Infectious biofilms are problematic in many healthcare-related devices, and are especially challenging and ubiquitous in urinary catheters. This report presents an on-demand fouling-release methodology to mechanically disrupt and remove biofilms, and proposes this method for the active removal of infectious biofilms from the previously-inaccessible main drainage lumen of urinary catheters. Mature Proteus mirabilis crystalline biofilms detach from silicone elastomer substrates upon application of strain to the substrate, and increasing the strain rate increases biofilm detachment. The study presents a quantitative relationship between applied strain rate and biofilm debonding through an analysis of biofilm segment length and the driving force for debonding. Based on this mechanism, hydraulic and pneumatic elastomer actuation was used to achieve surface strain selectively within the lumen of prototypes of sections of a fouling-release urinary catheter. Proof-of-concept prototypes of sections of active, fouling-release catheters were constructed using techniques typical to soft robotics including 3D printing and replica molding, and those prototypes demonstrate release of mature P. mirabilis crystalline biofilms (e.g., ≈90%) from strained surfaces. These results provide a basis for the development of a new urinary catheter technology in which infectious biofilms are effectively managed through new methods that are entirely complementary to existing approaches.

Biofilm removal from biomaterials is of fundamental importance, and is especially relevant when considering the problematic and deleterious impact of biofilm infections on the inner surfaces of urinary catheters. Catheter-associated urinary tract infections are the most common cause of hospital-acquired infections and there are over 30 million Foley urinary catheters used annually in the USA. In this paper, we present the design and optimization of urinary catheter prototypes capable of on-demand removal of biofilms from the inner luminal surface of catheters. The urinary catheters utilize 4 intra-wall inflation lumens that are pressure-actuated to generate region-selective strains in the elastomeric urine lumen, and thereby remove overlying biofilms. A combination of finite-element modeling and prototype fabrication was used to optimize the catheter design to generate greater than 30% strain in the majority of the luminal surface when subjected to pressure. The catheter prototypes are able to remove greater than 80% of a mixed community biofilm of Proteus mirabilis and Escherichia coli on-demand, and furthermore are able to remove the biofilm repeatedly. Additionally, experiments with the prototypes demonstrate that biofilm debonding can be achieved upon application of both tensile and compressive strains in the inner surface of the catheter. The fouling-release catheter offers the potential for a non-biologic, non-antibiotic method to remove biofilms and thereby for impacting the thus far intractable problem of catheter-associated infections.

Objective-To accelerate vein graft reendothelialization and reduce vein graft thrombosis by infusing human umbilical cord blood-derived endothelial cells (hCB-ECs) because loss of endothelium contributes to vein graft thrombosis and neointimal hyperplasia. Methods and Results-Under steady flow conditions in vitro, hCB-ECs adhered to smooth muscle cells 2.5 to 13 times more than ECs derived from peripheral blood or human aorta (PϽ0.05). Compared with peripheral blood and human aorta ECs, hCB-ECs had 1.4-fold more cell surface ␣ 5 ␤ 1 integrin heterodimers per cell (PϽ0.05) and proliferated on fibronectin 4-to 10-fold more rapidly (PϽ0.05). Therefore, we used hCB-ECs to enhance reendothelialization of carotid interposition vein grafts implanted in NOD.CB17-Prkdc scid /J mice. Two weeks postoperatively, vein grafts from hCB-EC-treated mice demonstrated approximately 55% reendothelialization and no luminal thrombosis. In contrast, vein grafts from sham-treated mice demonstrated luminal thrombosis in 75% of specimens (PϽ0.05) and only approximately 14% reendothelialization. In vein grafts from hCB-EC-treated mice, 33Ϯ10% of the endothelium was of human origin, as judged by human major histocompatibility class I expression. Key Words: endothelial function Ⅲ thrombosis Ⅲ vascular biology Ⅲ vascular surgery Ⅲ integrin S aphenous vein graft failure from thrombosis occurs with remarkable frequency: approximately 3% to 12% within the first postoperative month 1 and 28% within the first postoperative year. 2 Vein graft thrombosis is generally attributed to alterations in the vessel wall and flow dynamics, vein graft endothelial damage associated with both vein harvest and vein graft distension by arterial pressure, and consequent compromise of anticoagulant vessel properties. 1 Among these factors, the most practical target for therapy appears to be maintenance or restoration of the vein graft endothelium. Conclusion-TheReendothelialization of vein grafts is a relatively slow process that involves proliferation and migration of both graft-intrinsic endothelial cells (ECs) and graft-extrinsic ECs, 3 which may derive from adjacent arterial endothelium or circulating endothelial progenitor cells (EPCs). 4,5 Consequently, accelerating EC growth or increasing EC number with exogenous ECs may accelerate vein graft reendothelialization. Exogenous ECs derived from peripheral and umbilical cord blood EPCs are relatively easy to obtain and possess substantial replicative capacity. 6 Most studies that have examined adhesion of ECs to damaged vasculature have used ECs obtained from earlyoutgrowth cultures of EPCs, which are of a myeloid lineage and do not exhibit the antithrombotic properties of ECs. [7][8][9] Few vascular repair experiments have examined ECs derived from late-outgrowth cultures of EPCs isolated from adult or umbilical cord blood. These late-outgrowth EPCs, or endothelial colony-forming cells, exhibit characteristics only of ECs and not of monocytes. 10,11 ECs obtained from lateoutgrowth cultures of peripheral blood...