajtmh.17-0642 Acute conjunctivitis follows a seasonal pattern. Although its clinical course is typically self-limited, conjunctivitis epidemics incur a substantial economic burden because of missed school and work days. This study investigated seasonal and temporal trends of childhood conjunctivitis in the entire country of Burkina Faso from 2013 to 2016, using routine monthly surveillance from 2,444 government health facilities. A total of 783,314 cases were reported over the 4-year period. Conjunctivitis followed a seasonal pattern throughout the country, with a peak in April. A nationwide conjunctivitis outbreak with a peak in September 2016 was noted (P < 0.001), with an excess number of cases first detected in June 2016. Nationwide passive surveillance was able to detect an epidemic 3 months before its peak, which may aide in allocation of resources for containment and mitigation of transmission in future outbreaks. Sié Ali A Centre de Recherche en Sante de Nouna, Nouna, Burkina Faso. Diarra Abdramane A Centre de Recherche en Sante de Nouna, Nouna, Burkina Faso. Millogo Ourohiré O Centre de Recherche en Sante de Nouna, Nouna, Burkina Faso. Zongo Augustin A National Health Information System, Ministry of Health, Ouagadougou, Burkina Faso. Lebas Elodie E Francis I. Proctor Foundation, University of California San Francisco, San Francisco, California. Bärnighausen Till T Africa Health Research Institute, KwaZulu-Natal, South Africa. Department of Global Health and Population, Harvard T.H. Chan School of Public Health, Boston, Massachusetts. Heidelberg Institute of Public Health, Heidelberg University, Heidelberg, Germany. Chodosh James J Cornea and Refractive Surgery, Massachusetts Eye and Ear Hospital, Boston, Massachusetts. Porco Travis C TC Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, California. Department of Ophthalmology, University of California San Francisco, San Francisco, California. Francis I. Proctor Foundation, University of California San Francisco, San Francisco, California. Deiner Michael S MS Department of Ophthalmology, University of California San Francisco, San Francisco, California. Francis I. Proctor Foundation, University of California San Francisco, San Francisco, California. Lietman Thomas M TM Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, California. Department of Ophthalmology, University of California San Francisco, San Francisco, California. Francis I. Proctor Foundation, University of California San Francisco, San Francisco, California. Keenan Jeremy D JD Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, California. Department of Ophthalmology, University of California San Francisco, San Francisco, California. Francis I. Proctor Foundation, University of California San Francisco, San Francisco, California. Oldenburg Catherine E CE Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, California. Department of Ophthalmology, University of California San Francisco, San Francisco, California. Francis I. Proctor Foundation, University of California San Francisco, San Francisco, California. eng L40 EY028421 EY NEI NIH HHS United States R01 EY024608 EY NEI NIH HHS United States R25 MH083620 MH NIMH NIH HHS United States Journal Article 2018 05 14

United States Am J Trop Med Hyg 0370507 0002-9637 2018 5 16 6 0 2018 5 16 6 0 2018 5 16 6 0 aheadofprint 29761759 10.4269/ajtmh.17-0642 29621365 2018 05 25

2168-6173 136 5 2018 May 01 JAMA Ophthalmol Association of Hypovitaminosis D With Increased Risk of Uveitis in a Large Health Care Claims Database. 548-552 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

United States JAMA Ophthalmol 101589539 2168-6165 2018 4 6 6 0 2018 4 6 6 0 2018 4 6 6 0 ppublish 29621365 2677067 10.1001/jamaophthalmol.2018.0642 29633588 2018 06 20 2018 06 20

2162-0989 7 3 2018 May-Jun Asia Pac J Ophthalmol (Phila) Familial Exudative Vitreoretinopathy: Pathophysiology, Diagnosis, and Management. 176-182 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 Review 2018 04 09

China Asia Pac J Ophthalmol (Phila) 101583622 2162-0989 Familial Exudative Vitreoretinopathy IM Diagnostic Techniques, Ophthalmological Genetic Therapy methods Humans Retinal Diseases diagnosis physiopathology therapy Visual Acuity Vitreoretinal Surgery methods FEVR familial exudative vitreoretinopathy 2018 4 11 6 0 2018 6 21 6 0 2018 4 11 6 0 ppublish 29633588 10.22608/APO.201855 29427122 2018 05 12

1943-393X 80 4 2018 May Atten Percept Psychophys Visual search for changes in scenes creates long-term, incidental memory traces. 829-843 10.3758/s13414-018-1486-y Humans are very good at remembering large numbers of scenes over substantial periods of time. But how good are they at remembering changes to scenes? In this study, we tested scene memory and change detection two weeks after initial scene learning. In Experiments 1-3, scenes were learned incidentally during visual search for change. In Experiment 4, observers explicitly memorized scenes. At test, after two weeks observers were asked to discriminate old from new scenes, to recall a change that they had detected in the study phase, or to detect a newly introduced change in the memorization experiment. Next, they performed a change detection task, usually looking for the same change as in the study period. Scene recognition memory was found to be similar in all experiments, regardless of the study task. In Experiment 1, more difficult change detection produced better scene memory. Experiments 2 and 3 supported a "depth-of-processing" account for the effects of initial search and change detection on incidental memory for scenes. Of most interest, change detection was faster during the test phase than during the study phase, even when the observer had no explicit memory of having found that change previously. This result was replicated in two of our three change detection experiments. We conclude that scenes can be encoded incidentally as well as explicitly and that changes in those scenes can leave measurable traces even if they are not explicitly recalled. Utochkin Igor S IS Psychology Department, National Research University Higher School of Economics, Armyansky per., 4, room 419, Moscow, Russian Federation, 101000. isutochkin@inbox.ru. Wolfe Jeremy M JM Visual Attention Laboratory, Brigham & Women's Hospital, Cambridge, MA, USA. Departments of Radiology and Ophthalmology, Harvard Medical School, Boston, MA, USA. eng TZ-64 Program for Basic Research National Research University Higher School of Economics in 2016 Journal Article

United States Atten Percept Psychophys 101495384 1943-3921 Change blindness Incidental learning Long-term memory Visual search 2018 2 11 6 0 2018 2 11 6 0 2018 2 11 6 0 ppublish 29427122 10.3758/s13414-018-1486-y 10.3758/s13414-018-1486-y 29476725 2018 04 24

1879-1891 189 2018 May Am. J. Ophthalmol. The Effect of Botulinum Toxin Augmentation on Strabismus Surgery for Large-Angle Infantile Esotropia. 160-165 S0002-9394(18)30068-0 10.1016/j.ajo.2018.02.010 To determine whether botulinum toxin augments the effect of strabismus surgery in pediatric patients with large-angle infantile esotropia. Retrospective, comparative, case series. Setting: Tertiary-care pediatric hospital. Patients with large-angle infantile esotropia. Treatment with botulinum toxin-augmented bilateral medial rectus muscle recessions ("augmented-surgery group") or traditional bilateral medial rectus muscle recessions ("surgery-only group"). The effect of surgery on ocular alignment at 4 months, measured in prism diopters of change per mm of surgery (PD/mm). There were 14 patients in the augmented-surgery group and 16 patients in the surgery-only group. The mean effect on alignment was significantly greater in the augmented-surgery group compared to the surgery-only group at 4 months (5.7 ± 1.3 vs 4.0 ± 1.4 PD/mm, P = .002) and at 1 year (5.4 ± 1.2 vs 3.7 ± 1.2 PD/mm, P = .002). There was a partial loss of treatment effect between 4 months and 1 year in both groups, which was similar in magnitude (P = .57). On linear regression, there was a trend toward a positive correlation between botulinum toxin dose and treatment effect, but this was not statistically significant (P = .09). Botulinum toxin augments the surgical effect of medial rectus muscle recession. Botulinum toxin-augmented surgery may be an alternative to traditional options for large-angle infantile esotropia. A surgical dosing table is proposed for this technique. Copyright © 2018 Elsevier Inc. All rights reserved. Wan Michael J MJ Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts; Department of Ophthalmology, Boston Children's Hospital, Boston, Massachusetts. Gilbert Aubrey A Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts; Department of Ophthalmology, Boston Children's Hospital, Boston, Massachusetts. Kazlas Melanie M Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts; Department of Ophthalmology, Boston Children's Hospital, Boston, Massachusetts. Wu Carolyn C Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts; Department of Ophthalmology, Boston Children's Hospital, Boston, Massachusetts. Mantagos Iason S IS Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts; Department of Ophthalmology, Boston Children's Hospital, Boston, Massachusetts. Hunter David G DG Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts; Department of Ophthalmology, Boston Children's Hospital, Boston, Massachusetts. Shah Ankoor S AS Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts; Department of Ophthalmology, Boston Children's Hospital, Boston, Massachusetts. Electronic address: ankoor.shah@childrens.harvard.edu. eng Journal Article 2018 02 21

United States Am J Ophthalmol 0370500 0002-9394 2017 08 10 2018 02 11 2018 02 14 2018 2 25 6 0 2018 2 25 6 0 2018 2 25 6 0 ppublish 29476725 S0002-9394(18)30068-0 10.1016/j.ajo.2018.02.010 29470973 2018 04 24

1879-1891 189 2018 May Am. J. Ophthalmol. Long-term Surgical Outcomes for Large-angle Infantile Esotropia. 155-159 S0002-9394(17)30483-X 10.1016/j.ajo.2017.11.006 To report the long-term surgical outcomes for a cohort of children with large-angle infantile esotropia. Multicenter, nonrandomized clinical study. Setting: Two tertiary-care pediatric hospitals. Children with large-angle (≥55 prism diopters) infantile esotropia. Surgical treatment of infantile esotropia. Success rate at final follow-up (postoperative deviation ≤ 10 prism diopters and no need for retreatment). A total of 88 patients with large-angle infantile esotropia were treated during the 13-year study period. Treatment was bilateral medial rectus muscle recessions in 70 patients, botulinum toxin-augmented surgery in 15 patients, and 3-muscle surgery in 3 patients. After a mean follow-up of 40 months, 20 patients (23%) had a successful outcome compared to 68 treatment failures (77%). Of the 68 treatment failures, 59 had residual or recurrent esotropia and 9 had sequential exotropia. On multivariate logistic regression, treatment modality was the only factor significantly associated with a successful outcome. Specifically, patients treated with botulinum toxin-augmented surgery were more likely to have a successful outcome compared to patients treated with bilateral medial rectus muscle recessions. For the 26 patients (30%) who underwent retreatment, the mean number of procedures was 2.1, and 7 (27%) had a deviation of ≤10 prism diopters at final follow-up. The overall success rate for treatment of large-angle infantile esotropia was poor in this cohort, with most failures owing to recurrent or residual esotropia. Botulinum toxin-augmented surgery was associated with a higher success rate at final follow-up. Copyright © 2018 Elsevier Inc. All rights reserved. Wan Michael J MJ Department of Ophthalmology and Vision Sciences, Hospital for Sick Children and University of Toronto, Toronto, Canada; Department of Ophthalmology, Boston Children's Hospital and Harvard Medical School, Boston, Massachusetts. Chiu Hedva H Department of Ophthalmology and Vision Sciences, Hospital for Sick Children and University of Toronto, Toronto, Canada. Shah Ankoor S AS Department of Ophthalmology, Boston Children's Hospital and Harvard Medical School, Boston, Massachusetts. Hunter David G DG Department of Ophthalmology, Boston Children's Hospital and Harvard Medical School, Boston, Massachusetts. Electronic address: david.hunter@childrens.harvard.edu. eng Journal Article 2018 02 19

United States Am J Ophthalmol 0370500 0002-9394 2017 08 10 2017 11 02 2017 11 06 2018 2 23 6 0 2018 2 23 6 0 2018 2 23 6 0 ppublish 29470973 S0002-9394(17)30483-X 10.1016/j.ajo.2017.11.006 29775216 2018 05 22

1097-4547 2018 May 18 J. Neurosci. Res. Neuroimmflammation and microglia in glaucoma: time for a paradigm shift. 10.1002/jnr.24256 Glaucoma is a complex neurodegenerative disease with many clinical subtypes. Some of its rare forms include pigmentary glaucoma, uveitic glaucoma and congenital glaucoma. While they all share common features of progressive retinal ganglion cell (RGC) loss, optic nerve damage and corresponding visual field loss, the exact mechanisms underlying glaucomatous neuron loss are not clear. This has largely hindered the development of a real cure for this disease. Elevated intraocular pressure (IOP) is a known major risk factor of glaucoma; however, progressive degeneration of RGCs and axons can also be found in patients with a normal IOP, i.e., normal tension glaucoma (NTG). Interestingly, patients who carry the gain-of-function mutation of the pro-inflammatory gene TBK1 - tumor necrosis factor (TNF) receptor associated factor NF-κB activator (TANK) binding kinase 1 - are at increased risk to develop NTG. This finding suggests a causal link between neuroinflammatory processes and glaucoma. Various studies have reported the presence of neuroinflammatory responses by microglia, astrocytes and other blood-born immune cells in the optic nerve head (ONH) at early stages of experimental glaucoma. Inhibition of certain pro-inflammatory pathways, particularly those associated with microglial activation, appears to be neuroprotective. In this review, we will focus on the inflammatory responses, in particular the proposed roles of microglia, in the pathogenesis of glaucoma. © 2018 Wiley Periodicals, Inc. Wei Xin X Department of Ophthalmology, West China Hospital, Sichuan University, Chengdu, China. Department of Ophthalmology, Harvard Medical School, Schepens Eye Research Institute of Massachusetts Eye and Ear, Boston, Massachusetts. Cho Kin-Sang KS http://orcid.org/0000-0003-4285-615X Department of Ophthalmology, Harvard Medical School, Schepens Eye Research Institute of Massachusetts Eye and Ear, Boston, Massachusetts. Thee Eric F EF Department of Ophthalmology, Harvard Medical School, Schepens Eye Research Institute of Massachusetts Eye and Ear, Boston, Massachusetts. Department of Ophthalmology, Leiden University Medical Center, Leiden, the Netherlands. Jager Martine J MJ Department of Ophthalmology, Leiden University Medical Center, Leiden, the Netherlands. Chen Dong Feng DF http://orcid.org/0000-0001-6283-8843 Department of Ophthalmology, Harvard Medical School, Schepens Eye Research Institute of Massachusetts Eye and Ear, Boston, Massachusetts. eng R01 EY025259 EY NEI NIH HHS United States Journal Article Review 2018 05 18

United States J Neurosci Res 7600111 0360-4012 glaucoma inflammation microglia neurodegeneration 2018 01 31 2018 04 16 2018 04 19 2018 5 19 6 0 2018 5 19 6 0 2018 5 19 6 0 aheadofprint 29775216 10.1002/jnr.24256 29547466 2018 05 08

1537-2677 34 3 2018 May/Jun Ophthalmic Plast Reconstr Surg Dermalive Facial Filler Granulomas Masquerading as Neurofibromas. e99-e103 10.1097/IOP.0000000000001100 A 56-year-old woman presented with periocular nodules that were clinically suspected to be neurofibromas. Histopathologic examination of excised nodules revealed a pronounced granulomatous reaction to a foreign material that was composed of glossy polygonal palely eosinophilic fragments. These fragments were outlined in red with Masson trichrome, stained gray with the elastic stain, and were uniformly red with Gomori methenamine silver staining. The histopathologic appearance was consistent with a granulomatous reaction to Dermalive facial filler. Postoperatively the patient admitted that she had filler injections many years earlier in another country, and that nodules appeared 1 year after injection. Treatment with steroids, intralesional immunosuppressive agents and surgery had been previously attempted to eradicate the nodules. The literature pertaining to granulomatous reactions to Dermalive and related hybrid facial fillers is reviewed and treatment options are discussed. This report is the first to illustrate the unique histopathologic staining characteristics of Dermalive, which may be useful to ophthalmic pathologists in identifying this uncommon foreign material. Wolkow Natalie N David G. Cogan Laboratory of Ophthalmic Pathology. Jakobiec Frederick A FA David G. Cogan Laboratory of Ophthalmic Pathology. Yoon Michael K MK Ophthalmic Plastic and Reconstructive Surgery Service, Department of Ophthalmology of the Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts, U.S.A. eng Journal Article

United States Ophthalmic Plast Reconstr Surg 8508431 0740-9303 2018 3 17 6 0 2018 3 17 6 0 2018 3 17 6 0 ppublish 29547466 10.1097/IOP.0000000000001100 29346171 2018 05 08

1537-2677 34 3 2018 May/Jun Ophthalmic Plast Reconstr Surg A Common Procedure With an Uncommon Pathology: Triamcinolone Acetonide Eyelid Injection. e72-e73 10.1097/IOP.0000000000001045 Local corticosteroid injections are frequently employed by ophthalmologists to treat a variety of ocular, periocular, and orbital inflammatory conditions. Triamcinolone acetonide is a slowly dissolving crystalline corticosteroid that is often used for this purpose because of its prolonged anti-inflammatory effect. On occasion, previously injected corticosteroid material persists in tissues longer than anticipated, creating nodules that may masquerade as other disease conditions, or appearing incidentally in excised lesions on histopathologic examination. The histopathologic features of corticosteroid residues are unfamiliar to most ophthalmic pathologists and general pathologists. These features are described herein. Triamcinolone acetonide deposits in the skin appear as pale eosinophilic lakes of acellular frothy material on hematoxylin-eosin staining and are occasionally surrounded by a mild inflammatory reaction. Wolkow Natalie N Department of Ophthalmology, David G Cogan Laboratory of Ophthalmic Pathology, Massachusetts Eye and Ear Infirmary, Harvard Medical School. Jakobiec Frederick A FA Department of Ophthalmology, David G Cogan Laboratory of Ophthalmic Pathology, Massachusetts Eye and Ear Infirmary, Harvard Medical School. Hatton Mark P MP Harvard Medical School. Ophthalmic Consultants of Boston, Boston, Massachusetts, U.S.A. eng Journal Article

United States Ophthalmic Plast Reconstr Surg 8508431 0740-9303 2018 1 19 6 0 2018 1 19 6 0 2018 1 19 6 0 ppublish 29346171 10.1097/IOP.0000000000001045 29776671 2018 05 28

1549-4713 2018 May 24 Ophthalmology Guidelines on Diabetic Eye Care: The International Council of Ophthalmology Recommendations for Screening, Follow-up, Referral, and Treatment Based on Resource Settings. S0161-6420(17)33523-6 10.1016/j.ophtha.2018.04.007 Diabetes mellitus (DM) is a global epidemic and affects populations in both developing and developed countries, with differing health care and resource levels. Diabetic retinopathy (DR) is a major complication of DM and a leading cause of vision loss in working middle-aged adults. Vision loss from DR can be prevented with broad-level public health strategies, but these need to be tailored to a country's and population's resource setting. Designing DR screening programs, with appropriate and timely referral to facilities with trained eye care professionals, and using cost-effective treatment for vision-threatening levels of DR can prevent vision loss. The International Council of Ophthalmology Guidelines for Diabetic Eye Care 2017 summarize and offer a comprehensive guide for DR screening, referral and follow-up schedules for DR, and appropriate management of vision-threatening DR, including diabetic macular edema (DME) and proliferative DR, for countries with high- and low- or intermediate-resource settings. The guidelines include updated evidence on screening and referral criteria, the minimum requirements for a screening vision and retinal examination, follow-up care, and management of DR and DME, including laser photocoagulation and appropriate use of intravitreal anti-vascular endothelial growth factor inhibitors and, in specific situations, intravitreal corticosteroids. Recommendations for management of DR in patients during pregnancy and with concomitant cataract also are included. The guidelines offer suggestions for monitoring outcomes and indicators of success at a population level. Copyright © 2018 American Academy of Ophthalmology. All rights reserved. Wong Tien Y TY Singapore Eye Research Institute, Singapore National Eye Centre, Singapore, Republic of Singapore; Duke-NUS Medical School, National University of Singapore, Singapore, Republic of Singapore. Electronic address: wong.tien.yin@snec.com.sg. Sun Jennifer J Beetham Eye Institute, Joslin Diabetes Center, and Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts. Kawasaki Ryo R Department of Public Health, Yamagata University Graduate School of Medical Science, Yamagata, Japan. Ruamviboonsuk Paisan P Department of Ophthalmology, Rajavithi Hospital, Bangkok, Thailand. Gupta Neeru N Ophthalmology and Vision Sciences, St. Michael's Hospital, University of Toronto, and Dalla Lana School of Public Health, University of Toronto, Toronto, Canada. Lansingh Van Charles VC Help Me See and Instituto Mexicano de Oftalmologia, Queretaro, Mexico. Maia Mauricio M Department of Ophthalmology and Visual Sciences, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, Brazil. Mathenge Wanjiku W Rwanda International Institute of Ophthalmology, and Dr Agarwal's Eye Hospital, Kigali, Rwanda. Moreker Sunil S Apollo, Nanavati, Seven Hills, Fortis Hiranandani, Cumballa Hill, SL Raheja, Eyeris, Conwest Jain, Bhaktivedant, MGM Hospitals, Mumbai, India. Muqit Mahi M K MMK Vitreoretinal Service, Moorfields Eye Hospital, NIHR Moorfields Biomedical Research Centre (BRC), London, United Kingdom. Resnikoff Serge S Brien Holden Vision Institute and SOVS, University of New South Wales, Sydney, Australia. Verdaguer Juan J Los Andes Ophthalmologic Foundation, Los Andes University, Santiago, Chile. Zhao Peiquan P Department of Ophthalmology, Xin Hua Hospital affiliated with Shanghai Jiao Tong University School of Medicine, Shanghai, China. Ferris Frederick F National Eye Institute, National Institutes of Health, Bethesda, Maryland. Aiello Lloyd P LP Beetham Eye Institute, Joslin Diabetes Center, and Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts. Taylor Hugh R HR Melbourne School of Population and Global Health, University of Melbourne, Melbourne, Australia. eng Journal Article Review 2018 05 24

United States Ophthalmology 7802443 0161-6420 2017 12 08 2018 04 05 2018 04 05 2018 5 20 6 0 2018 5 20 6 0 2018 5 20 6 0 aheadofprint 29776671 S0161-6420(17)33523-6 10.1016/j.ophtha.2018.04.007