Search for: All records

Historically, physics education primarily consisted of lectures in which students have a largely passive role. Proponents of educational reform have rallied around active learning to increase engagement and retention in STEM fields, particularly advocating peer interactions to build a foundation of deep understanding. However, little is known about how students' prior preparation for introductory courses impacts their mastery of course material when instructors incorporate active learning. In the present study, we examine learning outcomes in two sections of an introductory mechanics course at an institution with a wide range of students' prior mathematics preparation as assessed by quantitative SAT scores. For each of three years, one section was taught using peer instruction in which much of the class time was spent in small-group discussions between students. The other section was taught by the same instructor using interactive lectures in which discussions primarily took place between volunteers from the class and the instructor. We find that students enrolled in the peer instruction sections earned lower grades in the course than did students in the interactive sections. We also find students in the peer instruction sections with lower quantitative SAT scores showed lower gains in understanding foundational concepts as assessed by the Force Concept Inventory and were less likely to earn an A in the course than comparable students in the interactive sections. While further research is needed to confirm these results, this study suggests that peer instruction might not be the optimal pedagogy for heterogeneous populations. 

Abstract Biofilms are ubiquitous surface-associated bacterial communities embedded in an extracellular matrix. It is commonly assumed that biofilm cells are glued together by the matrix; however, how the specific biochemistry of matrix components affects the cell-matrix interactions and how these interactions vary during biofilm growth remain unclear. Here, we investigate cell-matrix interactions inVibrio cholerae, the causative agent of cholera. We combine genetics, microscopy, simulations, and biochemical analyses to show thatV. choleraecells are not attracted to the main matrix component (Vibriopolysaccharide, VPS), but can be attached to each other and to the VPS network through surface-associated VPS and crosslinks formed by the protein Bap1. Downregulation of VPS production and surface trimming by the polysaccharide lyase RbmB cause surface remodeling as biofilms age, shifting the nature of cell-matrix interactions from attractive to repulsive and facilitating cell dispersal as aggregated groups. Our results shed light on the dynamics of diverse cell-matrix interactions as drivers of biofilm development. 

Biofilms are viscoelastic materials that are a prominent public health problem and a cause of most chronic bacterial infections, in large part due to their resistance to clearance by the immune system. Viscoelastic materials combine both solid-like and fluid-like mechanics, and the viscoelastic properties of biofilms are an emergent property of the intercellular cohesion characterizing the biofilm state (planktonic bacteria do not have an equivalent property). However, how the mechanical properties of biofilms are related to the recalcitrant disease that they cause, specifically to their resistance to phagocytic clearance by the immune system, remains almost entirely unstudied. We believe this is an important gap that is ripe for a large range of investigations. Here we present an overview of what is known about biofilm infections and their interactions with the immune system, biofilm mechanics and their potential relationship with phagocytosis, and we give an illustrative example of one important biofilm-pathogen ( Pseudomonas aeruginosa ) which is the most-studied in this context. We hope to inspire investment and growth in this relatively-untapped field of research, which has the potential to reveal mechanical properties of biofilms as targets for therapeutics meant to enhance the efficacy of the immune system. 

Abstract Attachment of bacteria onto a surface, consequent signaling, and accumulation and growth of the surface-bound bacterial population are key initial steps in the formation of pathogenic biofilms. While recent reports have hinted that surface mechanics may affect the accumulation of bacteria on that surface, the processes that underlie bacterial perception of surface mechanics and modulation of accumulation in response to surface mechanics remain largely unknown. We use thin and thick hydrogels coated on glass to create composite materials with different mechanics (higher elasticity for thin composites; lower elasticity for thick composites) but with the same surface adhesivity and chemistry. The mechanical cue stemming from surface mechanics is elucidated using experiments with the opportunistic human pathogenPseudomonas aeruginosacombined with finite-element modeling. Adhesion to thin composites results in greater changes in mechanical stress and strain in the bacterial envelope than does adhesion to thick composites with identical surface chemistry. Using quantitative microscopy, we find that adhesion to thin composites also results in higher cyclic-di-GMP levels, which in turn result in lower motility and less detachment, and thus greater accumulation of bacteria on the surface than does adhesion to thick composites. Mechanics-dependent c-di-GMP production is mediated by the cell-surface-exposed protein PilY1. The biofilm lag phase, which is longer for bacterial populations on thin composites than on thick composites, is also mediated by PilY1. This study shows clear evidence that bacteria actively regulate differential accumulation on surfaces of different stiffnessesviaperceiving varied mechanical stress and strain upon surface engagement. 

Biofilms are the cause of most chronic bacterial infections. Living within the biofilm matrix, which is made of extracellular substances, including polysaccharides, proteins, eDNA, lipids and other molecules, provides microorganisms protection from antimicrobials and the host immune response. Exopolysaccharides are major structural components of bacterial biofilms and are thought to be vital to numerous aspects of biofilm formation and persistence, including adherence to surfaces, coherence with other biofilm-associated cells, mechanical stability, protection against desiccation, binding of enzymes, and nutrient acquisition and storage, as well as protection against antimicrobials, host immune cells and molecules, and environmental stressors. However, the contribution of specific exopolysaccharide types to the pathogenesis of biofilm infection is not well understood. In this study we examined whether the absence of the two main exopolysaccharides produced by the biofilm former Pseudomonas aeruginosa would affect wound infection in a mouse model. Using P. aeruginosa mutants that do not produce the exopolysaccharides Pel and/or Psl we observed that the severity of wound infections was not grossly affected; both the bacterial load in the wounds and the wound closure rates were unchanged. However, the size and spatial distribution of biofilm aggregates in the wound tissue were significantly different when Pel and Psl were not produced, and the ability of the mutants to survive antibiotic treatment was also impaired. Taken together, our data suggest that while the production of Pel and Psl do not appear to affect P. aeruginosa pathogenesis in mouse wound infections, they may have an important implication for bacterial persistence in vivo. 

Abstract A new technique was used to measure the viscoelasticity of in vivoPseudomonas aeruginosabiofilms. This was done through ex vivo microrheology measurements of in vivo biofilms excised from mouse wound beds. To our knowledge, this is the first time that the mechanics of in vivo biofilms have been measured. In vivo results are then compared to typical in vitro measurements. Biofilms grown in vivo are more relatively elastic than those grown in a wound-like medium in vitro but exhibited similar compliance. Using various genetically mutatedP. aeruginosastrains, it is observed that the contributions of the exopolysaccharides Pel, Psl, and alginate to biofilm viscoelasticity were different for the biofilms grown in vitro and in vivo. In vitro experiments with collagen containing medium suggest this likely arises from the incorporation of host material, most notably collagen, into the matrix of the biofilm when it is grown in vivo. Taken together with earlier studies that examined the in vitro effects of collagen on mechanical properties, we conclude that collagen may, in some cases, be the dominant contributor to biofilm viscoelasticity in vivo. 

The growth of bacterial biofilms on implanted medical devices causes harmful infections and device failure. Biofilm development initiates when bacteria attach to and sense a surface. For the common nosocomial pathogen Pseudomonas aeruginosa and many others, the transition to the biofilm phenotype is controlled by the intracellular signal and second messenger cyclic-di-GMP (c-di-GMP). It is not known how biomedical materials might be adjusted to impede c-di-GMP signalling, and there are few extant methods for conducting such studies. Here, we develop such a method. We allowed P. aeruginosa to attach to the surfaces of poly(ethylene glycol) diacrylate (PEGDA) hydrogels. These bacteria contained a plasmid for a green fluorescent protein (GFP) reporter for c-di-GMP. We used laser-scanning confocal microscopy to measure the dynamics of the GFP reporter for 3 h, beginning 1 h after introducing bacteria to the hydrogel. We controlled for the effects of changes in bacterial metabolism using a promoterless plasmid for GFP, and for the effects of light passing through different hydrogels being differently attenuated by using fluorescent plastic beads as ‘standard candles’ for calibration. We demonstrate that this method can measure statistically significant differences in c-di-GMP signalling associated with different PEGDA gel types and with the surface-exposed protein PilY1.