The efficacy of the generation effect in improving new learning in persons with traumatic brain injury.

Objective: To evaluate the usefulness of the generation effect in improving learning and memory abilities in neurologically impaired individuals. The generation effect is the observation that items self-generated by participants are better remembered than items provided by the examiner. Although this effect has shown to be relatively robust in healthy adults, few studies have examined the usefulness of the generation effect in neurological populations. Participants: 18 individuals with moderate-severe traumatic brain injury (TBI) and 18 healthy adults. Main Outcome Measure: The measure was the generation effect protocol. Results: Results indicated recall and recognition of generated information was significantly higher than that of provided information across testing conditions. However, healthy adults showed greater benefit from the generation effect than did individuals with TBI. As expected, recall and recognition performance diminished over time (i.e., immediate recall, 30 min, 1 week) however, rates of forgetting did not differ between groups. Conclusion: Self-generation significantly improved verbal learning and memory in individuals with TBI. The results of self-generation in improving learning suggest that applying that technique may be beneficial in the cognitive rehabilitation of persons with TBI. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Antiapoptotic activity of the herpesvirus saimiri-encoded Bcl-2 homolog: stabilization of mitochondria and inhibition of caspase-3-like activity

Viruses have evolved different strategies to interfere with host cell apoptosis. Herpesvirus saimiri (HVS) and other lymphotropic herpesviruses code for proteins that are homologous to the cellular antiapoptotic Bcl-2. In this study HVS-Bcl-2 was stably expressed in the human leukemia cell line Jurkat and in the murine T-cell hybridoma DO to assess its antiapoptotic spectrum and to gain further insight into its mode of action. HVS- Bcl-2 prevented apoptosis that occurs as a result of a disturbance of intracellular homeostasis by, for example, DNA damage or menadione, which gives rise to oxygen radicals. In Jurkat cells, HVS-Bcl-2 also inhibited apoptosis mediated by the death receptor CD95. In DO cells, HVS-Bcl-2 did not interfere with CD95-mediated apoptosis but blocked dexamethasone-induced cell death. Mitochondrial damage is a central coordinating event in apoptosis induced by different stimuli. To assess the integrity of mitochondria, we used rhodamine 123, which is released upon disturbance of the mitochondrial membrane potential, and determined the release of cytochrome c into the cytosol. Both signs of mitochondrial damage were prevented by HVS-Bcl-2. This viral protein also inhibited the generation of caspase-3-like DEVDase activity and blocked the cleavage of poly(ADP-ribose) polymerase, a natural substrate of caspase-3-like proteases. In conclusion, HVS-Bcl-2 protects against a great variety of apoptotic stimuli, stabilizes mitochondria, and acts upstream of the generation of caspase-3-like activity.