Researchers at Massachusetts Eye and Ear/Harvard Medical School have identified inflammatory factors that contribute to optic nerve damage following keratoprosthesis (KPro) implantation in a mouse model. They have also shown that blocking one of the factors, TNFa, leads to a significant decrease in optic nerve cell death, suggesting a new direction for preventing optic nerve damage in patients with keratoprosthesis implants.
Mass. Eye and Ear/Harvard Medical School neuro-ophthalmologist and researcher awarded funding by the Department of Defense Congressionally Directed Medical Research Programs.
Joseph F. Rizzo III, MD, has been awarded grant funding as part of the Vision Prosthesis Pilot Study, a Congressionally Directed Medical Research Program of the United States Department of Defense. Director of Neuro-Ophthalmology at...
Mass. Eye and Ear researchers describe, for the first time, an association between a defective myogenic response of blood vessels in the retina and early, accelerated development of retinopathy in patients with type 1 diabetes. The findings may lead to the development of targeted therapies to delay or prevent the development of diabetic retinopathy in this population.
Mass. Eye and Ear and the Harvard Medical School Department of Ophthalmology are proud to be leading this important clinical trial. We look forward to reporting on safety and efficacy studies in the months and years to come.
ReNeuron announces first patient treated in US Phase I/II clinical trial inblindness-causing disease, retinitis pigmentosa
Marks initiation of ReNeuron’s clinical development activities in the US
ReNeuron Group plc (the “Company”) (AIM: RENE), a leading UK-based stem...
Mass. Eye and Ear researchers describe the role of endomucin, a molecule that – under healthy circumstances – resists the adhesion of white blood cells as they move through the circulatory system. These findings suggest that promoting the expression of endomucin (displayed in red in image) may prevent the collection of white blood cells that causes tissues to become inflamed.