Publications by authors named "K Labib"

Artificial intelligence (AI) is transforming ophthalmology by leveraging machine learning (ML) and deep learning (DL) techniques, particularly artificial neural networks (ANN) and convolutional neural networks (CNN) to mimic human brain functions and enhance accuracy through data exposure. These AI systems are particularly effective in analyzing ophthalmic images for early disease detection, improving diagnostic precision, streamlining clinical workflows, and ultimately enhancing patient outcomes. This study aims to explore the specific applications and impact of AI in the fields of glaucoma, corneal diseases, and oculoplastics.

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Artificial intelligence (AI) is reshaping ophthalmology by enhancing diagnostic precision and treatment strategies, particularly in retinal disorders and pediatric ophthalmology. This review examines AI's efficacy in diagnosing conditions such as diabetic retinopathy (DR) and age-related macular degeneration (AMD) using imaging techniques, such as optical coherence tomography (OCT) and fundus photography. AI also shows promise in pediatric care, aiding in the screening of retinopathy of prematurity (ROP) and the management of conditions, including pediatric cataracts and strabismus.

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Research Funding Organizations (RFOs) play an important role in promoting research integrity (RI). Not only do they allocate resources to research institutions and researchers, but they also set and monitor research standards in their funded projects. In spite of their crucial role, there is a paucity of guidance on how RFOs can promote research integrity.

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The CMG helicase is the stable core of the eukaryotic replisome and is ubiquitylated and disassembled during DNA replication termination. Fungi and animals use different enzymes to ubiquitylate the Mcm7 subunit of CMG, suggesting that CMG ubiquitylation arose repeatedly during eukaryotic evolution. Until now, it was unclear whether cells also have ubiquitin-independent pathways for helicase disassembly and whether CMG disassembly is essential for cell viability.

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Loss-of-function mutations in PTEN-induced kinase 1 (PINK1) are a frequent cause of early-onset Parkinson's disease (PD). Stabilization of PINK1 at the translocase of outer membrane (TOM) complex of damaged mitochondria is critical for its activation. The mechanism of how PINK1 is activated in the TOM complex is unclear.

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