29557828 2018 06 04

1536-481X 27 6 2018 Jun J. Glaucoma The Influence of Corneal Biomechanical Properties on Intraocular Pressure Measurements Using a Rebound Self-tonometer. 511-518 10.1097/IJG.0000000000000948 The purpose of this study was to examine the effect of corneal biomechanical properties on intraocular pressure (IOP) measurements obtained using a rebound self-tonometer (Icare HOME) compared with Goldmann applanation tonometry (GAT). An observational study of 100 patients with glaucoma or ocular hypertension. All had a comprehensive ophthalmic examination and standard automated perimetry. IOP was assessed by GAT, Icare HOME and Ocular Response Analyzer, which was also used to assess corneal hysteresis (CH) and corneal resistance factor (CRF). Central corneal thickness (CCT) was recorded. Mean (±SD) IOP measurements were 14.3±3.9 and 11.7±4.7 mm Hg using GAT and Icare HOME, respectively. Average CCT, CRF, and CH were 534.5±37.3 μm, 9.0±1.7 mm Hg, and 9.4±1.5 mm Hg, respectively. The mean difference between Icare HOME and GAT was -2.66±3.13 mm Hg, with 95% limits of agreement of -8.80 to 3.48 mm Hg, however, there was evidence of proportional bias. There was negative correlation between IOP and CH [5.17 mm Hg higher Icare HOME IOP (P=0.041, R=0.029) and 7.23 mm Hg higher GAT IOP (P=0.008, R=0.080) for each 10 mm Hg lower CH], whereas thinner CCT was significantly associated with lower IOP (P<0.001, R=0.14 for Icare HOME and P<0.001, R=0.08 for GAT). In multivariable analysis, although CRF and CH remained associated with IOP measured using either GAT or Icare HOME, CCT was no longer significant. IOP measurements obtained using a self-tonometer, similar to GAT, were more influenced by overall corneal biomechanics than CCT. Brown Lyndsay L Princess Alexandra Eye Pavilion, Department of Ophthalmology, University of Edinburgh, Edinburgh, UK. Foulsham William W Department of Ophthalmology, Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA. Pronin Savva S Princess Alexandra Eye Pavilion, Department of Ophthalmology, University of Edinburgh, Edinburgh, UK. Tatham Andrew J AJ Princess Alexandra Eye Pavilion, Department of Ophthalmology, University of Edinburgh, Edinburgh, UK. eng Journal Article

United States J Glaucoma 9300903 1057-0829 2018 3 21 6 0 2018 3 21 6 0 2018 3 21 6 0 ppublish 29557828 10.1097/IJG.0000000000000948 29953020 2018 06 28

1536-5964 97 26 2018 Jun Medicine (Baltimore) Trends in dacryocystitis in China: A STROBE-compliant article. e11318 10.1097/MD.0000000000011318 The aim of the study was to review the distribution, current trends, and microbiological characteristics of bacterial pathogens isolated from dacryocystitis patients in China during the last 15 years.This is a retrospective multiple-center noncomparative case series. The medical records of 15,452 consecutive patients from 7 cities diagnosed as having dacryocystitis between 2002 and 2016 were reviewed. The patients' demographics, microbiological data, and antibiotic sensitivity were reviewed and analyzed.A total of 3344 lacrimal sac content cultures were taken (21.6%) during the study period. A pathogen was identified in 1996 samples (59.7%), with bacterial isolates accounting for 1902 of the positive cultures (95.3%). Gram-positive isolates, gram-negative isolates, and anaerobic bacteria were found in 1218 (61.0%), 607 (30.4%), and 285 (14.3%) samples, respectively. An increase in gram-positive isolates over the study duration was found (P = .003). The predominant isolates were coagulase negative Staphylococci (485, 25.5%), Staphylococcus aureus (186, 9.8%), Pseudomonas aeruginosa (184, 9.7%), and Haemophilus influenzae (152, 9.0%). There was a trend toward increasing resistance to erythromycin from 10.5% during the first 5 years of the study to 20.7% during the last 5 years (P < .001). Antimicrobial susceptibility testing showed that gatifloxacin was the most effective drug against most of gram-positive, gram-negative, and anaerobic bacteria.The microbial culture rate of dacryocystitis in China is low. There was an increase in the percentage of gram-positive bacteria over time. The sensitivity of gram-positive isolates to tested antibiotics is relatively low compared with that of gram-negative isolates. Our data show that the empiric use of fourth-generation fluoroquinolones in refractory dacryocystitis may be justified. Chen Lijuan L People's Hospital of Putuo District, Shanghai. Fu Tongsheng T Department of Ophthalmology, People Hospital, Yangzhong. Gu Hao H Department of Ophthalmology, The Affiliated Hospital of Guizhou Medical University, Guiyang. Jie Ying Y Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Ophthalmology and Visual Science Key Laboratory Beijing, China. Sun Zhongmou Z Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA. Jiang Donghong D Department of Ophthalmology, The Second People Hospital, Taixing. Yu Jibing J The Affiliated Hospital of Ningbo University, Ningbo. Zhu Xinxing X Rudong Hospital of Traditional Chinese Medicine, Rudong. Xu Jianjiang J Department of Ophthalmology and Visual Science, Eye, and ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China. Hong Jiaxu J Department of Ophthalmology, The Affiliated Hospital of Guizhou Medical University, Guiyang. Department of Ophthalmology and Visual Science, Eye, and ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China. eng Journal Article

United States Medicine (Baltimore) 2985248R 0025-7974 2018 6 29 6 0 2018 6 29 6 0 2018 6 29 6 0 ppublish 29953020 10.1097/MD.0000000000011318 00005792-201806290-00083 29039719 2018 06 27

1931-8448 24 5 2018 Jun Microb. Drug Resist. Resistance in In Vitro Selected Tigecycline-Resistant Methicillin-Resistant Staphylococcus aureus Sequence Type 5 Is Driven by Mutations in mepR and mepA Genes. 519-526 10.1089/mdr.2017.0279 A tigecycline-susceptible (TGC-S) Sequence Type (ST) 5 clinical methicillin-resistant Staphylococcus aureus (MRSA) strain was cultured in escalating levels of tigecycline, yielding mutants eightfold more resistant. Their genomes were sequenced to identify genetic alterations, resulting in resistance. Alterations in rpsJ, commonly related to tigecycline resistance, were also investigated. Tigecycline resistance was mediated by loss-of-function mutations in the transcriptional repressor mepR, resulting in derepression of the efflux pump mepA. Increased levels of resistance were obtained by successive mutations in mepA itself. No alterations in RpsJ were observed in selected strains, but we observed a K57M substitution, previously correlated with resistance, among TGC-S clinical strains. Thus, the pathway to tigecycline resistance in CC5 MRSA in vitro appears to be derepression of mep operon as the result of mepR loss-of-function mutation, followed by alterations in MepA efflux pump. This shows that other evolutionary pathways, besides mutation of rpsJ, are available for evolving tigecycline resistance in CC5 MRSA. Dabul Andrei Nicoli Gebieluca ANG 1 Department of Physics and Interdisciplinary Science, São Carlos Institute of Physics, University of São Paulo , São Carlos, Brazil . Avaca-Crusca Juliana Sposto JS 1 Department of Physics and Interdisciplinary Science, São Carlos Institute of Physics, University of São Paulo , São Carlos, Brazil . Van Tyne Daria D 2 Department of Ophthalmology, Harvard Medical School , Massachusetts Eye and Ear Infirmary, Boston, Massachusetts. 3 Department of Microbiology and Immunobiology, Harvard Medical School , Boston, Massachusetts. Gilmore Michael S MS 2 Department of Ophthalmology, Harvard Medical School , Massachusetts Eye and Ear Infirmary, Boston, Massachusetts. 3 Department of Microbiology and Immunobiology, Harvard Medical School , Boston, Massachusetts. Camargo Ilana Lopes Baratella Cunha ILBC 1 Department of Physics and Interdisciplinary Science, São Carlos Institute of Physics, University of São Paulo , São Carlos, Brazil . eng K99 EY028222 EY NEI NIH HHS United States P01 AI083214 AI NIAID NIH HHS United States Journal Article 2017 10 17

United States Microb Drug Resist 9508567 1076-6294 MRSA MepA MepR tigecycline 2017 10 19 6 0 2017 10 19 6 0 2017 10 18 6 0 ppublish 29039719 10.1089/mdr.2017.0279 29946065 2018 06 29

2045-2322 8 1 2018 Jun 26 Sci Rep C3a triggers formation of sub-retinal pigment epithelium deposits via the ubiquitin proteasome pathway. 9679 10.1038/s41598-018-28143-0 The mechanisms that connect complement system activation and basal deposit formation in early stages of age-related macular degeneration (AMD) are insufficiently understood, which complicates the design of efficient therapies to prevent disease progression. Using human fetal (hf) retinal pigment epithelial (RPE) cells, we have established an in vitro model to investigate the effect of complement C3a on RPE cells and its role in the formation of sub-RPE deposits. The results of these studies revealed that C3a produced after C3 activation is sufficient to induce the formation of sub-RPE deposits via complement-driven proteasome inhibition. C3a binds the C3a receptor (C3aR), stimulates deposition of collagens IV and VI underneath the RPE, and impairs the extracellular matrix (ECM) turnover by increased MMP-2 activity, all mediated by downregulation of the ubiquitin proteasome pathway (UPP). The formation of basal deposits can be prevented by the addition of a C3aR antagonist, which restores the UPP activity and ECM turnover. These findings indicate that the cell-based model can be used to test potential therapeutic agents in vitro. The data suggest that modulation of C3aR-mediated events could be a therapeutic approach for treatment of early AMD. Fernandez-Godino Rosario R Ocular Genomics Institute, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, 02114, USA. rosario_godino@meei.harvard.edu. Pierce Eric A EA Ocular Genomics Institute, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, 02114, USA. eng P30 EY014104 EY NEI NIH HHS United States Journal Article 2018 06 26

England Sci Rep 101563288 2045-2322 2018 02 10 2018 06 15 2018 6 28 6 0 2018 6 28 6 0 2018 6 28 6 0 epublish 29946065 10.1038/s41598-018-28143-0 10.1038/s41598-018-28143-0 29784095 2018 05 22

1549-4713 125 6 2018 Jun Ophthalmology Pseudohemangioma in Nonarteritic Anterior Ischemic Optic Neuropathy. 903 S0161-6420(18)30169-6 10.1016/j.ophtha.2018.01.029 Fortin Elizabeth E Neuro-ophthalmology Service, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts. Gaier Eric D ED Neuro-ophthalmology Service, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts. eng Journal Article

United States Ophthalmology 7802443 0161-6420 2018 01 15 2018 01 22 2018 01 22 2018 5 23 6 0 2018 5 23 6 0 2018 5 23 6 0 ppublish 29784095 S0161-6420(18)30169-6 10.1016/j.ophtha.2018.01.029 29953490 2018 06 28

1932-6203 13 6 2018 PLoS ONE Quantitative analysis of optical coherence tomographic angiography (OCT-A) in patients with non-arteritic anterior ischemic optic neuropathy (NAION) corresponds to visual function. e0199793 10.1371/journal.pone.0199793 Non-arteritic anterior ischemic optic neuropathy (NAION) is the most common cause of non-glaucomatous optic neuropathy in older adults. Optical coherence tomographic angiography (OCT-A) is an emerging, non-invasive method to study the microvasculature of the posterior pole, including the optic nerve head. The goal of this study was to assess the vascular changes in the optic nerve head and peripapillary area associated with NAION using OCT-A. Retrospective comparative case series. We performed OCT-A in 25 eyes (7 acute and 18 non-acute) in 19 patients with NAION. Fellow, unaffected eyes were analyzed for comparison. Patent macro- and microvascular densities were quantified in the papillary and peripapillary regions of unaffected, acutely affected, and non-acutely affected eyes and compared across these groups according to laminar segment and capillary sampling region, and with respect to performance on automated visual field testing. In acutely affected eyes, OCT-A revealed a reduction in the signal from the major retinal vessels and dilation of patent superficial capillaries in the peripapillary area. By contrast, non-acutely affected eyes showed attenuation of patent capillaries. The peripapillary choriocapillaris was obscured by edema in acute cases, but was similar between non-acute and unaffected eyes. The degree of dilation of the superficial microvasculature in the acute phase and attenuation in the non-acute phase each correlated inversely with visual field performance. The region of reduced patent capillary density correlated with the location of visual field defects in 80% of acute cases and 80% of non-acute cases. OCT-A reveals a dynamic shift in the superficial capillary network of the optic nerve head with strong functional correlates in both the acute and non-acute phases of NAION. Further study may validate OCT-A as a useful adjunctive diagnostic tool in the evaluation of ischemic optic neuropathy. Gaier Eric D ED Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, United States of America. Wang Mengyu M Schepens Eye Research Institute, Harvard Medical School, Boston, MA, United States of America. Gilbert Aubrey L AL Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, United States of America. Rizzo Joseph F JF 3rd Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, United States of America. Cestari Dean M DM Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, United States of America. Miller John B JB Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, United States of America. eng Journal Article 2018 06 28

United States PLoS One 101285081 1932-6203 The authors have declared that no competing interests exist. 2017 12 08 2018 06 13 2018 6 29 6 0 2018 6 29 6 0 2018 6 29 6 0 epublish 29953490 10.1371/journal.pone.0199793 PONE-D-17-43106 29955180 2018 06 29

1546-1718 2018 Jun 28 Nat. Genet. Using an atlas of gene regulation across 44 human tissues to inform complex disease- and trait-associated variation. 10.1038/s41588-018-0154-4 We apply integrative approaches to expression quantitative loci (eQTLs) from 44 tissues from the Genotype-Tissue Expression project and genome-wide association study data. About 60% of known trait-associated loci are in linkage disequilibrium with a cis-eQTL, over half of which were not found in previous large-scale whole blood studies. Applying polygenic analyses to metabolic, cardiovascular, anthropometric, autoimmune, and neurodegenerative traits, we find that eQTLs are significantly enriched for trait associations in relevant pathogenic tissues and explain a substantial proportion of the heritability (40-80%). For most traits, tissue-shared eQTLs underlie a greater proportion of trait associations, although tissue-specific eQTLs have a greater contribution to some traits, such as blood pressure. By integrating information from biological pathways with eQTL target genes and applying a gene-based approach, we validate previously implicated causal genes and pathways, and propose new variant and gene associations for several complex traits, which we replicate in the UK BioBank and BioVU. Gamazon Eric R ER http://orcid.org/0000-0003-4204-8734 Division of Genetic Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA. egamazon@uchicago.edu. Clare Hall, University of Cambridge, Cambridge, UK. egamazon@uchicago.edu. Segrè Ayellet V AV http://orcid.org/0000-0001-6806-5845 The Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA, USA. asegre@broadinstitute.org. Department of Ophthalmology and Ocular Genomics Institute, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA, USA. asegre@broadinstitute.org. van de Bunt Martijn M http://orcid.org/0000-0002-6744-6125 Wellcome Centre for Human Genetics, Nuffield Department of Medicine, University of Oxford, Oxford, UK. Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, UK. Wen Xiaoquan X Department of Biostatistics, University of Michigan, Ann Arbor, MI, USA. Xi Hualin S HS Computational Sciences, Pfizer Inc, Cambridge, MA, USA. Hormozdiari Farhad F http://orcid.org/0000-0002-5617-6174 Department of Computer Science, University of California, Los Angeles, CA, USA. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA. Ongen Halit H http://orcid.org/0000-0002-4197-5790 Department of Genetic Medicine and Development, University of Geneva Medical School, Geneva, Switzerland. Institute for Genetics and Genomics in Geneva (iG3), University of Geneva, Geneva, Switzerland. Swiss Institute of Bioinformatics, Geneva, Switzerland. Konkashbaev Anuar A Division of Genetic Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA. Derks Eske M EM http://orcid.org/0000-0002-6292-6883 Translational Neurogenomics Group, QIMR Berghofer, Brisbane, Queensland, Australia. Aguet François F http://orcid.org/0000-0001-9414-300X The Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA, USA. Quan Jie J Computational Sciences, Pfizer Inc, Cambridge, MA, USA. GTEx Consortium Nicolae Dan L DL Section of Genetic Medicine, Department of Medicine, The University of Chicago, Chicago, IL, USA. Department of Statistics, The University of Chicago, Chicago, IL, USA. Department of Human Genetics, The University of Chicago, Chicago, IL, USA. Eskin Eleazar E Department of Computer Science, University of California, Los Angeles, CA, USA. Kellis Manolis M The Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA, USA. Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, Cambridge, MA, USA. Getz Gad G http://orcid.org/0000-0002-0936-0753 The Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA, USA. Massachusetts General Hospital Cancer Center and Department of Pathology, Massachusetts General Hospital, Boston, MA, USA. McCarthy Mark I MI http://orcid.org/0000-0002-4393-0510 Wellcome Centre for Human Genetics, Nuffield Department of Medicine, University of Oxford, Oxford, UK. Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, UK. Dermitzakis Emmanouil T ET http://orcid.org/0000-0002-9302-6490 Department of Genetic Medicine and Development, University of Geneva Medical School, Geneva, Switzerland. Institute for Genetics and Genomics in Geneva (iG3), University of Geneva, Geneva, Switzerland. Swiss Institute of Bioinformatics, Geneva, Switzerland. Cox Nancy J NJ Division of Genetic Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA. Ardlie Kristin G KG The Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA, USA. eng Journal Article 2018 06 28

United States Nat Genet 9216904 1061-4036 2017 07 04 2018 05 08 2018 6 30 6 0 2018 6 30 6 0 2018 6 30 6 0 aheadofprint 29955180 10.1038/s41588-018-0154-4 10.1038/s41588-018-0154-4 29659833 2018 06 08

1460-2083 27 11 2018 Jun 01 Hum. Mol. Genet. Ift172 conditional knock-out mice exhibit rapid retinal degeneration and protein trafficking defects. 2012-2024 10.1093/hmg/ddy109 Intraflagellar transport (IFT) is a bidirectional transport process that occurs along primary cilia and specialized sensory cilia, such as photoreceptor outersegments. Genes coding for various IFT components are associated with ciliopathies. Mutations in IFT172 lead to diseases ranging from isolated retinal degeneration to severe syndromic ciliopathies. In this study, we created a mouse model of IFT172-associated retinal degeneration to investigate the ocular disease mechanism. We found that depletion of IFT172 in rod photoreceptors leads to a rapid degeneration of the retina, with severely reduced electroretinography (ERG) responses by 1 month and complete outer-nuclear layer (ONL) degeneration by 2 months. We investigated molecular mechanisms of degeneration and show that IFT172 protein reduction leads to mislocalization of specific photoreceptor outersegment (OS) proteins (RHO, RP1, IFT139), aberrant light-driven translocation of alpha transducin and altered localization of glioma-associated oncogene family member 1 (GLI1). This mouse model exhibits key features of the retinal phenotype observed in patients with IFT172-associated blindness and can be used for in vivo testing of ciliopathy therapies. Gupta Priya R PR Department of Ophthalmology, Ocular Genomics Institute, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA 02114, USA. Weill Cornell Medical College, New York, NY 10021, USA. Pendse Nachiket N Department of Ophthalmology, Ocular Genomics Institute, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA 02114, USA. Greenwald Scott H SH Department of Ophthalmology, Ocular Genomics Institute, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA 02114, USA. Leon Mihoko M Department of Ophthalmology, Ocular Genomics Institute, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA 02114, USA. Liu Qin Q Department of Ophthalmology, Ocular Genomics Institute, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA 02114, USA. Pierce Eric A EA Department of Ophthalmology, Ocular Genomics Institute, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA 02114, USA. Bujakowska Kinga M KM Department of Ophthalmology, Ocular Genomics Institute, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA 02114, USA. eng P30 EY014104 EY NEI NIH HHS United States R01 EY012910 EY NEI NIH HHS United States Journal Article

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1536-481X 2018 Jun 26 J. Glaucoma Juvenile Open Angle Glaucoma with Non Bullous Congenital Ichthyosiform Erythroderma. 10.1097/IJG.0000000000001016 Glaucoma in patients with Non Bullous Congenital Ichthyosiform Erythroderma (NBCIE) is a rare entity that has not been described in a histologically confirmed case. We present a unique case of coexisting glaucoma, ichthyosis and dwarfism that has not been previously described. We present a case of NBCIE with glaucoma and dwarfism that presented to our outpatient department. The patient was referred for watering and photophobia that were due to an epithelial defect that was subsequently managed conservatively. Investigations revealed the existence of a constellation of findings that are presented here. NBCIE, glaucoma and dwarfism represent a spectrum of diseases that seem to have a syndromic association. More gene linkage based analysis are however needed to further confirm our observations. NBCIE, glaucoma and dwarfism can often occur together and need to be assessed and managed individually. Early diagnosis of this spectrum can help improve patient management and quality of life. Dermatologists must get an ocular examination done for icthyoses patients. Ichhpujani Parul P Department of Ophthalmology, Government Medical College and Hospital, Sector-32, Chandigarh, India. Thakur Sahil S Department of Ophthalmology, Government Medical College and Hospital, Sector-32, Chandigarh, India. Kumar Suresh S Department of Ophthalmology, Government Medical College and Hospital, Sector-32, Chandigarh, India. Singh Rohan Bir RB Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston MA 02114, USA. eng Journal Article 2018 06 26

United States J Glaucoma 9300903 1057-0829 2018 6 29 6 0 2018 6 29 6 0 2018 6 29 6 0 aheadofprint 29952820 10.1097/IJG.0000000000001016 29784156 2018 05 22

1715-3360 53 3 2018 Jun Can. J. Ophthalmol. Lower ocular pulse amplitude with dynamic contour tonometry is associated with biopsy-proven giant cell arteritis. 215-221 S0008-4182(17)30621-X 10.1016/j.jcjo.2017.10.027 To determine the role of the ocular pulse amplitude (OPA) from Pascal dynamic contour tonometry in predicting the temporal artery biopsy (TABx) result in patients with suspected giant cell arteritis (GCA). Prospective validation study. Adults aged 50 years or older who underwent TABx from March 2015 to April 2017. Subjects on high-dose glucocorticoids more than 14 days or without serology before glucocorticoid initiation were excluded. The OPA from both eyes was obtained and averaged just before TABx of the predominantly symptomatic side. The variables chosen for the a priori prediction model were age, average OPA, and C-reactive protein (CRP). Erythrocyte sedimentation rate (ESR), platelets, jaw claudication, and eye findings were also recorded. In this study, subjects with a negative biopsy were considered not to have GCA, and contralateral biopsy was performed if the clinical suspicion for GCA remained high. An external validation set (XVAL) was obtained. Of 109 TABx, 19 were positive and 90 were negative. On univariate logistic regression, the average OPA had 0.60 odds for positive TABx (p = 0.03), with no statistically significant difference in age, sex, CRP, ESR, or jaw claudication. In suspected GCA, an OPA of 1 mm Hg had positive likelihood ratio 4.74 and negative likelihood ratio 0.87 for positive TABx. Multivariate regression of the prediction model using optimal mathematical transforms (inverse OPA, log CRP, age >65 years) had area under the receiver operating characteristic curve (AUROC) = 0.85 and AUROC_XVAL = 0.81. OPA is lower in subjects with biopsy-proven GCA and is a statistically significant predictor of GCA. Copyright © 2018 Canadian Ophthalmological Society. Published by Elsevier Inc. All rights reserved. Ing Edsel E Department of Ophthalmology and Vision Sciences, University of Toronto Medical School, Toronto, Ont. Electronic address: edinglidstrab@gmail.com. Pagnoux Christian C Department of Medicine, Rheumatology, University of Toronto Medical School, Toronto, Ont. Tyndel Felix F Department of Medicine, Neurology, University of Toronto Medical School, Toronto, Ont. Sundaram Arun A Department of Medicine, Neurology, University of Toronto Medical School, Toronto, Ont. Hershenfeld Seymour S Department of Ophthalmology and Vision Sciences, University of Toronto Medical School, Toronto, Ont. Ranalli Paul P Department of Medicine, Neurology, University of Toronto Medical School, Toronto, Ont. Chow Shirley S Department of Medicine, Rheumatology, University of Toronto Medical School, Toronto, Ont. Le Tran T Department of Ophthalmology and Vision Sciences, University of Toronto Medical School, Toronto, Ont. Lutchman Carla C Department of Ophthalmology and Vision Sciences, University of Toronto Medical School, Toronto, Ont. Rutherford Susan S Department of Ophthalmology and Vision Sciences, University of Toronto Medical School, Toronto, Ont. Lam Kay K Department of Ophthalmology and Vision Sciences, University of Toronto Medical School, Toronto, Ont. Bedi Harleen H Department of Ophthalmology and Vision Sciences, University of Toronto Medical School, Toronto, Ont. Torun Nurhan N Harvard Medical School, Beth Israel Deaconess Hospital, Boston Department of Ophthalmology, Boston, MA. eng Journal Article 2017 12 26

England Can J Ophthalmol 0045312 0008-4182 2017 06 17 2017 08 29 2017 10 10 2018 5 23 6 0 2018 5 23 6 0 2018 5 23 6 0 ppublish 29784156 S0008-4182(17)30621-X 10.1016/j.jcjo.2017.10.027 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 29895550 2018 06 13

1757-790X 2018 2018 Jun 11 BMJ Case Rep Traumatic corneal perforation with exteriorisation of Ahmed glaucoma valve tube. bcr-2018-225181 10.1136/bcr-2018-225181 We report a rare case of traumatic corneal perforation with Ahmed glaucoma valve (AGV) tube. A 5-year-old female child, diagnosed with refractory glaucoma, had undergone AGV implantation, presented with the posterior migration of AGV tube after trauma to the eye. The detailed ocular history, ophthalmic findings, clinical course and surgical management are discussed. © BMJ Publishing Group Ltd (unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted. Kumar Suresh S Department of Ophthalmology, Government Medical College and Hospital, Chandigarh, India. Ichhpujani Parul P Department of Ophthalmology, Government Medical College and Hospital, Chandigarh, India. Thakur Sahil S Department of Ophthalmology, Government Medical College and Hospital, Chandigarh, India. Singh Rohan Bir RB http://orcid.org/0000-0002-2426-3900 Department of Ophthalmology, Government Medical College and Hospital, Chandigarh, India. Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. eng Journal Article 2018 06 11

England BMJ Case Rep 101526291 1757-790X anterior chamber glaucoma iris ophthalmology Competing interests: None declared. 2018 6 14 6 0 2018 6 14 6 0 2018 6 14 6 0 epublish 29895550 bcr-2018-225181 10.1136/bcr-2018-225181 29621510 2018 05 25

1879-1891 190 2018 Jun Am. J. Ophthalmol. Peripheral Changes Associated With Delayed Dark Adaptation in Age-related Macular Degeneration. 113-124 S0002-9394(18)30150-8 10.1016/j.ajo.2018.03.035 To study the association between peripheral changes in age-related macular degeneration (AMD) and dark adaptation (DA). Prospective, cross-sectional study. We recruited patients with AMD and a control group (>50 years) without any vitreoretinal disease. Ultra-widefield (UWF) pseudocolor and fundus autofluorescence (FAF) were obtained, and were assessed by 2 graders for the presence of several peripheral changes in perimacular, midperipheral, and far-peripheral zones. All participants were also imaged with 7-field color fundus photographs used for AMD staging (Age-Related Eye Disease Study classification system). Both eyes of study participants were tested with a dark adaptation (DA) extended protocol (20 minutes). Multilevel mixed-effect models (accounting for correlated outcomes between 2 eyes) were used for analyses. We included 128 eyes (n = 72 patients), 75% with AMD and the remainder controls. The presence of reticular pigmentary changes in the midperipheral (ß = 4.3, P = .012) and far-peripheral zones (ß = 8.4, P < .001) was associated with delayed rod-intercept times (RITs), even after adjusting for confounding factors. The presence, number, and extent of peripheral classic drusen did not show a similar association (P ≥ .148). The presence of a mottled decreased FAF pattern in the midperipheral zone was also associated with prolonged RITs (β = 4.4, P = .031). Our results suggest an association between DA and the presence of peripheral reticular pigmentary changes, as well as the presence of a peripheral mottled decreased FAF pattern. This provides new insights on the clinical significance of peripheral changes in AMD, and their contribution to impairments on DA. Copyright © 2018 Elsevier Inc. All rights reserved. Laíns Inês I Retina Service, Massachusetts Eye and Ear, Harvard Ophthalmology AMD Center of Excellence, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Park Dong Ho DH Retina Service, Massachusetts Eye and Ear, Harvard Ophthalmology AMD Center of Excellence, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Mukai Ryo R Retina Service, Massachusetts Eye and Ear, Harvard Ophthalmology AMD Center of Excellence, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Silverman Rebecca R Retina Service, Massachusetts Eye and Ear, Harvard Ophthalmology AMD Center of Excellence, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Oellers Patrick P Retina Service, Massachusetts Eye and Ear, Harvard Ophthalmology AMD Center of Excellence, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Mach Steven S Retina Service, Massachusetts Eye and Ear, Harvard Ophthalmology AMD Center of Excellence, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Kim Ivana K IK Retina Service, Massachusetts Eye and Ear, Harvard Ophthalmology AMD Center of Excellence, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Vavvas Demetrios G DG Retina Service, Massachusetts Eye and Ear, Harvard Ophthalmology AMD Center of Excellence, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Miller Joan W JW Retina Service, Massachusetts Eye and Ear, Harvard Ophthalmology AMD Center of Excellence, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Miller John B JB Retina Service, Massachusetts Eye and Ear, Harvard Ophthalmology AMD Center of Excellence, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Husain Deeba D Retina Service, Massachusetts Eye and Ear, Harvard Ophthalmology AMD Center of Excellence, Department of Ophthalmology, Harvard Medical School, Boston, MA, United States. Electronic address: Deeba_Husain@meei.harvard.edu. eng Journal Article 2018 04 03

United States Am J Ophthalmol 0370500 0002-9394 2018 01 10 2018 03 14 2018 03 22 2018 4 6 6 0 2018 4 6 6 0 2018 4 6 6 0 ppublish 29621510 S0002-9394(18)30150-8 10.1016/j.ajo.2018.03.035 28452839 2018 06 14

1539-2864 38 6 2018 Jun Retina (Philadelphia, Pa.) HEALTH CONDITIONS LINKED TO AGE-RELATED MACULAR DEGENERATION ASSOCIATED WITH DARK ADAPTATION. 1145-1155 10.1097/IAE.0000000000001659 To determine the association between dark adaption (DA) and different health conditions linked with age-related macular degeneration (AMD). Cross-sectional study, including patients with AMD and a control group. Age-related macular degeneration was graded according to the Age-Related Eye Disease Study (AREDS) classification. We obtained data on medical history, medications, and lifestyle. Dark adaption was assessed with the extended protocol (20 minutes) of AdaptDx (MacuLogix). For analyses, the right eye or the eye with more advanced AMD was selected. Multivariate linear and logistic regressions were performed, accounting for age and AMD stage. Seventy-eight subjects (75.6% AMD; 24.4% controls) were included. Multivariate assessments revealed that body mass index (BMI; β = 0.30, P = 0.045), taking AREDS vitamins (β = 5.51, P < 0.001), and family history of AMD (β = 2.68, P = 0.039) were significantly associated with worse rod intercept times. Abnormal DA (rod intercept time ≥ 6.5 minutes) was significantly associated with family history of AMD (β = 1.84, P = 0.006), taking AREDS supplements (β = 1.67, P = 0.021) and alcohol intake (β = 0.07, P = 0.017). Besides age and AMD stage, a higher body mass index, higher alcohol intake, and a family history of AMD seem to impair DA. In this cohort, the use of AREDS vitamins was also statistically linked with impaired DA, most likely because of an increased severity of disease in subjects taking them. Laíns Inês I Retina Service, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts. Department of Ophthalmology, Faculty of Medicine, University of Coimbra, Coimbra, Portugal. Miller John B JB Retina Service, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts. Mukai Ryo R Retina Service, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts. Mach Steven S Retina Service, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts. Vavvas Demetrios D Retina Service, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts. Kim Ivana K IK Retina Service, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts. Miller Joan W JW Retina Service, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts. Husain Deeba D Retina Service, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts. eng Journal Article

United States Retina 8309919 0275-004X 2017 4 30 6 0 2017 4 30 6 0 2017 4 29 6 0 ppublish 28452839 10.1097/IAE.0000000000001659 29462403 2018 06 08

1460-2091 73 6 2018 Jun 01 J. Antimicrob. Chemother. Transferable vancomycin resistance in clade B commensal-type Enterococcus faecium. 1479-1486 10.1093/jac/dky039 Vancomycin-resistant Enterococcus faecium is a leading cause of MDR hospital infection. Two genetically definable populations of E. faecium have been identified: hospital-adapted MDR isolates (clade A) and vancomycin-susceptible commensal strains (clade B). VanN-type vancomycin resistance was identified in two isolates of E. faecium recovered from blood and faeces of an immunocompromised patient. To understand the genomic context in which VanN occurred in the hospitalized patient, the risk it posed for transmission in the hospital and its origins, it was of interest to determine where these strains placed within the E. faecium population structure. We obtained the genome sequence of the VanN isolates and performed comparative and functional genomics of the chromosome and plasmid content. We show that, in these strains, VanN occurs in a genetic background that clusters with clade B E. faecium, which is highly unusual. We characterized the chromosome and the conjugative plasmid that carries VanN resistance in these strains, pUV24. This plasmid exhibits signatures of in-host selection on the vanN operon regulatory system, which are associated with a constitutive expression of vancomycin resistance. VanN resistance in clade B strains may go undetected by current methods. We report a case of vancomycin resistance in a commensal lineage of E. faecium responsible for an atypical bacteraemia in an immunocompromised patient. A reservoir of transferable glycopeptide resistance in the community could pose a concern for public health. Lebreton François F Departments of Ophthalmology, Microbiology and Immunobiology, Harvard Medical School, Boston, MA, USA. Infectious Disease & Microbiome Program, The Broad Institute, Cambridge, MA, USA. Valentino Michael D MD Departments of Ophthalmology, Microbiology and Immunobiology, Harvard Medical School, Boston, MA, USA. Infectious Disease & Microbiome Program, The Broad Institute, Cambridge, MA, USA. Schaufler Katharina K Departments of Ophthalmology, Microbiology and Immunobiology, Harvard Medical School, Boston, MA, USA. Infectious Disease & Microbiome Program, The Broad Institute, Cambridge, MA, USA. Earl Ashlee M AM Infectious Disease & Microbiome Program, The Broad Institute, Cambridge, MA, USA. Cattoir Vincent V Université de Caen Basse-Normandie, EA4655 U2RM (équipe 'Antibio-résistance'), Caen, France. CHU de Caen, Service de Microbiologie, Caen, France. Gilmore Michael S MS Departments of Ophthalmology, Microbiology and Immunobiology, Harvard Medical School, Boston, MA, USA. Infectious Disease & Microbiome Program, The Broad Institute, Cambridge, MA, USA. eng HHSN272200900018C AI NIAID NIH HHS United States P01 AI083214 AI NIAID NIH HHS United States R01 AI072360 AI NIAID NIH HHS United States U19 AI110818 AI NIAID NIH HHS United States Journal Article

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2379-5042 3 3 2018 Jun 27 mSphere Bacterial RecA Protein Promotes Adenoviral Recombination during In Vitro Infection. e00105-18 10.1128/mSphere.00105-18 Adenovirus infections in humans are common and sometimes lethal. Adenovirus-derived vectors are also commonly chosen for gene therapy in human clinical trials. We have shown in previous work that homologous recombination between adenoviral genomes of human adenovirus species D (HAdV-D), the largest and fastest growing HAdV species, is responsible for the rapid evolution of this species. Because adenovirus infection initiates in mucosal epithelia, particularly at the gastrointestinal, respiratory, genitourinary, and ocular surfaces, we sought to determine a possible role for mucosal microbiota in adenovirus genome diversity. By analysis of known recombination hot spots across 38 human adenovirus genomes in species D (HAdV-D), we identified nucleotide sequence motifs similar to bacterial Chi sequences, which facilitate homologous recombination in the presence of bacterial Rec enzymes. These motifs, referred to here as Chi_AD, were identified immediately 5' to the sequence encoding penton base hypervariable loop 2, which expresses the arginine-glycine-aspartate moiety critical to adenoviral cellular entry. Coinfection with two HAdV-Ds in the presence of an Escherichia coli lysate increased recombination; this was blocked in a RecA mutant strain, E. coli DH5α, or upon RecA depletion. Recombination increased in the presence of E. coli lysate despite a general reduction in viral replication. RecA colocalized with viral DNA in HAdV-D-infected cell nuclei and was shown to bind specifically to Chi_AD sequences. These results indicate that adenoviruses may repurpose bacterial recombination machinery, a sharing of evolutionary mechanisms across a diverse microbiota, and unique example of viral commensalism.IMPORTANCE Adenoviruses are common human mucosal pathogens of the gastrointestinal, respiratory, and genitourinary tracts and ocular surface. Here, we report finding Chi-like sequences in adenovirus recombination hot spots. Adenovirus coinfection in the presence of bacterial RecA protein facilitated homologous recombination between viruses. Genetic recombination led to evolution of an important external feature on the adenoviral capsid, namely, the penton base protein hypervariable loop 2, which contains the arginine-glycine-aspartic acid motif critical to viral internalization. We speculate that free Rec proteins present in gastrointestinal secretions upon bacterial cell death facilitate the evolution of human adenoviruses through homologous recombination, an example of viral commensalism and the complexity of virus-host interactions, including regional microbiota. Copyright © 2018 Lee et al. Lee Jeong Yoon JY Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, USA. Lee Ji Sun JS Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, USA. Materne Emma C EC Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, USA. Rajala Rahul R Department of Chemistry and Biochemistry, University of Oklahoma, Norman, Oklahoma, USA. Ismail Ashrafali M AM Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, USA. Seto Donald D Bioinformatics and Computational Biology Program, School of Systems Biology, George Mason University, Manassas, Virginia, USA. Dyer David W DW Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA. Rajaiya Jaya J Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, USA jaya_rajaiya@meei.harvard.edu james_chodosh@meei.harvard.edu. Chodosh James J Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, USA jaya_rajaiya@meei.harvard.edu james_chodosh@meei.harvard.edu. eng P30 EY014104 EY NEI NIH HHS United States R01 EY013124 EY NEI NIH HHS United States R01 EY021558 EY NEI NIH HHS United States Journal Article 2018 06 20

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1460-2202 43 6 2018 Jun Curr. Eye Res. The Effect of Solithromycin, a Cationic Amphiphilic Drug, on the Proliferation and Differentiation of Human Meibomian Gland Epithelial Cells. 683-688 10.1080/02713683.2017.1418894 We previously discovered that azithromycin (AZM) acts directly on immortalized human meibomian gland epithelial cells (IHMGECs) to stimulate their lipid and lysosome accumulation and overall differentiation. We hypothesize that this phospholipidosis-like effect is due to AZM's cationic amphiphilic drug (CAD) nature. If our hypothesis is correct, then other CADs (e.g., solithromycin [SOL]) should be able to duplicate AZM's action on IHMGECs. Our purpose was to test this hypothesis. IHMGECs were cultured in the presence of vehicle or SOL (2, 10, or 20 µg/ml) for up to 7 days under proliferating or differentiating conditions. Positive (epidermal growth factor and bovine pituitary extract for proliferation; AZM for differentiation) and negative (vehicle) controls were included with the experiments. IHMGECs were evaluated for cell number, neutral lipid content, and lysosome accumulation. Our results demonstrate that SOL induces a rapid and dose-dependent increase in the accumulation of neutral lipids and lysosomes in HMGECs. The lysosomal effects were most prominent with the 10 and 20 µg/ml doses, and occurred earlier (i.e., 1 day) with SOL than with the AZM (10 µg/ml) control. The effects of SOL and AZM on IHMGEC differentiation were essentially the same after 3 days of culture. SOL did not influence the proliferation of HMGECs during a 7-day time period. Our results support our hypothesis that SOL, a CAD, is able to reproduce AZM's impact on lysosome and lipid accumulation, as well as the differentiation, of HMGECs. The effect of SOL on lysosome appearance was faster than that of AZM. Liu Yang Y a Schepens Eye Research Institute, Massachusetts Eye and Ear, and Department of Ophthalmology , Harvard Medical School , Boston , MA , USA. Kam Wendy R WR a Schepens Eye Research Institute, Massachusetts Eye and Ear, and Department of Ophthalmology , Harvard Medical School , Boston , MA , USA. Fernandes Prabhavathi P b Cempra Pharmaceuticals , Chapel Hill , NC , USA. Sullivan David A DA a Schepens Eye Research Institute, Massachusetts Eye and Ear, and Department of Ophthalmology , Harvard Medical School , Boston , MA , USA. eng Journal Article 2017 12 28

England Curr Eye Res 8104312 0271-3683 Solithromycin azithromycin cationic amphiphilic drug dry eye disease meibomian gland dysfunction phospholipidosis 2017 12 29 6 0 2017 12 29 6 0 2017 12 29 6 0 ppublish 29283676 10.1080/02713683.2017.1418894 29886125 2018 06 10

1879-3304 2018 Jun 07 Surv Ophthalmol Update on the Ophthalmic Management of Facial Paralysis. S0039-6257(18)30093-6 10.1016/j.survophthal.2018.06.001 Bell palsy is the most common neurologic condition affecting the cranial nerves. Lagophthalmos, exposure keratopathy, and corneal ulceration are potential complications. In this review, we evaluate various causes of facial paralysis as well as the level 1 evidence supporting the use of a short course of oral steroids for idiopathic Bell palsy to improve functional outcomes. Various surgical and nonsurgical techniques are also discussed for the management of residual facial dysfunction. Copyright © 2018. Published by Elsevier Inc. MacIntosh Peter W PW Illinois Eye and Ear Infirmary, University of Illinois at Chicago, Chicago, IL, USA. Electronic address: pmacint1@uic.edu. Fay Aaron M AM Department of Ophthalmology, Harvard Medical School, Boston, MA. eng Journal Article Review 2018 06 07

United States Surv Ophthalmol 0404551 0039-6257 2018 03 27 2018 05 30 2018 06 04 2018 6 11 6 0 2018 6 11 6 0 2018 6 11 6 0 aheadofprint 29886125 S0039-6257(18)30093-6 10.1016/j.survophthal.2018.06.001 29252689 2018 05 11

1536-5166 38 2 2018 Jun J Neuroophthalmol Rehabilitation of Visual Loss: Where We Are and Where We Need to Be. 223-229 10.1097/WNO.0000000000000594 Spontaneous recovery of visual loss resulting from injury to the brain is variable. A variety of traditional rehabilitative strategies, including the use of prisms or compensatory saccadic eye movements, have been used successfully to improve visual function and quality-of-life for patients with homonymous hemianopia. More recently, repetitive visual stimulation of the blind area has been reported to be of benefit in expanding the field of vision. We performed a literature review with main focus on clinical studies spanning from 1963 to 2016, including 52 peer-reviewed articles, relevant cross-referenced citations, editorials, and reviews. Repetitive visual stimulation is reported to expand the visual field, although the interpretation of results is confounded by a variety of methodological factors and conflicting outcomes from different research groups. Many studies used subjective assessments of vision and did not include a sufficient number of subjects or controls. The available clinical evidence does not strongly support claims of visual restoration using repetitive visual stimulation beyond the time that spontaneous visual recovery might occur. This lack of firm supportive evidence does not preclude the potential of real benefit demonstrated in laboratories. Additional well-designed clinical studies with adequate controls and methods to record ocular fixation are needed. Mansouri Behzad B Neurology Section (BM, MR), Department of Internal Medicine, Department of Ophthalmology, and Biomedical Engineering Program, University of Manitoba, Winnipeg, Manitoba, Canada; Neuro-Ophthalmology Service (JFR), Department of Ophthalmology, Harvard Medical School and the Massachusetts Eye and Ear Infirmary, Boston, Massachusetts; Department of Neurology (SP), Brigham and Women's Hospital, Boston, Massachusetts; and Harvard Medical School (JFR, SP), Boston, Massachusetts. Roznik Marinya M Rizzo Joseph F JF 3rd Prasad Sashank S eng Journal Article

United States J Neuroophthalmol 9431308 1070-8022 2017 12 19 6 0 2017 12 19 6 0 2017 12 19 6 0 ppublish 29252689 10.1097/WNO.0000000000000594 29444356 2018 05 31

1651-2227 107 6 2018 Jun Acta Paediatr. Long-chain polyunsaturated fatty acids decline rapidly in milk from mothers delivering extremely preterm indicating the need for supplementation. 1020-1027 10.1111/apa.14275 Our aim was to perform an in-depth analysis of the composition of fatty acids in milk from mothers delivering extremely preterm babies. We investigated longitudinal changes in milk fatty acid profiles and the relationship between several types of fatty acids, including omega-3 and omega-6. Milk samples were collected at three stages of lactation from 78 mothers who delivered at less than 28 weeks of pregnancy at the Sahlgrenska University Hospital, Gothenburg, Sweden, from April 2013 to September 2015. Fatty acid composition was analysed by gas chromatography-mass spectrometry. A reduction in long-chain polyunsaturated fatty acids (LCPUFAs) was observed during the lactation period. The concentrations of arachidonic acid and docosahexaenoic acid declined from medians of 0.34 to 0.22 mol% and 0.29 to 0.15 mol%, respectively, between postnatal day 7 and a postmenstrual age of 40 weeks. Strong correlations were found between the intermediates of several classes of fatty acids, including omega-3, omega-6 and omega-9. A rapid reduction in LCPUFA content in the mother's milk during the lactation period emphasises the importance of fatty acid supplementation to infants born extremely preterm, at least during the period corresponding to the third trimester, when rapid development of the brain and adipose tissue requires high levels of LCPUFAs. ©2018 The Authors. Acta Paediatrica published by John Wiley & Sons Ltd on behalf of Foundation Acta Paediatrica. Nilsson Anders K AK Section for Ophthalmology, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Löfqvist Chatarina C Section for Ophthalmology, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Najm Svetlana S Department of Paediatrics, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Hellgren Gunnel G Section for Ophthalmology, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Sävman Karin K Department of Paediatrics, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Andersson Mats X MX Department of Biology and Environmental Sciences, The Faculty of Science, University of Gothenburg, Gothenburg, Sweden. Smith Lois E H LEH The 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 2018 03 13

Norway Acta Paediatr 9205968 0803-5253 Semin Fetal Neonatal Med. 2017 Feb;22(1):8-14 27599697 Pediatr Res. 2016 May;79(5):723-30 26761122 Eur J Clin Nutr. 2013 Sep;67(9):966-71 23695208 J Pediatr. 2013 Mar;162(3 Suppl):S37-47 23445847 Prostaglandins Leukot Essent Fatty Acids. 2013 Sep;89(4):241-4 23870193 Ann Nutr Metab. 2007;51(6):550-6 18227623 Clin Nutr. 2017 Dec;36(6):1593-1600 27756480 Int J Food Sci Nutr. 2012 May;63(3):318-25 22023571 Am J Clin Nutr. 2007 Jun;85(6):1457-64 17556680 J Clin Invest. 1959 Feb;38(2):443-50 13631077 Cochrane Database Syst Rev. 2016 Sep 30;9:CD005252 27689716 Am J Clin Nutr. 1983 Aug;38(2):300-12 6881084 Am J Clin Nutr. 2014 Mar;99(3):734S-41S 24500153 Chang Gung Med J. 2005 Oct;28(10):708-15 16382755 Prostaglandins Leukot Essent Fatty Acids. 2009 Aug-Sep;81(2-3):143-50 19577914 J Matern Fetal Neonatal Med. 2016 Mar;29(5):832-5 25758615 Int Breastfeed J. 2017 Jan 28;12 :7 28149321 J Nutr. 2008 Nov;138(11):2222-8 18936223 Lipids Health Dis. 2009 Jun 10;8:20 19515230 Am J Clin Nutr. 2007 Nov;86(5):1323-30 17991642 J Pediatr Gastroenterol Nutr. 1994 Apr;18(3):355-60 8057221 Clin Nutr. 2011 Feb;30(1):116-23 20800325 Eur J Pediatr. 1997 Feb;156(2):142-7 9039520 J Pediatr Gastroenterol Nutr. 2015 Jul;61(1):8-17 25883056 Eur J Nutr. 2017 Jun;56(4):1733-1742 27164830 Clin Nutr ESPEN. 2017 Aug;20:17-23 29072164 Pediatr Neurol. 2016 Jun;59:54-61.e1 27318249 Pediatrics. 2013 Jan;131(1):e262-72 23248232 Early Hum Dev. 1996 Mar 22;44(3):215-23 8654314 Arachidonic acid Docosahexaenoic acid Extremely preterm infants Human milk Long-chain polyunsaturated fatty acids 2017 09 19 2018 02 08 2018 2 15 6 0 2018 2 15 6 0 2018 2 15 6 0 ppublish 29444356 10.1111/apa.14275 PMC5969106 29905657 2018 06 15

1872-6623 2018 Jun 12 Pain Color-Selective Photophobia in Ictal vs. Interictal Migraineurs and in Healthy Controls. 10.1097/j.pain.0000000000001303 Aversion to light is common among migraineurs undergoing acute attacks. Using psychophysical assessments in episodic migraine patients, we reported that white, blue, amber and red lights exacerbate migraine headache in a significantly larger percentage of patients and to a greater extent compared to green light. This study aimed at determining whether these findings are phase-dependent - namely, manifested exclusively during migraine (ictally) but not in its absence (interictally), or condition-dependent - i.e., expressed uniquely in migraineurs but not in healthy controls. To determine whether the color-preference of migraine-type photophobia is phase- or condition-dependent, we compared the effects of each color of light in each intensity between migraineurs during and in-between attacks and healthy controls. During the ictal and interictal phases, the proportion of migraineurs reporting changes in headache severity when exposed to the different colors of light increased in accordance with elevated light intensities. During the ictal phase, white, blue, amber and red lights exacerbated headaches in ∼80% of the patients; however, during the interictal phase light initiated headache in only 16-19%. Notably, green light exacerbated headaches in 40% and triggered headaches in 3% of the patients studied during the ictal and interictal phases, respectively. With one exception (highest red light intensity), no control subject reported headache in response to the light stimuli. These findings suggest that color preference is unique to migraineurs - as it was not found in control subjects - and that it is independent of whether or not the patients are in their ictal or interictal phase. Nir Rony-Reuven RR Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, Boston MA 02115. Harvard Medical School, Boston, MA 02215. Lee Alice J AJ Harvard Catalyst Clinical Research Center, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. Huntington Shaelah S Harvard Catalyst Clinical Research Center, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. Noseda Rodrigo R Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, Boston MA 02115. Harvard Medical School, Boston, MA 02215. Bernstein Carolyn A CA Harvard Medical School, Boston, MA 02215. Department of Neurology, Brigham and Women's Faulkner Hospital, Boston MA 02130. Fulton Anne B AB Harvard Medical School, Boston, MA 02215. Department of Ophthalmology, Children's Hospital Boston, Boston MA 02115. Bertisch Suzanne M SM Harvard Medical School, Boston, MA 02215. Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02115. Hovaguimian Alexandra A Harvard Medical School, Boston, MA 02215. Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA 02115. Buettner Catherine C Harvard Medical School, Boston, MA 02215. Department of Medicine, Mount Auburn Hospital, Cambridge MA 02138. Borsook David D Harvard Medical School, Boston, MA 02215. Center for Pain and the Brain, Department of Anesthesia Critical Care and Pain Medicine, Boston Children's Hospital, Boston, MA 02115 and. Burstein Rami R Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, Boston MA 02115. Harvard Medical School, Boston, MA 02215. eng Journal Article 2018 06 12

United States Pain 7508686 0304-3959 2018 6 16 6 0 2018 6 16 6 0 2018 6 16 6 0 aheadofprint 29905657 10.1097/j.pain.0000000000001303 29909964 2018 06 21

1537-6605 2018 Jun 04 Am. J. Hum. Genet. Neonatal-Onset Chronic Diarrhea Caused by Homozygous Nonsense WNT2B Mutations. S0002-9297(18)30168-X 10.1016/j.ajhg.2018.05.007 Homozygous nonsense mutations in WNT2B were identified in three individuals from two unrelated families with severe, neonatal-onset osmotic diarrhea after whole-exome sequencing was performed on trios from the two families. Intestinal biopsy samples from affected individuals were used for histology and immunofluorescence and to generate enteroids ex vivo. Histopathologic evaluation demonstrated chronic inflammatory changes in the stomach, duodenum, and colon. Immunofluorescence demonstrated diminished staining for OLFM4, a marker for intestinal stem cells (ISCs). The enteroids generated from WNT2B-deficient intestinal epithelium could not be expanded and did not survive passage. Addition of CHIR-99021 (a GSK3A and GSK3B inhibitor and activator of canonical WNT/β-CATENIN signaling) could not rescue WNT2B-deficient enteroids. Addition of supplemental recombinant murine WNT2B was able to perpetuate small enteroids for multiple passages but failed to expand their number. Enteroids showed a 10-fold increase in the expression of LEF1 mRNA and a 100-fold reduction in TLR4 expression, compared with controls by quantitative RT-PCR, indicating alterations in canonical WNT and microbial pattern-recognition signaling. In summary, individuals with homozygous nonsense mutations in WNT2B demonstrate severe intestinal dysregulation associated with decreased ISC number and function, likely explaining their diarrheal phenotype. WNT2B deficiency should be considered for individuals with neonatal-onset diarrhea. Copyright © 2018 American Society of Human Genetics. Published by Elsevier Inc. All rights reserved. O'Connell Amy E AE Division of Newborn Medicine, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA. Electronic address: amy.oconnell@childrens.harvard.edu. Zhou Fanny F Division of Endocrinology, Boston Children's Hospital, Boston, MA 02115, USA. Shah Manasvi S MS Division of Endocrinology, Boston Children's Hospital, Boston, MA 02115, USA. Murphy Quinn Q Division of Genetics and Genomics, Boston Children's Hospital, Boston, MA 02115, USA; The Manton Center for Orphan Disease Research, Boston Children's Hospital, Boston, MA 02115, USA. Rickner Hannah H Division of Endocrinology, Boston Children's Hospital, Boston, MA 02115, USA. Kelsen Judith J Division of Genetics, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA. Boyle John J Division of Gastroenterology, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA. Doyle Jefferson J JJ Department of Ophthalmology, Boston Children's Hospital, Boston, MA 02115, USA. Gangwani Bharti B Department of Ophthalmology, Boston Children's Hospital, Boston, MA 02115, USA. Thiagarajah Jay R JR Division of Gastroenterology, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA. Kamin Daniel S DS Division of Gastroenterology, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA. Goldsmith Jeffrey D JD Department of Pathology, Boston Children's Hospital, Boston, MA 02115, USA. Richmond Camilla C Division of Gastroenterology, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA. Breault David T DT Division of Endocrinology, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA; Harvard Stem Cell Institute, Cambridge, MA 02138, USA. Agrawal Pankaj B PB Division of Newborn Medicine, Boston Children's Hospital, Boston, MA 02115, USA; Division of Genetics and Genomics, Boston Children's Hospital, Boston, MA 02115, USA; The Manton Center for Orphan Disease Research, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA. Electronic address: pagrawal@enders.tch.harvard.edu. eng KL2 TR001100 TR NCATS NIH HHS United States R01 AR068429 AR NIAMS NIH HHS United States Journal Article 2018 06 04

United States Am J Hum Genet 0370475 0002-9297 CODE Lgr5 OLFM4 TLR4 WNT2B congenital diarrhea and enteropathy diarrhea intestinal stem cells 2018 03 08 2018 05 17 2018 6 19 6 0 2018 6 19 6 0 2018 6 19 6 0 aheadofprint 29909964 S0002-9297(18)30168-X 10.1016/j.ajhg.2018.05.007 29552665 2018 03 21

2451-9936 10 2018 Jun Am J Ophthalmol Case Rep Hemorrhagic choroidal melanoma. 105-107 10.1016/j.ajoc.2018.02.001 To demonstrate the clinical pathologic correlation in a hemorrhagic choroidal melanoma. A 52 year old patient presented with a large choroidal mass associated with vitreous and retinal hemorrhage. The eye was enucleated and histopathology demonstrated epithelioid-type MART1 positive tumor cells consistent with choroidal melanoma. The tumor had broken through Bruch's membrane, which led to localized vascular compression with bleeding into the subretinal space, retina and vitreous. Choroidal melanoma rarely presents with hemorrhage. Tumor rupture through Bruch's membrane may result in a tourniquet effect on the tumor vasculature leading to massive hemorrhage, as in this case. A high level of clinical suspicion is required to make the diagnosis. Oellers Patrick P Retina Service, Department of Ophthalmology, Mass Eye and Ear, Harvard Medical School, Boston, MA, USA. Wolkow Natalie N David G. Cogan Laboratory of Ophthalmic Pathology, Department of Ophthalmology, Mass Eye and Ear, Boston, MA, USA. Jakobiec Frederick A FA David G. Cogan Laboratory of Ophthalmic Pathology, Department of Ophthalmology, Mass Eye and Ear, Boston, MA, USA. Kim Ivana K IK Retina Service, Department of Ophthalmology, Mass Eye and Ear, Harvard Medical School, Boston, MA, USA. eng Journal Article 2018 02 07

United States Am J Ophthalmol Case Rep 101679941 2451-9936 Am J Ophthalmol. 2004 Mar;137(3):574-7 15013891 Arch Ophthalmol. 1979 Jul;97(7):1311-4 313204 Choroidal melanoma Hemorrhagic melanoma 2017 11 03 2018 02 05 2018 3 20 6 0 2018 3 20 6 0 2018 3 20 6 1 epublish 29552665 10.1016/j.ajoc.2018.02.001 S2451-9936(17)30338-9 PMC5852264 29915052 2018 06 29

1091-6490 2018 Jun 18 Proc. Natl. Acad. Sci. U.S.A. Microglia inhibit photoreceptor cell death and regulate immune cell infiltration in response to retinal detachment. 201719601 10.1073/pnas.1719601115 Retinal detachment (RD) is a sight-threatening complication common in many highly prevalent retinal disorders. RD rapidly leads to photoreceptor cell death beginning within 12 h following detachment. In patients with sustained RD, progressive visual decline due to photoreceptor cell death is common, leading to significant and permanent loss of vision. Microglia are the resident immune cells of the central nervous system, including the retina, and function in the homeostatic maintenance of the neuro-retinal microenvironment. It is known that microglia become activated and change their morphology in retinal diseases. However, the function of activated microglia in RD is incompletely understood, in part because of the lack of microglia-specific markers. Here, using the newly identified microglia marker P2ry12 and microglial depletion strategies, we demonstrate that retinal microglia are rapidly activated in response to RD and migrate into the injured area within 24 h post-RD, where they closely associate with infiltrating macrophages, a population distinct from microglia. Once in the injured photoreceptor layer, activated microglia can be observed to contain autofluorescence within their cell bodies, suggesting they function to phagocytose injured or dying photoreceptors. Depletion of retinal microglia results in increased disease severity and inhibition of macrophage infiltration, suggesting that microglia are involved in regulating neuroinflammation in the retina. Our work identifies that microglia mediate photoreceptor survival in RD and suggests that this effect may be due to microglial regulation of immune cells and photoreceptor phagocytosis. Copyright © 2018 the Author(s). Published by PNAS. Okunuki Yoko Y http://orcid.org/0000-0002-1612-7925 Angiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA 02114. Mukai Ryo R Angiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA 02114. Pearsall Elizabeth A EA Angiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA 02114. Klokman Garrett G Angiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA 02114. Husain Deeba D Angiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA 02114. Park Dong-Ho DH Angiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA 02114. Korobkina Ekaterina E Schepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114. Weiner Howard L HL Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115. Evergrande Center for Immunologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115. Butovsky Oleg O Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115. Evergrande Center for Immunologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115. Ksander Bruce R BR Schepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114. Miller Joan W JW http://orcid.org/0000-0003-2046-3996 Angiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA 02114. Connor Kip M KM http://orcid.org/0000-0002-2048-9080 Angiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA 02114; kip_connor@meei.harvard.edu. eng P30 EY014104 EY NEI NIH HHS United States Journal Article 2018 06 18

United States Proc Natl Acad Sci U S A 7505876 0027-8424 macrophages microglia phagocytosis photoreceptor cell death retinal detachment The authors declare no conflict of interest. 2018 6 20 6 0 2018 6 20 6 0 2018 6 20 6 0 aheadofprint 29915052 1719601115 10.1073/pnas.1719601115 29555514 2018 06 12

1528-3933 22 3 2018 Jun J AAPOS Congenital muscular dystrophy-dystroglycanopathy, type A, featuring bilateral retinal dysplasia and vertical angle kappa. 242-244.e1 S1091-8531(17)30444-5 10.1016/j.jaapos.2017.12.011 Muscular dystrophy-dystroglycanopathy type A (MDDGA3), one of a group of diseases collectively known as congenital muscular dystrophies, is an alpha-dystroglycanopathy with characteristic brain and ocular abnormalities. We report the case of a 9-month-old boy with developmental delay whose family sought evaluation for esotropia. Subsequent examination, imaging, and testing revealed significant motor and cognitive delay, marked weakness with appendicular spasticity, and a diffuse brain malformation. In addition, the patient had poor visual acuity, nystagmus, optic nerve hypoplasia, bilateral retinal dysplasia and retinal dragging with a large vertical angle kappa, and an avascular peripheral retina. Genetic testing revealed two known heterozygous mutations in the POMGnT1 gene confirming MDDGA3. He was treated with botulinum toxin injections for his strabismus and continues to be followed, with planned laser ablation of the peripheral avascular retina. Copyright © 2018 American Association for Pediatric Ophthalmology and Strabismus. Published by Elsevier Inc. All rights reserved. Peiris Timothy J TJ Rutgers New Jersey Medical School, Newark, New Jersey. Indaram Maanasa M Department of Ophthalmology, Boston Children's Hospital, Boston, Massachusetts; Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts. Koo Euna E Department of Ophthalmology, Boston Children's Hospital, Boston, Massachusetts; Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts. Soul Janet S JS Department of Neurology, Boston Children's Hospital, Boston, Massachusetts; Department of Neurology, Harvard Medical School, Boston, Massachusetts. Hunter David G DG Department of Ophthalmology, Boston Children's Hospital, Boston, Massachusetts; Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts. Electronic address: david.hunter@childrens.harvard.edu. eng Journal Article 2018 03 16

United States J AAPOS 9710011 1091-8531 2017 06 01 2017 12 17 2017 12 19 2018 3 21 6 0 2018 3 21 6 0 2018 3 21 6 0 ppublish 29555514 S1091-8531(17)30444-5 10.1016/j.jaapos.2017.12.011 29420328 2018 05 11

1536-5166 38 2 2018 Jun J Neuroophthalmol Tacrolimus Optic Neuropathy. 160-166 10.1097/WNO.0000000000000635 Tacrolimus (FK506, Prograf) is a potent immunosuppressant, which inhibits cytokine synthesis and blocks T-cell development. Optic neuropathy from tacrolimus toxicity is very uncommon but, when present, can result in severe vision loss. Case series and review of the literature. We present 3 patients with tacrolimus optic neuropathy after bone marrow transplantation complicated by graft-vs-host disease and demonstrate the differing clinical and radiologic presentation of this presumed toxic optic neuropathy. Tacrolimus optic neuropathy can manifest in a multitude of clinical presentations and can have devastating visual consequences. Rasool Nailyn N Department of Ophthalmology (NR), Harkness Eye Institute, Columbia University, New York, New York; Deartment of Ophthalmology (KB), University of Montreal, Montreal, Quebec, Canada; Department of Ophthalmology (SL, DMC), Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts; and Department of Ophthalmology (SP), Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts. Boudreault Katherine K Lessell Simmons S Prasad Sashank S Cestari Dean M DM eng Journal Article

United States J Neuroophthalmol 9431308 1070-8022 2018 2 9 6 0 2018 2 9 6 0 2018 2 9 6 0 ppublish 29420328 10.1097/WNO.0000000000000635 29796050 2018 05 31

0165-8107 42 3 2018 Jun Neuroophthalmology Angiographic Findings in the Tolosa-Hunt Syndrome and Resolution after Corticosteroid Treatment. 159-163 10.1080/01658107.2017.1365268 The Tolosa-Hunt syndrome is a rare clinical condition characterized by painful opthalmoparesis associated with idiopathic granulomatous inflammation of the orbital apex and cavernous sinus. Historically, this condition was thought to result from arteritic changes in the internal carotid artery and cavernous sinus. Modern digital angiographic techniques were unavailable when THS was initially described, and few reports exist on its high-resolution angiographic findings. Painful ophthalmoparesis, especially of the oculomotor nerve, warrants vascular imaging because of the concern for an underlying aneurysm. Here, we describe angiographic findings of THS which may be useful for clinicians when encountering patients presenting with painful ophthalmoplegia. Ravindran Krishnan K The Royal Melbourne Hospital, Parkville, VIC, Australia. Schmalz Philip P Department of Neurosurgery, University of Alabama at Birmingham, Birmingham, Alabama, USA. Neurosurgical Service, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA. Torun Nurhan N Division of Ophthalmology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA. Ronthal Michael M Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA. Chang Yu-Ming YM Department of Radiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA. Thomas Ajith J AJ Neurosurgical Service, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA. eng Journal Article 2017 09 06

England Neuroophthalmology 8408966 0165-8107 Neurol Sci. 2010 Dec;31(6):777-9 20198499 AJR Am J Roentgenol. 1979 Jul;133(1):31-4 110066 Surg Neurol. 2006 Mar;65(3):304-7; discussion 307 16488259 Curr Pain Headache Rep. 2007 Aug;11(4):317-25 17686398 Headache. 1999 May;39(5):321-5 11279911 J Neurol Neurosurg Psychiatry. 1954 Nov;17(4):300-2 13212421 Cephalalgia. 1999 Dec;19 Suppl 25:36-8 10668118 Surv Ophthalmol. 1982 Sep-Oct;27(2):79-95 6755785 Surg Neurol Int. 2016 Nov 11;7(Suppl 30):S779-S784 27920936 Am J Ophthalmol. 1966 Jun;61(6):1466-72 5938314 Cephalalgia. 2013 Jul;33(9):629-808 23771276 Neurology. 1961 Jan;11:56-62 13716871 Radiology. 1973 Jan;106(1):105-12 4682706 Eur Radiol. 2003 Jan;13(1):17-28 12541106 Cephalalgia. 2014 Jul;34(8):624-32 24477599 J Neurol Neurosurg Psychiatry. 2001 Nov;71(5):577-82 11606665 J Med Imaging Radiat Oncol. 2008 Oct;52(5):447-51 19032389 Angiography Tolosa–Hunt syndrome cavernous sinus headache disorders neuroimaging oculomotor nerve 2017 07 11 2017 08 04 2017 08 05 2018 09 06 2018 5 26 6 0 2018 5 26 6 0 2018 5 26 6 1 epublish 29796050 10.1080/01658107.2017.1365268 1365268 PMC5958970 29946119 2018 06 27

2045-2322 8 1 2018 Jun 26 Sci Rep Optimization of Optomotor Response-based Visual Function Assessment in Mice. 9708 10.1038/s41598-018-27329-w Optomotor response/reflex (OMR) assays are emerging as a powerful and versatile tool for phenotypic study and new drug discovery for eye and brain disorders. Yet efficient OMR assessment for visual performance in mice remains a challenge. Existing OMR testing devices for mice require a lengthy procedure and may be subject to bias due to use of artificial criteria. We developed an optimized staircase protocol that utilizes mouse head pausing behavior as a novel indicator for the absence of OMR, to allow rapid and unambiguous vision assessment. It provided a highly sensitive and reliable method that can be easily implemented into automated or manual OMR systems to allow quick and unbiased assessment for visual acuity and contrast sensitivity in mice. The sensitivity and quantitative capacity of the protocol were validated using wild type mice and an inherited mouse model of retinal degeneration - mice carrying rhodopsin deficiency and exhibiting progressive loss of photoreceptors. Our OMR system with this protocol was capable of detecting progressive visual function decline that was closely correlated with the loss of photoreceptors in rhodopsin deficient mice. It provides significant advances over the existing methods in the currently available OMR devices in terms of sensitivity, accuracy and efficiency. Shi Cong C Schepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. cong_shi@meei.harvard.edu. Yuan Xuedong X College of Computer Science, Sichuan University, Chengdu, China. Chang Karen K Schepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Graduate Institute of Clinical Dentistry, School of Medicine, National Taiwan University, Taipei, Taiwan. Cho Kin-Sang KS Schepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Xie Xinmin Simon XS AfaSci Research Laboratories, Redwood City, CA, USA. Chen Dong Feng DF Schepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Luo Gang G Schepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. eng Journal Article 2018 06 26

England Sci Rep 101563288 2045-2322 2017 11 16 2018 05 21 2018 6 28 6 0 2018 6 28 6 0 2018 6 28 6 0 epublish 29946119 10.1038/s41598-018-27329-w 10.1038/s41598-018-27329-w 29923968 2018 06 20

1537-2677 2018 Jun 18 Ophthalmic Plast Reconstr Surg Epibulbar Mass With Upper Eyelid Cleft and Focal Scalp Alopecia in a Neonate: A New Case of Oculoectodermal Syndrome. 10.1097/IOP.0000000000001151 A female neonate presented with a pedunculated left lateral epibulbar mass protruding through the eyelids that originated from the temporal cornea and superolateral bulbar and palpebral conjunctiva. She had a cleft in the ipsilateral central upper eyelid with horizontal kink of the tarsus lateral to the cleft and focal patches of alopecia on the scalp. Histopathology of the epibulbar mass revealed conjunctival epithelium with underlying connective tissue, cartilage, bone, adipose, and lacrimal gland consistent with epibulbar dermoid. Genetic testing of the surgical specimen was positive for a KRAS mutation at position 146. MRI showed subarachnoid asymmetry around the left temporal lobe and a C1-C2 enhancing lesion. These clinical and molecular findings suggest that this patient has a new clinical variant of oculoectodermal syndrome, a rare disorder associated with somatic KRAS gene mutations and characterized clinically by epibulbar dermoids, alopecia, aplasia cutis, brain anomalies, umbilical hernias, and congenital heart defects. Shoji Marissa K MK Harvard Medical School, Boston, Massachusetts, U.S.A. Saeed Hajirah N HN Harvard Medical School, Boston, Massachusetts, U.S.A. Cornea Service, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, U.S.A. Habib Larissa A LA Harvard Medical School, Boston, Massachusetts, U.S.A. Ophthalmic Plastic Surgery Service, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, U.S.A. Freitag Suzanne K SK Harvard Medical School, Boston, Massachusetts, U.S.A. Ophthalmic Plastic Surgery Service, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, U.S.A. eng Journal Article 2018 06 18

United States Ophthalmic Plast Reconstr Surg 8508431 0740-9303 2018 6 21 6 0 2018 6 21 6 0 2018 6 21 6 0 aheadofprint 29923968 10.1097/IOP.0000000000001151 29907530 2018 06 19

1879-307X 22 7 2018 Jul Trends Cogn. Sci. (Regul. Ed.) Why Does the Cortex Reorganize after Sensory Loss? 569-582 S1364-6613(18)30095-0 10.1016/j.tics.2018.04.004 A growing body of evidence demonstrates that the brain can reorganize dramatically following sensory loss. Although the existence of such neuroplastic crossmodal changes is not in doubt, the functional significance of these changes remains unclear. The dominant belief is that reorganization is compensatory. However, results thus far do not unequivocally indicate that sensory deprivation results in markedly enhanced abilities in other senses. Here, we consider alternative reasons besides sensory compensation that might drive the brain to reorganize after sensory loss. One such possibility is that the cortex reorganizes not to confer functional benefits, but to avoid undesirable physiological consequences of sensory deafferentation. Empirical assessment of the validity of this and other possibilities defines a rich program for future research. Copyright © 2018 Elsevier Ltd. All rights reserved. Singh Amy Kalia AK Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA. Phillips Flip F Department of Psychology and Neuroscience, Skidmore College, Saratoga Springs, NY, USA. Merabet Lotfi B LB Laboratory for Visual Neuroplasticity, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, USA. Sinha Pawan P Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA. Electronic address: psinha@mit.edu. eng Journal Article Review 2018 06 12

England Trends Cogn Sci 9708669 1364-6613 cortical reorganization multimodal activations plasticity sensory compensation sensory loss 2018 02 02 2018 04 01 2018 04 17 2018 6 17 6 0 2018 6 17 6 0 2018 6 17 6 0 ppublish 29907530 S1364-6613(18)30095-0 10.1016/j.tics.2018.04.004 29953303 2018 06 28

1744-5078 2018 Jun 28 Ocul. Immunol. Inflamm. Vogt-Koyanagi-Harada Disease Associated with Hepatitis B Vaccination. 1-4 10.1080/09273948.2018.1483520 To report a case of Vogt-Koyanagi-Harada (VKH) disease associated with hepatitis B vaccination. Case report. A 43-year-old Caucasian male presented with a three-week history of blurry vision, pain, photophobia, and redness in both eyes. Three days prior to the onset of symptoms, he had received the hepatitis B virus vaccine. Clinical evaluation revealed multifocal placoid lesions in the posterior pole, choroidal thickening, and serous macular detachment. Targeted laboratory investigations were negative for infectious or autoimmune markers. After treatment with oral corticosteroids, the patient had resolution of symptoms with near-total recovery of visual function. The patient later reported systemic findings of hearing loss, tinnitus, and integumentary changes. A diagnosis of VKH disease was made and inflammation was managed with oral corticosteroids followed by methotrexate for long-term disease control. VKH disease is an inflammatory condition primarily affecting the choroid, retinal pigment epithelium, and outer retina. The underlying etiology is unclear, but it can be associated with a viral prodrome suggesting an infectious trigger in a genetically susceptible individual. Our case suggests that hepatitis B vaccination may trigger a similar inflammatory response. Sood Arjun B AB a Massachusetts Eye and Ear Infirmary, Department of Ophthalmology , Harvard Medical School , Boston , Massachusetts , USA. O'Keefe Ghazala G b Emory Eye Center, Department of Ophthalmology , Emory University School of Medicine , Atlanta , Georgia , USA. Bui Diem D c Barnet Dulaney Perkins Eye Center , Phoenix , Arizona , USA. Jain Nieraj N b Emory Eye Center, Department of Ophthalmology , Emory University School of Medicine , Atlanta , Georgia , USA. eng Journal Article 2018 06 28

England Ocul Immunol Inflamm 9312169 0927-3948 Imaging Vogt–Koyanagi–Harada immunomodulators uveitis vaccine 2018 6 29 6 0 2018 6 29 6 0 2018 6 29 6 0 aheadofprint 29953303 10.1080/09273948.2018.1483520 29859174 2018 06 02

1875-9777 22 6 2018 Jun 01 Cell Stem Cell Regenerating Eye Tissues to Preserve and Restore Vision. 834-849 S1934-5909(18)30231-5 10.1016/j.stem.2018.05.013 Ocular regenerative therapies are on track to revolutionize treatment of numerous blinding disorders, including corneal disease, cataract, glaucoma, retinitis pigmentosa, and age-related macular degeneration. A variety of transplantable products, delivered as cell suspensions or as preformed 3D structures combining cells and natural or artificial substrates, are in the pipeline. Here we review the status of clinical and preclinical studies for stem cell-based repair, covering key eye tissues from front to back, from cornea to retina, and including bioengineering approaches that advance cell product manufacturing. While recognizing the challenges, we look forward to a deep portfolio of sight-restoring, stem cell-based medicine. VIDEO ABSTRACT. Copyright © 2018 Elsevier Inc. All rights reserved. Stern Jeffrey H JH Neural Stem Cell Institute, Rensselaer, NY 12144, USA; Kellogg Eye Center, University of Michigan, Ann Arbor, MI 48105, USA. Tian Yangzi Y Colleges of Nanoscale Science and Engineering, SUNY Polytechnic Institute, 257 Fuller Road, Albany, NY 12203, USA. Funderburgh James J Department of Ophthalmology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA. Pellegrini Graziella G Centre for Regenerative Medicine, University of Modena and Reggio Emilia, via G.Gottardi 100, 41125 Modena, Italy. Zhang Kang K Shiley Eye Institute and Institute for Engineering in Medicine, University of California, San Diego, La Jolla, CA 92093, USA; State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University and Guangzhou Regenerative Medicine and Health Laboratory, Guangzhou 510060, China. Goldberg Jeffrey L JL Byers Eye Institute at Stanford University, 2452 Watson Court, Palo Alto, CA 94303, USA. Ali Robin R RR Department of Genetics, University College London Institute of Ophthalmology, 11-43 Bath Street, London EC1V 9EL, UK; NIHR Biomedical Research Centre at Moorfields Eye Hospital NHS Foundation Trust and UCL Institute of Ophthalmology, City Road, London EC1V 2PD, UK; Kellogg Eye Center, University of Michigan, Ann Arbor, MI 48105, USA. Young Michael M The Schepens Eye Research Institute, Massachusetts Eye and Ear, an affiliate of Harvard Medical School, Boston, MA 02114, USA. Xie Yubing Y Colleges of Nanoscale Science and Engineering, SUNY Polytechnic Institute, 257 Fuller Road, Albany, NY 12203, USA. Temple Sally S Neural Stem Cell Institute, Rensselaer, NY 12144, USA; Kellogg Eye Center, University of Michigan, Ann Arbor, MI 48105, USA. Electronic address: sallytemple@neuralsci.org. eng Journal Article Review

United States Cell Stem Cell 101311472 1875-9777 cornea eye lens limbal ocular ophthalmology optic nerve photoreceptors regenerative medicine retina retinal ganglion cells retinal pigment epithelium stem cells trabecular meshwork 2018 6 3 6 0 2018 6 3 6 0 2018 6 3 6 0 ppublish 29859174 S1934-5909(18)30231-5 10.1016/j.stem.2018.05.013 29940588 2018 06 25

1423-0259 2018 Jun 25 Ophthalmic Res. Scotopic Microperimetric Assessment of Rod Function in Stargardt Disease (SMART) Study: Design and Baseline Characteristics (Report No. 1). 1-8 10.1159/000488711 To describe the study design and characteristics at first visit of participants in the longitudinal Scotopic Microperimetric Assessment of Rod Function in Stargardt Disease (SMART) study. Scotopic microperimetry (sMP) was performed in one designated study eye in a subset of participants with molecularly proven ABCA4-associated Stargardt disease (STGD1) enrolled in a multicenter natural history study (ProgStar). Study visits were every 6 months over a period ranging from 6 to 24 months, and also included fundus autofluorescence (FAF). SMART enrolled 118 participants (118 eyes). At the first visit of SMART, the mean sensitivity in mesopic microperimetry was 11.48 (±5.05; range 0.00-19.88) dB and in sMP 11.25 (±5.26; 0-19.25) dB. For FAF, all eyes had a lesion of decreased autofluorescence (mean lesion size 3.62 [±3.48; 0.10-21.46] mm2), and a total of 76 eyes (65.5%) had a lesion of definitely decreased autofluorescence with a mean lesion size of 3.46 (±3.60; 0.21-21.46) mm2. Rod function is impaired in STGD1 and can be assessed by sMP. Testing rod function may serve as a potential outcome measure for future clinical treatment trials. This is evaluated in the SMART study. © 2018 S. Karger AG, Basel. Strauss Rupert W RW Wilmer Eye Institute, Johns Hopkins University, Baltimore, Maryland, USA. Moorfields Eye Hospital NHS Foundation Trust, and UCL Institute of Ophthalmology, University College London, London, United Kingdom. Department of Ophthalmology, Kepler University Clinic and Kepler University Linz, Linz, Austria. Department of Ophthalmology, Medical University Graz, Graz, Austria. Kong Xiangrong X Wilmer Eye Institute, Johns Hopkins University, Baltimore, Maryland, USA. Department of Biostatistics and Epidemiology, University of Massachusetts-Amherst, Amherst, Massachusetts, USA. Bittencourt Millena G MG Wilmer Eye Institute, Johns Hopkins University, Baltimore, Maryland, USA. Ho Alexander A Doheny Eye Institute, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California, USA. Jha Anamika A Doheny Eye Institute, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California, USA. Schönbach Etienne M EM Wilmer Eye Institute, Johns Hopkins University, Baltimore, Maryland, USA. Ahmed Mohamed I MI Wilmer Eye Institute, Johns Hopkins University, Baltimore, Maryland, USA. Muñoz Beatriz B Wilmer Eye Institute, Johns Hopkins University, Baltimore, Maryland, USA. Ervin Ann-Margret AM Wilmer Eye Institute, Johns Hopkins University, Baltimore, Maryland, USA. Michaelides Michel M Moorfields Eye Hospital NHS Foundation Trust, and UCL Institute of Ophthalmology, University College London, London, United Kingdom. Birch David G DG Retina Foundation of the Southwest, Dallas, Texas, USA. Sahel José-Alain JA Sorbonne Universités, University Pierre et Marie Curie (UPMC) Université de Paris 06, Institut National de la Santé et de la Recherche Médicale (INSERM), Centre National de la Recherche Scientifique (CNRS), Institut de la Vision, Centre Hospitalier National d'Ophtalmologie (CHNO) des Quinze-Vingts, Paris, France. Sunness Janet S JS Hoover Low Vision Rehabilitation Services, Greater Baltimore Medical Center and University of Maryland School of Medicine, Baltimore, Maryland, USA. Zrenner Eberhart E Center for Ophthalmology, Eberhard-Karls University Hospital, Tübingen, Germany. Bagheri Saghar S Wilmer Eye Institute, Johns Hopkins University, Baltimore, Maryland, USA. Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, USA. Ip Michael M Doheny Eye Institute, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California, USA. Sadda SriniVas S Doheny Eye Institute, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California, USA. West Sheila S Wilmer Eye Institute, Johns Hopkins University, Baltimore, Maryland, USA. Scholl Hendrik P N HPN Wilmer Eye Institute, Johns Hopkins University, Baltimore, Maryland, USA. Department of Ophthalmology, University of Basel, Basel, Switzerland. Institute of Molecular and Clinical Ophthalmology Basel, Basel, Switzerland. for the SMART Study Group eng Journal Article 2018 06 25

Switzerland Ophthalmic Res 0267442 0030-3747 Clinical trials Endpoints Mesopic microperimetry Scotopic microperimetry Stargardt disease 2018 03 16 2018 03 22 2018 6 26 6 0 2018 6 26 6 0 2018 6 26 6 0 aheadofprint 29940588 000488711 10.1159/000488711 29929908 2018 06 22

1879-1883 2018 Jun 12 Am. J. Surg. Novel techniques of engineering 3D vasculature tissue for surgical procedures. S0002-9610(18)30762-1 10.1016/j.amjsurg.2018.06.004 Thomas Daniel D 3Dynamic Systems Tissue Engineering, Heol Ty Gwyn, UK. Electronic address: daniel.thomas@engineer.com. Singh Deepti D Department of Ophthalmology, Schepens Eye Research Institute, Harvard Medical School, Boston, MA, 02114, USA. Electronic address: deepti_singh@meei.harvard.edu. eng Letter 2018 06 12

United States Am J Surg 0370473 0002-9610 2018 05 28 2018 06 05 2018 6 23 6 0 2018 6 23 6 0 2018 6 23 6 0 aheadofprint 29929908 S0002-9610(18)30762-1 10.1016/j.amjsurg.2018.06.004 29880713 2018 06 27

1091-6490 115 25 2018 Jun 19 Proc. Natl. Acad. Sci. U.S.A. Reply to Vickers: Pharmacogenetics and progression to neovascular age-related macular degeneration-Evidence supporting practice change. E5640-E5641 10.1073/pnas.1804781115 Vavvas Demetrios G DG Department of Ophthalmology Retina Service, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA 02114. Small Kent W KW Macula and Retina Institute, Los Angeles, CA 90048. Awh Carl C Tennessee Retina, Nashville, TN 37203. Zanke Brent W BW ArcticDx, Toronto, ON M5G 1M1, Canada. Tibshirani Robert J RJ Department of Statistics, Stanford University, Stanford, CA 94305; tibs@stanford.edu. Department of Biomedical Data Science, Stanford University, Stanford, CA 94305. Kustra Rafal R Dalla Lana School of Public Health, University of Toronto, Toronto, ON M5T 3M7, Canada. eng Journal Article 2018 06 07

United States Proc Natl Acad Sci U S A 7505876 0027-8424 Proc Natl Acad Sci U S A. 2018 Jan 23;115(4):E696-E704 29311295 Proc Natl Acad Sci U S A. 2018 Jun 19;115(25):E5639 29880714 Ophthalmology. 2014 Nov;121(11):2173-80 24974817 Ophthalmology. 2015 Jan;122(1):162-9 25200399 Ophthalmology. 2018 Mar;125(3):391-397 29032853 Br J Ophthalmol. 2016 Dec;100(12 ):1731-1737 27471039 Ophthalmology. 2018 May;125(5):e34-e35 29681304 Arch Ophthalmol. 2001 Oct;119(10):1417-36 11594942 Conflict of interest statement: B.W.Z. is an officer of ArcticDx, which holds patents relevant to results. C.A. and R.K. are technical consultants of ArcticDx. 2018 12 19 2018 6 9 6 0 2018 6 9 6 0 2018 6 9 6 0 ppublish 29880713 1804781115 10.1073/pnas.1804781115 PMC6016766 29887334 2018 06 11

1549-4713 2018 Jun 07 Ophthalmology A Dosing Study of Bevacizumab for Retinopathy of Prematurity: Late Recurrences and Additional Treatments. S0161-6420(18)30491-3 10.1016/j.ophtha.2018.05.001 Intravitreal bevacizumab is increasingly used to treat severe retinopathy of prematurity (ROP), but it enters the bloodstream, and there is concern that it may alter development of other organs. Previously we reported short-term outcomes of 61 infants enrolled in a dose de-escalation study, and we report the late recurrences and additional treatments. Masked, multicenter, dose de-escalation study. A total of 61 premature infants with type 1 ROP. If type 1 ROP was bilateral at enrollment, then the study eye was randomly selected. In the study eye, bevacizumab intravitreal injections were given at de-escalating doses of 0.25 mg, 0.125 mg, 0.063 mg, or 0.031 mg; if needed, fellow eyes received 1 dose level higher: 0.625 mg, 0.25 mg, 0.125 mg, or 0.063 mg, respectively. After 4 weeks, additional treatment was at the discretion of the investigator. Early and late ROP recurrences, additional treatments, and structural outcomes after 6 months. Of 61 study eyes, 25 (41%; 95% confidence interval [CI], 29%-54%) received additional treatment: 3 (5%; 95% CI, 1%-14%) for early failure (within 4 weeks), 11 (18%; 95% CI, 9%-30%) for late recurrence of ROP (after 4 weeks), and 11 (18%; 95% CI, 9%-30%) for persistent avascular retina. Re-treatment for early failure or late recurrence occurred in 2 of 11 eyes (18%; 95% CI, 2%-52%) treated with 0.25 mg, 4 of 16 eyes (25%; 95% CI, 7%-52%) treated with 0.125 mg, 8 of 24 eyes (33%; 95% CI, 16%-55%) treated with 0.063 mg, and 0 (0%; 95% CI, 0%-31%) of 10 eyes treated with 0.031 mg. By 6 months corrected age, 56 of 61 study eyes had regression of ROP with normal posterior poles, 1 study eye had developed a Stage 5 retinal detachment, and 4 infants had died of preexisting medical conditions. Retinal structural outcomes are very good after low-dose bevacizumab treatment for ROP, although many eyes received additional treatment. Copyright © 2018 American Academy of Ophthalmology. Published by Elsevier Inc. All rights reserved. Wallace David K DK Indiana University, Indianapolis, Indiana. Electronic address: dwallac@iu.edu. Dean Trevano W TW Jaeb Center for Health Research, Tampa, Florida. Hartnett Mary Elizabeth ME John A. Moran Eye Center, Salt Lake City, Utah. Kong Lingkun L Texas Tech University Health Science Center, Lubbock, Texas. Smith Lois E LE Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts. Hubbard G Baker GB The Emory Eye Center, Atlanta, Georgia. McGregor Mary Lou ML Pediatric Ophthalmology Associates, Columbus, Ohio. Jordan Catherine O CO Pediatric Ophthalmology Associates, Columbus, Ohio. Mantagos Iason S IS Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts. Bell Edward F EF University of Iowa, Iowa City, Iowa. Kraker Raymond T RT Jaeb Center for Health Research, Tampa, Florida. Pediatric Eye Disease Investigator Group eng Journal Article 2018 06 07

United States Ophthalmology 7802443 0161-6420 2018 02 20 2018 04 30 2018 05 01 2018 6 12 6 0 2018 6 12 6 0 2018 6 12 6 0 aheadofprint 29887334 S0161-6420(18)30491-3 10.1016/j.ophtha.2018.05.001 29784167 2018 05 22

1715-3360 53 3 2018 Jun Can. J. Ophthalmol. Outcomes of Boston keratoprosthesis type 1 reimplantation: multicentre study results. 284-290 S0008-4182(17)30640-3 10.1016/j.jcjo.2017.10.021 To investigate the visual and anatomical outcomes of Boston keratoprosthesis (Kpro) type 1 reimplantation. Subgroup analysis of multicentre prospective cohort study. Of 303 eyes that underwent Kpro implantation between January 2003 and July 2008 by 1 of 19 surgeons at 18 medical centres, 13 eyes of 13 patients who underwent reimplantation of Boston Kpro type 1 were compared with 13 eyes of 13 diagnosis-matched patients who underwent initial implantation. Forms reporting preoperative, intraoperative, and postoperative parameters were prospectively collected and analyzed. Main outcome measures were Kpro retention and logMAR visual acuity. After a mean follow-up time of 17.1 ± 17.6 months, the retention of both initial and repeat Kpro implantation was 92.3% (12/13 in both groups), and 62% of initial implantation and 58% of repeat implantation eyes achieved visual acuity better than 20/200. Vision worse than 20/200 was often due to glaucoma or posterior segment pathology. Best-recorded logMAR visual acuity was significantly improved postoperatively in both groups (p < 0.001), and there was no statistically significant difference in final logMAR visual acuity between the 2 groups (p = 0.89). Sterile keratolysis (n = 4) and fungal infection (n = 5) were the most common causes of initial Kpro failure in the repeat Kpro group. The single failure in the repeat Kpro implantation group was due to fungal keratitis, and in the control group it was related to Kpro extrusion. Repeat Kpro implantation is a viable option after failed initial Kpro, with visual and anatomical outcomes comparable to those of initial procedures. Copyright © 2018 Canadian Ophthalmological Society. Published by Elsevier Inc. All rights reserved. Wang Jay C JC Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA. Rudnisky Christopher J CJ Department of Ophthalmology, University of Alberta, Edmonton, Alta. Belin Michael W MW Department of Ophthalmology, University of Arizona, Tucson, AZ. Ciolino Joseph B JB Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA. Electronic address: joseph_ciolino@meei.harvard.edu. Boston Type 1 Keratoprosthesis Study Group eng Journal Article 2017 12 11

England Can J Ophthalmol 0045312 0008-4182 2017 06 25 2017 10 04 2017 10 10 2018 5 23 6 0 2018 5 23 6 0 2018 5 23 6 0 ppublish 29784167 S0008-4182(17)30640-3 10.1016/j.jcjo.2017.10.021 29572107 2018 05 25

1879-1891 190 2018 Jun Am. J. Ophthalmol. Reduced Efficacy of Low-dose Topical Steroids in Dry Eye Disease Associated With Graft-versus-Host Disease. 17-23 S0002-9394(18)30125-9 10.1016/j.ajo.2018.03.024 To compare the response of dry eye disease (DED) to treatment with topical steroid in patients with and without graft-vs-host disease (GVHD). Post hoc analysis of a double-masked, randomized clinical trial. This single-center study included 42 patients with moderate-to-severe DED associated with (n = 21) or without (n = 21) chronic GVHD. In each group, patients received either loteprednol etabonate 0.5% ophthalmic suspension or artificial tears twice daily for 4 weeks. Clinical data, including Ocular Surface Disease Index (OSDI) questionnaire, corneal fluorescein staining (CFS), conjunctival lissamine green staining, tear break-up time (TBUT), and Schirmer test, were evaluated before and after treatment. There were no significant differences in signs and symptoms of DED between the groups at baseline. In non-GVHD patients receiving loteprednol treatment, the average OSDI score decreased by 34% from 49.5 ± 5.9 to 32.6 ± 4.8 (mean ± standard error of the mean, P = .001) and the average CFS score decreased by 41% from 5.6 ± 0.6 to 3.3 ± 0.9 (P = .02). On the other hand, loteprednol treatment in GVHD patients resulted in minimal change in OSDI (59.2 ± 6.7 to 61.1 ± 7.1, 3% increase, P = .66) and CFS (5.5 ± 0.5 to 5.3 ± 1.1, 4% decrease, P = .85) scores. Treatment with artificial tears resulted in 22% decrease of OSDI (P = .10) and 32% decrease of CFS (P = .02) scores in non-GVHD patients, and had minimal effect in patients with GVHD. DED patients with ocular GVHD have a less favorable response to a low-dose topical steroid regimen compared with those without ocular GVHD even with similar baseline disease severity. Copyright © 2018 Elsevier Inc. All rights reserved. Yin Jia J Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Kheirkhah Ahmad A Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Dohlman Thomas T Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Saboo Ujwala U Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Dana Reza R Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Electronic address: Reza_Dana@meei.harvard.edu. eng Journal Article 2018 03 20

United States Am J Ophthalmol 0370500 0002-9394 2017 12 08 2018 02 21 2018 03 11 2018 3 25 6 0 2018 3 25 6 0 2018 3 25 6 0 ppublish 29572107 S0002-9394(18)30125-9 10.1016/j.ajo.2018.03.024 28471890 2018 06 14

1539-2864 38 6 2018 Jun Retina (Philadelphia, Pa.) PROGRESSIVE RETINAL DETACHMENT IN INFANTS WITH RETINOPATHY OF PREMATURITY TREATED WITH INTRAVITREAL BEVACIZUMAB OR RANIBIZUMAB. 1079-1083 10.1097/IAE.0000000000001685 Fibrovascular contraction and tractional retinal detachment (TRD) are recognized complications associated with the use of anti-vascular endothelial growth factor agents in vasoproliferative vitreoretinopathies. The authors characterize TRDs that developed after intravitreal bevacizumab or ranibizumab therapy for vascularly active retinopathy of prematurity. This is an international, multicenter, interventional, retrospective, case series. Thirty-five eyes from 23 infants were included. Inclusion required anti-vascular endothelial growth factor treatment of Type 1 retinopathy of prematurity with progression to TRD. Mean gestational age was 26 ± 2 weeks, and mean birth weight was 873 ± 341 g. Mean postmenstrual age on the day of injection was 35 ± 2 weeks. Retinal detachment was noted a mean of 70 days (median, 34; range, 4-335) after injection. Eleven percent detached within 1 week, 23% within 2 weeks, and 49% within 4 weeks. The highest stage of retinopathy of prematurity noted was 4A in 29%, 4B in 37%, and 5 in 34% of eyes. Time to RD negatively correlated with postmenstrual age at the time of injection (Rho = -0.54; P < 0.01). Three TRD configurations were observed: 1) conventional peripheral elevated ridge or volcano-shaped Stage 5 detachment, 2) midperipheral detachment with tight circumferential vectors, and 3) very posterior detachment with prepapillary contraction. Full or partial reattachment was achieved with surgical intervention in 86% of eyes. Progressive atypical TRD may occur after anti-vascular endothelial growth factor injections for retinopathy of prematurity. The configuration of the detachment varies with the extent of primary retinal vascularization present at the time of treatment. Yonekawa Yoshihiro Y Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts. Pediatric Retina Surgery Service, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts. Wu Wei-Chi WC Department of Ophthalmology, Chang Gung Memorial Hospital and Chang Gung University, College of Medicine, Taoyuan, Taiwan. Nitulescu Cristina E CE Department of Ophthalmology, National Institute for Mother and Child Health Alessandrescu-Rusescu, Bucharest, Romania. Chan R V Paul RVP Retina Service, Department of Ophthalmology, Illinois Eye and Ear Infirmary, University of Illinois College of Medicine, Chicago, Illinois. Thanos Aristomenis A Associated Retinal Consultants, Royal Oak, Michigan. Department of Ophthalmology, Oakland University William Beaumont School of Medicine, Rochester, Michigan. Thomas Benjamin J BJ Florida Retina Institute, Jacksonville, Florida. Todorich Bozho B Associated Retinal Consultants, Royal Oak, Michigan. Department of Ophthalmology, Oakland University William Beaumont School of Medicine, Rochester, Michigan. Drenser Kimberly A KA Associated Retinal Consultants, Royal Oak, Michigan. Department of Ophthalmology, Oakland University William Beaumont School of Medicine, Rochester, Michigan. Trese Michael T MT Associated Retinal Consultants, Royal Oak, Michigan. Department of Ophthalmology, Oakland University William Beaumont School of Medicine, Rochester, Michigan. Capone Antonio A Jr Associated Retinal Consultants, Royal Oak, Michigan. Department of Ophthalmology, Oakland University William Beaumont School of Medicine, Rochester, Michigan. eng Journal Article

United States Retina 8309919 0275-004X 2017 5 5 6 0 2017 5 5 6 0 2017 5 5 6 0 ppublish 28471890 10.1097/IAE.0000000000001685