The role of semantic memory in the recognition of emotional valence conveyed by written words.

The main goal of this study was to examine the role of semantic memory in the recognition of emotional valence conveyed by words. Eight participants presenting with the semantic variant of primary progressive aphasia (svPPA) and 33 healthy control participants were administered three tasks designed to investigate the formal association between the recognition of emotional valence conveyed by words and the lexical and semantic processing of these words. Results revealed that individuals with svPPA showed deficits in the recognition of negative emotional valence conveyed by words. Moreover, results evidenced that their performance in the recognition of emotional valence was better for correctly than for incorrectly retrieved lexical entries of words, while their performance was comparable for words that were correctly or incorrectly associated with semantic concepts. These results suggest that the recognition of emotional valence conveyed by words relies on the retrieval of lexical, but not semantic, representations of words.

Repeated exposure to others' pain reduces vicarious pain intensity estimation.

BACKGROUND: Pain perception in others can be influenced by different contextual factors. In clinical settings, the repeated exposure to others' pain has been proposed as a factor that could explain underestimation of patients' pain by health care providers. Previous research supported this idea by showing that repeated exposure to persons in pain biases the subsequent willingness to impute pain in others. However, it remains unclear if the effect of repeated exposure on the detection of pain extends to deliberate pain estimation of stimuli presented for a longer period. METHOD: Therefore, in a first experiment, healthy participants were either exposed to clips of facial expressions of intense pain or neutral expressions before estimating the intensity of other individuals' pain expressions. To test the specificity of this effect with regard to the pain content, a second study was conducted with healthy adults, which compared the effect of exposure to fear, pain and neutral videos on subsequent pain assessment in others. RESULTS: Results from the first experiment indicated that repeated exposure to others' pain diminished the subsequent estimation of the intensity of pain in others. Results from the second experiment suggested that exposure to fear could bias pain estimation in a similar manner. However, the absence of difference in ratings between the exposure to fear and neutral groups warrants caution in the interpretation of these findings. CONCLUSION: By demonstrating that repeated exposure to others' pain diminished subsequent pain estimation in others, this study adds relevant information on the factors that could contribute to pain underestimation in health care professionals. WHAT DOES THIS STUDY ADD?: Repeated exposure to facial expressions of intense pain not only biases pain detection, but also pain estimation in others. Prior exposure to facial expressions of pain compared to exposure to neutral ones leads to a reduced estimation of others' pain. This effect is not specific to pain as exposure to another negative emotion (fear) also biases subsequent pain estimation. These results support the interpretation that the underestimation of patients' pain by health care professionals could be related to repeated exposure to other's pain.

Mechanisms associated with thymocyte apoptosis induced by simian immunodeficiency virus.

Despite considerable research, the mechanisms by which HIV disrupts thymic function remain controversial. We have described the phenotypic changes that occur in the thymus of SIV-infected macaques during acute SIV infection. In this study, we analyzed the effects of SIV infection on apoptotic pathways in thymic tissue from newborn macaques infected with SIV. Thymocyte apoptosis was accompanied by a modest increase in surface Fas expression, a profound decrease in the frequency of bcl-2-positive cells, as well as the amount of bcl-2 per cell. With control of viral replication, levels of bcl-2 and Fas returned to baseline together with a return to basal levels of apoptosis. In the thymus, SIV infection resulted in depletion of CD4+CD8+ thymocytes, an increase in apoptosis of thymocytes, and a down-regulation of MHC class I molecules. These changes peaked 14-21 days after infection at or just after peak viremia. This data further suggests disruption of the antiapoptotic pathway regulated by bcl-2 plays a critical role in SIV-induced apoptosis of thymocytes.