Publications by authors named "D V Gowda"

Background: Over a century ago, Virchow proposed that cancer represents a chronically inflamed, poorly healing wound. Normal wound healing is represented by a transitory phase of inflammation, followed by a pro-resolution phase, with prostaglandin (PGE2/PGD2)-induced 'lipid class switching' producing inflammation-quenching lipoxins (LXA4, LXB4).

Objective: We explored if lipid dysregulation in colorectal cancers (CRCs) is driven by a failure to resolve inflammation.

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  • Artificial intelligence (AI) is set to transform healthcare, particularly in critical and acute care medicine, with a focus on digital twin (DT) technology.
  • DTs enhance medical education, research, and support clinical decisions, thanks to improved computational power and validation processes.
  • While DTs offer significant benefits for efficiency in critical care, they also present challenges like data safety, privacy issues, and potential increases in healthcare disparities, making stakeholder investment crucial for successful implementation.
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  • Scientists created new chemicals to fight cancer, specifically focusing on colon cancer.
  • They tested how well these compounds could stop cancer cells from growing and found some that worked really well compared to a standard medicine called Gefitinib.
  • The team plans to keep improving these compounds to develop better ways to treat cancer in the future.
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Sorghum, a globally grown gluten-free cereal, is used mainly as an animal feed in developed countries regardless of its potential for human consumption. In this study, we utilized nontargeted lipidomics to thoroughly analyze, compare, and characterize whole-grain lipids in six sorghum cultivars (cv) grown in a single field trial in Australia: Buster, Bazley, Cracker, Liberty, MR43, and Tiger. In total, 194 lipid molecular species representing five major lipid classes were identified.

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Introduction: Hepatocellular carcinoma (HCC) is a fatal cancer that is often diagnosed at the advanced stages which limits the available therapeutic options. The interaction of HGF with c-MET (a receptor tyrosine kinase) results in the activation of c-MET which subsequently triggers the PI3K/Akt/mTOR axis. Overexpression of c-MET in HCC tissues has been demonstrated to contribute to tumor progression and metastasis.

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