Inconsistent seduction: Addressing confounds and methodological issues in the study of the seductive detail effect

Introduction: The inclusion of interesting but irrelevant details in instructional materials may interfere with recall and application of the core content. Although this seductive detail effect is well researched, recent research highlights factors that may influence the effect size. Objectives: The current study discusses confounds and methodological issues in the study of seductive details and outlines strategies for over coming them. These practices were then applied in a study that examined the role of learning objectives on the seductive detail effect. Met hods: Seductive details were selected on the basis of interest and importance level and matched forword count and reading level. The 3×2 between subjects design presented 132 undergraduate students with a lesson on plate tectonics; participants completed tests on both recall and transfer. Results: Results did not reveal a consistent detrimental effect of high-interest details on core content recall and transfer. On the recall test, contrary to expectation, the seductive detail effect obtained only when objectives were provided. A similar pattern emerged on the transfer task. Conclusion: These findings highlight the difficulty of consistently eliciting the seductive detail effect. We discuss outstanding issues that must be addressed in order to develop practical guidelines on the inclusion of seductive details in educational materials

Molecular Beams

Contains research objectives and reports on one research project.Lincoln Laboratory, Purchase Order DDL B-00306U. S. ArmyU. S. NavyU. S. Air Force under Air Force Contract AF19(604)-520

Effects of the Mutant TP53 Reactivator APR-246 on Therapeutic Sensitivity of Pancreatic Cancer Cells in the Presence and Absence of WT-TP53

The TP53 tumor suppressor is mutated in ~75% of pancreatic cancers. The mutant TP53 protein in pancreatic ductal adenocarcinomas (PDAC) promotes tumor growth and metastasis. Attempts have been made to develop molecules that restore at least some of the properties of wildtype (WT) TP53. APR-246 is one such molecule, and it is referred to as a mutant TP53 reactivator. To understand the potential of APR-246 to sensitize PDAC cells to chemotherapy, we introduced a vector encoding WT-TP53 into two PDAC cell lines, one lacking the expression of TP53 (PANC-28) and one with a gain-of-function (GOF) mutant TP53 (MIA-PaCa-2). APR-246 increased drug sensitivity in the cells containing either a WT or mutant TP53 protein with GOF activity, but not in cells that lacked TP53. The introduction of WT-T53 into PANC-28 cells increased their sensitivity to the TP53 reactivator, chemotherapeutic drugs, and signal transduction inhibitors. The addition of WT-TP53 to PDAC cells with GOF TP53 also increased their sensitivity to the drugs and therapeutics, indicating that APR-246 could function in cells with WT-TP53 and GOF TP53. These results highlight the importance of knowledge of the type of TP53 mutation that is present in cancer patients before the administration of drugs which function through the reactivation of TP53

Molecular Beams

Contains research objectives and reports on four research projects.Lincoln Laboratory, Purchase Order DDL B-00306U. S. ArmyU. S. NavyU. S. Air Force under Air Force Contract AF19(604)-740

NON-DESTRUCTIVE RADIOCARBON DATING: NATURALLY MUMMIFIED INFANT BUNDLE FROM SW TEXAS

Plasma oxidation was used to obtain radiocarbon dates on six different materials from a naturally mummified baby bundle from the Lower Pecos River region of southwest Texas. This bundle was selected because it was thought to represent a single event and would illustrate the accuracy and precision of the plasma oxidation method. Five of the materials were clearly components of the original bundle with 13 dates combined to yield a weighted average of 2135 {+-} 11 B.P. Six dates from a wooden stick of Desert Ash averaged 939 {+-} 14 B.P., indicating that this artifact was not part of the original burial. Plasma oxidation is shown to be a virtually non-destructive alternative to combustion. Because only sub-milligram amounts of material are removed from an artifact over its exposed surface, no visible change in fragile materials has been observed, even under magnification. The method is best applied when natural organic contamination is unlikely and serious consideration of this issue is needed in all cases. If organic contamination is present, it will have to be removed before plasma oxidation to obtain accurate radiocarbon dates

Molecular Beams

Contains reports on five research projects

Targeting GSK3 and Associated Signaling Pathways Involved in Cancer

Glycogen synthase kinase 3 (GSK-3) is a serine/threonine (S/T) protein kinase. Although GSK-3 originally was identified to have functions in regulation of glycogen synthase, it was subsequently determined to have roles in multiple normal biochemical processes as well as various disease conditions. GSK-3 is sometimes referred to as a moonlighting protein due to the multiple substrates and processes which it controls. Frequently, when GSK-3 phosphorylates proteins, they are targeted for degradation. GSK-3 is often considered a component of the PI3K/PTEN/AKT/GSK-3/mTORC1 pathway as GSK-3 is frequently phosphorylated by AKT which regulates its inactivation. AKT is often active in human cancer and hence, GSK-3 is often inactivated. Moreover, GSK-3 also interacts with WNT/\u3b2-catenin signaling and \u3b2-catenin and other proteins in this pathway are targets of GSK-3. GSK-3 can modify NF-\u3baB activity which is often expressed at high levels in cancer cells. Multiple pharmaceutical companies developed small molecule inhibitors to suppress GSK-3 activity. In addition, various natural products will modify GSK-3 activity. This review will focus on the effects of small molecule inhibitors and natural products on GSK-3 activity and provide examples where these compounds were effective in suppressing cancer growth

Targeting the leukemic stem cell: the Holy Grail of leukemia therapy

Since the discovery of leukemic stem cells (LSCs) over a decade ago, many of their critical biological properties have been elucidated, including their distinct replicative properties, cell surface phenotypes, their increased resistance to chemo-therapeutic drugs and the involvement of growthpromoting chromosomal translocations. Of particular importance is their ability to transfer malignancy to non-obese diabetic-severe combined immunodeficient (NOD-SCID) mice. Furthermore, numerous studies demonstrate that acute myeloid leukemia arises from mutations at the level of stem cell, and chronic myeloid leukemia is also a stem cell disease. In this review, we will evaluate the main characteristics of LSCs elucidated in several well-documented leukemias. In addition, we will discuss points of therapeutic intervention. Promising therapeutic approaches include the targeting of key signal transduction pathways (for example, PI3K, Rac and Wnt) with smallmolecule inhibitors and specific cell surface molecules (for example, CD33, CD44 and CD123), with effective cytotoxic antibodies. Also, statins, which are already widely therapeutically used for a variety of diseases, show potential in targeting LSCs. In addition, drugs that inhibit ATP-binding cassette transporter proteins are being extensively studied, as they are important in drug resistance â a frequent characteristic of LSCs. Although the specific targeting of LSCs is a relatively new field, it is a highly promising battleground that may reveal the Holy Grail of cancer therapy. Originally published Leukemia, Vol. 23, No. 1, Jan 200