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12. Societal Boundaries

Author

Brand, Ulrich, Muraca, Barbara, Pineault, Éric, Sahakian, Marlyne, Schaffartzik, Anke, Novy, Andreas, Streissler, Christoph, Haberl, Helmut, Asara, Viviana, Dietz, Kristina, Lang, Miriam, Kothari, Ashish, Smith, Tone, Spash, Clive, Brad, Alina, Pichler, Melanie, Plank, Christina, Velegrakis, Giorgos, Jahn, Thomas, Carter, Angela, Huan, Qingzhi, Kallis, Giorgos, Alier, Joan Martínez, Riva, Gabriel, Satgar, Vishwas, Mantovani, Emiliano Teran, Williams, Michelle, Wissen, Markus, Görg, Christoph, Wallenhorst, Nathanaël, editor, and Wulf, Christoph, editor

Published
2023
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13. Planetary Boundaries

Author

Brand, Ulrich, Muraca, Barbara, Pineault, Éric, Sahakian, Marlyne, Schaffartzik, Anke, Novy, Andreas, Streissler, Christoph, Haberl, Helmut, Asara, Viviana, Dietz, Kristina, Lang, Miriam, Kothari, Ashish, Smith, Tone, Spash, Clive, Brad, Alina, Pichler, Melanie, Plank, Christina, Velegrakis, Giorgos, Jahn, Thomas, Carter, Angela, Huan, Qingzhi, Kallis, Giorgos, Alier, Joan Martínez, Riva, Gabriel, Satgar, Vishwas, Mantovani, Emiliano Teran, Williams, Michelle, Wissen, Markus, Görg, Christoph, Wallenhorst, Nathanaël, editor, and Wulf, Christoph, editor

Published
2023
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19. Phosphoprotein-based biomarkers as predictors for cancer therapy

Author

Carter, Angela M., Tan, Chunfeng, Pozo, Karine, Telange, Rahul, Molinaro, Roberto, Guo, Ailan, De Rosa, Enrica, Martinez, Jonathan O., Zhang, Shanrong, Kumar, Nilesh, Takahashi, Masaya, Wiederhold, Thorsten, Ghayee, Hans K., Oltmann, Sarah C., Pacak, Karel, Woltering, Eugene A., Hatanpaa, Kimmo J., Nwariaku, Fiemu E., Grubbs, Elizabeth G., Gill, Anthony J., Robinson, Bruce, Gillardon, Frank, Reddy, Sushanth, Jaskula-Sztul, Renata, Mobley, James A., Mukhtar, M. Shahid, Tasciotti, Ennio, Chen, Herbert, and Bibb, James A.

Published
2020

20. Causal Effect of Plasminogen Activator Inhibitor Type 1 on Coronary Heart Disease

Author

Song, Ci, Burgess, Stephen, Eicher, John D, O'Donnell, Christopher J, Johnson, Andrew D, Huang, Jie, Sabater‐Lleal, Maria, Asselbergs, Folkert W, Tregouet, David, Shin, So‐Youn, Ding, Jingzhong, Baumert, Jens, Oudot‐Mellakh, Tiphaine, Folkersen, Lasse, Smith, Nicholas L, Williams, Scott M, Ikram, Mohammad A, Kleber, Marcus E, Becker, Diane M, Truong, Vinh, Mychaleckyj, Josyf C, Tang, Weihong, Yang, Qiong, Sennblad, Bengt, Moore, Jason H, Williams, Frances MK, Dehghan, Abbas, Silbernagel, Günther, Schrijvers, Elisabeth MC, Smith, Shelly, Karakas, Mahir, Tofler, Geoffrey H, Silveira, Angela, Navis, Gerjan J, Lohman, Kurt, Chen, Ming‐Huei, Peters, Annette, Goel, Anuj, Hopewell, Jemma C, Chambers, John C, Saleheen, Danish, Lundmark, Per, Psaty, Bruce M, Strawbridge, Rona J, Boehm, Bernhard O, Carter, Angela M, Meisinger, Christa, Peden, John F, Bis, Joshua C, McKnight, Barbara, Öhrvik, John, Taylor, Kent, Franzosi, Maria Grazia, Seedorf, Udo, Collins, Rory, Franco‐Cereceda, Anders, Syvänen, Ann‐Christine, Goodall, Alison H, Yanek, Lisa R, Cushman, Mary, Müller‐Nurasyid, Martina, Folsom, Aaron R, Basu, Saonli, Matijevic, Nena, van Gilst, Wiek H, Kooner, Jaspal S, Hofman, Albert, Danesh, John, Clarke, Robert, Meigs, James B, Kathiresan, Sekar, Reilly, Muredach P, Klopp, Norman, Harris, Tamara B, Winkelmann, Bernhard R, Grant, Peter J, Hillege, Hans L, Watkins, Hugh, Spector, Timothy D, Becker, Lewis C, Tracy, Russell P, März, Winfried, Uitterlinden, Andre G, Eriksson, Per, Cambien, Francois, Morange, Pierre‐Emmanuel, Koenig, Wolfgang, Soranzo, Nicole, van der Harst, Pim, Liu, Yongmei, Hamsten, Anders, Ehret, Georg B, Munroe, Patricia B, Rice, Kenneth M, Bochud, Murielle, Chasman, Daniel I, Smith, Albert V, Tobin, Martin D, and Verwoert, Germaine C

Subjects
Clinical Research, Heart Disease - Coronary Heart Disease, Cardiovascular, Heart Disease, Aging, Biomarkers, Blood Glucose, Coronary Disease, Fibrinolysis, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Incidence, Lipoproteins, HDL, Mendelian Randomization Analysis, Multivariate Analysis, Observational Studies as Topic, Odds Ratio, Plasminogen Activator Inhibitor 1, Polymorphism, Single Nucleotide, Risk Assessment, Risk Factors, coronary heart disease, genome-wide association study, Mendelian randomization, plasminogen activator inhibitor type 1, single nucleotide polymorphism, genome‐wide association study, Cardiorespiratory Medicine and Haematology
Abstract

Plasminogen activator inhibitor type 1 (PAI-1) plays an essential role in the fibrinolysis system and thrombosis. Population studies have reported that blood PAI-1 levels are associated with increased risk of coronary heart disease (CHD). However, it is unclear whether the association reflects a causal influence of PAI-1 on CHD risk. To evaluate the association between PAI-1 and CHD, we applied a 3-step strategy. First, we investigated the observational association between PAI-1 and CHD incidence using a systematic review based on a literature search for PAI-1 and CHD studies. Second, we explored the causal association between PAI-1 and CHD using a Mendelian randomization approach using summary statistics from large genome-wide association studies. Finally, we explored the causal effect of PAI-1 on cardiovascular risk factors including metabolic and subclinical atherosclerosis measures. In the systematic meta-analysis, the highest quantile of blood PAI-1 level was associated with higher CHD risk comparing with the lowest quantile (odds ratio=2.17; 95% CI: 1.53, 3.07) in an age- and sex-adjusted model. The effect size was reduced in studies using a multivariable-adjusted model (odds ratio=1.46; 95% CI: 1.13, 1.88). The Mendelian randomization analyses suggested a causal effect of increased PAI-1 level on CHD risk (odds ratio=1.22 per unit increase of log-transformed PAI-1; 95% CI: 1.01, 1.47). In addition, we also detected a causal effect of PAI-1 on elevating blood glucose and high-density lipoprotein cholesterol. Our study indicates a causal effect of elevated PAI-1 level on CHD risk, which may be mediated by glucose dysfunction.

Published
2017

21. What Can Be Learned from Action Learning Coaching? Learnings of Novice Action Learners and Their Coach

Author

Carter, Angela Danielle

Abstract

Action learning coaching (ALC), a form of action learning that integrates leadership coaching, is suggested as a method and ethos to build future capacity, specifically in novice HRD practitioners. The purpose of this article is to offer an account of learning from the perspectives of novice action learners, who were new to the field of human resource development (HRD) and to the concept of ALC, as well as their similarly noviced coach. Data from budding practitioners and their coach, participants in an action learning action research (ALAR) study, are analyzed to show how they used action and generative learning through ambiguity to apply learning to their new roles. Action learning coaching elevated participants' skills, self-concept, efficaciousness, professionalism, commitment to action, and capacity for learning and growth. Participants changed themselves, their practice, and ultimately the way they approached human resource development as novices.

Published
2019
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23. Cdk5 drives formation of heterogeneous pancreatic neuroendocrine tumors

Author

Carter, Angela M., Kumar, Nilesh, Herring, Brendon, Tan, Chunfeng, Guenter, Rachael, Telange, Rahul, Howse, Wayne, Viol, Fabrice, McCaw, Tyler R., Bickerton, Hayden H., Gupta, Priyanka, Gillardon, Frank, Woltering, Eugene A., Dhall, Deepti, Totenhagen, John, Banerjee, Ronadip R., Kurian, Elizabeth M., Reddy, Sushanth, Chen, Herbert, Schrader, Joerg, Bart Rose, J., Mukhtar, M. Shahid, and Bibb, James A.

Published
2021
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26. Editorial

Author

Rus, Diana, primary, Carter, Angela, additional, and Okay-Somerville, Belgin, additional

Published
2023
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29. Who Are We Not Calling On? A Study of Classroom Participation and the Implementation of the Name Card Method.

Author

Carter, Angela

Abstract

This study involved observing a second-grade classroom to investigate how the teacher called on students, noting whether the teacher gave enough attention to students who raised their hands frequently by calling on them and examining students' responses when called on. Researchers implemented a new method of calling on students using name cards, which involves placing each student's name on an index card. When the teacher asks a question, a card is chosen for a response. Students were observed over 5 weeks, and the teacher was introduced to name cards. Students completed surveys asking which method of being called on they preferred. Overall, the teacher did not call on students who raised their hands as frequently as students chose to participate. This did not discourage students from continuing to raise their hands, though they appeared frustrated. The teacher mainly called on students whose hands were raised. Using name cards, the teacher called on all 21 students. Students had the same frustrated responses to not being called on when name cards were used, though less frequently. Most of the students preferred the name card method. An appendix contains observation transcripts, survey questions and results, and teacher interview guideline questions. (SM)

Published
2000

31. Feds should not waste their $15-billion Canada Growth Fund on carbon capture for oil

Author

Cameron, Laura and Carter, Angela

Subjects
Stock funds -- Investments, Petroleum industry -- Environmental aspects, Carbon sequestration -- Government finance, Company investment, General interest, News, opinion and commentary
Abstract

Byline: LAURA CAMERON, ANGELA CARTER Laura Cameron is a senior policy adviser at the International Institute for Sustainable Development. Angela Carter is a professor at the University of Waterloo and [...]

Published
2023

37. Faulty Metabolism: A Potential Instigator of an Aggressive Phenotype in Cdk5-dependent Medullary Thyroid Carcinoma

Author

Gupta, Priyanka, Herring, Brendon, Kumar, Nilesh, Telange, Rahul, Garcia-Buntley, Sandra S., Caceres, Tessa W., Colantonio, Simona, Williams, Ford, Kurup, Pradeep, Carter, Angela M., Lin, Diana, Chen, Herbert, Rose, Bart, Jaskula-Sztul, Renata, Mukhtar, Shahid, Reddy, Sushanth, and Bibb, James A.

Subjects
Article
Abstract

Mechanistic modeling of cancers such as Medullary Thyroid Carcinoma (MTC) to emulate patient-specific phenotypes is challenging. The discovery of potential diagnostic markers and druggable targets in MTC urgently requires clinically relevant animal models. Here we established orthotopic mouse models of MTC driven by aberrantly active Cdk5 using cell-specific promoters. Each of the two models elicits distinct growth differences that recapitulate the less or more aggressive forms of human tumors. The comparative mutational and transcriptomic landscape of tumors revealed significant alterations in mitotic cell cycle processes coupled with the slow-growing tumor phenotype. Conversely, perturbation in metabolic pathways emerged as critical for aggressive tumor growth. Moreover, an overlapping mutational profile was identified between mouse and human tumors. Gene prioritization revealed putative downstream effectors of Cdk5 which may contribute to the slow and aggressive growth in the mouse MTC models. In addition, Cdk5/p25 phosphorylation sites identified as biomarkers for Cdk5-driven neuroendocrine tumors (NETs) were detected in both slow and rapid onset models and were also histologically present in human MTC. Thus, this study directly relates mouse and human MTC models and uncovers vulnerable pathways potentially responsible for differential tumor growth rates. Functional validation of our findings may lead to better prediction of patient-specific personalized combinational therapies. GRAPHICAL ABSTRACT: HIGHLIGHTS: CGRP driven aberrant Cdk5 activation develops early onset aggressive MTC. Genetic alterations in mouse and human tumors disrupt common pathways. Aggressive tumor model characterized by alterations in metabolic pathways. Slow growing tumor model elicits disruption of mitotic spindle assembly.

Published
2023

44. Syntaxin 1 Ser 14 phosphorylation is required for nonvesicular dopamine release

Author

Shekar, Aparna, primary, Mabry, Samuel J., additional, Cheng, Mary H., additional, Aguilar, Jenny I., additional, Patel, Shalin, additional, Zanella, Daniele, additional, Saleeby, David P., additional, Zhu, Yanqi, additional, Romanazzi, Tiziana, additional, Ulery-Reynolds, Paula, additional, Bahar, Ivet, additional, Carter, Angela M., additional, Matthies, Heinrich J. G., additional, and Galli, Aurelio, additional

Published
2023
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49. However the pandemic unfolds, it's time for oil use to peak—and society to prepare for the fallout.

Author

Strauch, Yonatan, Carter, Angela, and Homer-Dixon, Thomas

Subjects
*COVID-19 pandemic, *FOSSIL fuels, *TIME management, *PANDEMICS, *CLIMATE change
Abstract

The decline of oil's dominance will start with a peak in demand. Reaching that peak quickly is an essential goal, even if things will likely spin out of control from there. If humanity is to avoid staggering harm from climate change, carbon emissions must fall sharply very soon, which implies that humanity's use of fossil fuels must start to decline soon. As people grasp this imperative, they'll work to seize this moment when the oil industry has stumbled. The coronavirus pandemic presents activists with several openings to keep oil demand from ever returning to its pre-pandemic peak. [ABSTRACT FROM AUTHOR]

Published
2020
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