Resources for Teaching and Assessing the Vision and Change Biology Core Concepts

The Vision and Change report called for the biology community to mobilize around teaching the core concepts of biology. This essay describes a collection of resources developed by several different groups that can be used to respond to the report’s call to transform undergraduate education at both the individual course and departmental levels. First, we present two frameworks that help articulate the Vision and Change core concepts, the BioCore Guide and the Conceptual Elements (CE) Framework, which can be used in mapping the core concepts onto existing curricula and designing new curricula that teach the biology core concepts. Second, we describe how the BioCore Guide and the CE Framework can be used alongside the Partnership for Undergraduate Life Sciences Education curricular rubric as a way for departments to self-assess their teaching of the core concepts. Finally, we highlight three sets of instruments that can be used to directly assess student learning of the core concepts: the Biology Card Sorting Task, the Biology Core Concept Instruments, and the Biology—Measuring Achievement and Progression in Science instruments. Approaches to using these resources independently and synergistically are discussed

NUDT2 Disruption Elevates Diadenosine Tetraphosphate (Ap4A) and Down-Regulates Immune Response and Cancer Promotion Genes.

Regulation of gene expression is one of several roles proposed for the stress-induced nucleotide diadenosine tetraphosphate (Ap4A). We have examined this directly by a comparative RNA-Seq analysis of KBM-7 chronic myelogenous leukemia cells and KBM-7 cells in which the NUDT2 Ap4A hydrolase gene had been disrupted (NuKO cells), causing a 175-fold increase in intracellular Ap4A. 6,288 differentially expressed genes were identified with P < 0.05. Of these, 980 were up-regulated and 705 down-regulated in NuKO cells with a fold-change ≥ 2. Ingenuity® Pathway Analysis (IPA®) was used to assign these genes to known canonical pathways and functional networks. Pathways associated with interferon responses, pattern recognition receptors and inflammation scored highly in the down-regulated set of genes while functions associated with MHC class II antigens were prominent among the up-regulated genes, which otherwise showed little organization into major functional gene sets. Tryptophan catabolism was also strongly down-regulated as were numerous genes known to be involved in tumor promotion in other systems, with roles in the epithelial-mesenchymal transition, proliferation, invasion and metastasis. Conversely, some pro-apoptotic genes were up-regulated. Major upstream factors predicted by IPA® for gene down-regulation included NFκB, STAT1/2, IRF3/4 and SP1 but no major factors controlling gene up-regulation were identified. Potential mechanisms for gene regulation mediated by Ap4A and/or NUDT2 disruption include binding of Ap4A to the HINT1 co-repressor, autocrine activation of purinoceptors by Ap4A, chromatin remodeling, effects of NUDT2 loss on transcript stability, and inhibition of ATP-dependent regulatory factors such as protein kinases by Ap4A. Existing evidence favors the last of these as the most probable mechanism. Regardless, our results suggest that the NUDT2 protein could be a novel cancer chemotherapeutic target, with its inhibition potentially exerting strong anti-tumor effects via multiple pathways involving metastasis, invasion, immunosuppression and apoptosis

Correction to: Cluster identification, selection, and description in Cluster randomized crossover trials: the PREP-IT trials

An amendment to this paper has been published and can be accessed via the original article

Prediction model for adult height of small for gestational age children at the start of growth hormone treatment

Context: GH treatment is approved for short children born small for gestational age (SGA). The optimal dose is not yet established. Objective: Our objective was to develop a model for prediction of height at the onset of puberty and of adult height (AH). Design and Setting: Two GH studies were performed in short SGA children. Patients/Intervention: A total of 150 SGA children with height SD scores (SDS) less than -2, age 3 yr or older, no signs of catch-up growth, available height at the onset of puberty, and at least 1 yr of GH treatment before the onset of puberty were studied. In one study, patients were randomly assigned to either 0.033 or 0.067 mg/kg·d; in the other study all received 0.033 mg/kg·d. In 71 children, AH was reached. Main Outcome Measures: Height SDS at the onset of puberty and AH SDS were calculated. Results: Determinants positively related to height SDS at the onset of puberty were: height SDS at the start; target height SDS; and GH dose, whereas age at the start and female gender were negatively related. Positively related to AHSDS were: height SDS and chronological age - bone age at the start; target height SDS; and GH dose, whereas serum IGF binding protein (IGFBP)-3 SDS at the start was negatively related. There was a significant interaction between GH dose and IGFBP-3 SDS, indicating a smaller GH dose effect for higher levels of IGFBP-3. The final model explained 57% of the variance in height SDS at the onset of puberty and 41% of AH SDS. Conclusions: The prediction model for height SDS at the onset of puberty and AH SDS of short SGA children treated with GH provides useful information about the expected long-term growth. Because GH dosage is one of the determinants, the model aids in determining the optimal GH dose for each child. Copyrigh