Publications by authors named "D Y Gao"

Increased entropy is a common cause of disease and aging. Lifespan entropy is the overall increase in disorder caused by a person over their lifetime. Aging leads to the excessive production of reactive oxygen species (ROS), which damage the antioxidant system and disrupt redox balance.

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Investigations have indicated that there is a correlation between thyroid nodules and patients'negative emotions. Nevertheless, the risk factors contributing to the development of negative emotions in thyroid nodule patients remain unidentified. This cross-sectional study recruited 150 patients diagnosed with thyroid nodules through ultrasound examination from January 2022 to January 2023 at Jinan Central Hospital, the Second Affiliated Hospital of Shandong First Medical University, and Qingyun County Maternal and Child Health Hospital as the case group, which were categorized based on their levels of anxiety and depression.

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Organoid technology provides a transformative approach to understand human physiology and pathology, offering valuable insights for scientific research and therapeutic development. Human gastric organoids, in particular, have gained significant interest for applications in disease modeling, drug discovery, and studies of tissue regeneration and homeostasis. However, the lack of standardized quality control has limited their extensive clinical applications.

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Rechargeable Mg batteries are promising candidates for achieving considerable high-energy-density. Enhancing the energy density can be achieved by integrating metallic Mg anodes with conversion-type cathode materials, which are characterized by multi-electron transfer process and elevated specific capacities in contrast to intercalation-type materials. Despite these advantages, the conversion-type cathodes still have some challenges of substantial volume expansion, sluggish diffusion kinetics and intricate mesophase evolution during repeated electrochemical reactions.

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Members of the KMT2C/D-KDM6A complex are recurrently mutated in urothelial carcinoma and in histologically normal urothelium. Here, using genetically engineered mouse models, we demonstrate that Kmt2c/d knockout in the urothelium led to impaired differentiation, augmented responses to growth and inflammatory stimuli and sensitization to oncogenic transformation by carcinogen and oncogenes. Mechanistically, KMT2D localized to active enhancers and CpG-poor promoters that preferentially regulate the urothelial lineage program and Kmt2c/d knockout led to diminished H3K4me1, H3K27ac and nascent RNA transcription at these sites, which leads to impaired differentiation.

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