Twitter Journal Club

Curatorial note from Digital Pedagogy in the Humanities: Laura Gogia started Twitter Journal Club (originally #tjc15) while she was a graduate student; people agree to read an article together at a designated time period and live tweet as they go (occasionally with the author responding on Twitter). A hashtag on Twitter allows anyone to observe at any time and jump in whenever they like; they do not need to be part of the community, nor does using a hashtag make them part of the community if they do not wish to use it regularly. Discussion can be synchronous, planned or spontaneous, or asynchronous over an extended time period. Participation does not require membership in a community, but helps build a PLN, as Shelly Terrell explains (Rheingold). This artifact serves as both a model and a tutorial. See this article by Gogia and Warren in Hybrid Pedagogy for the backstory behind #TJC

Open Learning Recipe

Curatorial note from Digital Pedagogy in the Humanities: This is a crowdsourced document in which participants in a rhizomatic, connectivist open course (#rhizo15) worked together in the first week to create a recipe for open learning. It was created in an open Google Docs document where different participants entered the tips they felt would be helpful to someone new to the arena of open learning. Because participants could see one another’s tips, they could add to what already existed, add comments (viewable in the margins), and ask for clarification. The document is a good example of crowdsourcing knowledge in a network and can be adapted for a variety of different learning contexts. The #rhizo15 MOOC participants: Maha Bali, Dave Cormier, Helen DeWaard, Barry Dyck, Ann Gagne, Dilrukshi Gamage, Kevin Hodgson, Rebecca J. Hogue, Sarah Honeychurch, Keesa V. Johnson, Scott Johnson, James Kerr, Daniel Lynds, Laura Pasquini, Sandra Sinfield, Lenandlar Singh, Wendy Taleo, Lee Skallerup Bessette, Sandra Rennie, Blair Vessey, Susan Watson, Wafa Nichol

Peeragogy Handbook

Curatorial note from Digital Pedagogy in the Humanities: A “how-to-do-it” resource on how a group of self-learners can organize via networked colearning. The Peeragogy Handbook is a crowdsourced and collaboratively annotated compendium for any group of people who want to colearn any subject together using the tools and knowledge available online. When students are given an open group research project, this handbook guides the colearners in identifying shared purpose and defining self-determined learning outcomes. The term “peeragogy” comes from Howard Rheingold and collaborators via his Social Media Classroom. Rheingold instigated this project, serving as a catalyst for the creation of this peer-created guide to pure peer-to-peer learning in the networked era. Peeragogy is a flexible framework of techniques for peer learning and peer knowledge production. Whereas pedagogy deals with the transmission of knowledge from teachers to students, peeragogy is what people use to produce and apply knowledge together. The strength of peeragogy is its flexibility and scalability through networked learning

Marginal Syllabus

Curatorial note from Digital Pedagogy in the Humanities: Digital annotation can expand our understanding of what is possible when we read together. The social annotation tool Hypothesis facilitates the act of shared reading. It leverages group annotation to enable sentence-level critique and multimodal note-taking on any text found on the Internet. An example of the networked use of this tool comes from Marginal Syllabus, which hosts monthly “annotatathons” on preselected articles. The 2017–18 Syllabus was co-organized with the National Writing Project. Students can participate in any of the scheduled annotatathons and experience networked learning in action, discussing articles with other students and educators globally. The Marginal Syllabus is a multistakeholder collaboration between Hypothesis, a nonprofit organization building an open platform for discussion on the Web; Aurora Public Schools in Aurora, Colorado; and researchers and teacher educators from the University of Colorado Denver School of Education and Human Development in Denver, Colorado

Salted roads lead to oedema and reduced locomotor function in amphibian populations

Human activities have caused massive losses of natural populations across the globe. Like many groups, amphibians have experienced substantial declines worldwide, driven by environmental changes such as habitat conversion, pollution, and disease emergence. Each of these drivers is often found in close association with the presence of roads. Here we report a novel consequence of roads affecting an amphibian native to much of North America, the wood frog (Rana sylvatica). Across 38 populations distributed from southern to central New England, we found that adult wood frogs living adjacent to roads had higher incidence and severity of oedema (indicated by obvious bloating caused by subcutaneous fluid accumulation) during the breeding season than frogs living away from the influence of roads. This effect was best explained by increased conductivity of breeding ponds, prob-ably caused by runoff pollution from road salt used for de-icing. Oedema severity was negatively correlated with locomotor performance in more northerly populations. Interestingly, northern populations experience more intense winters, which tends to result in more de-icing salt runoff and increased energetic demands associated with overwintering cryoprotection needs. Thus, this emerging consequence of roads appears to impose potential fitness costs associated with locomotion, and these effects might be most impactful on populations living in regions where de-icing is most intense.Together, our findings reveal a novel set of impacts of roads and runoff pollution on wood frog physiology and performance, which seem likely to contribute to population decline. Given the global prevalence of roads and increasing salinisation of freshwater habitats, oedema and related impacts could be widespread consequences faced by amphibian populations across much of the planet's temperate zonesThis work was supported by Mianus River Gorge Preserve, Elm City Innovation Collaborative, Yale Institute for Biospheric Studies, EEES Graduate fellowship and Cramer funds, Guarini School of Graduate and Advanced Studies McCulloch Fellowship, CAPES graduate fellowship (SwB 13442/13-9), the Margarita Salas Fellowship, and the National Science Foundation (DEB #1011335, DEB #1655092).Peer reviewe

Assessing interactions between the associations of common genetic susceptibility variants, reproductive history and body mass index with breast cancer risk in the breast cancer association consortium: a combined case-control study.

INTRODUCTION: Several common breast cancer genetic susceptibility variants have recently been identified. We aimed to determine how these variants combine with a subset of other known risk factors to influence breast cancer risk in white women of European ancestry using case-control studies participating in the Breast Cancer Association Consortium. METHODS: We evaluated two-way interactions between each of age at menarche, ever having had a live birth, number of live births, age at first birth and body mass index (BMI) and each of 12 single nucleotide polymorphisms (SNPs) (10q26-rs2981582 (FGFR2), 8q24-rs13281615, 11p15-rs3817198 (LSP1), 5q11-rs889312 (MAP3K1), 16q12-rs3803662 (TOX3), 2q35-rs13387042, 5p12-rs10941679 (MRPS30), 17q23-rs6504950 (COX11), 3p24-rs4973768 (SLC4A7), CASP8-rs17468277, TGFB1-rs1982073 and ESR1-rs3020314). Interactions were tested for by fitting logistic regression models including per-allele and linear trend main effects for SNPs and risk factors, respectively, and single-parameter interaction terms for linear departure from independent multiplicative effects. RESULTS: These analyses were applied to data for up to 26,349 invasive breast cancer cases and up to 32,208 controls from 21 case-control studies. No statistical evidence of interaction was observed beyond that expected by chance. Analyses were repeated using data from 11 population-based studies, and results were very similar. CONCLUSIONS: The relative risks for breast cancer associated with the common susceptibility variants identified to date do not appear to vary across women with different reproductive histories or body mass index (BMI). The assumption of multiplicative combined effects for these established genetic and other risk factors in risk prediction models appears justified.RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are

Genome-wide association analysis of more than 120,000 individuals identifies 15 new susceptibility loci for breast cancer.

Genome-wide association studies (GWAS) and large-scale replication studies have identified common variants in 79 loci associated with breast cancer, explaining ∼14% of the familial risk of the disease. To identify new susceptibility loci, we performed a meta-analysis of 11 GWAS, comprising 15,748 breast cancer cases and 18,084 controls together with 46,785 cases and 42,892 controls from 41 studies genotyped on a 211,155-marker custom array (iCOGS). Analyses were restricted to women of European ancestry. We generated genotypes for more than 11 million SNPs by imputation using the 1000 Genomes Project reference panel, and we identified 15 new loci associated with breast cancer at P < 5 × 10(-8). Combining association analysis with ChIP-seq chromatin binding data in mammary cell lines and ChIA-PET chromatin interaction data from ENCODE, we identified likely target genes in two regions: SETBP1 at 18q12.3 and RNF115 and PDZK1 at 1q21.1. One association appears to be driven by an amino acid substitution encoded in EXO1.BCAC is funded by Cancer Research UK (C1287/A10118, C1287/A12014) and by the European Community's Seventh Framework Programme under grant agreement 223175 (HEALTH-F2-2009-223175) (COGS). Meetings of the BCAC have been funded by the European Union COST programme (BM0606). Genotyping on the iCOGS array was funded by the European Union (HEALTH-F2-2009-223175), Cancer Research UK (C1287/A10710, C8197/A16565), the Canadian Institutes of Health Research (CIHR) for the CIHR Team in Familial Risks of Breast Cancer program and the Ministry of Economic Development, Innovation and Export Trade of Quebec, grant PSR-SIIRI-701. Combination of the GWAS data was supported in part by the US National Institutes of Health (NIH) Cancer Post-Cancer GWAS initiative, grant 1 U19 CA148065-01 (DRIVE, part of the GAME-ON initiative). For a full description of funding and acknowledgments, see the Supplementary Note.This is the author accepted manuscript. The final version is available from NPG via http://dx.doi.org/10.1038/ng.324

Characterizing Mutational Signatures in Human Cancer Cell Lines Reveals Episodic APOBEC Mutagenesis.

Multiple signatures of somatic mutations have been identified in cancer genomes. Exome sequences of 1,001 human cancer cell lines and 577 xenografts revealed most common mutational signatures, indicating past activity of the underlying processes, usually in appropriate cancer types. To investigate ongoing patterns of mutational-signature generation, cell lines were cultured for extended periods and subsequently DNA sequenced. Signatures of discontinued exposures, including tobacco smoke and ultraviolet light, were not generated in vitro. Signatures of normal and defective DNA repair and replication continued to be generated at roughly stable mutation rates. Signatures of APOBEC cytidine deaminase DNA-editing exhibited substantial fluctuations in mutation rate over time with episodic bursts of mutations. The initiating factors for the bursts are unclear, although retrotransposon mobilization may contribute. The examined cell lines constitute a resource of live experimental models of mutational processes, which potentially retain patterns of activity and regulation operative in primary human cancers.This work was supported by Wellcome grants 098051 and 206194; Cancer Research UK Grand Challenge Award C98/A24032 to L.B.A. and B.O.; the Li Ka Shing Foundation and National Institute for Health Research Oxford Biomedical Research Centre to D.C.W.; ED481A-2016/151 from Xunta de Galicia to B.R.–M

Identification of four novel susceptibility loci for oestrogen receptor negative breast cancer

Common variants in 94 loci have been associated with breast cancer including 15 loci with genome-wide significant associations (P<5 × 10−8) with oestrogen receptor (ER)-negative breast cancer and BRCA1-associated breast cancer risk. In this study, to identify new ER-negative susceptibility loci, we performed a meta-analysis of 11 genome-wide association studies (GWAS) consisting of 4,939 ER-negative cases and 14,352 controls, combined with 7,333 ER-negative cases and 42,468 controls and 15,252 BRCA1 mutation carriers genotyped on the iCOGS array. We identify four previously unidentified loci including two loci at 13q22 near KLF5, a 2p23.2 locus near WDR43 and a 2q33 locus near PPIL3 that display genome-wide significant associations with ER-negative breast cancer. In addition, 19 known breast cancer risk loci have genome-wide significant associations and 40 had moderate associations (P<0.05) with ER-negative disease. Using functional and eQTL studies we implicate TRMT61B and WDR43 at 2p23.2 and PPIL3 at 2q33 in ER-negative breast cancer aetiology. All ER-negative loci combined account for ∼11% of familial relative risk for ER-negative disease and may contribute to improved ER-negative and BRCA1 breast cancer risk prediction