Previous research often revealed detrimental effects of seductive details on learning with multimedia instruction, but there are mixed findings regarding how to best explain these detrimental effects. We investigated whether the detrimental effects of seductive details are mainly mediated by the cognitive processes of diversion (deeper processing of seductive details rather than pertinent content) or disruption (unsuccessful attempts to integrate seductive details with pertinent content) by assessing the effects of instructional prompts. In an online learning experiment, participants ( = 247) learned either without seductive details (control condition) or with seductive details in one of three conditions: Participants received either a prompt informing them about the irrelevance of seductive details (irrelevance-prompt), a prompt to process seductive details and pertinent content separately (separation-prompt), or no prompt within their task instruction.
View Article and Find Full Text PDFBackground: Collision lesions as two independent and unrelated skin tumors often manifest an atypical morphology.
Objective: To determine the combinations of collision skin lesions (CSLs).
Methods: Twenty-one pigmented lesion clinics in nine countries included 77 histopathologically proven CSLs in this retrospective observational study.
Despite recent advances in understanding the relevance of cell adhesion-related signaling in the pathogenesis of ischemic cardiomyopathy (ICM) in animal models, substantial questions remain unanswered in the human setting. We have previously shown that the neural cell adhesion molecule CD56 [neural cell adhesion molecule (NCAM1)] is specifically overexpressed in ICM; it was the aim of the current study to further elucidate the role of CD56 in the pathogenesis of human ICM. We used quantitative real-time PCR and IHC in human ICM and a rat model of coronary obstruction to demonstrate that CD56(140kD), the only extraneuronally expressed NCAM1 isoform with a cytoplasmic protein domain capable of inducing intracellular signaling, is the only up-regulated CD56 isoform in failing cardiomyocytes in human ICM in vivo.
View Article and Find Full Text PDFChromosomal instability (CIN) is a major hallmark of human cancer and might contribute to tumorigenesis. Genes required for the normal progression of mitosis represent potential CIN genes and, as such, are important tumour suppressors. The Chk2 kinase and its downstream targets p53 and Brca1 are tumour suppressors that have been functionally linked to the DNA damage response pathway.
View Article and Find Full Text PDFThe mitotic spindle checkpoint represents a signal transduction pathway that prevents the onset of anaphase until all chromosomes are properly aligned on a metaphase plate. Partial inactivation of this checkpoint allows premature separation of sister chromatids and results in aneuploidy, which might contribute to tumorigenesis. Unlike other cell cycle checkpoints, the spindle checkpoint is essential for cell viability, giving rise to the idea that the spindle checkpoint itself might represent a valuable target for anticancer therapy.
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