Publications by authors named "Braaten B"

Radio frequency (RF) biosensors are an expanding field of interest because of the ability to design noninvasive, label-free, low-production-cost sensing devices. Previous works identified the need for smaller experimental devices, requiring nanoliter to milliliter sampling volumes and increased capability of repeatable and sensitive measurement capability. The following work aims to verify a millimeter-sized, microstrip transmission line biosensor design with a microliter well operating on a broadband radio frequency range of 1.

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Objectives: The objectives of this review were to review the current literature on escape rooms in pharmacy education, determine their impact on educational outcomes, and identify areas for future research.

Findings: A literature search retrieved 14 reports, of which 10 studies met all of the study criteria. The majority of the studies used the escape room to review previously taught content (90%).

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The rapid growth of wireless spectrum access through cellular and IoT devices, for example, requires antennas with more capabilities such as being conformal and self-adapting beamforming. In this paper, the adaptive beamforming patterns of microstrip patch antenna arrays on changing flexible (or conformal) curved surfaces are developed by deriving array coefficients based on the projection method that includes the mutual coupling between elements. A linear four-element microstrip patch antenna array is then embedded on two deformed conformal surfaces to investigate the projection method for desired beamforming patterns.

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The phenomenon of contact-dependent growth inhibition (CDI) and the genes required for CDI () were identified and isolated in 2005 from an isolate (EC93) from rats. Although the locus has been the focus of extensive research during the past 15 years, little is known about the EC93 isolate from which it originates. Here we sequenced the EC93 genome and find two complete and functional loci (including the previously identified locus), both carried on a large 127 kb plasmid.

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Recently, interest in the effects of radio frequency (RF) on biological systems has increased and is partially due to the advancements and increased implementations of RF into technology. As research in this area has progressed, the reliability and reproducibility of the experiments has not crossed multidisciplinary boundaries. Therefore, as researchers, it is imperative to understand the various exposure systems available as well as the aspects, both electromagnetic and biological, needed to produce a sound exposure experiment.

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Many studies have been performed on exploring the effects of radio-frequency (RF) energy on biological function in vivo. In particular, gene expression results have been inconclusive due, in part, to a lack of a standardized experimental procedure. This research describes a new far field RF exposure system for unrestrained murine models that reduces experimental error.

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Unlabelled: Goal: The aim of this study is to develop a novel fully wireless and batteryless technology for cardiac pacing.

Methods: This technology uses radio frequency (RF) energy to power the implanted electrode in the heart. An implantable electrode antenna was designed for 1.

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With the prevalence of wireless radio frequency (RF) devices, interest is growing to more fully understand the effect of RF on biological tissue. This research explores how ?DNA interacts with RF energy. By sweeping a radio frequency range from 1 GHz to 8.

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Clonally derived bacterial populations exhibit significant genotypic and phenotypic diversity that contribute to fitness in rapidly changing environments. Here, we show that serial passage of Salmonella enterica serovar Typhimurium LT2 (StLT2) in broth, or within a mouse host, results in selection of an evolved population that inhibits the growth of ancestral cells by direct contact. Cells within each evolved population gain the ability to express and deploy a cryptic "orphan" toxin encoded within the rearrangement hotspot (rhs) locus.

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Bacterial contact-dependent growth inhibition (CDI) is mediated by the CdiA/CdiB family of two-partner secretion proteins. Each CdiA protein exhibits a distinct growth inhibition activity, which resides in the polymorphic C-terminal region (CdiA-CT). CDI(+) cells also express unique CdiI immunity proteins that specifically block the activity of cognate CdiA-CT, thereby protecting the cell from autoinhibition.

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Bacteria have developed mechanisms to communicate and compete with one another in diverse environments. A new form of intercellular communication, contact-dependent growth inhibition (CDI), was discovered recently in Escherichia coli. CDI is mediated by the CdiB/CdiA two-partner secretion (TPS) system.

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Contact-dependent growth inhibition (CDI) is a mechanism identified in Escherichia coli by which bacteria expressing two-partner secretion proteins encoded by cdiA and cdiB bind to BamA in the outer membranes of target cells and inhibit their growth. A third gene in the cluster, cdiI, encodes a small protein that is necessary and sufficient to confer immunity to CDI, thereby preventing cells expressing the cdiBA genes from inhibiting their own growth. In this study, the cdiI gene was placed under araBAD promoter control to modulate levels of the immunity protein and thereby induce CDI by removal of arabinose.

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Contact-dependent growth inhibition (CDI) is a phenomenon by which bacterial cell growth is regulated by direct cell-to-cell contact via the CdiA/CdiB two-partner secretion system. Characterization of mutants resistant to CDI allowed us to identify BamA (YaeT) as the outer membrane receptor for CDI and AcrB as a potential downstream target. Notably, both BamA and AcrB are part of distinct multi-component machines.

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Bacteria have developed mechanisms to communicate and compete with each other for limited environmental resources. We found that certain Escherichia coli, including uropathogenic strains, contained a bacterial growth-inhibition system that uses direct cell-to-cell contact. Inhibition was conditional, dependent upon the growth state of the inhibitory cell and the pili expression state of the target cell.

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Pap pili gene expression is controlled by a reversible OFF/ON phase switch that is orchestrated by binding of Lrp to pap pilin promoter proximal sites 1, 2, and 3 (OFF) or pap promoter distal sites 4, 5, and 6 (ON). Movement of Lrp between proximal and distal sites controls pap pilin transcription and is modulated by PapI and DNA adenine methylase. Here we show that activation of the environmentally responsive CpxAR two-component regulatory system inhibits Pap phase variation by generation of phosphorylated CpxR (CpxR-P).

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Bacteria have developed epigenetic mechanisms to control the reversible Off-to-On switching of cell surface structures such as pyelonephritis-associated pili (PAP). The pap pili switch is primarily controlled by the global regulator leucine-responsive regulatory protein (Lrp), the local regulator PapI, and DNA adenine methylase (Dam). There are two sets of binding sites for Lrp in the pap regulatory region: promoter proximal sites 1,2,3 and promoter distal sites 4,5,6.

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The expression of pyelonephritis-associated pili (Pap) in uropathogenic Escherichia coli is epigenetically controlled by a reversible OFF to ON switch. In phase OFF cells, the global regulator Lrp is bound to pap sites proximal to the pilin promoter, whereas in phase ON cells, Lrp is bound to promoter distal sites. We have found that the local regulator PapI increases the affinity of Lrp for the sequence "ACGATC," which contains the target "GATC" site for DNA adenine methylase (Dam) and is present in both promoter proximal and distal sites.

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Bacteria have developed an epigenetic phase variation mechanism to control cell surface pili-adhesin complexes between heritable expression (phase ON) and nonexpression (phase OFF) states. In the pyelonephritis-associated pili (pap) system, global regulators [catabolite gene activator protein (CAP), leucine-responsive regulatory protein (Lrp), DNA adenine methylase (Dam)] and local regulators (PapI and PapB) control phase switching. Lrp binds cooperatively to three pap DNA binding sites, sites 1-3, proximal to the papBA pilin promoter in phase OFF cells, whereas Lrp is bound to sites 4-6 distal to papBA in phase ON cells.

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Catabolite gene activator protein (CAP) is essential for the expression of Pap pili by uropathogenic Escherichia coli. Both in vitro and in vivo analyses indicate that binding of cAMP-CAP centred at 215.5 bp upstream of the papBA promoter is essential for activation of transcription.

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Pap pili play an important role in the pathogenesis of upper urinary tract infections by enabling uropathogenic Escherichia coli to adhere to host epithelial cells. Pap pili are coded for by the pyelonephritis-associated pili (pap) operon, which consists of 11 genes required for the expression and assembly of Pap pili. Expression of Pap pili is regulated by a phase variation mechanism in which the pili expression state of the bacterial population is skewed between phase-on (expression positive) and phase-off (expression negative) states.

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The expression of Pap pili that facilitate the attachment of Escherichia coli to uroepithelial cells is shut off outside the host at temperatures below 26 degrees C. Ribonuclease protection analysis showed that this thermoregulatory response was rapid as evidenced by the absence of papBA transcripts, coding for Pap pilin, after only one generation of growth at 23 degrees C. The histone-like nucleoid structuring protein H-NS and DNA sequences within papB were required for thermoregulation, but the PapB and PapI regulatory proteins were not.

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The global regulator Lrp plays a central role as both a repressor and an activator in Pap phase variation. Unlike most other members of the Lrp regulon such as ilvIH, activation of papBA transcription requires the coregulator PapI and is methylation dependent. We developed a two-color genetic screen to identify Lrp mutations that inhibit Pap phase variation but still activate ilvIH transcription, reasoning that such mutations might identify PapI binding or methylation-responsive domains.

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Expression of the pyelonephritis-associated pilus (pap) operon in Escherichia coli is regulated by a complex epigenetic phase-variation mechanism involving the formation of differential DNA-methylation patterns. This review discusses how DNA-methylation patterns are formed by protein-DNA interactions and how methylation patterns, in turn, control pap gene expression.

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Pyelonephritis-associated pili (Pap) expression in Escherichia coli is subject to a phase variation control mechanism that is regulated by the leucine-responsive regulatory protein (Lrp), PapI, and deoxyadenosine methylase (Dam). In previous work, we found that the differential Dam methylation of two target sites in pap regulatory DNA, GATC-I and GATC II, is essential for the transition between active and inactive pap transcriptional states. Here, we identify six Lrp binding sites within the pap regulatory DNA, each separated by about three helical turns.

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Expression of pyelonephritis-associated pili (Pap) varies between transcriptionally active (ON) and inactive (OFF) phase states. Pap phase variation is controlled by the binding of leucine-responsive regulatory protein (Lrp) to two pap regulatory DNA regions, each containing a deoxyadenosine methylase site and designated GATC-I and GATC-II. Methylation of these GATC sites modulates binding of Lrp and plays an essential role in phase variation.

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