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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dc="http://purl.org/dc/elements/1.1/"><rdf:Description rdf:about="https://repozitorij.uni-lj.si/IzpisGradiva.php?id=176478"><dc:title>Spatiotemporal analysis of Escherichia coli membrane permeabilization and uptake kinetics induced by a single microbubble cavitation event</dc:title><dc:creator>Drab,	Mitja	(Avtor)
	</dc:creator><dc:creator>Iglič,	Aleš	(Avtor)
	</dc:creator><dc:creator>Stopar,	David	(Avtor)
	</dc:creator><dc:creator>Pandur,	Žiga	(Avtor)
	</dc:creator><dc:subject>cavitation</dc:subject><dc:subject>bacterial cells</dc:subject><dc:subject>poration</dc:subject><dc:subject>propidium iodide uptake</dc:subject><dc:subject>Goldman equation</dc:subject><dc:description>A single cavitation microbubble can transiently disrupt the cellular membrane, providing a chemicalfree, targeted drug delivery mechanism. Here, we investigate the spatiotemporal dynamics of membrane permeabilization in an Escherichia coli (E. coli) monolayer exposed to a single cavitation event. Using high-resolution fluorescence microscopy and propidium iodide (PI) uptake as a marker of membrane disruption, we tracked the response of 5565 individual cells around the center of the cavitation event over timescales from microseconds to minutes and spatial scales from 1 to 165 µm. PI uptake rates exhibited a strong spatial dependence, with cells closer to the cavitation center showing rapid and extensive permeabilization. A modified Goldman equation describing PI concentrations inside and outside the cells was used and related to the spatiotemporal measurements of fluorescence intensity. The model accurately captured the first-order PI uptake kinetics, which resulted in saturated fluorescence intensity profiles. Additionally, the model predicted an exponential decay of permeability post-cavitation, implicitly suggesting that pore-resealing dynamics were taking place. Membrane permeability decreased with distance as 1/r, with a characteristic decay time of approximately 3.4 min. Our model thus predicts cell damage induced by a single cavitation event in both space and time. In the present case, where the cavitation bubble reached maximum radius of 29.7 µm, we found that at a distance of 11 µm from the cavitation center,~50% of cell membranes are damaged and permeable to PI, but a pore-resealing mechanism reduces this damage to~1% after 10 min. Our results are consistent with existing sonoporation studies and offer novel insights for optimizing cavitationassisted drug delivery and biofilm disruption strategies.</dc:description><dc:date>2025</dc:date><dc:date>2025-12-02 09:59:31</dc:date><dc:type>Članek v reviji</dc:type><dc:identifier>176478</dc:identifier><dc:language>sl</dc:language></rdf:Description></rdf:RDF>
