Publications by authors named "C Di Bari"

Purpose Of Review: Giant cell arteritis (GCA) is an age-related autoimmune disease with a complex pathogenesis that involves several pathogenic mechanisms. This review provides recent critical insights into novel aspects of GCA pathogenesis.

Recent Findings: The use of novel approaches, including multiomic techniques, has uncovered notable findings that broaden the understanding of GCA pathogenesis.

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Background: Bacterial antimicrobial resistance (AMR) is a global threat to both humans and livestock. Despite this, there is limited global consensus on data-informed, priority areas for intervention in both sectors. We compare current livestock AMR data collection efforts with other variables pertinent to human and livestock AMR to identify critical data gaps and mutual priorities.

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Quantifying the impact of poor animal health outcomes on human health represents a complex challenge. Using the disability-adjusted life year (DALY) metric as an endpoint, this article discusses how animal health outcomes can impact humans through three key processes: directly through zoonotic disease, indirectly via changes in yields and their impacts on nutrition and wealth, and finally, through indirect features associated with the agricultural industry, such as pharmaceuticals and climate change. For each process, the current state of the art and feasibility of global DALY-associated estimates are discussed.

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Article Synopsis
  • Neutrophil activation needs careful control to prevent diseases, as uncontrolled neutrophil extracellular traps (NETs) can cause more harm than good.
  • A receptor called MICL helps keep this process in check by recognizing DNA in NETs, and when it doesn't work properly, it can lead to too many NETs being formed.
  • In diseases like rheumatoid arthritis and lupus, there are autoantibodies that block MICL, which worsens the disease, but during certain infections, like with a fungus, having more NETs can actually help fight off the infection.
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Objective: Obesity increases osteoarthritis (OA) risk due to adipose tissue dysfunction with associated metabolic syndrome and excess weight. Lipodystrophy syndromes exhibit systemic metabolic and inflammatory abnormalities similar to obesity without biomechanical overloading. Here, we used lipodystrophy mouse models to investigate the effects of systemic versus intra-articular adipose tissue dysfunction on the knee.

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