Harvard Ophthalmology and Mass Eye and Ear
9TH MILITARY VISION SYMPOSIUM
NOVEL TECHNOLOGY AND VISION RESTORATION
February 27-28, 2025
Boston, MA
CO-CHAIRS
Dong Feng Chen, MD, PhD
Associate Professor of Ophthalmology, Harvard Medical School
Co-chair, International Research and Training Program, Harvard Ophthalmology
Associate Scientist, Mass Eye and Ear
Leo A. Kim, MD, PhD
Associate Professor of Ophthalmology, Harvard Medical School
Monte J. Wallace Ophthalmology Chair in Retina, Mass Eye and Ear
Assistant Scientist, Mass Eye and Ear
Jia Yin, MD, PhD, MPH
Assistant Professor of Ophthalmology, Harvard Medical School
Fellowship Director, Cornea and Refractive Service, Mass Eye and Ear
Assistant Scientist, Mass Eye and Ear
Thursday, February 27, 2025
7:30-8:00 AM - BREAKFAST (Starr Center, Breakout Space)
8:00 AM Welcome & Opening Address
Reza Dana, MD, MSc, MPH - Claes H. Dohlman Professor of Ophthalmology, Harvard Medical School
Session 1 - Military Vision Care – Epidemiology and Trends
Moderators: Reza Dana, MD, MSc, MPH and Lina Kubli, PhD
Contrasting Mechanisms of Ocular Injuries and Treatment Between Military and Civilian Settings
8:20 AM
Marisa Tieger, MD - Assistant Professor of Ophthalmology, Tufts University School of Medicine
8:40 AM Ocular Trauma Characteristics in Current Warfare
Charisma Evangelista, MD - RR&D Scientific Program Manager for Sensory Systems, US Department of Veterans Affairs
9:00 AM Chronic Sequalae of Visual Dysfunction
Brittany Powell, MD - Ophthalmologist, Lackland Air Force Base, US Air Force
Exploring Rehabilitation for Visual Impairment
9:20 AM
9:40 AM
William Boules, MS - Section Lead, Low Vision Rehabilitation, Vision Center of Excellence, Department of Defense
Sally H. Dang, OD, MPH - Branch Chief, Vision Center of Excellence Washington DC, Department of Defense
Specifics of Providing Specialized Ophthalmic Care in the Armed Forces of Ukraine During the Full-Scale Invasion of the Russian Federation
Colonel Igor Khramov - Head of Ophthalmology Department, National Military Medical Clinical Center
Captain Andrii Kovalov - Resident, Ophthalmology Department, National Military Medical Clinical Center
9:55 AM Panel Discussion
10:10-10:30 AM - MORNING BREAK (Starr Center, Breakout Space)
Trainee Research Contest - Morning Session
Judges: Daniel Sun, PhD; Thomas H. Dohlman, MD; Inês Laíns, MD, PhD; and Menglu Yang, MD, PhD
1. Advancing Supersaturated Oxygen Emulsion as a Topical Treatment for Ocular Alkali Burn in Rabbits - Hennaav Dhillon, MD
2. Electrical Stimulation as the Therapeutic Modality of Accidental Laser Injuries - Farris ElZaridi, BS
3. Restoring Vision in Chemical Warfare: The Potential of Mdivi-1 - Arpan G. Mazumder, MS, PhD
4. DNA Methylation Modifier Delays Photoreceptor Loss in a Mouse Model of Retinal Degeneration - Lu Huang, MD
10:30 AM
5. Mitigating Nitrogen Mustard-Induced Corneal Injury: Anti-Inflammatory and Anti-Apoptotic Benefits of alpha-MSH Therapy - Francesca Kahale, MD
6. Single-cell Transcriptome Comparison of Myeloid Cells in the Retina in Response to Transplantation of Human StemCell Derived Neurons and to Ocular Damage Reveals the Reversibility of the Microglia Activation - Emil Kriukov, MD
7. Differentiation and Characterization of Induced Pluripotent Stem Cell (iPSC)-derived Limbal Stem Cells (LSCs) - Vinay Kumar Pulimamidi, PhD
Session 2 - Whole Eye Transplantation
Moderators: Leo A. Kim, MD, PhD and Dong Feng Chen, MD, PhD
10:50 AM Challenges in Eye Transplantation
Vaidehi S. Dedania, MD - Associate Professor of Ophthalmology, NYU Langone
11:10 AM Ocular Preservation and Neuroregeneration Strategies for Eye Transplantation
Jeff Goldberg, MD, PhD - Professor and Chair of Ophthalmology, Byers Eye Institute, Stanford University
11:30 AM Assessment of the Vision in Animals Based on their Innate Behaviors
Gang Luo, PhD - Associate Professor of Ophthalmology, Harvard Medical School
11:50 AM Panel Discussion
12:00-1:30 PM - LUNCH & EXHIBITS (Wyndham Boston Beacon Hill, 15th Floor)
SCHEDULE
Thursday, February 27, 2025 (Continued)
Trainee Research Contest - Afternoon Session
Judges: Daniel Sun, PhD; Thomas H. Dohlman, MD; Inês Laíns, MD, PhD; and Menglu Yang, MD, PhD
8. Targeting the Rho-kinase Pathway for the Treatment of Proliferative Vitreoretinopathy: Netarsudil as a Therapeutic Candidate - Jeysson Sanchez Suarez, PhD
9. Development of a Hyaluronic Acid and Plasma Rich in Growth Factors (PRGF) Product for the Treatment of Ocular Burns - Jared Tallo, MD, MS
10. Wait, a Hazard? Enhancing Blind-Side Hazard Detection in Drivers With Hemianopia Through Scanning Training Yi Ni Toh, PhD
1:30 PM
11. Enhancing Optic Nerve Regeneration and Neuroprotection in Mouse Glaucoma Models Through Anti-Lipid Peroxidation Strategies - Ming Yang, MD, PhD
12. Analyzing Retinal Circuitry In Vivo During Traumatic Optic Neuropathy in Preclinical Animal Models - Brent Young, PhD
13. Understanding the Pathophysiology of Traumatic Ocular Conditions Through Biology: An Integrative Phenome- and Genome-wide Analysis of Epiretinal Membranes Across >1 Million Individuals From the Million Veterans Program and Others - Maryam Zekavat, MD, PhD
Session 3 - Post-traumatic Ocular and Brain Inflammation
Moderator: Joseph B. Ciolino, MD
1:50 PM Toxic Effects of Reactive Organic Vapors on the Anterior Eye
Patrick McNutt, PhD - Associate Professor, Institute for Regenerative Medicine, Wake Forest University
2:10 PM Models of Combat-Related Ocular Trauma: Insight Into the Posterior Segment
Heuy-Ching Hetty Wang, PhD - Director, Combat Casualty Care & Operational Medicine, Naval Medical Research Unit
2:30 PM Inflammation in Post-traumatic Brain Injury
Stephanie S. Sloley, PhD - Chief, Research Support Cell, Research Section, Traumatic Brain Injury Center of Excellence (TBICoE), Research Support Division, Research and Engineering Directorate, Defense Health Agency
2:50 PM Panel Discussion
3:00-3:20 PM - AFTERNOON BREAK (Starr Center, Breakout Space)
Vision Injury Research Forum - Short Talks
Moderator: Leo A. Kim, MD, PhD
• Ocular Motor Function and Related Outcomes in Military Veterans with Extended History of Mild Traumatic Brain Injury - Jeffrey R. Hebert, PhD, PT (University of Colorado, School of Medicine)
• Phase 1/2 Clinical Study of Locally Delivered Allogeneic Mesenchymal Stromal Cells for Corneal Repair - Esther Kwon, MA (University of Illinois College of Medicine at Chicago)
3:20 PM
• Chemically Induced In Vivo Retinal Neuron Reprogramming Restores Vision - Biraj Mahato, PhD (Children’s Hospital Los Angeles, University of Southern California)
• Defense and Veterans Eye Injury and Vision Registry (DVEIVR): Epidemiology of Traumatic Ocular Injury Among US Service Members in Theater, 2001-2024 - Frances M. Silva, OD, MS, PhD (U.S. Army Institute of Surgical Research)
Session 4 - Diagnosis and Mitigation of Eye Injury
Moderators: Jia Yin, MD, PhD, MPH and Mariia Viswanathan, MD, PhD
3:40 PM Army’s Teleophthalmology Program
Gary L. Legault, MD - Director, Virtual Medical Center Uniformed Services University, San Antonio Military Medical Center
General AI in Ocular Diagnosis and Treatment
4:00 PM
4:20 PM
CDR Peter B. Walker, PhD - Deputy Branch Chief, Science and Technology Portfolio Management, Science & Technology Enterprise Integration Division, Defense Health Agency
New Directions for the Treatment of Proliferative Vitreoretinopathy
Leo A. Kim, MD, PhD - Associate Professor of Ophthalmology, Harvard Medical School
4:40 PM Panel Discussion
(Schedule continued on next page)
Thursday, February 27, 2025 (Continued)
4:50 PM Introduction to Day 1 Keynote Lecture - Leo A. Kim, MD, PhD - HMS Conference Co-chair
4:55 PM Photoreceptor Cell Death: Life Hanging in the Balance
David Zacks, MD, PhD - Professor and Edna H. Perkiss Research Professor, Ophthalmology and Visual Sciences, University of Michigan
5:25 PM Adjourn - Dong Feng Chen, MD, PhD - HMS Conference Co-chair
5:30-7:30 PM - RECEPTION & EXHIBITS (Wyndham Boston Beacon Hill, 15th Floor)
Friday, February 28, 2025
7:30-8:00 AM - BREAKFAST (Starr Center, Breakout Space)
8:00 AM Welcome Back - Jia Yin, MD, PhD, MPH - HMS Conference Co-chair
Session 5 - Vision Restoration through Regeneration
Moderators: Eleftherios Paschalis Ilios, PhD and Petr Baranov, MD, PhD
8:05 AM Ocular Surface Treatment With Autologous Stem Cells
Ula V. Jurkunas, MD - Professor of Ophthalmology, Harvard Medical School
8:25 AM Axonal Mitochondria Motility in Optic Nerve Regeneration
Yang Hu, MD, PhD - Associate Professor of Ophthalmology, Bayers Eye Institute, Stanford University
8:45 AM Stem-cell Derived Retinal Pigment Epithelium for Advanced Dry Age-Related Macular Degeneration
Amir Kashani, MD, PhD - Boone Pickens Professor of Ophthalmology, Johns Hopkins Medicine
9:05 AM Panel Discussion
9:15 AM Introduction to Day 2 Keynote Lecture
Michael S. Gilmore, PhD - Sir William Osler Professor of Ophthalmology, Harvard Medical School
A Hitchhiker’s and Backpacker’s Approach to Drug Delivery
9:20 AM
Samir Mitragotri, PhD - Hiller Professor of Bioengineering and Hansjorg Wyss Professor of Biologically Inspired Engineering, Wyss Institute, Harvard University
9:50 AM Conference Survey - Jia Yin, MD, PhD, MPH - HMS Conference Co-chair
9:55-10:20 AM - MORNING BREAK (Starr Center, Breakout Space)
Session 6 - Panel: Initiatives to Advance Vision Research Moderators: Michael Gilmore, PhD and Jia Yin, MD, PhD
10:20 AM CDMRP Vision Research Program
Tian Wang, PhD - Program Manager, CDMRP Vision Research Program, Department of Defense
10:30 AM Educating and Advocating for Vision Research Funding
Dan Ignaszewski - Executive Director, NAEVR/AEVR
10:40 AM VA Office of Research & Development
Lina Kubli, MD - RR&D Scientific Program Manager for Sensory Systems, US Department of Veterans Affairs
10:50 AM Panel Discussion
11:40 AM Trainee Research Contest Awards, Travel Awards, and Closing Remarks
Dong Feng Chen, MD, PhD; Leo A. Kim, MD, PhD; and Jia Yin, MD, PhD, MPH - HMS Conference Co-chairs
11:45 AM - ADJOURN
TRAINEE CONTEST
Trainee Research Abstracts - Morning Session
Advancing Supersaturated Oxygen Emulsion as a Topical Treatment for Ocular Alkali Burn in Rabbits
Hennaav K. Dhillon, Zhirong Lin, Asmaa A. Zidan, Sheyda Najafi, Bhupender Verma, Kate Pate, Jia Yin
Purpose: Ocular chemical injury is one of the ophthalmic medical emergencies with limited treatment options. We have engineered a perfluorodecalin (PFD)-based supersaturated oxygen emulsion (SSOE) to deliver high levels of oxygen to the eye. We previously showed that SSOE is safe and effective in treating ocular chemical injuries in mice. In this study, we aim to establish the safety and determine the efficacy of SSOE in treating ocular alkali burn in rabbits.
Methods: For safety study, adult New Zealand White rabbits were given topical application of SSOE or unoxygenated vehicle emulsion once daily for one week. For efficacy study, corneal burn was induced by applying an 8mm filter paper soaked in 2M sodium hydroxide solution to the central cornea for 20 seconds, followed by a 15-minute wash with PBS. SSOE or vehicle emulsion (unoxygenated emulsion with PFD) was given either once immediately after wash or once daily for one week. Rabbits with burned and untreated corneas served as controls. Imaging was conducted using a slit lamp, OCT, and in vivo confocal microscopy. After 28 days, tissues were collected, and histopathological analysis was performed using hematoxylin and eosin (H&E), and immunohistochemistry of CD45, alpha-smooth muscle actin (α-SMA), and TUNEL.
Results: There were no ocular changes including eyelid abnormality, conjunctival injection/chemosis, corneal fluorescein staining, anterior segment reaction, or corneal microstructure after daily application of SSOE or vehicle control, determined by slit lamp photography and IVCM. Similarly, OCT revealed no changes in corneal or retinal thickness or structure, as confirmed by the H&E analysis, thereby establishing the safety of SSOE use in rabbits. Following alkali burn, there was a significant reduction in corneal neovascularized area in the single (5.91±3.88%) and daily (9.62±5.81%) application SSOE groups, compared to the untreated controls (17.17±6.43%) at day 7. Daily application of SSOE significantly reduced corneal opacity (opacity score 2.4±5.4 vs 4±0, p<0.0001, unpaired t-test) and central corneal thickness (976±70.72µ vs 1119±107.8µ, p=0.0239, unpaired t-test) at day 21. There were no significant differences in corneal epithelial wound healing among the groups. On H&E staining, the SSOE group showed well-preserved tissue integrity in both the cornea and retina, whereas the untreated and vehicle controls showed epithelial discontinuity and lack of re-epithelialization and numerous inflammatory cells in the stroma. There was reduction in α-SMA, CD45, and TUNEL staining in the SSOE treated-corneas, demonstrating less corneal fibrosis, leukocyte infiltration, and apoptosis, compared to the controls.
Conclusion: SSOE is safe as a topical treatment in rabbits. After alkali burn, SSOE prevents corneal neovascularization, opacification, fibrosis, inflammation, and apoptosis, leading to preserved ocular tissue integrity. SSOE represents a novel therapeutic to meet the unmet medical needs in acute ocular chemical injury.
Electrical Stimulation as the Therapeutic Modality of Accidental Laser Injuries
Farris ElZaridi, Matthijs Tsonas, Anton Lennikov, Dong Feng Chen
Purpose: Lasers have become an increasingly important component of military, telecom, industrial, and medical applications, increasing the number of laser eye injuries. There is an urgent need to develop an immediate treatment to limit visual loss after a laser eye injury. Noninvasive microcurrent electric stimulation (ES) is emerging as a potential therapeutic modality for eye diseases. This study aims to create an accidental laser exposure injury model (AOLIM) in vivo and evaluate the efficacy of non-invasive electric stimulation in limiting laser injury to the retina.
Methods: AOLIM was induced in adult C57BL/6 mice with a 532-nm laser (150 mW, pulse: 50 ms, with unfocused beam). The mice were then subjected to the daily ES (biphasic ramp, 300 µA, 20 Hz, transpalpebral, 4 min) or sham treatment for 7 days. Optometric response (OMR) was recorded after 5 days, and fluorescein angiography (FA) and optic coherence tomography (OCT) were performed after 7 days after AOLIM. Immunolabeling of RPE/Choroidal whole mounts (Lycopersicon esculentum lectin, IBA1, Vegfa) and RT-PCR analysis of retinal RNA extracts (Cox2, Tnfα, Ang2, Vegfa, Il1β) were used to determine inflammatory and angiogenic responses. The safety profile of ES was established by ES (sham, biphasic ramp, 20 Hz, transpalpebral, 4 min; 300 µA, 500 µA) for 7 days in C57BL/6 mice with an evaluation of OMR, ERG, and by immunolabeling of retinal ganglion cells (RGC) by Brn3a and photoreceptors by peanut agglutinin (PNA).
Results: Unfocused laser injury demonstrated diffuse damage to all retinal layers, marked FA leakages, and significantly reduced functional vision. ES-treated eyes significantly reduced lesion size (OCT) and fluorescein leakages. Immunolabeling of RPE/Choroidal complexes indicated the reduction of vascularized area, IBA1+ inflammatory cell infiltration, and reduced Vegfa expression. RT-PCR analysis further confirmed the significant reduction of inflammatory and angiogenic cytokines. Safety profile evaluation determined no significant difference in OMR, ERG responses, or RGC or photoreceptor cell numbers between sham, ES 300, and 500 µA stimulations.
Conclusion: The results of this study demonstrated a novel model of accidental laser exposure, providing a robust platform for further studies. The ES ameliorated inflammatory and angiogenic responses in AOLIM mice, demonstrating high safety to retinal neurons. These studies lay the foundation for further studies of ES application in clinical settings to reduce laser injury.
TRAINEE CONTEST
Restoring Vision in Chemical Warfare: The Potential of Mdivi-1
Arpan G. Mazumder, Tat Fong NG, M. Elizabeth Fini
Purpose: Exposure to vesicants like nitrogen mustard (NM) in chemical warfare causes ocular damage through alkylation, triggering a biphasic response. The early phase includes photophobia, blistering, and corneal edema, while the later phase results in dry eye, epithelial defects, limbal stem cell deficiency, and corneal neovascularization. Mitochondrial Division Inhibitor-1 (Mdivi-1), an inhibitor of mitochondrial dynamin DRP1, shows promise in addressing such damage. This study evaluates the potential of Mdivi-1 to prevent mitochondrial dysfunction, reduce oxidative stress, and preserve corneal integrity, offering a targeted treatment for NM-induced corneal damage in chemical warfare.
Methods: Immortalized human corneal limbal epithelial cells (HCLE) were exposed to nitrogen mustard (NM) to induce ocular damage. Following NM exposure, the cells were treated with varying concentrations of Mdivi-1. Cell viability was assessed under different conditions, and mitochondrial damage was evaluated by measuring mitochondrial reactive oxygen species (ROS) levels using Mitosox staining, along with mitochondrial membrane potential through JC-1 staining. To further investigate mitochondrial damage and cellular maintenance, mitophagy was also assessed. Mitochondrial dysfunction and oxidative stress were further analyzed by transfecting the cells with a Mito-Timer plasmid, enabling the tracking of the fluorescence shift from green to red, a marker of mitochondrial dysfunction and oxidative stress following NM exposure and Mdivi-1 treatment. Mitochondrial function was comprehensively studied by measuring key metabolic parameters using the Seahorse XF96 analyzer. This included assessing oxygen consumption rate (OCR) and extracellular acidification rate (ECAR), along with mitochondrial parameters such as basal and maximal respiration, spare respiratory capacity, proton leak, and metabolic shift. These analyses provided a deeper understanding of mitochondrial activity and cellular energy status in response to NM exposure and Mdivi-1 treatment. For in vivo validation, C57BL/6 mouse corneas were exposed to NM and treated with either dexamethasone (positive control) or Mdivi-1. Corneal healing and integrity were monitored through fluorescein staining and imaging with a Micron IV microscope over a 28-day period to assess the therapeutic potential of Mdivi-1.
Results: Mdivi-1 treatment at 25 µM and 50 µM significantly enhanced HCLE cell viability following 200 µM NM exposure. MitoSox staining intensity was significantly reduced, indicating a decrease in mitochondrial oxidative stress. JC-1 staining revealed that Mdivi-1 preserved mitochondrial membrane potential, demonstrated by an increased red/green fluorescence ratio. At 50 µM, Mdivi-1 promoted mitophagy, facilitating the degradation of dysfunctional mitochondria and the formation of autophagolysosomes. Seahorse analysis indicated that Mdivi-1 restored mitochondrial function, shifting ATP production from glycolysis to oxidative phosphorylation. In vivo, Mdivi-1 improved corneal epithelial healing, surpassing the efficacy of 0.1% dexamethasone as a positive control.
Conclusion: Mdivi-1 significantly improves HCLE cell viability and mitochondrial function after exposure to NM, a model chemical warfare agent. It reduces oxidative stress, preserves mitochondrial membrane potential, and promotes mitophagy, protecting against mitochondrial dysfunction induced by NM. Seahorse metabolic flux analysis demonstrated the restoration of mitochondrial function, while in vivo studies showed enhanced corneal epithelial healing. These results suggest the potential of Mdivi-1 as a promising therapeutic strategy for mitigating damage from chemical warfare agents and other conditions involving mitochondrial dysfunction and corneal injury.
DNA Methylation Modifier Delays Photoreceptor
Loss in a Mouse Model of Retinal Degeneration
Lu Huang, Wai Lydia Tai, Kin-Sang Cho, Ajay Ashok, Maximilian Braun, Menglu Yang, Karen Chang, Anton Lennikov, Sarita Pooranawattanakul, Farris Elzaridi, Hio Tong Kam, Yizhen Tang, Dong Feng Chen
Purpose: Outer retinal damage as a result of concussion or laser-based injuries is a common cause of acute vision loss in the battlefield and younger populations. Laser weapons are central to the US military’s directed energy arsenal, with a 300-kilowatt system planned for 2025. Despite genetic and symptomatic diversity, photoreceptor (PR) loss is common in outer retinal disorders, yet treatments remain limited, with only one approved gene therapy addressing a small subset of cases. DNA methylation exhibits dynamic changes associated with photoreceptor degeneration. To identify neuroprotective agents for photoreceptors, we evaluated the effects of DNA methyltransferase (DNMT) inhibitor decitabine in both rhodopsin-deficient mice (Rho-/-) and laser-induced retinal injury models.
Methods: All animal procedures complied with ARVO/IACUC guidelines. We assessed DNMT expression by qPCR and immunofluorescence and evaluated DNA methylation via 5mC and 5hmC using immunolabeling and ELISA in Rho-/- mouse retinas and retinas with laser injury. To determine whether DNMTs play a role in photoreceptor degeneration, we performed weekly intravitreal injections of Decitabine (100 µmol) or PBS vehicle for four weeks in Rho-/- mice, starting when they were 6 weeks old – before the detectable cone dysfunction occurred. Photoreceptor and visual functions were examined by optomotor response (OMR) and photopic electroretinography (ERG). Retinal structure and cone survival were evaluated using optical coherence tomography (OCT) and immunofluorescence on retinal sections.
Results: Results of qPCR, ELISA, and immunostaining revealed elevated levels of DNMTs and DNA methylation associated with cone loss. Decitabine treatment significantly improved visual functions in outer retinal degeneration models, as shown by OMR-based visual acuity and contrast sensitivity assessment. Results of photopic ERG indicated enhanced cone function, while OCT and immunofluorescence revealed a thickened photoreceptor cell layer and structural preservation in decitabine-treated degeneration models. Immunohistochemistry further confirmed reduced DNA methylation following Decitabine treatment.
Conclusion: Decitabine treatment delayed cone photoreceptor loss and preserved visual function in mice with photoreceptor degeneration, underscoring the therapeutic potential of epigenetic modulation for outer retinal damage. These findings pave the way for improved treatment and prevention strategies in combat-related retinal injuries.
TRAINEE CONTEST
Mitigating Nitrogen Mustard-Induced Corneal Injury: Anti-Inflammatory and Anti-Apoptotic Benefits of alpha-MSH Therapy
Francesca Kahale, Pier Luigi Surico, Rohan Bir Singh, Parisa Dashti, Swatilekha Hazra, Reza Dana
Purpose: We investigate the therapeutic potential of alpha-melanocyte-stimulating hormone (α-MSH) in mitigating nitrogen mustard (NM)-induced corneal injury. α-MSH is known for its antioxidative, anti-inflammatory, and anti-apoptotic properties, and this research aims to assess its efficacy in preserving corneal integrity and reducing corneal endothelial cell damage following NM exposure.
Methods: C57BL/6 mice were subjected to NM-induced corneal injury. Post-injury, mice received intraperitoneal α-MSH injections three times per week over a 28-day period. Corneal health was evaluated through slit lamp bi-microscopy, anterior segment optical coherence tomography (AS-OCT), histological analysis, and TUNEL assays to measure epithelial integrity, stromal thickness, corneal endothelial cell (CEnC) density, and apoptosis levels. Control and treated groups were compared for corneal opacity, epithelial cell damage, and endothelial morphological changes.
Results: α-MSH treatment significantly reduced corneal epithelial staining (CFS) scores and stromal edema compared to untreated controls (Day 28 CFS: 2.6±0.7 vs. 9.8±1.4, p<0.01; CST: 68.8±1.4 μm vs. 115±15.9 μm, p<0.05). Histological analysis showed that treated corneas had greater epithelial thickness (21.08 ± 2.3 μm) and better-preserved CEnC density, morphology, and hexagonality than untreated corneas. TUNEL assays revealed a significant reduction in apoptosis in both the central and limbal cornea of α-MSH-treated mice (Day 28: central 11.66% vs. 28%, p<0.0001; limbal 9.41% vs. 20%, p<0.01).
Conclusion: α-MSH demonstrates significant anti-inflammatory and cytoprotective effects in NM-induced corneal injury. Treatment preserved epithelial and endothelial integrity, reduced apoptosis, and maintained corneal transparency, highlighting α-MSH’s potential as a therapeutic option for managing chemical ocular injuries.
Single-cell Transcriptome Comparison of Myeloid Cells in the Retina in Response to Transplantation of Human Stem-Cell Derived Neurons and to Ocular Damage Reveals the Reversibility of the Microglia Activation
Emil Kriukov, Anthony Mukwaya, Paul Cullen, George Baldwin, Volha Malechka, Nasrin Refaian, Nikita Bagaev, Everett Labrecque, Sthavir Vinjamuri, Milica Margeta and Petr Baranov
Purpose: Retinal ganglion cells relay visual signals from the retina to the brain. Optic neuropathies cause permanent RGC loss in mammals. Transplantation strategies aim to restore these cells and recover vision. However, activated microglia can hinder donor RGC survival. Understanding and modulating microglia behavior is crucial for successful neuroregenerative therapies in the retina. We would like to investigate host microglia parameters upon donor human induced pluripotent stem cell derived retinal ganglion cells transplantation into the mouse retina. Profiling the host microglia changes upon transplantation supports our understanding of donor RGC survival and integration mechanisms for better transplant success.
Methods: The CX3CR1-GFP mice were used as a host in the study. The H9-BRN3B:tdTomatoThy1.2-hESCs were differentiated into retinal ganglion cells following the laboratory protocol. Using a glass pipette, 20,000 viable tdTomato+ve human ES-derived RGCs in 1µl was injected into one eye of each mouse. One drop of Neomycin and Polymyxin B Sulfates and Bacitracin Zinc Ophthalmic ointment was applied onto the surface of injected eye following the procedure. Three days following RGC transplantation, mice were euthanized, eyes enucleated and retinal tissue isolated and transferred into a tube containing PBS with 0.04% BSA on ice. TdTomato+ and GFP+ cells were sorted and sent for sequencing. Of the sorted cells, up to 10,000 viable cells per sample were used for single cell RNA library preparation following the 10x genomics Chromium Next GEM Single Cell 3ʹ Reagent Kits v3.1 protocol. Single-cell RNA-sequencing data was further processed using Cell ranger, R- and Python- based environments and packages. Commitment score, as a novel metric of downstream RNA Velocity, was defined and available in the code repository on GitHub. Multiconditional atlas integration was performed using scVI from the publicly available GEO datasets (95 datasets, 121 batch) and available on CELLxGENE through https://cellxgene.cziscience.com/collections/7dd7e8a1-f7c2-4213-9f23-dd52afb7ee16. Raw sequencing data generated in this study is available on GEO under the accession number GSE285564.
Results: Our scRNAseq dataset analysis demonstrates microglia activation to be a bi-directional and reversible process. Multiple genes were correlated with the resting and activated states of microglia, including P2ry12, Tmem119, and Apoe, Igf1, Cd74, respectively. We profile the continuity of microglia activation, with the transitory states, along the resting-to-inflammatory and inflammatory-to-resting trajectory. umulative score analysis demonstrates microglia in host-upon-transplantation (HUT) conditions tends to transit towards the resting state. Upon multiconditional comparison (HUT, developing retina, healthy adult retina, MB-induced glaucoma retina, and optic nerve crush retina of mouse), we observe HUT microglia to have highest enrichment score in the inflammation-related pathways.
Conclusion: We built and characterized the atlases of mouse healthy developing and adult, MB-induced glaucoma and optic nerve crush models, mouse retinas in single cell resolution. We demonstrate the changes host microglia undergoes upon the transplantation of hIPSC-derived neurons. Our findings confirm that microglia, being in a balance between the resting and activated states, is highly shifted towards the activatory state in the host upon transplantation. Cell transplantation for host microglia, inflammation-wise, is the strongest stress, compared to both chronic and acute injury mouse models. Meanwhile, developing microglia has the lowest inflammatory potential, being the most promising condition for successful neurons transplantation.
Differentiation and Characterization of Induced Pluripotent Stem Cell (iPSC)-derived Limbal Stem Cells (LSCs)
Vinay
Pulimamidi, Olufemi Folorunso, Lei Xi, Nishant Sinha, Kanika Arora, Meghanashree Shreenivas, John Fallon, and Sunil Chauhan
Purpose: Limbal stem cells (LSCs) play a crucial role in corneal tissue homeostasis. Limbal stem cell deficiency (LSCD), often resulting from severe ocular trauma or chemical burns, is a significant challenge in vision restoration, particularly for military personnel exposed to such combat-related ocular injuries. Autologous limbal grafts have been widely used to treat unilateral limbal stem cell deficiency (LSCD). However, for patients suffering from bilateral LSCD, induced pluripotent stem cells (iPSC)-derived LSCs could be a promising alternative to allogeneic limbal grafts. This study aimed to differentiate iPSCs into LSCs using defined culture conditions.
Methods: Human fibroblast-derived iPSC line was purchased from Wi Cell (Madison, WI). iPSCs were cultured on Matrigel-coated tissue culture dishes in mTeSR1 medium. The iPSC line was characterized by its expression of pluripotency markers (Oct4, Nanog, and SSEA4) and its capacity to form trilineage differentiation potential. Pluripotency was also evaluated by the teratoma formation assay in immunodeficient mice. The iPSCs were differentiated into LSCs using defined culture conditions. The iPSC-derived LSCs were characterized based on the expression of LSC-specific markers by qRT-PCR and immunofluorescence. Human leukocyte antigens (HLAs) expression was also evaluated by flow cytometry.
Results: The iPSC line expressed the pluripotency markers Oct4, Nanog, and SSEA4. The iPSCs were differentiated into the three germ layers and expressed ectoderm (OTX2), endoderm (SOX2), and mesoderm (Brachyury) specific markers. In the teratoma assay, we observed the presence of tissues from all three germ layers. At D9, pluripotency markers Oct4 (p=0.0002), and Nanog (p=0.0001) were significantly downregulated in iPSC-derived LSCs, while the eye-specific transcription factors PAX6 (p=0.0003) and p63α (p=0.0001) were significantly upregulated. On Day 24, the iPSC-derived LSCs showed increased expression of putative LSC markers PAX6 (p=0.0001), p63α (p=0.0001), ABCB5 (p=0.01), KRT 14 (p=0.0001), and KRT 15 (p=0.0001). Post-thaw iPSC-derived LSCs also retained the expression of LSC-specific markers. The expression of HLA molecules was maintained in iPSC-derived LSCs which was moderately lower compared to the corneolimbal epithelial cell line.
Conclusion: Our data suggest that human iPSC-derived limbal stem cells could provide a promising alternative for the treatment of limbal stem cell deficiency. Further, preclinical proof-of-concept studies are warran ted to explore their translational potential.
TRAINEE CONTEST
Trainee Research Abstracts - Afternoon Session
Targeting the Rho-kinase Pathway for the Treatment of Proliferative Vitreoretinopathy: Netarsudil as a Therapeutic Candidate
Jeysson Sanchez-Suarez, Anil Upreti, Aruvi Vijikumar, William Miller, Yvonne Adu-Rutledge, Karim Barake, Rose Lin, Max Semegran, Dhanesh Amarnani, David Doobin, Michael O’Hare, Leo Kim
Purpose: Proliferative vitreoretinopathy (PVR) is a severe complication of retinal detachment for which effective therapeutic options are absent, thus leaving surgery as the primary treatment option. The pathogenesis of PVR is fundamentally linked to the epithelial-mesenchymal transition (EMT), a process heavily influenced by the Rho-kinase pathway. By targeting this pathway, netarsudil, a ROCK1/2 inhibitor, has the potential to serve as a pharmacological intervention. The present study aims to characterize the cellular and molecular responses to Rho-kinase inhibition using a patient-derived in vitro and ex vivo PVR model, providing insights into its therapeutic potential.
Methods: Primary cells derived from patients with PVR (C-PVR) were cultured to create an in vitro model for studying netarsudil, a ROCK1/2 inhibitor. The effects of netarsudil on proliferation, migration, and TGF-β2-induced contractility were assessed after the drug was applied at a concentration of 2.5 µM for 48 hours. Immunoblotting and immunofluorescence techniques were employed to measure downstream targets, such as phosphorylated PTEN (pPTEN) and myosin light chain 2 (pMLC2), to evaluate molecular changes. Single-cell RNA sequencing (scRNA-seq) was utilized to generate a comprehensive profile of cellular subpopulations, with a particular focus on alterations in extracellular matrix cells, fibroblasts, and RPE cells. Furthermore, differential gene expression analysis was conducted to identify pivotal genes regulated by netarsudil, including PEG10, IL33, CXCL12, BMP4, and ALDH1A3. These comprehensive approaches offer a multi-dimensional understanding of netarsudil’s impact on PVR-related cellular processes.
Results: Netarsudil significantly inhibited key PVR-related processes, reducing proliferation by 45.1%, migration by 47.1%, and TGF-β2-induced contractility by 58.4–71.5% (p<0.01). Molecular analysis showed reduced levels of pPTEN and pMLC2 (p<0.05). The distribution of pMLC2 within the cytoskeleton of C-PVR cells was extensive, and its decrease was discernible following treatment. ScRNA-seq revealed changes in cell subpopulations, including reduced extracellular matrix cells, fibroblasts, and RPE cells. Key genes implicated in PVR pathogenesis, such as PEG10, IL33, CXCL12, BMP4, and ALDH1A3, were significantly regulated, highlighting the broad molecular effects of Rho-kinase inhibition.
Conclusion: Netarsudil has been shown to disrupt the pathogenesis of PVR by inhibiting critical processes such as proliferation, migration, and contraction. Molecularly, it modulates PTEN and MLC2 activation, resulting in favorable changes in cell populations and gene regulation. These findings underscore the potential of netarsudil as a therapeutic agent against PVR.
Development of a Hyaluronic Acid and Plasma Rich in Growth Factors (PRGF) Product for the Treatment of Ocular Burns
Jared Tallo, Brittany
Powell, Dorian Houser, Eric Jensen
Purpose: Chemical and thermal ocular burns present a significant clinical challenge due to their complex healing process, high risk of morbidity, and subsequent complications, such as corneal disease. Within the military, there is significant burden of ocular burns related to wartime and occupational hazards, making up over 2% of all ocular injuries. Utilizing animal models, a novel, topical application of chitosan and plasma-rich growth factors (PRGF), which both have antimicrobial and regenerative properties, can improve the corneal surface and aid in corneal remodeling that could dramatically change the treatment of corneal disease. It could allow for earlier intervention, alleviating the need for repeated procedures, salvaging vision, and relieving eye pain.
Methods: While developing the topical gel fortified with chitosan-PRGF, Navy Ophthalmologists were asked to help care for the marine working mammals charged with harbor security. The dolphins specifically tend to develop a neurotrophic keratitis complicated by corneal ulcers and perforation, despite fortified antimicrobial therapy and repeated sedated corneal graft procedures. The previously developed topical formulation was used as a framework to create a similar therapeutic for these marine mammals. Feasibility of the therapeutic product was evaluated using a rodent model (n=16) wherein the healing times of corneal abrasions was measured across four groups with percent healing at 24 hours. The chitosan was administered four times daily leading to 93.5% healing, as compared to 63.9% with hydroxypropyl cellulose drops, 41.7% with saline drops, and 16% with no treatment.
Results: Currently, variations of the therapeutic have been developed to determine what formulation has the ideal corneal adherence to ensure optimized drug delivery and enhance bioavailability. In marine mammals, this provides a unique challenge given their underwater environment. An in vivo model using corneal cell lines demonstrated safety of these therapeutics, suggesting this will be safe to use in human subjects. While evaluating the pertinent characteristics of dolphins, it was found that they had several differences in factor quantities when compared with human plasma, resulting in a unique formulation used in product development.
Conclusion: As an emerging technology, the chitosan-PRGF formulation, particularly in gel and patch forms, is anticipated to enhance healing rates and reduce inflammation in cases of ocular burns. The chitosan-PRGF product has the potential to be a less invasive and more effective treatment than current modalities, such as amniotic membrane grafts and standard topical antibiotics/anti-inflammatories. Next steps will be to apply the therapeutic to the marine mammals and evaluate effectiveness, as well as any evidence of toxicity Further investigations include further animal model experiments this summer, followed by human clinical trials next year.
Wait, a Hazard? Enhancing Blind-Side Hazard Detection in Drivers With Hemianopia Through Scanning Training
Yi Ni Toh, Patrick Baker, Jing Xu, Alex Bowers
Purpose: Traumatic brain injury and stroke are major health concerns for military personnel and veterans, often leading to hemianopic field loss—the loss of half the visual field. This condition may increase collision risk by impairing blind-side hazard detection, a critical safety challenge for drivers with hemianopia, permitted to drive in many states. Driving is a vital rehabilitation goal, as it restores independence and improves quality of life. This open-label clinical trial evaluates a novel training program that uses auditory reminder cues to encourage early, large head scans toward the blind side on approach to intersections. Does the training improve scanning behaviors and blind-side hazard detection?
Methods: Participants with hemianopia completed training and evaluation sessions in a high-fidelity driving simulator equipped with head and eye tracking, driving along city routes with frequent intersections and traffic. During training, head movements were monitored, and if participants did not make a sufficiently large head scan (>20°) toward their blind side early enough, a reminder beep sounded from a loudspeaker on that side when they were 20 meters from the intersection. Evaluation drives, which included hazardous motorcycle events at 38% of intersections (requiring participants to press the horn upon detection), did not include reminder beeps. Importantly, detection tasks were only part of evaluation drives, not the training sessions. To assess the effectiveness of the training, hazard detection performance was measured at three time points: pre-training baseline, one week after training, and at least one month after training. Of the 20 participants screened, 4 were ineligible, 6 are mid-study, and 10 have completed the study.
Results: Training significantly improved the detection of motorcycles approaching from the blind side. Missed detections on the blind side dropped from 45% at baseline to 18% one week after training (p < .0001) and remained lower at 24% after one month (p < .0001). These gains were primarily driven by enhanced compensatory scanning: blind-side misses due to insufficient or absent head scanning decreased from 33% at baseline to 12% one week after training, with a slight increase to 20% after one month. Blind-side detection safety also improved significantly. Safe detection of motorcycles approaching from the blind side increased from 35% at baseline to 63% one week post-training (p < .0001) and were maintained at 54% after one month (p = .05). Post-training, blind-side detection safety approached the levels of the seeing side (73% and 69%, smallest p = 0.21).
Conclusion: Our findings highlight a promising outcome: although limited visual fields impair blind-side hazard detection, this challenge can be mitigated by adopting large, deliberate head scans before entering intersections. Encouragingly, this behavior can be trained through three reminder-cue scanning training sessions in a driving simulator, with detection benefits observed in the simulator lasting at least a month. Early results from this open-label clinical trial suggest that post-training improvements were primarily driven by enhanced scanning, demonstrating the potential of this training to rehabilitate deficits in blind-side hazard detection.
Enhancing Optic Nerve Regeneration and Neuroprotection in Mouse Glaucoma Models Through Anti-Lipid Peroxidation Strategies
Ming Yang, Liang Li, Xue Feng, Haoliang Huang, Liang Liu, Dong Liu, Fuyun Bian, Roopa Dalal, Hang Yang, Frank Cao, Petrina Ong, Alexandria Luo, Yang Hu
Purpose: This study investigates the role of lipid peroxidation in retinal ganglion cell (RGC) survival and optic nerve (ON) regeneration under conditions of trauma and glaucoma in mouse models.
Methods: Through retrograde regenerating axon tracing, Smart-Seq2 single-cell sequencing, and RGC-specific RiboTag-RNA sequencing, we identified GPX4, a key enzyme in anti-lipid peroxidation, as significantly upregulated in regenerating and glaucomatous RGCs. Using an AAV2 vector driven by the mouse Sncg promoter for RGC-specific gene expression, we assessed axon regeneration following optic nerve crush (ONC) injury and the neuroprotective effects of GPX4 overexpression in a silicone oil-induced ocular hypertension (SOHU) glaucoma model. Additionally, the lipid peroxidation inhibitor Liproxstatin-1 was employed to evaluate its role in ON regeneration and neuroprotection. Assessments included histological analyses, CTB-traced regenerating axons, optokinetic tracking response (OKR) for visual function, in vivo optical coherence tomography (OCT), and pattern electroretinogram (PERG) to measure electrophysiological RGC function.
Results: The anti-lipid peroxidation enzyme GPX4 was markedly upregulated in both regenerating and glaucomatous RGCs. AAV2mediated RGC-specific overexpression of mitochondrial (MitoGPX4) and cytosolic (CytoGPX4) GPX4 significantly enhanced ON regeneration in the ONC model (p < 0.0001), with CytoGPX4 demonstrating superior efficacy compared to MitoGPX4. Intraperitoneal administration of Liproxstatin-1 also promoted axon regeneration (p < 0.0001). In the SOHU glaucoma model, RGC-specific overexpression of CytoGPX4 provided more robust neuroprotection (p < 0.001) than MitoGPX4 (p < 0.01), preserving RGC somata and axons as shown by OCT imaging and histological quantification. Functional visual improvements were confirmed through OKR and PERG analyses.
Conclusion: Lipid peroxidation plays a critical role in neurodegeneration following traumatic and glaucomatous optic nerve injuries. Targeting lipid peroxidation through GPX4 gene modulation or chemical inhibition represents a promising therapeutic strategy for promoting axon regeneration and neuroprotection in glaucoma and other central nervous system axonopathies.
TRAINEE CONTEST
Analyzing Retinal Circuitry In Vivo During Traumatic Optic Neuropathy in Preclinical Animal Models
Brent Young, Ziyu Yu, Kathleen Heng, Chantel George, Jeffrey Goldberg
Purpose: Traumatic injury is a common cause of vision loss in those in active military service. Often, this traumatic injury can lead to traumatic optic neuropathy, due to the loss of neurons known as retinal ganglion cells (RGCs), which causes irreversible vision loss with no approved treatments. The Yucatan minipig is an excellent preclinical model of traumatic optic neuropathy due to its similarity in size and vasculature to humans. However, the analysis of potential therapeutics is complicated by the difficulty of visualizing RGCs in vivo. Therefore, we sought to develop a system to image RGCs in vivo to track cell survival during injury and treatment.
Methods: We utilized the Yucatan minipig from 6 months to 1 year of age for this study. The eyes were injected with AAV2-CAG-tdTomato viral construct in the nasal and temporal portion of the eye 4-8 weeks before imaging. A two-photon microscope was used with a 4x objective and an Electrotunable lens for imaging in vivo. Pigs were anesthetized and laid on their side during imaging. Multiple areas were imaged with a laser power previously measured to be safe for retinal tissue. Following imaging, pigs were either recovered for follow-up imaging or euthanized for further histological analysis.
Results: The two-photon imaging system allowed for repeated imaging in vivo and observation of RGCs at a single cell level. Furthermore, we were able to use blood vessel patterns within the retina to identify the same fluorescently labeled RGCs imaged during in vivo imaging following tissue collection and immunohistochemistry.
Conclusion: Fluorescent labeling of RGCs, combined with two-photon fluorescent imaging is sufficient to allow for in vivo imaging of RGCs. Furthermore, the single cell resolution enabled us to identify the same cell population pre- and post-tissue fixation. In the future, this will allow us to monitor RGC numbers and potential treatments following traumatic optic neuropathy in the minipig model.
Understanding the Pathophysiology of Traumatic Ocular Conditions Through Biology: An Integrative Phenome- and Genome-wide Analysis of Epiretinal Membranes Across >1 Million Individuals From the Million Veterans Program and Others
Seyedeh Maryam Zekavat, William Miller, Bryan Gorman, Joel Rämö, Bryan Kaplan, Yuyang Luo, Satoshi Koyama, Yoon Kim, Anna M. Stagner, Neal S. Peachey, Leo A. Kim, Pradeep Natarajan, Sudha K. Iyengar, Elizabeth J. Rossin
Purpose: Epiretinal membrane (ERM) is a poorly understood phenotype resulting in visual decline for which we have no preventative options and limited benefit from surgery. Several clinical co-morbidities are thought so contribute to ERM, including trauma, age, diabetes, central retinal vein occlusion, uveitis, and AMD; however, over 50% of ERM remains “idiopathic.” For military veterans, trauma from combat plays a significant role in ERM risk. Here, we explore phenome- and genome-wide contributions to ERM across >1 million individuals, with downstream immunostaining of patient-derived ERM tissue to understand the biology of ERM. These analyses will address gaps in knowledge regarding clinical risk factors for ERM and identify associated genes that point to biological targets for possible ERM therapeutics.
Methods: We conducted ERM cross-phenotype analyses in the UK Biobank, a cohort of ~500,000 participants. ERM cases were identified using the C80.1 procedure code ‘Peel of epiretinal fibroglial membrane’ (1,266 cases, 450,342 controls). Analyses covered 1,866 ICD-based Phecode Map groupings and 88 quantitative biomarkers, using logistic regression adjusted for age, age², sex, smoking status, and genetic ancestry. Bonferroni correction determined significance (P<0.05/88 for quantitative tests, P<0.05/107 for disease analyses). We also performed a meta-analysis of ICD-based ERM genome-wide association study (GWAS) from the Million Veteran’s Program (38,232 cases, 557,988 controls), FinnGen (3,576 cases, 344,569 controls), and Mass-General-Brigham (1,216 cases, 52,090 controls), with replication in the UK Biobank. Immunostaining of patient-derived ERM tissue identified candidate genes from top GWAS loci. An ERM polygenic risk score (PRS) was created in the UK Biobank using 52 genome-wide significant, independent variants. Mendelian randomization identified potential causal links between disease and ERM.
Results: Significant associations with ERM were detected for retinal detachments and defects (OR 7.4, P=2.4x10-38), macular degeneration (OR 12.2, P=4.4x10-37), diabetic retinopathy (OR 9.3, P=4x10-22), cataract (OR 2.9, P=4.3x10-22), inflammation of the eye (OR 2.8, P=3.7x10-5), as well as type 1 diabetes (OR 4, P=5.6x10-12), type 2 diabetes (OR 1.9, P=1.7x10-6), and hypertension (OR 1.43, P=9.5x10-6). ERM GWAS meta-analysis (total 43,024 cases and 954,647 controls) identified 52 independent, genome-wide significant loci. Immunostaining of patient-derived ERM suggests that DHX36 is causal at the top locus. The ERM PRS was significantly associated with ERM surgery in the UK Biobank (OR=1.4, P=3.9x10-32). Mendelian randomization identified significant association of AMD risk variants with ERM (IVW OR 1.06, P=2.2x10-34) with CFH being a shared genome-wide significant locus for both.
Conclusion: Through phenome-wide association analyses, we identified multiple cardio-metabolic and ocular conditions associated with ERM, with evidence of a causal link between AMD and ERM driven by the CFH locus. Through genome-wide association analyses, we identified 52 independent regions of the genome linked to ERM, with immunostaining of patient-derived ERM supporting that the enzyme DHX36 (DEAH-box helicase 36) at the top locus, also linked to BMI, is causal towards ERM pathogenesis. Overall, this work highlights clinical and biological ties to ERM pathogenesis across multiple large biobanks, improving understanding of the pathophysiology of ERM and identifying possible targets for therapeutics.
Gold Level
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CLAREON® VIVITY® The first and only non-diffractive PCIOL with monofocalquality distance visual acuity, excellence intermediate vision and functional near vision4-6†‡
*Based on worldwide sales of AcrySof PanOptix® and AcrySof IQ Vivity® and Clareon® PanOptix® and Clareon® Vivity® IOLs
** Defined as modified Miyata grade 0, <25mv/mm2 over 3 years (n=138), and over 9 years (n=20), respectively. PCIOL=Presbyopia Correcting IOL.
† Results from a prospective, randomized, parallel group, subject- and assessor-masked, multisite trial of 107 subjects bilaterally implanted with the AcrySof® IQ Vivity® Extended Vision IOL and 113 with the AcrySof® IQ IOL with 6 months follow-up.
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‡ Snellen VA was converted from logMAR VA. A Snellen notation of 20/20-2 or better indicates a logMAR VA of 0.04 or better, which means 3 or more of the 5 ETDRS chart letters in the line were identified correctly. Learn more at ClareonIOL.com
Silver Level
9TH MILITARY VISION SYMPOSIUM
Planning
Committee & Facilitators
PLANNING COMMITTEE
Dong Feng Chen, MD, PhD*
Associate Professor of Ophthalmology, Harvard Medical School and Co-chair, International Research and Training Program, Harvard Ophthalmology
Associate Scientist, Mass Eye and Ear
Reza Dana, MD, MSc, MPH*
Claes H. Dohlman Professor of Ophthalmology, Harvard Medical School
Vice Chair, Academic Programs; Director, Harvard-Vision Clinical Scientist Development Program; and Co-director, Cornea Center of Excellence, Harvard Ophthalmology
Senior Scientist; Director, Cornea and Refractive Surgery Service; and Associate Chief for Academic Programs, Mass Eye and Ear
Leo A. Kim, MD, PhD*
Associate Professor of Ophthalmology, Harvard Medical School
Assistant Scientist and Monte J. Wallace Ophthalmology Chair in Retina, Mass Eye and Ear
Dan Ignaszewski
Executive Director, National Alliance for Eye and Vision Research (NAEVR) and Alliance for Eye and Vision Research (AEVR)
Mariia Viswanathan, MD, PhD*
Clinical Care and Integration Section Chief, Vision Center of Excellence, Defense Health Agency
Tian Wang, PhD
Vision Research Program Manager, Congressionally Directed Medical Research Programs
Jia Yin, MD, PhD, MPH*
Assistant Professor of Ophthalmology, Harvard Medical School
Assistant Scientist and Fellowship Director, Cornea and Refractive Service, Mass Eye and Ear
*Also participating as a session moderator
SESSION MODERATORS
Lina Kubli, PhD
RR&D Scientific Program Manager for Sensory Systems US Department of Veterans Affairs
Eleftherios Paschalis Ilios, PhD
Assistant Professor of Ophthalmology, Harvard Medical School
Assistant Scientist and Director, Boston Keratoprosthesis Research, Development, and Regulatory Affairs, Mass Eye and Ear
Joseph B. Ciolino, MD
Associate Professor of Ophthalmology, Harvard Medical School
Associate Scientist and Henry Freeman Allen Cornea Scholar, Mass Eye and Ear
Petr Baranov, MD, PhD
Assistant Professor of Ophthalmology and Associate Director, Ocular Regenerative Medicine Institute, Harvard Medical School
Assistant Scientist, Mass Eye and Ear
Michael S. Gilmore, PhD
Sir William Osler Professor of Ophthalmology (Microbiology and Immunobiology), Harvard Medical School
Director, Infectious Disease Institute, Harvard Ophthalmology Chief Scientific Officer, Mass Eye and Ear
TRAINEE RESEARCH CONTEST JUDGES
Daniel Sun, PhD
Assistant Professor of Ophthalmology, Harvard Medical School Assistant Scientist, Mass Eye and Ear
Thomas H. Dohlman, MD
Assistant Professor of Ophthalmology, Harvard Medical School
Assistant Scientist and Medical Director, Boston Keratoprosthesis Program, Mass Eye and Ear
Inês Maria De Carvalho Laíns, MD, PhD
Instructor in Ophthalmology, Harvard Medical School Investigator, Mass Eye and Ear
Menglu Yang, MD, PhD Instructor in Ophthalmology, Harvard Medical School Investigator, Mass Eye and Ear
Funding for this conference was made possible (in part) by grants from the National Eye Institute (grant # 1R13EY037175-01) from the National Alliance for Eye and Vision Research.
The views expressed in written conference materials and by speakers and moderators do not necessarily reflect the official policies of the Department of Health and Human Services; nor does mention by trade names, commercial practices, or organizations imply endorsement by the U.S. Government.