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1. Can Peer Review Be Kinder? Supportive Peer Review: A Re-Commitment to Kindness and a Call to Action

Author

Clase, Catherine M, Dicks, Elizabeth, Holden, Rachel, Sood, Manish M, Levin, Adeera, Kalantar-Zadeh, Kamyar, Moore, Linda W, Bartlett, Susan J, Bello, Aminu K, Bohm, Clara, Bridgewater, Darren, Bouchard, Josee, Burger, Dylan, Carrero, Juan Jesús, Donald, Maoliosa, Elliott, Meghan, Goldenberg, Maya J, Jardine, Meg, Lam, Ngan N, Maddigan, W Joy, Madore, François, Mavrakanas, Thomas A, Molnar, Amber O, Prasad, GV Ramesh, Rigatto, Claudio, Tennankore, Karthik K, Torban, Elena, Trainor, Laurel, White, Christine A, and Hartwig, Sunny

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Good Health and Well Being, humility, kindness, peer review, supportive review, truth, Clinical sciences
Abstract

Peer review aims to select articles for publication and to improve articles before publication. We believe that this process can be infused by kindness without losing rigor. In 2014, the founding editorial team of the Canadian Journal of Kidney Health and Disease (CJKHD) made an explicit commitment to treat authors as we would wish to be treated ourselves. This broader group of authors reaffirms this principle, for which we suggest the terminology "supportive review."

Published
2022

4. Involving Patient Partners in the KRESCENT Peer Review: Intent, Process, Challenges, and Opportunities

Author

Fowler, Elisabeth A., primary, Bell, Karin, additional, Burns, Kevin, additional, Chiazzese, Angela, additional, DeSerres, Sacha A., additional, Foster, Bethany J., additional, Hartwig, Sunny, additional, Herrington, Gwen, additional, James, Matthew T., additional, Jensen, Victor, additional, Jones, Nina, additional, Kidston, Sandi, additional, Lemay, Serge, additional, Levin, Adeera, additional, MacPhee, Anne, additional, McCutcheon, Shanda, additional, Ravani, Pietro, additional, Samuel, Susan, additional, Scholey, James, additional, Takano, Tomoko, additional, Tangri, Navdeep, additional, Verdin, Nancy, additional, Alexander, R. Todd, additional, and Clase, Catherine M., additional

Published
2022
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5. Advancing Discovery Research in Nephrology in Canada: A Conference Report From the 2021 Molecules and Mechanisms Mediating Kidney Health and Disease (M3K) Scientific Meeting and Investigator Summit

Author

Burger, Dylan, primary, Abdelrasoul, Amira, additional, Alexander, R. Todd, additional, Ballermann, Barbara, additional, Bridgewater, Darren, additional, Chan, John S. D., additional, Cunanan, Joanna, additional, Cybulsky, Andrey V., additional, Gerarduzzi, Casimiro, additional, Gunaratnam, Lakshman, additional, Hartwig, Sunny, additional, Kapus, Andras, additional, Kennedy, Christopher R. J., additional, Lamarche, Caroline, additional, Myette, Robert L., additional, Nmecha, Ifeanyi Kennedy, additional, Stalker, Leanne, additional, Szaszi, Katalin, additional, Torban, Elena, additional, Zhang, Shao Ling, additional, and Takano, Tomoko, additional

Published
2022
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6. Can Peer Review Be Kinder? Supportive Peer Review: A Re-Commitment to Kindness and a Call to Action

Author

Clase, Catherine M., primary, Dicks, Elizabeth, additional, Holden, Rachel, additional, Sood, Manish M., additional, Levin, Adeera, additional, Kalantar-Zadeh, Kamyar, additional, Moore, Linda W, additional, Bartlett, Susan J., additional, Bello, Aminu K., additional, Bohm, Clara, additional, Bridgewater, Darren, additional, Bouchard, Josee, additional, Burger, Dylan, additional, Carrero, Juan Jesús, additional, Donald, Maoliosa, additional, Elliott, Meghan, additional, Goldenberg, Maya J., additional, Jardine, Meg, additional, Lam, Ngan N., additional, Maddigan, W. Joy, additional, Madore, François, additional, Mavrakanas, Thomas A., additional, Molnar, Amber O., additional, Prasad, G. V. Ramesh, additional, Rigatto, Claudio, additional, Tennankore, Karthik K., additional, Torban, Elena, additional, Trainor, Laurel, additional, White, Christine A., additional, and Hartwig, Sunny, additional

Published
2022
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7. Table 1

Author

Bourassi, Emilia, Savidge, Christine, Foley, Peter, and Hartwig, Sunny

Subjects
70706 Veterinary Medicine, animal diseases, FOS: Veterinary sciences, mental disorders, bacteria, bacterial infections and mycoses
Abstract

Distribution of the negative and positive microscopic agglutination tests for Leptospira species per location in 200 feral cats on Prince Edward Island

Published
2021
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8. Table 2

Author

Bourassi, Emilia, Savidge, Christine, Foley, Peter, and Hartwig, Sunny

Subjects
70706 Veterinary Medicine, FOS: Veterinary sciences, bacteria, bacterial infections and mycoses
Abstract

Demographic, geographic and laboratory characteristics of 20 cats positive for Leptospira species on Prince Edward Island, based on microscopic agglutination test

Published
2021
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9. sj-docx-1-cjk-10.1177_20543581211033405 – Supplemental material for Training Programs for Fundamental and Clinician-Scientists: Balanced Outcomes for Graduates by Gender

Author

Rampersad, Christie, Alexander, Todd, Fowler, Elisabeth, Hartwig, Sunny, Levin, Adeera, Rosenblum, Norman D., Samuel, Susan, Wiebe, Chris, and Ho, Julie

Subjects
Medicine
Abstract

Supplemental material, sj-docx-1-cjk-10.1177_20543581211033405 for Training Programs for Fundamental and Clinician-Scientists: Balanced Outcomes for Graduates by Gender by Christie Rampersad, Todd Alexander, Elisabeth Fowler, Sunny Hartwig, Adeera Levin, Norman D. Rosenblum, Susan Samuel, Chris Wiebe and Julie Ho in Canadian Journal of Kidney Health and Disease

Published
2021
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12. Contributors

Author

Antignac, Corinne, primary, Aronson, Peter S., additional, Asch, William S., additional, Baum, Michel, additional, Beerman, Isabel, additional, Bergeron, Anne, additional, Biber, Jürg, additional, Bichet, Daniel G., additional, Bleyer, Anthony J., additional, Bowden, Donald W., additional, Boyden, Lynn M., additional, Brown, Edward M., additional, Cantley, Lloyd G., additional, Chou, Janice Y., additional, Coca, Steven G., additional, Cox, Timothy M., additional, Cramer, Scott D., additional, Cremers, Cor WJR., additional, Deen, Peter M.T., additional, Desnick, Robert J., additional, Endou, Hitoshi, additional, Esquivel, Ernie L., additional, Forster, Ian C., additional, Freedman, Barry I., additional, Geller, David S., additional, Gharavi, Ali, additional, Giebisch, Gerhard H., additional, Grubb, Robert L., additional, Guay-Woodford, Lisa M., additional, Hariri, Ali, additional, Hart, Thomas C., additional, Hartwig, Sunny, additional, Hebert, Steven C., additional, Hernando, Nati, additional, Hildebrandt, Friedhelm, additional, Hosoya, Tatsuo, additional, Hosoyamada, Makoto, additional, Ichida, Kimiyoshi, additional, Igarashi, Peter, additional, Jorquera, Rossana, additional, Kahle, Kristopher T., additional, Kalatzis, Vasiliki, additional, Karet, Fiona E., additional, Klotman, Paul E., additional, Knoers, Nine V.A.M., additional, Kreidberg, Jordan A., additional, Kwiatkowski, David Joseph, additional, Lee, Brendan, additional, Lifton, Richard P., additional, Lin, Fangming, additional, Marston Linehan, W., additional, Mansfield, Brian C., additional, Marlier, Arnaud, additional, Mistry, Pramod Kumar, additional, Moe, Orson W., additional, Mohan, Chandra, additional, Morello, Roy, additional, Murer, Heini, additional, Palacin, Manuel, additional, Patel, Vishal, additional, Patrakka, Jaakko, additional, Pollak, Martin R., additional, Polu, Krishna R., additional, Reilly, Robert F., additional, Rich, Stephen S., additional, Rossier, Bernard C., additional, Scheinman, Steven J., additional, Schild, Laurent, additional, Schilsky, Michael L., additional, Scholl, Ute I., additional, Scolari, Francesco, additional, Scott, Daryl, additional, Seldin, Donald W., additional, Somlo, Stefan, additional, Takayama, Tatsuya, additional, Tanguay, Robert M., additional, Tryggvason, Karl, additional, Wagner, Carsten A., additional, Wakeland, Edward K., additional, Walther, McClellan M., additional, Wang, Andrew, additional, Weinstein, David A., additional, White, Perrin C., additional, Wilson, Frederick H., additional, Wright, Ernest M., additional, Wyatt, Christina M., additional, and van Os, Carel H., additional

Published
2009
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20. WT1 targetsGas1to maintain nephron progenitor cells by modulating FGF signals

Author

Kann, Martin, primary, Bae, Eunnyung, additional, Lenz, Maximilian O., additional, Li, Liangji, additional, Trannguyen, BaoTran, additional, Schumacher, Valerie A., additional, Taglienti, Mary E., additional, Bordeianou, Liliana, additional, Hartwig, Sunny, additional, Rinschen, Markus M., additional, Schermer, Bernhard, additional, Benzing, Thomas, additional, Fan, Chen-Ming, additional, and Kreidberg, Jordan A., additional

Published
2015
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21. The transcription factor sry-related HMG box-4 (SOX4) is required for normal renal developmentin vivo

Author

Huang, Jez, primary, Arsenault, Michel, additional, Kann, Martin, additional, Lopez-Mendez, Carlos, additional, Saleh, Monique, additional, Wadowska, Dorota, additional, Taglienti, Mary, additional, Ho, Jacqueline, additional, Miao, Yuan, additional, Sims, David, additional, Spears, Jonathan, additional, Lopez, Alfonso, additional, Wright, Glenda, additional, and Hartwig, Sunny, additional

Published
2015
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25. Canadian Journal of Kidney Health and Disease: A Unique Launch of a Unique Journal

Author

Levin, Adeera, primary, Clase, Catherine M, additional, Sood, Manish M, additional, Dicks, Elizabeth, additional, Fortin, Marie-Chantal, additional, Hartwig, Sunny, additional, Holden, Rachel, additional, Lafrance, Jean-Philippe, additional, Molzahn, Anita, additional, Rosenblum, Norman, additional, Samuel, Susan, additional, and Soroka, Steven, additional

Published
2014
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26. The transcription factor sry‐related HMG box‐4 (SOX4) is required for normal renal development in vivo

Author

Huang, Jez, primary, Arsenault, Michel, additional, Kann, Martin, additional, Lopez‐Mendez, Carlos, additional, Saleh, Monique, additional, Wadowska, Dorota, additional, Taglienti, Mary, additional, Ho, Jacqueline, additional, Miao, Yuan, additional, Sims, David, additional, Spears, Jonathan, additional, Lopez, Alfonso, additional, Wright, Glenda, additional, and Hartwig, Sunny, additional

Published
2013
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29. WT1 targets Gas1 to maintain nephron progenitor cells by modulating FGF signals.

Author

Kann, Martin, Eunnyung Bae, Lenz, Maximilian O., Liangji Li, BaoTran Trannguyen, Schumacher, Valerie A., Taglienti, Mary E., Bordeianou, Liliana, Hartwig, Sunny, Rinschen, Markus M., Schermer, Bernhard, Benzing, Thomas, Chen-Ming Fan, and Kreidberg, Jordan A.

Subjects
KIDNEY tubules, PROGENITOR cells, TRANSCRIPTION factors, TUMOR suppressor genes, GENE expression, MESSENGER RNA
Abstract

Development of the metanephric kidney depends on tightly regulated interplay between self-renewal and differentiation of a nephron progenitor cell (NPC) pool. Several key factors required for the survival of NPCs have been identified, including fibroblast growth factor (FGF) signaling and the transcription factor Wilms' tumor suppressor 1 (WT1). Here, we present evidence that WT1 modulates FGF signaling by activating the expression of growth arrest-specific 1 (Gas1), a novel WT1 target gene and novel modulator of FGF signaling. We show that WT1 directly binds to a conserved DNA binding motif within the Gas1 promoter and activates Gas1 mRNA transcription in NPCs. We confirm that WT1 is required for Gas1 expression in kidneys in vivo. Loss of function of GAS1 in vivo results in hypoplastic kidneys with reduced nephron mass due to premature depletion of NPCs. Although kidney development in Gas1 knockout mice progresses normally until E15.5, NPCs show decreased rates of proliferation at this stage and are depleted as of E17.5. Lastly, we show that Gas1 is selectively required for FGF-stimulated AKT signaling in vitro. In summary, our data suggest a model in which WT1 modulates receptor tyrosine kinase signaling in NPCs by directing the expression of Gas1. [ABSTRACT FROM AUTHOR]

Published
2015
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33. Integrin-Linked Kinase Mediates Bone Morphogenetic Protein 7-Dependent Renal Epithelial Cell Morphogenesis.

Author

Chungyee Leung-Hagesteijn, Ming Chang Hu, Mahendra, Ahalya S., Hartwig, Sunny, Klamut, Henry J., Rosenblum, Norman D., and Hannigan, Gregory E.

Subjects
BONE morphogenetic proteins, MITOGENS, EPITHELIAL cells, KIDNEYS, MOLECULES
Abstract

Bone morphogenetic protein 7 (BMP7) stimulates renal branching morphogenesis via p38 mitogen-activated protein kinase (p38MAPK) and activating transcription factor 2 (ATF-2) (M. C. Hu, D. Wasserman, S. Hartwig, and N. B. Rosenblum, 1 Biol. Chem. 279:12051-12059, 2004). Here, we demonstrate a novel role for integrinlinked kinase (ILK) in mediating renal epithelial cell morphogenesis in embryonic kidney explants and identify p38MAPK as a target of ILK signaling in a cell culture model of renal epithelial morphogenesis. The spatial and temporal expression of ILK in embryonic mouse kidney cells suggested a role in branching morphogenesis. Adenovirus-mediated expression of ILK stimulated and expression of a dominant negative ILK mutant inhibited ureteric bud branching in embryonic mouse kidney explants. BMP7 increased ILK kinase activity in inner medullary collecting duct 3 (IMCD-3) cells, and adenovirus-mediated expression of ILK increased IMCD-3 cell morphogenesis in a three-dimensional culture model. In contrast, treatment with a small molecule ILK inhibitor or expression of a dominant negative-acting ILK (ILKE359K) inhibited epithelial cell morphogenesis. Further, expression of ILKE359K abrogated BMP7-dependent stimulation. To investigate the role of ILK in BMP7 signaling, we showed that ILK overexpression increased basal and BMP7-induced levels of phospho-p38MAPK and phospho-ATF-2. Consistent with its inhibitory effects on IMCD-3 cell morphogenesis, expression of ILKE359K blocked BMP7-dependent increases in phospho-p38MAPK and phospho-ATF-2. Inhibition of p38MAPK activity with the specific inhibitor, SB203580, failed to inhibit BMP7-dependent stimulation of ILK activity, suggesting that ILK functions upstream of p38MAPK during BMP7 signaling. We conclude that ILK functions in a BMP7/p38MAPK/ATF-2 signaling pathway and stimulates epithelial cell morphogenesis. [ABSTRACT FROM AUTHOR]

Published
2005
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37. P38MAPK Acts in the BMP7-dependent Stimulatory Pathway during Epithelial Cell Morphogenesis and Is Regulated by Smadl1.

Author

Ming Chang Hu, Wasserman, David, Hartwig, Sunny, and osenblum, Norman D.

Subjects
*EPITHELIAL cells, *MORPHOGENESIS, *TRANSFORMING growth factors-beta, *GLYCOPROTEINS, *PEPTIDE hormones, *PHOSPHORYLATION, *GROWTH factors, *PROTEIN kinases
Abstract

Bone morphogenetic protein (BMP)-7 exerts dose-dependent stimulatory and inhibitory effects during renal branching morphogenesis. Previously, we identified an inhibitory role for activin-like kinase receptors and Smad1 in BMP-dependent inhibition (Piscione, T. D., Phan, T., and Rosenblum, N. D. (2001) Am. J. Physiol. 280, F19-F33). Here we demonstrate a novel role for p38 mitogen-activated kinase (p38MAPK) in BMP7-dependent stimulatory signaling. Stimulatory doses (0.25 nM) of BMP7 increased p38MAPK activity and stimulated phosphorylation of endogenous activating transcription factot 2 (ATF2) in a p38MAPK-dependent manner in murine inner medullary collecting duct (mIMCD-3) cells. In contrast, high doses (10 nM) of BMP7 inhibited p38MAPK activity and phosphorylation of endogenous ATF2. Treatment with BMP7 exerted no significant effect on the levels of the phosphorylated forms of endogenous SAPK/JNK or p44 and p42 (ERK1 and ERK2) protein kinases. To investigate the functional importance of p38MAPK signaling, we showed that SB203580, a p38MAPK inhibitor, blocked the stimulatory effect of BMP7 on mIMCD-3 cell morphogenesis but had no effect on BMP7dependent inhibition in a three-dimensional culture model. To identify mechanisms by which BMP7-dependent inhibitory signaling suppresses p38MAPK activity, we measured p38MAPK activity in ligand independent mIMCD-3 models of enhanced and suppressed Smad signaling. Basal activity of p38MAPK was decreased in mIMCD-3 cells and in embryonic kidney tissue expressing a constitutively active activin-like kinase receptor, but was increased in mIMCD-3 cells stably expressing a dominant negative form of Smad1. We conclude that BMP7 stimulates renal epithelial cell morphogenesis via p38MAPK and that p38MAPK activity is negatively regulated by Smad1. [ABSTRACT FROM AUTHOR]

Published
2004
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