This more detailed method, employing both dynamic analysis and joint kinematics simultaneously, was found to be a reliable approach for the quantification of gait in rats.

We report the development of a rodent model of primary blast limb trauma that is the first to highlight an important role played by blast wave duration and magnitude in initiating acute inflammatory response following limb injury in the absence of limb fracture or penetrating trauma. The combined biological and mechanical method developed can be used to further understand the complex effects of blast waves in a range of different tissues and organs in vivo.

BackgroundExplosive blast trauma occurs by four mechanisms: primary injuries are due to the isolated effect of the blast wave on the human body, secondary injuries are due to damage from fragments energised from the explosion, tertiary injuries result from acceleration of the body against an object or through the explosion energising hard materials in a solid form (not fragments) and encroaching upon the person, and quaternary injuries describe other physical insults, including burns and smoke inhalation 1 .Gas-containing organs such as the lungs are particularly susceptible to barotrauma, and 'Primary Blast Lung Injury' (PBLI) is a commonly reported injury amongst blast casualties. A review of terrorist bombings worldwide found the incidence of PBLI in immediate fatalities to be as high as 47% 2 ; whilst in a review of military blast casualties that survived to emergency admission, PBLI was found in 11.2% of 648 blast casualties. In this series, 16.2% of mounted and 17.1% of dismounted injuries developed PBLI, which was significantly associated with increased mortality 3,4 .Laboratory investigations of PBLI have sought to recapitulate the injury under experimental conditions. Studies investigating the subsequent immune response have been reported most commonly in rats 5-10 , mice [11][12][13][14][15] and swine 16,17 . These studies have offered overwhelming evidence of the neutrophil response to PBLI in animal models, with increases in circulating and broncho-alveolar lavage fluid (BALF) neutrophils, increases in Myeloperoxidase (MPO) activity in the lung, and neutrophil staining by histology [9][10][11][12]14,18,19 . However, the immune response to tissue damage differs depending on the type of organ injured and their local physiology; it remains unclear what specific contribution blast injuries to different parts of the body make to the inflammatory response that ensues. Whilst most clinically blast injured patients are polytraumatised, discerning these interacting immune responses experimentally is necessary for translational studies seeking to better understand, monitor or attenuate the immune response in blast trauma.Further, knowledge of the role played by other immune cells to PBLI is limited -no study has characterised the full repertoire of immune cells in PBLI; specifically, the involvement of monocytes in PBLI remains unclear. These cells are frequently recruited to sites of inflammation; in humans they are characterised by differential CD14 and CD16 expression 20 , in mice by CCR2, CX3CR1 and Ly6C 21,22 and in rats by CD43 alone or in conjunction with His48 23 . In rats, CD43 Hi and Lo monocytes are considered to be analogous to the Ly6C Lo (Non-classical) and Ly6C Hi (Classical) murine monocytes respectively. Classical Ly6C Hi monocytes are recruited to tissues in sterile 24 and infectious 25 models of inflammation. There, they can differentiate into inflammatory macrophages and dendritic cells, amplifying or resolving inflammation. In rats, circulating monocyte subsets are activated by inflammator...