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In the current research-focused climate, academics are facing increasing pressure to produce research outputs. This pressure can prove particularly daunting for early career (EC) academics, who are simultaneously attempting to master new teaching and administrative demands while establishing their own independent research trajectories. Previous reports suggest that academic writing retreats can be an effective way of increasing research outputs. Such retreats generally involve academics from a range of career stages and require expert facilitators. Through organising a series of structured writing events, this project aims to cultivate an enduring community of practice for academic writers. Reflecting on our EC retreat and subsequent writing days with academics from different career stages, we suggest that success hinged on three key factors: (1) "A formal structure" comprising bounded periods of intense writing, flanked by group reviewing and goal-setting; (2) "Co-located writing" with participants based in a shared space, away from their usual workstation and distractions; (3) "Peer discussions" involving participants at a similar career stage. Specifically we found that writing amongst "equals" increased productivity and confidence amongst EC academics.

The effect of test-induced priming on false recognition was investigated in children aged 5, 7, 9, and 11 years using lists of semantic associates, category exemplars, and phonological associates. In line with effects previously observed in adults, nine- and eleven-year-olds showed increased levels of false recognition when critical lures were preceded by four studied items. This pattern was present with all three list types. In contrast, no effects of test-induced priming were observed in five- or seven-year-olds with any list type. The results also support those of previous studies in showing a developmental shift from phonological to semantic false memories. The findings are discussed in terms of current theories of children's false memories. (Contains 2 tables.)

Caspase 8 has been found to play a required role in T-cell homeostasis and in T-cell-mediated immunity. Mice with a targeted caspase 8 mutation restricted to the T-cell lineage were generated to study the role. Although normal thymocyte development was seen, so were a distinct decrease in the number of peripheral T-cells and impaired ex vivo T-cell response to activation stimuli . Death receptor-mediated apoptosis problems are linked to cancer and autoimmune disease.

Treatment of NB4 acute promyelocytic leukemia cells with 1,25-dihydroxyvitamin D3 (1,25D3) or analogs 20-epi-22-oxa-24a,26a,27a-trihomo-1α,25-dihydroxyvitamin D3, 1,24-dihydroxy-22-ene-24-cyclopropylvitamin D3, 1α,25-dihydroxylumisterol3, or 1α,25(OH)2-d5-previtamin D3 in combination with TPA induces monocytic differentiation. The role of 1,25D3 in the induction of maturation has been shown to be a priming effect. Differentiation in response to these agents requires VDR-independent signaling of 1,25D3, PKC signaling, intracellular calcium, and calpain activity. In this study we identify the NFκB/IκB signaling pathway as a target of 1,25D3 and TPA action. One of the priming effects of 1,25D3 appears to be the rapid phosphorylation of serine residues on IκBα. On their own, 1,25D3, its analogs, and TPA do not alter IκBα expression; however, combinations of analogs with TPA result in a synergistic decrease in IκBα expression. Decreased expression of IκBα likely results from enhanced degradation, which allows the observed subsequent nuclear translocation of NFκB subunit p65. Since nuclear-localized NFκB was observed only in combination-treated cells, it is proposed that nuclear targets of NFκB are required for monocytic differentiation. Intracellular calcium and proteolytic activity are both necessary for the induction of IκB regulation and translocation of NFκB and are critical components of the nongenomic signaling cascades of the 1,25D3-induced differentiation pathway. [Copyright &y& Elsevier]