Analysis of injury mechanism of the elderly and non-elderly groups in minor motor vehicle accidents.

OBJECTIVE: The purpose of this study is to investigate the injury patterns of noncatastrophic accidents by individual age groups. METHODS: Data were collected from the Korean In-Depth Accident Study database based on actual accident investigation. The noncatastrophic criteria were classified according to U.S. experts from the Centers for Disease Control and Prevention's recommendations for field triage guidelines of high-risk automobile crash criteria by vehicle intrusions more than 12 in. on occupant sites (including the roof) and more than 18 in. on any site. The Abbreviated Injury Scale (AIS) was used to determine injury patterns for each body region. Severely injured patients were classified as Maximum Abbreviated Injury Scale (MAIS) 3 or higher. RESULTS: In this study, the most significant injury regions were the head and neck, extremities, and thorax. In addition, the incidence of severe injury among elderly patients was nearly 1.6 times higher than that of non-elderly patients. According to age group, injured body regions among the elderly were the thorax, head and neck, and extremities, in that order. For the non-elderly groups, these were head and neck, extremities, and thorax. Severe injury rates were slightly different for the elderly group (head and neck, abdomen) and non-elderly group (thorax, head and neck). CONCLUSIONS: In both age groups, the rate of severe injury is proportional to an increase in crush extent zone. Front airbag deployment may have a relatively significant relationship to severe injuries.

The heat-shock protein-70-induced renoprotective effect is partially mediated by CD4+ CD25+ Foxp3 + regulatory T cells in ischemia/reperfusion-induced acute kidney injury.

Recent reports suggest the presence of heat-shock protein (HSP)-reactive T cells with a regulatory phenotype in various inflammatory diseases. To test whether HSP exerts renoprotective effects through regulatory T cells (Tregs), ischemia/reperfusion injury was done with or without heat preconditioning in mice. Splenocytes from heat-preconditioned mice had Treg expansion and a reduced proliferative response upon mitogenic stimulus. T cells from heat-preconditioned mice failed to reconstitute postischemic injury when adoptively transferred to T cell-deficient nu/nu mice in contrast to those from control mice. Tregs were also increased in heat-preconditioned ischemic kidneys. Depleting Tregs before heat preconditioning abolished the renoprotective effect, while adoptive transfer of these cells back into Treg-depleted mice partially restored the beneficial effect of heat preconditioning. Inhibition of HSP70 by quercetin suppressed Treg expansion, as well as renoprotective effects. Transferring Tregs in quercetin-treated heat-preconditioned mice partially restored the beneficial effect of heat preconditioning. The specificity of immune cell HSP70 in renoprotection was confirmed by partial restoration of kidney injury when T cells from HSP70-deficient heat preconditioned mice were adoptively transferred to nu/nu mice. Thus, the renoprotective effect of HSP70 may be partially mediated by a direct immunomodulatory effect through Tregs. Better understanding of immunomodulatory mechanisms of various stress proteins might facilitate discovery of new preventive strategies in acute kidney injury.