Publications by authors named "Joshua McCall"

Research over the past several decades has revealed that non-linguistic cognitive impairments can appear alongside language deficits in individuals with aphasia. One vulnerable cognitive domain is executive function, an umbrella term for the higher-level cognitive processes that allow us to direct our behavior towards a goal. Studies in healthy adults reveal that executive function abilities are supported by inner speech, the ability to use language silently in one's head.

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Despite the many mistakes we make while speaking, people can effectively communicate because we monitor our speech errors. However, the cognitive abilities and brain structures that support speech error monitoring are unclear. There may be different abilities and brain regions that support monitoring phonological speech errors versus monitoring semantic speech errors.

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People use cognitive control across many contexts in daily life, yet it remains unclear how cognitive control is used in contexts involving language. Distinguishing language-specific cognitive control components may be critical to understanding aphasia, which can co-occur with cognitive control deficits. For example, deficits in control of semantic representations (i.

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Optimal performance in any task relies on the ability to detect and correct errors. The anterior cingulate cortex and the broader posterior medial frontal cortex (pMFC) are active during error processing. However, it is unclear whether damage to the pMFC impairs error monitoring.

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Anosognosia, or lack of self-awareness, is often present following neurological injury and can result in poor functional outcomes. The specific phenomenon of intellectual awareness, the knowledge that a function is impaired in oneself, has not been widely studied in post-stroke aphasia. We aim to identify behavioral and neural correlates of intellectual awareness by comparing stroke survivors' self-reports of anomia to objective naming performance and examining lesion sites.

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Methods to precisely control growth factor presentation in a local and sustained fashion are of increasing interest for a number of complex tissue engineering applications. The cytokine transforming growth factor beta (TGFβ) plays a key role in promoting the chondrogenic differentiation of human mesenchymal stem cells (hMSCs). Traditional chondrogenic approaches utilize soluble delivery, an approach with limited application for clinical translation.

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Photoinitiated polymerization remains a robust method for fabrication of hydrogels, as these reactions allow facile spatial and temporal control of gelation and high compatibility for encapsulation of cells and biologics. The chain-growth reaction of macromolecular monomers, such as acrylated PEG and hyaluronan, is commonly used to form hydrogels, but there is growing interest in step-growth photopolymerizations, such as the thiol-ene "click" reaction, as an alternative. Thiol-ene reactions are not susceptible to oxygen inhibition and rapidly form hydrogels using low initiator concentrations.

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Transforming growth factor beta (TGFβ(1)) influences a host of cellular fates, including proliferation, migration, and differentiation. Due to its short half-life and cross reactivity with a variety of cells, clinical application of TGFβ(1) may benefit from a localized delivery strategy. Photoencapsulation of proteins in polymeric matrices offers such an opportunity; however, the reactions forming polymer networks often result in lowered protein bioactivity.

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We report the first use of a polymerization-based ELISA substrate solution employing enzymatically mediated radical polymerization as a dual-mode amplification strategy. Enzymes are selectively coupled to surfaces to generate radicals that subsequently lead to polymerization-based amplification (PBA) and biodetection. Sensitivity and amplification of the polymerization-based detection system were optimized in a microwell strip format using a biotinylated microwell surface with a glucose oxidase (GOx)-avidin conjugate.

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