Publications by authors named "Allison R Cutri"

Bacterial communities exhibit complex self-organization that contributes to their survival. To better understand the molecules that contribute to transforming a small number of cells into a heterogeneous surface biofilm community, we studied acellular aggregates, structures seen by light microscopy in colony biofilms using light microscopy and chemical imaging. These structures differ from cellular aggregates, cohesive clusters of cells important for biofilm formation, in that they are visually distinct from cells using light microscopy and are reliant on metabolites for assembly.

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is an opportunistic human pathogen capable of causing a wide range of diseases in immunocompromised patients. In order to better understand behavior and virulence and to advance drug therapies to combat infection, it would be beneficial to understand how cells survive stressful conditions, especially environmental stressors. Here, we report on a strategy that measures potential-dependent fluorescence of individual cells, as a sentinel, for cellular response to starvation, hunger, and oxidative stress.

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In this study, we use nanopore arrays as a platform for detecting and characterizing individual nanoparticles (NPs) in real time. Dark-field imaging of nanopores with dimensions smaller than the wavelength of light occurs under conditions where trans-illumination is blocked, while the scattered light propagates to the far-field, making it possible to identify nanopores. The intensity of scattering increases dramatically during insertion of AgNPs into empty nanopores, owing to their plasmonic properties.

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is a Gram-negative opportunistic human pathogen responsible for a number of healthcare-associated infection. It is currently difficult to assess single cell behaviors of that might contribute to acquisition of antibiotic resistance, intercellular communication, biofilm development, or virulence, because mechanistic behavior is inferred from ensemble collections of cells, thus averaging effects over a population. Here, we develop and characterize a device that can capture and trap arrays of single cells in individual micropores in order to study their behaviors using spectroelectrochemistry.

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() is commonly implicated in hospital-acquired infections where its capacity to form biofilms on a variety of surfaces and the resulting enhanced antibiotic resistance seriously limit treatment choices. Because surface attachment sensitizes to quorum sensing (QS) and induces virulence through both chemical and mechanical cues, we investigate the effect of surface properties through spatially patterned mucin, combined with sub-inhibitory concentrations of tobramycin on QS and virulence factors in both mucoid and non-mucoid strains using multi-modal chemical imaging combining confocal Raman microscopy and matrix-assisted laser desorption/ionization-mass spectrometry. Samples comprise surface-adherent static biofilms at a solid-water interface, supernatant liquid, and pellicle biofilms at an air-water interface at various time points.

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Indium-tin oxide (ITO) is used in a variety of applications due to its electrical conductivity and optical transparency. Moreover, ITO coated glass is a common working electrode for spectroelectrochemistry. Thus, the ITO substrates should exhibit well-understood spectroscopic characteristics.

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produces a number of phenazine metabolites, including pyocyanin (PYO), phenazine-1-carboxamide (PCN), and phenazine-1-carboxylic acid (PCA). Among these, PYO has been most widely studied as a biomarker of infection. However, despite its broad-spectrum antibiotic properties and its role as a precursor in the biosynthetic route leading to other secondary phenazines, PCA has attracted less attention, partially due to its relatively low concentration and interference from other highly abundant phenazines.

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Mitochondrial Ca(2+) Uniporter (MCU)-dependent mitochondrial Ca(2+) uptake is the primary mechanism for increasing matrix Ca(2+) in most cell types. However, a limited understanding of the MCU complex assembly impedes the comprehension of the precise mechanisms underlying MCU activity. Here, we report that mouse cardiomyocytes and endothelial cells lacking MCU regulator 1 (MCUR1) have severely impaired [Ca(2+)]m uptake and IMCU current.

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