Effectiveness of installing overhead ceiling lifts. Reducing musculoskeletal injuries in an extended care hospital unit.

The effectiveness of replacing floor lifts with mechanical ceiling lifts was evaluated in the extended care unit of a British Columbia hospital. Sixty-five ceiling lifts were installed between April and August 1998. Injury data were abstracted from injury reports for all staff musculoskeletal injuries (MSI) occurring in the unit during a 3 year period prior to installation and a 1.5 year follow up period. Descriptive statistics were calculated for injuries pre- versus post-installation. Rates were calculated as number of injuries per 100,000 worked hours. Rates for three pre- and three post-installation intervals were compared using Poisson regression. The rate of MSI caused by lifting/transferring patients was significantly reduced (58% reduction, p = .011) after installation, but rates of all MSI and MSI caused by repositioning did not statistically decline (p > .05). Further follow up is necessary to determine whether or not ceiling lifts also can be effective for decreasing injuries related to repositioning patients on this unit.

Implicating calpain in tau-mediated toxicity in vivo.

Alzheimer's disease and other related neurodegenerative disorders known as tauopathies are characterized by the accumulation of abnormally phosphorylated and aggregated forms of the microtubule-associated protein tau. Several laboratories have identified a 17 kD proteolytic fragment of tau in degenerating neurons and in numerous cell culture models that is generated by calpain cleavage and speculated to contribute to tau toxicity. In the current study, we employed a Drosophila tauopathy model to investigate the importance of calpain-mediated tau proteolysis in contributing to tau neurotoxicity in an animal model of human neurodegenerative disease. We found that mutations that disrupted endogenous calpainA or calpainB activity in transgenic flies suppressed tau toxicity. Expression of a calpain-resistant form of tau in Drosophila revealed that mutating the putative calpain cleavage sites that produce the 17 kD fragment was sufficient to abrogate tau toxicity in vivo. Furthermore, we found significant toxicity in the fly retina associated with expression of only the 17 kD tau fragment. Collectively, our data implicate calpain-mediated proteolysis of tau as an important pathway mediating tau neurotoxicity in vivo.