Publications by authors named "N G Deshpande"

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.

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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.

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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.

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CD163, a scavenger receptor with anti-inflammatory function expressed exclusively on monocytes/macrophages, is dysregulated in cases of diabetes complications. This study aimed to characterize circulating CD163+ monocytes in the presence (D) or absence (D) of diabetes-related complications. RNA-sequencing and mass cytometry were conducted on CD163+ monocytes in adults with long-duration diabetes and D or D.

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Article Synopsis
  • Epidemiological studies indicate that cigarette smoking worsens corneal endothelial dysfunction, but the exact reasons are not well understood.
  • The research found that prolonged exposure to smoke activates the aryl hydrocarbon receptor (AhR), which increases the expression of CYP1B1 and leads to aging and scarring in corneal cells, possibly as a way to adapt to damage.
  • While these changes suggest early signs of dysfunction, no severe damage was detected, implying that developing a serious condition like Fuchs endothelial corneal dystrophy requires other environmental or genetic influences beyond just smoking.
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