Microcystic macular edema (MME) represents a pathological change that can be observed in the inner layer of the retina in patients diagnosed with glaucoma. This phenomenon is particularly prevalent in individuals with moderate to advanced glaucoma. The majority of research in this field has focused on primary open-angle glaucoma. The occurrence of MME in glaucoma has been demonstrated to be associated with younger age, advanced stage and disease progression. MME occurs in the parafoveal region, most frequently located in the inferior perimacular region, which corresponded with the most vulnerable area of ganglion cells in glaucoma. The presence of MME may affect the automatic layering of optical coherence tomography images, suggesting that clinicians should be mindful of the occurrence of MME to avoid misdiagnosis of the disease. It is hypothesised that the occurrence of MME in glaucoma may be related to macular vitreous traction, mechanical stress of the stent, and Müller cell dysfunction. A comprehensive investigation of the precise pathophysiological mechanism of MME in glaucoma will facilitate the development of a novel perspective and a scientific foundation for the diagnosis, disease monitoring and evaluation of treatment efficacy in glaucoma.

Allergic rhinitis (AR), a globally prevalent immune-mediated inflammatory condition, is still an incurable disease. In the present study, we have validated the impact of the Kelch-like ECH associated protein 1 (Keap1)-related oxidative stress and inflammatory response in clinical AR patient peripheral blood and nasal swab samples, emphasizing the biological relevance of Keap1 and AR. Targeting Keap1 -nuclear factor erythroid 2-related factor 2 (Nrf2) related anti-oxidative stress may be effective for AR intervention. Drawing inspiration from the Keap1 homodimerization and the E3 ligase characteristics, we herein present a design of novel bivalent molecules for chemical knockdown of Keap1. For the first time, we characterized ternary complexes of Keap1 dimer and one molecule of bivalent compounds. The best bivalent molecule 8 encompasses robust capacity to degrade Keap1 as a homoPROTAC^KEAP1. It efficaciously suppresses inflammatory cytokines in extensively different cells, including human nasal epithelial cells. Moreover, in an AR mouse model, we confirmed that the chemical degradation induced by homoPROTAC^KEAP1 led to therapeutic benefits in managing AR symptoms, oxidative stress and inflammation. In summary, our findings underscore the efficacy of targeting the Keap1 system through the homoPROTAC-ing technology as an innovative and promising treatment strategy for the incurable allergic disorders.

Microcystic macular edema (MME) represents a pathological change that can be observed in the inner layer of the retina in patients diagnosed with glaucoma. This phenomenon is particularly prevalent in individuals with moderate to advanced glaucoma. The majority of research in this field has focused on primary open-angle glaucoma. The occurrence of MME in glaucoma has been demonstrated to be associated with younger age, advanced stage and disease progression. MME occurs in the parafoveal region, most frequently located in the inferior perimacular region, which corresponded with the most vulnerable area of ganglion cells in glaucoma. The presence of MME may affect the automatic layering of optical coherence tomography images, suggesting that clinicians should be mindful of the occurrence of MME to avoid misdiagnosis of the disease. It is hypothesised that the occurrence of MME in glaucoma may be related to macular vitreous traction, mechanical stress of the stent, and Müller cell dysfunction. A comprehensive investigation of the precise pathophysiological mechanism of MME in glaucoma will facilitate the development of a novel perspective and a scientific foundation for the diagnosis, disease monitoring and evaluation of treatment efficacy in glaucoma.

0.05). But the amplitudes of the PhNR were significantly reduced in group of primary optic nerve atrophy (P