ABSTRACT
BACKGROUND: With an increasing life expectancy and more active elderly population, management of geriatric trauma patients continues to evolve. The aim was to describe the mechanism and injuries of severely injured geriatric patients and to identify risk factors associated with mortality. METHODS: The Trauma Registry at a Canadian Level I trauma center was queried for all trauma patients older than 65 years and injury severity score >15 from 2004 to 2006, resulting in a retrospective chart review of 276 patients. The data were subsequently analyzed using univariate and multivariate analysis. RESULTS: Average age was 81.5 years (mean injury severity score of 25). Most common comorbid illness was hypertension (57.3%) and most frequent mechanism of injury was falls (72.3%). The overall mortality was comparable with the US National Trauma Data Bank (26.8% vs. 32.0%, confidence interval, 0.00-0.10). Geriatric patients requiring intubation, blood transfusions, or suffering from head, C-spine, or chest trauma had an increased likelihood of death. In-hospital respiratory, gastrointestinal, or infectious complications also had higher likelihood of death. CONCLUSIONS: Falls continue to be the most frequent mechanism of injury in severely injured geriatric patients. Risk factors associated with a higher likelihood of death are identified. More research is needed to better understand this important and increasing group of trauma patients.
Subject(s)
Accidental Falls/statistics & numerical data , Brain Injuries/epidemiology , Cause of Death , Fractures, Bone/epidemiology , Hospital Mortality , Age Distribution , Aged , Aged, 80 and over , Brain Injuries/diagnosis , Brain Injuries/therapy , Cohort Studies , Female , Fractures, Bone/diagnosis , Fractures, Bone/therapy , Geriatric Assessment , Humans , Injury Severity Score , Male , Ontario/epidemiology , Prevalence , Registries , Retrospective Studies , Risk Assessment , Sex Distribution , Survival Analysis , Trauma CentersABSTRACT
Mutations in the gene encoding parkin cause an autosomal recessive juvenile-onset form of Parkinson's disease. Parkin functions as a RING-type E3 ubiquitin-ligase, coordinating the transfer of ubiquitin to substrate proteins and thereby targeting them for degradation by the proteasome. We now report that the extreme C terminus of parkin, which is selectively truncated by a Parkinson's disease-causing mutation, functions as a class II PDZ-binding motif that binds CASK, the mammalian homolog of Caenorhabditis elegans Lin-2, but not other PDZ proteins in brain extracts. Importantly, parkin co-localizes with CASK at synapses in cultured cortical neurons as well as in postsynaptic densities and lipid rafts in brain. Further, parkin associates not only with CASK but also with other postsynaptic proteins in the N-methyl d-aspartate (NMDA) receptor-signaling complex, in rat brain in vivo. Finally, despite exhibiting E2-dependent ubiquitin ligase activity, rat brain parkin does not ubiquitinate CASK, suggesting that CASK may function in targeting or scaffolding parkin within the postsynaptic complex rather than as a direct substrate for parkin-mediated ubiquitination. These data implicate for the first time a PDZ-mediated interaction between parkin and CASK in neurodegeneration and possibly in ubiquitination of proteins involved in synaptic transmission and plasticity.
