Publications by authors named "D L Brand"

Background: Recommendations from a trusted healthcare provider have been shown to be the most effective intervention for encouraging patients to be vaccinated. However, providers have reported feeling less prepared to address vaccination questions and having less time to discuss vaccines with patients than before the COVID-19 pandemic. Providers may benefit from a brief update about the available influenza vaccines and vaccination guidelines.

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Objective: Investigational cell therapies have been developed as disease-modifying agents for the treatment of osteoarthritis (OA), including those that inducibly respond to inflammatory factors driving OA progression. However, dysregulated inflammatory cascades do not specifically signify the presence of OA. Here, we deploy a synthetic receptor platform that regulates cell behaviors in an arthritis-specific fashion to confine transgene expression to sites of cartilage degeneration.

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Mitotic activity is an important feature for grading several cancer types. However, counting mitotic figures (cells in division) is a time-consuming and laborious task prone to inter-observer variation. Inaccurate recognition of MFs can lead to incorrect grading and hence potential suboptimal treatment.

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Article Synopsis
  • - Neurotrauma in limbs causes long-lasting neuroinflammation that interferes with nerve structure and slows down nerve repair, despite some inflammatory processes being beneficial for clearing damaged tissue.
  • - Peripheral nerve injuries lead to increased expression of secreted frizzled-related protein 1 (sFRP1) by Schwann cells, which interacts with heat shock protein 90 (HSP90) in macrophages, causing excessive inflammation.
  • - Targeted deletion of sFRP1 from Schwann cells or HSP90 from macrophages can reduce neuroinflammation and hinder nerve damage progression, highlighting the harmful role of macrophage response to sFRP1 in nerve injuries.
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When IL-1 receptor antagonist (IL-1rn) is knocked out, mice have shown strain background dependent and major QTL regulated susceptibility to spontaneously inflammatory arthritis disease (SAD). The impact on bone properties resulting from the interactions of IL-1rn, genomic background strains, and the QTL locus, is unknown. Bone properties in the four specifically bred mouse strains with mutation of IL-1rn and variations in genomic components were investigated with high-resolution MicroCT and genomic analytical tools.

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