Electrically driven dielectric elastomers (DEs) suffer from an electromechanical instability (EMI) when the applied potential difference reaches a critical value. A majority of the past investigations address the mechanics of this operational instability by restricting the kinematics to homogeneous deformations. However, a DE membrane comprising both active and inactive electric regions undergoes inhomogeneous deformation, thus necessitating the solution of a complex boundary value problem. This paper reports the numerical and experimental investigation of such DE actuators with a particular emphasis on the EMI in quasistatic mode of actuation. The numerical simulations are performed using an in-house finite element framework developed based on the field theory of deformable dielectrics. Experiments are performed on the commercially available acrylic elastomer (VHB 4910) at varying levels of prestretch and proportions of the active to inactive areas. In particular, two salient features associated with the electromechanical response are addressed: the effect of the flexible boundary constraint and the locus of the dielectric breakdown point. To highlight the influence of the flexible boundary constraint, the estimates of the threshold value of potential difference on the onset of electromechanical instability are compared with the experimental observations and with those obtained using the lumped parameter models reported previously. Additionally, a locus of localized thinning, near the boundary of the active electric region, is identified using the numerical simulations and ascertained through the experimental observations. Finally, an approach based on the Airy stress function is suggested to justify the phenomenon of localized thinning leading to the dielectric breakdown.

Lyme disease is a tick‐borne disease prevalent in North America, Europe, and Asia. Despite the accumulated knowledge from epidemiological, in vitro, and in animal studies, the understanding of dissemination of vector‐borne pathogens, such as Borrelia burgdorferi (Bb), remains incomplete with several important knowledge gaps, especially related to invasion and intravasation into circulation. To elucidate the mechanistic details of these processes a tissue‐engineered human dermal microvessel model is developed. Fluorescently labeled Bb are injected into the extracellular matrix (ECM) to mimic tick inoculation. High resolution, confocal imaging is performed to visualize the sub‐acute phase of infection. From analysis of migration paths no evidence to support adhesin‐mediated interactions between Bb and ECM components is found, suggesting that collagen fibers serve as inert obstacles to migration. Intravasation occurs at cell–cell junctions and is relatively fast, consistent with Bb swimming in ECM. In addition, it is found that Bb alone can induce endothelium activation, resulting in increased immune cell adhesion but no changes in global or local permeability. Together these results provide new insight into the minimum requirements for Bb dissemination and highlight how tissue‐engineered models are complementary to animal models in visualizing dynamic processes associated with vector‐borne pathogens.

Lyme disease is a tick-borne disease prevalent in North America, Europe, and Asia. Dissemination of vector-borne pathogens, such as Borrelia burgdorferi (Bb), results in infection of distant tissues and is the main contributor to poor outcomes. Despite the accumulated knowledge from epidemiological, in vitro, and in animal studies, the understanding of dissemination remains incomplete with several important knowledge gaps, especially related to invasion and intravasation at the site of a tick bite, which cannot be readily studied in animal models or humans. To elucidate the mechanistic details of these processes we developed a tissue-engineered human dermal microvessel model. Fluorescently-labeled Bb (B31 strain) were injected into the extracellular matrix (ECM) of the model to mimic tick inoculation. High resolution, confocal imaging was performed to visualize Bb migration in the ECM and intravasation into circulation. From analysis of migration paths we found no evidence to support adhesin-mediated interactions between Bb and components of the ECM or basement membrane, suggesting that collagen fibers serve as inert obstacles to migration. Transendothelial migration occurred at cell-cell junctions and was relatively fast, consistent with Bbswimming in ECM. In addition, we found that Bb alone can induce endothelium activation, resulting in increased immune cell adhesion but no changes in global or local permeability. Together these results provide new insight into the minimum requirements for dissemination of Bb at the site of a tick bite, and highlight how tissue-engineered models are complementary to animal models in visualizing dynamic processes associated with vector-borne pathogens.