Anti-UBB monoclonal antibody, clone 21D3-3

It is critical to understand the relationship between under-body blast (UBB) loading and occupant response to provide optimal protection to the warfighter from serious injuries, many of which affect the spine. Previous studies have examined component and whole body response to accelerative based UBB loading. While these studies both informed injury prediction efforts and examined the shortcomings of traditional anthropomorphic test devices in the evaluation of human injury, few studies provide response data against which future models could be compared and evaluated. The current study examines four different loading conditions on a seated occupant that demonstrate the effects of changes in the floor, seat, personal protective equipment (PPE), and reclined posture on whole body post-mortem human surrogate (PMHS) spinal response in a sub-injurious loading range. Twelve PMHS were tested across floor velocities and time-to-peak (TTP) that ranged from 4.0 to 8.0 m/s and 2 to 5 ms, respectively. To focus on sub-injurious response, seat velocities were kept at 4.0 m/s and TTP ranged from 5 to 35 ms. Results demonstrated that spine response is sensitive to changes in TTP and the presence of PPE. However, spine response is largely insensitive to changes in floor loading. Data from these experiments have also served to develop response corridors that can be used to assess the performance and predictive capability of new test models used as human surrogates in high-rate vertical loading experiments.

UBB+1 is a mutant ubiquitin which accumulates in the hallmarks of tauopathies, including Alzheimer's disease. Transgenic mice expressing high levels of neuronal UBB+1 exhibit moderately decreased proteasome activity and spatial reference memory deficits at 9 months of age. In the present study, we characterized the behavioral phenotype of male UBB+1 transgenic mice at different ages. We show that UBB+1 transgenic mice displayed an age-related functional decline similar to wild-type littermates, without gross neurological abnormalities or alterations in procedural motor-learning and motor coordination. At 15 months of age, a transgene-specific spatial learning deficit was dependent on the period of training in the Morris watermaze. This deficit could be eliminated after additional training. We conclude that the previously reported spatial reference memory deficits of UBB+1 transgenic mice persist during aging. In addition, our results demonstrate that the subtle defect in spatial reference memory formation, caused by a decrease in forebrain proteasome activity, is a persistent defect and not a structural defect. (C) 2010 Elsevier Inc. All rights reserved.