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Biology subjects

Krauss, T. D.

Publications and source records attributed to Krauss, T. D..

3 recordsLinked to original sources

Transforming dairy waste into hydrogen fuel using alginate-encapsulated bacterial co-cultures

Dairy waste, such as whey resulting from cheese production, is produced in massive volumes worldwide and is regarded as environmentally difficult to dispose of due to its high organic content1. Harnessing the potential of this waste material to support the synthesis of valuable products such as hydrogen fuel or reduced graphene oxide, which may be utilized for conductive thin films and energy storage2,3, can reduce waste and add revenue streams for dairy farmers. Here, we demonstrate a circular bioeconomy using alginate-encapsulated co-cultures of Shewanella oneidensis together with lactic-acid-producing bacteria Klebsiella pneumoniae. These co-cultures can directly metabolize unprocessed cheese-making waste as an electron source instead of costly, environmentally high-impact lactic acid4,5. Alginate-encapsulated co-cultures fed unprocessed dairy waste showed a 2-to-3-fold higher graphene oxide reduction rate compared to S. oneidensis monocultures with no supplemental electron source. Encapsulated co-cultures were able to be recycled for more than 30 days with no measurable decrease in graphene oxide reduction efficiency, showing compatibility with future industrial scaling. Photocatalytic hydrogen generation with cadmium selenide quantum dots as the catalyst resulted in 6-fold increases in hydrogen produced by co-cultures using milk as an electron source precursor for the system in comparison to S. oneidensis monocultures without any added electron sources. Thus, dairy waste may be processed to drive the synthesis of valuable products utilizing microbial electron transfer processes, converting a significant fluvial environmental pollutant into a valuable renewable energy resource that could provide a robust alternative revenue stream for dairy farmers in a volatile industry.

microbiology↗

Hybrid Amyloid Quantum Dot Nanoassemblies to Probe Neuroinflammatory Damage

Various oligomeric species of amyloid-beta have been proposed to play different immunogenic roles in the cellular pathology of Alzheimers Disease. However, investigating the role of a homogenous single oligomeric species has been difficult due to highly dynamic oligomerization and fibril formation kinetics that convert between many species. Here we report the design and construction of a quantum dot mimetic for larger spherical oligomeric amyloid species as an "endogenously" fluorescent proxy for this cytotoxic species to investigate its role in inducing inflammatory and stress response states in neuronal and glial cell types.

neuroscience↗

A Quantum Dot Biomimetic for SARS-CoV-2 to Interrogate Dysregulation of the Neurovascular Unit Relevant to Brain Inflammation

Despite limited evidence for competent infection and viral replication of SARS-CoV-2 in the central nervous system (CNS), neurologic dysfunction is a common post-acute medical condition reported in "recovered" COVID-19 patients. To identify a potential noninfectious route for SARS-CoV-2-mediated neurological damage, we constructed colloidal nanocrystal quantum dots linked to micelles decorated with spike protein (COVID-QDs) as a biomimetic to interrogate how blood-brain barrier (BBB) dysregulation may subsequently induce neuroinflammation in the absence of infection. In transwell co-culture of endothelial bEnd.3 monolayers and primary neuroglia, we exposed only the bEnd.3 monolayers to COVID-QDs and examined by fluorescence microscopy whether such treatment led to (i) increased inflammation and leakage across the bEnd.3 monolayers, (ii) permeability of the COVID-QDs across the monolayers, and (iii) induction of neuroinflammation in neuroglial cultures. The results of our study provide evidence of neuroinflammatory hallmarks in cultured neurons and astrocytes without direct exposure to SARS-CoV-2-like nanoparticles. Additionally, we found that pre-treatment of our co-cultures with a small-molecule, broad-spectrum inhibitor of mixed lineage and leucine rich repeat kinases led to reversal of the observed dysregulation in endothelial monolayers and resulted in neuroglial protection. The results reported here may serve to guide future studies into the potential mechanisms by which SARS-CoV-2 mediates neurologic dysfunction.

neuroscience↗