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Wrede, A. H.

Publications and source records attributed to Wrede, A. H..

2 recordsLinked to original sources

Behavior of Neural Cells Post Manufacturing and After Prolonged Encapsulation within Conductive Graphene-Laden Alginate Microfibers

Engineering conductive 3D cell scaffoldings offer unique advantages towards the creation of physiologically relevant platforms with integrated real-time sensing capabilities. Toward this goal, rat dopaminergic neural cells were encapsulated into graphene-laden alginate microfibers using a microfluidic fiber fabrication approach, which is unmatched for creating continuous, highly tunable microfibers. Incorporating graphene increases the conductivity of the alginate microfibers 148%, creating a similar conductivity to native brain tissue. Graphene leads to an increase in the cross-sectional sizes and porosities of the fibers, while reducing the roughness of the fiber surface. The cell encapsulation procedure has an efficiency rate of 50%, and of those cells, approximately 30% remain for the entire 6-day observation period. To understand how encapsulation effects cell genetics, the genes IL-1{beta}, TH, TNF-, and TUBB-3 are analyzed, both after manufacturing and after encapsulation for six days. The manufacturing process and combination with alginate leads to an upregulation of TH, and the introduction of graphene further increases its levels; however, the inverse trend is true of TUBB-3. Long-term encapsulation shows continued upregulation of TH and of TNF-, and six-day exposure to graphene leads to the upregulation of TUBB-3 and IL-1{beta}, which indicates increased inflammation.

bioengineering

How do neuroglial cells respond to ultrasound induced cavitation?

Reactive astrocytes are known to play a vital role in the overall response of the brain during a traumatic brain injury (TBI). Modern studies have speculated the existence of cavitation in the skull during a TBI, which has alarming potential to cause detrimental damages. Previous studies have confirmed the upregulation of various harmful genes in neurodegenerative diseases. Studying the longitudinal presence of these harmful genes in response to cavitation allows for optimized understanding and treatment methods in cavitation exposure. We seek to characterize the longitudinal genetic expression levels that astrocytes exhibit after exposure to cavitation and further elucidate the startling presence of cranial cavitation. Astrocytic expression levels of various common genes that have been documented in TBI research are our target of interest, like, TNF, IL-1{beta}, and NOS1. Results summarize specific gene trends from 1-48 hours after cavitation. Our data concludes that maximum expression is not consistently exhibited immediately after cavitation exposure, and most genes have individualized genetic trends. IL-1{beta} shows a decreasing expression over 48 hours, and TNF shows upregulation until the 6 hour time point but then begins to decrease in expression. The upregulation of NOS1 has been documented in neurodegenerative diseases, like Alzheimers and Parkinsons disease. This study has shown a consistent upregulation in NOS1 expression from 0-48 hours. These results postulate a possible linkage between cavitation damage and neurodegenerative diseases. This analysis also provides novelty in optimizing treatments for astrocytic function post-TBI and legitimizing the concern of cranial cavitation existence. These results add motivation for future studies of cavitation elimination or minimization via advanced helmet and airbag engineering.

bioengineering