Nanofluidic platforms offering tunable material transport are applicable in biosensing, chemical detection, and filtration. Prior studies have achieved selective and controllable ion transport through electrical, optical, or chemical gating of complex nanostructures. https://www.selleckchem.com/products/prt543.html Here, we mechanically control nanofluidic transport using nanobubbles. When plugging nanochannels, nanobubbles rectify and occasionally enhance ionic currents in a geometry-dependent manner. These conductance effects arise from nanobubbles inducing surface-governed ion transport through interfacial electrolyte films residing between nanobubble surfaces and nanopipette walls. The nanobubbles investigated here are mechanically generated, made metastable by surface pinning, and verified with cryogenic transmission electron microscopy. Our findings are relevant to nanofluidic device engineering, three-phase interface properties, and nanopipette-based applications.Super-soft elastomers derived from bottlebrush polymers show promise as advanced materials for biomimetic tissue and device applications, but current processing strategies are restricted to simple molding. Here, we introduce a design concept that enables the three-dimensional (3D) printing of super-soft and solvent-free bottlebrush elastomers at room temperature. The key advance is a class of inks comprising statistical bottlebrush polymers that self-assemble into well-ordered body-centered cubic sphere phases. These soft solids undergo sharp and reversible yielding at 20°C in response to shear with a yield stress that can be tuned by manipulating the length scale of microphase separation. The addition of a soluble photocrosslinker allows complete ultraviolet curing after extrusion to form super-soft elastomers with near-perfect recoverable elasticity well beyond the yield strain. These structure-property design rules create exciting opportunities to tailor the performance of 3D-printed elastomers in ways that are not possible with current materials and processes.Devices that perform cardiac mapping and ablation to treat atrial fibrillation provide an effective means of treatment. Current devices, however, have limitations that either require tedious point-by-point mapping of a cardiac chamber or have limited ability to conform to the complex anatomy of a patient's cardiac chamber. In this work, a detailed, scalable, and manufacturable technique is reported for fabrication of a multielectrode, soft robotic sensor array. These devices exhibit high conformability (~85 to 90%) and are equipped with an array of stretchable electronic sensors for voltage mapping. The form factor of the device is intended to match that of the entire left atrium and has a hydraulically actuated soft robotic structure whose profile facilitates deployment from a 13.5-Fr catheter. We anticipate that the methods described in this paper will serve a new generation of conformable medical devices that leverage the unique characteristics of stretchable electronics and soft robotics.Elevated blood/tissue glucose is a hallmark feature of advanced diabetes, and people with diabetes are prone to more frequent and invasive infections with Staphylococcus aureus. Phagocytes must markedly increase glucose consumption during infection to generate and oxidative burst and kill invading bacteria. Similarly, glucose is essential for S. aureus survival in an infection and competition with the host, for this limited resource is reminiscent of nutritional immunity. Here, we show that infiltrating phagocytes do not express their high-efficiency glucose transporters in modeled diabetic infections, resulting in a diminished respiratory burst and increased glucose availability for S. aureus We show that excess glucose in these hyperglycemic abscesses significantly enhances S. aureus virulence potential, resulting in worse infection outcomes. Last, we show that two glucose transporters recently acquired by S. aureus are essential for excess virulence factor production and the concomitant increase in disease severity in hyperglycemic infections.Gray wolves are a premier example of how predators can transform ecosystems through trophic cascades. However, whether wolves change ecosystems as drastically as previously suggested has been increasingly questioned. We demonstrate how wolves alter wetland creation and recolonization by killing dispersing beavers. Beavers are ecosystem engineers that generate most wetland creation throughout boreal ecosystems. By studying beaver pond creation and recolonization patterns coupled with wolf predation on beavers, we determined that 84% of newly created and recolonized beaver ponds remained occupied until the fall, whereas 0% of newly created and recolonized ponds remained active after a wolf killed the dispersing beaver that colonized that pond. By affecting where and when beavers engineer ecosystems, wolves alter all of the ecological processes (e.g., water storage, nutrient cycling, and forest succession) that occur due to beaver-created impoundments. Our study demonstrates how predators have an outsized effect on ecosystems when they kill ecosystem engineers.Vascular plant pathogens travel long distances through host veins, leading to life-threatening, systemic infections. In contrast, nonvascular pathogens remain restricted to infection sites, triggering localized symptom development. The contrasting features of vascular and nonvascular diseases suggest distinct etiologies, but the basis for each remains unclear. Here, we show that the hydrolase CbsA acts as a phenotypic switch between vascular and nonvascular plant pathogenesis. cbsA was enriched in genomes of vascular phytopathogenic bacteria in the family Xanthomonadaceae and absent in most nonvascular species. CbsA expression allowed nonvascular Xanthomonas to cause vascular blight, while cbsA mutagenesis resulted in reduction of vascular or enhanced nonvascular symptom development. Phylogenetic hypothesis testing further revealed that cbsA was lost in multiple nonvascular lineages and more recently gained by some vascular subgroups, suggesting that vascular pathogenesis is ancestral. Our results overall demonstrate how the gain and loss of single loci can facilitate the evolution of complex ecological traits.