These included patient age, number of rib fractures, chronic lung disease and pre-injury anti-coagulant use. This is the first study in which pre-injury anti-platelet use has been reported as a risk factor for complications following isolated blunt chest wall trauma. Pathophysiological mechanisms differ substantially between blunt poly-trauma patients suffering trauma-induced coagulopathy and isolated blunt chest trauma patients and as a result, comparisons between such studies are not appropriate. The results of this study are therefore distinctive from any previous research and should be considered by emergency physicians managing isolated blunt chest trauma. Anti-platelet therapy is now a well-recognised risk factor for potential poor outcomes following Ganoderic-acid-F severe traumatic head Notoginsenoside-Fe injuries and trauma clinicians are becoming increasingly aware of its negative impact in the elderly trauma patient. Despite the limitations associated with a single centre retrospective study, this results of this study have highlighted an important clinical finding that trauma clinicians should 
consider when managing the blunt chest wall trauma patient in the ED. A prospective multi-centre study is planned to further investigate the impact of pre-injury anti-platelet use on outcomes in blunt chest wall trauma patients. Microtubules are one of the major cytoskeletal components and play critical roles in diverse cellular events. While the dynamic property of microtubules is important for many microtubulemediated cellular events such as cell division and migration, the stability of microtubules is also important, especially for intracellular transport and the maintenance of cell polarity. Deregulation of microtubule stability can lead to severe consequences such as developmental defects and neurodegenerative diseases. In cells, microtubule stability is controlled by a number of proteins interacting with microtubules and/or its tubulin subunits, collectively known as microtubule-associated proteins. The level of Mdp3 varies significantly in different tissues, with relatively high expression in skeletal muscle and lung tissues. In addition, Mdp3 expression undergoes dramatic changes during the cell cycle, with lower expression in the G2 phase compared with its expression in the other phases of the cell cycle. It has been demonstrated previously that Mdp3 plays an important role in the regulation of microtubule stability. However, the molecular mechanisms underlying this function of Mdp3 remain unclear. In this study, we provide the first evidence that Mdp3 modulates microtubule stability via two different mechanisms, direct binding to microtubules/tubulin and regulating histone deacetylase 6 -mediated tubulin deacetylation. Proteins of the MAP family are key players in the regulation of microtubule stability. Abnormal expression or posttranslational modification of MAPs has been implicated in the pathogenesis of human diseases especially neurodegenerative diseases.