The Rationale for Consuming Cognitive Enhancement Drugs in University Students and Teachers

Sattler S, Sauer C, Mehlkop G, Graeff P. The Rationale for Consuming Cognitive Enhancement Drugs in University Students and Teachers. PLoS ONE. 2013;8(7): e68821.Cognitive enhancement (CE) is the pharmaceutical augmentation of mental abilities (e.g., learning or memory) without medical necessity. This topic has recently attracted widespread attention in scientific and social circles. However, knowledge regarding the mechanisms that underlie the decision to use CE medication is limited. To analyze these decisions, we used data from two online surveys of randomly sampled university teachers (N = 1,406) and students (N = 3,486). Each respondent evaluated one randomly selected vignette with regard to a hypothetical CE drug. We experimentally varied the characteristics of the drugs among vignettes and distributed them among respondents. In addition, the respondent’s internalization of social norms with respect to CE drug use was measured. Our results revealed that students were more willing to enhance cognitive performance via drugs than university teachers, although the overall willingness was low. The probability of side effects and their strength reduced the willingness to use CE drugs among students and university teachers, whereas higher likelihoods and magnitudes of CE increased this propensity. In addition, the internalized norm against CE drug use influenced decision making: Higher internalization decreased the willingness to use such medications. Students’ internalized norms more strongly affected CE abstinence compared with those of university teachers. Furthermore, internalized norms negatively interacted with the instrumental incentives for taking CE medication. This internalization limited the influence of and deliberation on instrumental incentives. This study is the first to provide empirical evidence regarding the importance of social norms and their influence on rational decision making with regard to CE. We identified previously undiscovered decision-making patterns concerning CE. Thus, this study provides insight into the motivators and inhibitors of CE drug use. These findings have implications for contending with CE behavior by highlighting the magnitude of potential side effects and by informing the debate regarding the ethics of CE use

Phospho-specific flow cytometry identifies aberrant signaling in indolent B-cell lymphoma

<p>Abstract</p> <p>Background</p> <p>Knowledge about signaling pathways in malignant cells may provide prognostic and diagnostic information in addition to identify potential molecular targets for therapy. B-cell receptor (BCR) and co-receptor CD40 signaling is essential for normal B cells, and there is increasing evidence that signaling via BCR and CD40 plays an important role in the pathogenesis of B-cell lymphoma. The aim of this study was to investigate basal and induced signaling in lymphoma B cells and infiltrating T cells in single-cell suspensions of biopsies from small cell lymphocytic lymphoma/chronic lymphocytic leukemia (SLL/CLL) and marginal zone lymphoma (MZL) patients.</p> <p>Methods</p> <p>Samples from untreated SLL/CLL and MZL patients were examined for basal and activation induced signaling by phospho-specific flow cytometry. A panel of 9 stimulation conditions targeting B and T cells, including crosslinking of the B cell receptor (BCR), CD40 ligand and interleukins in combination with 12 matching phospho-protein readouts was used to study signaling.</p> <p>Results</p> <p>Malignant B cells from SLL/CLL patients had higher basal levels of phosphorylated (p)-SFKs, p-PLCγ, p-ERK, p-p38, p-p65 (NF-κB), p-STAT5 and p-STAT6, compared to healthy donor B cells. In contrast, anti-BCR induced signaling was highly impaired in SLL/CLL and MZL B cells as determined by low p-SFK, p-SYK and p-PLCγ levels. Impaired anti-BCR-induced p-PLCγ was associated with reduced surface expression of IgM and CD79b. Similarly, CD40L-induced p-ERK and p-p38 were also significantly reduced in lymphoma B cells, whereas p-p65 (NF-κB) was equal to that of normal B cells. In contrast, IL-2, IL-7 and IL-15 induced p-STAT5 in tumor-infiltrating T cells were not different from normal T cells.</p> <p>Conclusions</p> <p>BCR signaling and CD40L-induced p-p38 was suppressed in malignant B cells from SLL/CLL and MZL patients. Single-cell phospho-specific flow cytometry for detection of basal as well as activation-induced phosphorylation of signaling proteins in distinct cell populations can be used to identify aberrant signaling pathways.</p