Flagellated bacteria have been employed as microactuators in low Reynolds number fluidic environments. SU-8 microstructures have been fabricated and released on the surface of swarming Serratia marcescens, and the flagella propel the structures along the swarm surface. Phototactic control of these structures is demonstrated by exposing the localized regions of the swarm to ultraviolet light. The authors additionally discuss the control of microstructures in an open channel powered by bacteria which have been docked through a blotting technique. A tracking algorithm has been developed to analyze swarming patterns of the bacteria as well as the kinematics of the microstructures.

The rate of vascular injury in modern combat is higher than that reported in previous wars. Open reconstruction is performed in half of cases, although ligation is an important damage control option, especially for minor or distal vessel injuries. Angiographic techniques are increasingly being used and documented within wartime registries more than ever. Proficiency with open and endovascular methods of vascular injury management remains a critical need for the U.S. military and will require partnership with civilian institutions to attain and maintain.

The flagellated bacteria Serratia marcescens have been employed as fluidic actuators to propel custom designed microstructures through the use of a swarm blotting technique. The novel methodology for microfabrication, manipulation, and experimentation is described in detail, and the advantages and drawbacks of alternative techniques are considered. Our results with PDMS and silicon microstructures led to the discovery of SU-8 as a suitable material. A microstructure-tracking algorithm was developed to quantify the motion. The methodology is applied in a study of effects of microstructure geometry on velocity and trajectory in an open fluidic channel. Additionally, relationships between structure dimension and velocity are discussed.

The thoracic outlet syndrome occurs when the neurovascular structures are compressed as they traverse the thoracic outlet. Degenerative changes can occur in the subclavian artery and the vessel may become a source of embolism with the risk of acute or chronic upper limb ischaemia. Rarely, distal thromboembolism in the thoracic outlet syndrome may be associated with retrograde flow when there is the added risk of cerebral thromboembolism.