IASDR 2017 Workshop
Design now faces with new challenges that have made us rethink about our current design paradigm. It motivated us to organize a forum called, Design 3.0 Forum at KAIST in 2016, where we invited globally renowned design researchers and practitioners from different countries to discuss about important agenda for emerging challenges. The agenda we extracted from this forum can be summarized as follows: 1) envisioning of designers' future roles on open creativity and design; 2) dissemination and evaluation of design research outcomes by keeping deep design values; and 3) post education and practice that moves beyond the current use-centered perspectives by thinking big toward social innovation and large-scale impact.
As the result of the Design 3.0 forum, we all agreed that we must continue to develop and extend these agenda and collaboratively make executable actions to carry them out in the design community. In this special session at IASDR 2017, not only the organizers of the previous Design 3.0 forum (i.e. Youn-kyung Lim, Ron Wakkary, Kun-pyo Lee, and Tek-jin Nam), we invite the people who have not participated in the previous forum but can provide important insights on these issues. For the format of the session, we will take the panel format where the invited participants will present their positions first, and then have in-depth discussion on them among the participants and the audience. Through this special session, we expect to advance the initial Design 3.0 agenda and can generate more concrete and executable action items for Design 3.0.
Please follow developments of this work at http://design3-0.org/2017iasdr/
IASDR 2017 Guest Speaker
Mark Hallerberg is Dean and Professor of Public Management and Political Economy at the Hertie School of Governance, a private public policy School in Berlin, Germany. His research focuses on fiscal governance, tax competition, financial crises, public sector innovation, and European Union politics.
He previously held academic positions at Emory University, where he maintains an affiliation with the political science department, as well as at the University of Pittsburgh and Georgia Institute of Technology. He received his PhD from UCLA in 1995.
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Seattle Cancer Care Alliance and Premera Blue Cross show you how we conducted design research to build a collective understanding of the cancer care experience. We will provide detailed instructions, with checklists, on how to recreate a similar collaboration, including how we worked and what we worked on. You will walk away knowing how we shared skills and resources, built credibility and equal playing fields, and delivered research insights to both our organizations from multiple perspectives and vantage points.
Seattle Cancer Care Alliance (SCCA) brings together the leading research teams and cancer specialists from Fred Hutchinson Cancer Research Center, Seattle Children's and UW Medicine. Based in Seattle, SCCA is one of the top five Adult Cancer Care facilities in the United States as ranked by U.S. News & World Report. Shay Ghassemian, User Experience Designer in Digital Health, and Katie Rehfield, Patient Experience Specialist, will be facilitating this workshop.
Premera Blue Cross is a not-for-profit health insurance company serving 2 million people across the United States. As the largest health plan in the Pacific Northwest, Premera offers a wide range of products for individuals and families, Medicare recipients, and employers ranging from small business to Fortune 100 companies. Irish Malig, Senior Manager of Experience Strategy, Robert Racadio, Design Research Manager, Design Strategists Sara Bell, Paul Braun, and Ryan Rosensweig, and Darci Brown, Healthcare Implementation Manager in Provider Experience, will all be facilitating this workshop.
Presented by Shay Ghassemian and Robert Racadio
This paper expounds the background of Chinese design education as well as the orientation of the design education of Tongji University in the new times, it also collects 458 master thesis of College of Design and Innovation during 2010-2016 as analyzed sample. Based on the coding of subject classification, quantitative analysis and content analysis are made in order to understand the interdisciplinary education status of College of Design and Innovation from the two perspectives: the overall cross-disciplinary performance and the relationship between different cross-disciplinary directions.
Science teachers are often charged with providing discipline-specific literacy instruction. However, little is known about the reading and writing genres, or text types, typically found in these classrooms. In particular, there is a lack of knowledge about what opportunities adolescents have to engage with the genres privileged in science to learn the discipline's specialized ways of making meaning and communicating knowledge. This article reports on a case study of the reading and writing genres found within four middle-grade science classrooms in one small all-female school. Results suggest that although a variety of text genres were present, there was little discussion of how and why science content was presented in particular ways. Notably, students also had far more opportunities to read than write extended nonfiction. Teachers can cultivate a more reciprocal relation between reading and writing in science by using genres that students read as models for their writing.
Overnight, room temperature hold
(ONH) of whole blood before component processing
offers several benefits. This study evaluated the storage
and in vivo recovery characteristics of ONH red blood
cells (RBCs) stored in additive solution-7 (AS-7).
Wu et al. map an Nf1-Stat3-Arid1b/ b-catenin pathway that initiates
Neurofibromatosis type 1 (Nf1) neurofibromas, using unbiased
insertional mutagenesis screening. Stat3 transcriptionally represses Gsk3b and Arid1b, thereby activating b-catenin in Schwann cell precursors and resulting in neurofibroma initiation and maintenance.
Stat3-mediated modification plays a role in early tumorigenesis.
PM-18. EGFR-STAT3 ACTIVATES b-CATENIN SIGNALING TO
DRIVE NEUROFIBROMA INITIATION IN NF1, AND PLAYS A
ROLE IN TUMOR MAINTENANCE
Nancy Ratner1, Vincent Keng2, Deanna M. Patmore1, Jed K. Kendall1,
Edwin Jousma1, Kwangmin Choi1, Danhua Fan2, Eric B. Schwartz2, James
R. Fuchs2, Yuanshu Zou2, Mi-Ok Kim1, Eva Dombi5, David E. Levy6, Jose
A. Cancelas1, Anat Stemmer-Rachamimov4, Robert J. Spinner3, and David
Cincinnati Children’s, Cincinnati, OH, USA; 2
Minnesota, Minneapolis, MN, USA; 3
Mayo Clinic, Rochester, MN, USA; 4
Massachusetts General Hospital, Boston, MA, USA; 5
Institute Pediatric Branch, Bethesda, MD, USA; 6
New York University School
of Medicine, New York, NY, USA
To identify genes and signaling pathways that drive peripheral nerve tumor
initiationand growth beyond the Ras-MAPK pathwaywe used unbiased insertional
mutagenesis screening. We identified Stat3 as a potential driver of
Neurofibromatosis type 1 neurofibroma. Targeted genetic deletion of Stat3
in Schwann cell precursors (SCPs) and Schwann cells (SCs) largely prevented
neurofibroma formation, and self-renewal of tumor initiating cells. Genetic
gain- and loss-of-function identified EGFR as the major upstream regulator
of P-Stat3 in mouse and human neurofibroma SCP and in neurofibroma initiation;
IL-6 reinforced EGFR/Jak/Stat signaling. Preclinical tests of a Jak2/
Stat3 inhibitor reduced established neurofibroma growth, supporting an additional
role for Stat3 in benign nerve tumor maintenance. Unexpectedly, downstream
of Stat3, we identified b-catenin, and b-catenin expression rescued
phenotypic effects of Stat3 loss in SCPs. Phosphorylated STAT3 (Y705) and
b-catenin were strongly correlated in NF1 human plexiform neurofibromas.
The data support testing of JAK/STAT inhibition and Wnt/ b-catenin
pathway inhibition in neurofibroma therapeutic trials. Supported by: NIH
R01 NS28840 to N.R. and NIH P50 NS057531 to N.R. and D.L.), a
DAMD New Investigator Award (W81XWH-11-1-0259) and an Ohio State
University Comprehensive Cancer Center Pelotonia Idea Grant (to J.W.).
The American Cancer Society (IRG-67-003-44) supported J.R.F.