Publications by authors named "Yunna L Sinskey"

Article Synopsis
  • - Pediatric limb loss or deficiency is rare in the U.S., happening at a rate of 1 in 1943 live births, primarily affecting upper limbs more than lower limbs and often stemming from congenital issues or trauma.
  • - Amniotic band syndrome is a significant cause of congenital limb loss due to vascular disruption, posing unique medical and rehabilitation challenges for affected children.
  • - Prosthetic development for children with limb differences needs a personalized approach, considering various factors like amputation level, cognitive development, family goals, and resources, rather than using a standardized method.
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Introduction: Partial thickness burns not undergoing surgical excision are treated with topical silver products including silver sulfadiazine (SSD) and Mepilex Ag. Skin allograft is a more costly alternative that acts as definitive wound coverage until autogenous epithelialization. Economic constraints and the movement toward value-based care demand cost and outcome justification prior to adopting more costly products.

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The effect of tumor necrosis factor-α (TNFα) on cartilage matrix degradation is mediated by its transport and binding within the extracellular matrix (ECM) of the tissue, which mediates availability to cell receptors. Since the bioactive form of TNFα is a homotrimer of monomeric subunits, conversion between trimeric and monomeric forms during intratissue transport may affect binding to ECM and, thereby, bioactivity within cartilage. We studied the transport and binding of TNFα in cartilage, considering the quaternary structure of this cytokine.

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The efficacy of biological therapeutics against cartilage degradation in osteoarthritis is restricted by the limited transport of macromolecules through the dense, avascular extracellular matrix. The availability of biologics to cell surface and matrix targets is limited by steric hindrance of the matrix, and the microstructure of matrix itself can be dramatically altered by joint injury and the subsequent inflammatory response. We studied the transport into cartilage of a 48 kDa anti-IL-6 antigen binding fragment (Fab) using an in vitro model of joint injury to quantify the transport of Fab fragments into normal and mechanically injured cartilage.

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