Mitochondria-Targeted Antioxidant (MitoQ) and Nontargeted Antioxidant (Idebenone) Mitigate Mitochondrial Dysfunction in Corneal Endothelial Cells.

Purpose: To investigate the effectiveness of mitochondrial-targeted antioxidant mitoquinone (MitoQ) and nontargeted antioxidant idebenone (Idb) in alleviating mitochondrial dysfunction in corneal endothelial cells (CEnCs).

Methods: In vitro experiments were conducted using immortalized normal human corneal endothelial cells (HCEnC-21T; SVN1-67F) and Fuchs endothelial corneal dystrophy (FECD) cells (SVF5-54F; SVF3-76M). Cells were pretreated with MitoQ or Idb and then exposed to menadione (MN) with simultaneous antioxidant treatment.

Take Charge of Your Professional Network of Colleagues to Succeed in Academic Medicine.

Instead of relying on a single, dyadic mentor for career advice, we suggest creating and intentionally cultivating a professional network of colleagues (PNC) to guide your academic career. There are four archetypes to help clinician educators succeed in academic medicine: a traditional mentor, a sponsor, a coach, and a connector.1 However, these roles are not discrete, and overlap occurs.

Microscopy image reconstruction with physics-informed denoising diffusion probabilistic model.

Light microscopy is a practical tool for advancing biomedical research and diagnostics, offering invaluable insights into the cellular and subcellular structures of living organisms. However, diffraction and optical imperfections actively hinder the attainment of high-quality images. In recent years, there has been a growing interest in applying deep learning techniques to overcome these challenges in light microscopy imaging.

Modulation of ATM enhances DNA repair in G2/M phase of cell cycle and averts senescence in Fuchs endothelial corneal dystrophy.

Fuchs Endothelial Corneal Dystrophy (FECD) is an aging disorder characterized by expedited loss of corneal endothelial cells (CEnCs) and heightened DNA damage compared to normal CEnCs. We previously established that ultraviolet-A (UVA) light causes DNA damage and leads to FECD phenotype in a non-genetic mouse model. Here, we demonstrate that acute treatment with chemical stressor, menadione, or physiological stressors, UVA, and catechol estrogen (4-OHE), results in an early and increased activation of ATM-mediated DNA damage response in FECD compared to normal CEnCs.