Publications by authors named "R Kevin Tindell"

Musculoskeletal interfacial tissues consist of complex gradients in structure, cell phenotype, and biochemical signaling that are important for function. Designing tissue engineering strategies to mimic these types of gradients is an ongoing challenge. In particular, new fabrication techniques that enable precise spatial control over fiber alignment are needed to better mimic the structural gradients present in interfacial tissues, such as the tendon-bone interface.

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The lamina propria within the vocal fold (VF) is a complex multilayered tissue that increases in stiffness from the superficial to deep layer, where this characteristic is crucial for VF sound production. Tissue-engineered scaffolds designed for VF repair must mimic the biophysical nature of the native vocal fold and promote cell viability, cell spreading, and vibration with air flow. In this study, we present a unique trilayered, partially degradable hydrogel scaffold that mimics the multilayered structure of the VF lamina propria.

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The trace element selenium (Se) contributes to redox signaling, antioxidant defense, and immune responses in critically ill neonatal and adult patients. Se is required for the synthesis and function of selenoenzymes including thioredoxin (Trx) reductase-1 (TXNRD1) and glutathione peroxidases (GPx). We have previously identified TXNRD1, primarily expressed by airway epithelia, as a promising therapeutic target to prevent lung injury, likely via nuclear factor E2-related factor 2 (Nrf2)-dependent mechanisms.

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Extremely preterm infants are at high risk for morbidities including bronchopulmonary dysplasia, intraventricular hemorrhage, and retinopathy of prematurity likely related to their exposure to reactive oxygen and nitrogen species early in life. Selenium is a trace mineral contributes to the proper function of multiple systems including immunity, redox regulation, and inflammation via the "selenoenzymes" glutathione peroxidase, thioredoxin reductase, and selenoprotein P. Given that selenium accretion via the placenta occurs primarily during the third trimester, preterm neonates are born selenium deficient.

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