Search

Your search keyword '"Kwak, Brenda R"' showing total 577 results
Start Over Author "Kwak, Brenda R"
577 results on '"Kwak, Brenda R"'

1. IMproving Preclinical Assessment of Cardioprotective Therapies (IMPACT): a small animal acute myocardial infarction randomized-controlled multicenter study on the effect of ischemic preconditioning

Author

Hernandez-Resendiz, Sauri, Vilskersts, Reinis, Aluja, David, Andreadou, Ioanna, Bencsik, Péter, Dambrova, Maija, Efentakis, Panagiotis, Gao, Fei, Giricz, Zoltán, Inserte, Javier, Kelly-Laubscher, Roisin, Kiss, Attila, Krieg, Thomas, Kwak, Brenda R., Lecour, Sandrine, Lopaschuk, Gary, Mączewski, Michał, Waszkiewicz, Michał, Oknińska, Marta, Pagliaro, Pasquale, Podesser, Bruno, Prag, Hiran A., Ruiz-Meana, Marisol, Szabados, Tamara, Zuurbier, Coert J., Ferdinandy, Péter, and Hausenloy, Derek J.

Published
2025
Full Text
View/download PDF

3. Unravelling molecular mechanisms in atherosclerosis using cellular models and omics technologies

Author

Kardassis, Dimitris, Vindis, Cécile, Stancu, Camelia Sorina, Toma, Laura, Gafencu, Anca Violeta, Georgescu, Adriana, Alexandru-Moise, Nicoleta, Molica, Filippo, Kwak, Brenda R., Burlacu, Alexandrina, Hall, Ignacio Fernando, Butoi, Elena, Magni, Paolo, Wu, Junxi, Novella, Susana, Gamon, Luke F., Davies, Michael J., Caporali, Andrea, de la Cuesta, Fernando, and Mitić, Tijana

Published
2025
Full Text
View/download PDF

7. Consensus guidelines for the use and interpretation of angiogenesis assays

Author

Nowak-Sliwinska, Patrycja, Alitalo, Kari, Allen, Elizabeth, Anisimov, Andrey, Aplin, Alfred C, Auerbach, Robert, Augustin, Hellmut G, Bates, David O, van Beijnum, Judy R, Bender, R Hugh F, Bergers, Gabriele, Bikfalvi, Andreas, Bischoff, Joyce, Böck, Barbara C, Brooks, Peter C, Bussolino, Federico, Cakir, Bertan, Carmeliet, Peter, Castranova, Daniel, Cimpean, Anca M, Cleaver, Ondine, Coukos, George, Davis, George E, De Palma, Michele, Dimberg, Anna, Dings, Ruud PM, Djonov, Valentin, Dudley, Andrew C, Dufton, Neil P, Fendt, Sarah-Maria, Ferrara, Napoleone, Fruttiger, Marcus, Fukumura, Dai, Ghesquière, Bart, Gong, Yan, Griffin, Robert J, Harris, Adrian L, Hughes, Christopher CW, Hultgren, Nan W, Iruela-Arispe, M Luisa, Irving, Melita, Jain, Rakesh K, Kalluri, Raghu, Kalucka, Joanna, Kerbel, Robert S, Kitajewski, Jan, Klaassen, Ingeborg, Kleinmann, Hynda K, Koolwijk, Pieter, Kuczynski, Elisabeth, Kwak, Brenda R, Marien, Koen, Melero-Martin, Juan M, Munn, Lance L, Nicosia, Roberto F, Noel, Agnes, Nurro, Jussi, Olsson, Anna-Karin, Petrova, Tatiana V, Pietras, Kristian, Pili, Roberto, Pollard, Jeffrey W, Post, Mark J, Quax, Paul HA, Rabinovich, Gabriel A, Raica, Marius, Randi, Anna M, Ribatti, Domenico, Ruegg, Curzio, Schlingemann, Reinier O, Schulte-Merker, Stefan, Smith, Lois EH, Song, Jonathan W, Stacker, Steven A, Stalin, Jimmy, Stratman, Amber N, Van de Velde, Maureen, van Hinsbergh, Victor WM, Vermeulen, Peter B, Waltenberger, Johannes, Weinstein, Brant M, Xin, Hong, Yetkin-Arik, Bahar, Yla-Herttuala, Seppo, Yoder, Mervin C, and Griffioen, Arjan W

Subjects
Biochemistry and Cell Biology, Biological Sciences, Cardiovascular, Animals, Biological Assay, Guidelines as Topic, Humans, Mice, Neoplasms, Neovascularization, Pathologic, Angiogenesis, Aortic ring, Endothelial cell migration, Proliferation, Microfluidic, Zebrafish, Chorioallantoic membrane, Vascular network, Intussusceptive angiogenesis, Retinal vasculature, Corneal angiogenesis, Hindlimb ischemia, Myocardial angiogenesis, Recombinant proteins, Tip cells, Plug assay, Vessel co-option, Clinical Sciences, Pharmacology and Pharmaceutical Sciences, Oncology & Carcinogenesis, Biochemistry and cell biology
Abstract

The formation of new blood vessels, or angiogenesis, is a complex process that plays important roles in growth and development, tissue and organ regeneration, as well as numerous pathological conditions. Angiogenesis undergoes multiple discrete steps that can be individually evaluated and quantified by a large number of bioassays. These independent assessments hold advantages but also have limitations. This article describes in vivo, ex vivo, and in vitro bioassays that are available for the evaluation of angiogenesis and highlights critical aspects that are relevant for their execution and proper interpretation. As such, this collaborative work is the first edition of consensus guidelines on angiogenesis bioassays to serve for current and future reference.

Published
2018

8. Protective role of Pannexin1 in lymphatic endothelial cells in the progression of atherosclerosis in female mice.

Author

Ehrlich, Avigail, Pelli, Graziano, Foglia, Bernard, Molica, Filippo, and Kwak, Brenda R.

Subjects
HIGH cholesterol diet, ATHEROSCLEROTIC plaque, ARTERIAL diseases, FREE fatty acids, BLOOD cholesterol
Abstract

Atherosclerosis is a progressive arterial disease arising from imbalanced lipid metabolism and a maladaptive immune response. The lymphatic system ensures tissue fluid homeostasis, absorption of dietary fats and trafficking of immune cells to draining lymph nodes, thereby potentially affecting atherogenesis. Endothelial cell-specific deletion of Pannexin1 (Panx1) in apolipoprotein E-deficient (Apoe-/-) mice increased atherosclerosis, suggesting a protective role for Panx1 channels in arterial endothelial function. Here, we investigated the role of Panx1 in lymphatic endothelial cells (LECs) in the initiation and the progression of atherosclerosis. Male or female Prox1-CreERT2+Panx1fl/flApoe-/- and Panx1fl/flApoe-/- mice were fed a high cholesterol diet (HCD) for 6 or 10 weeks. Tamoxifen-induced deletion of Panx1 was performed before or after 4 weeks of HCD. Body weight and serum lipid profiles were determined. The atherosclerotic plaque burden was assessed by Sudan-IV staining on thoracic-abdominal aortas and in aortic roots. Plaque composition was determined by immunohistochemistry. No differences in serum cholesterol, LDL and HDL were observed between genotypes and between sexes after HCD. Bodyweight, serum triglycerides and free fatty acid levels were higher before and after 6 weeks of HCD in male Prox1-CreERT2+Panx1fl/flApoe-/- and control Panx1fl/flApoe-/- mice compared to females of the same genotypes, which was associated with more lipids and inflammatory cells in their atherosclerotic plaques. In contrast, the atherosclerotic plaque burden was higher in female mice. The progression of atherosclerosis in male mice was not different between genotypes. However, female Prox1-CreERT2+Panx1fl/flApoe-/- mice showed enhanced progression of atherosclerosis compared to Panx1fl/flApoe-/- controls of the same sex. In addition, atherosclerotic lesions in female, but not in male, Prox1-CreERT2+Panx1fl/flApoe-/- mice showed T cell enrichment. Altogether, our results reveal differential sex-dependent effects of Panx1 in lymphatic endothelium on the progression of atherosclerosis. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

9. Non-canonical roles of connexins

Author

Van Campenhout, Raf, Cooreman, Axelle, Leroy, Kaat, Rusiecka, Olga M., Van Brantegem, Pieter, Annaert, Pieter, Muyldermans, Serge, Devoogdt, Nick, Cogliati, Bruno, Kwak, Brenda R., and Vinken, Mathieu

Published
2020
Full Text
View/download PDF

15. Cold Exposure Rejuvenates the Metabolic Phenotype of Panx1 −/− Mice.

Author

Molica, Filippo, Ehrlich, Avigail, Pelli, Graziano, Rusiecka, Olga M., Montessuit, Christophe, Chanson, Marc, and Kwak, Brenda R.

Subjects
WHITE adipose tissue, FATTY acid oxidation, ADIPOSE tissues, INSULIN sensitivity, FAT cells
Abstract

Pannexin1 (Panx1) ATP channels are important in adipocyte biology, potentially influencing energy storage and expenditure. We compared the metabolic phenotype of young (14 weeks old) and mature (20 weeks old) wild-type (WT) and Panx1−/− mice exposed or not to cold (6 °C) during 28 days, a condition promoting adipocyte browning. Young Panx1−/− mice weighed less and exhibited increased fat mass, improved glucose tolerance, and lower insulin sensitivity than WT mice. Their energy expenditure and respiratory exchange ratio (RER) were increased, and their fatty acid oxidation decreased. These metabolic effects were no longer observed in mature Panx1−/− mice. The exposure of mature mice to cold exacerbated their younger metabolic phenotype. The white adipose tissue (WAT) of cold-exposed Panx1−/− mice contained more small-sized adipocytes, but, in contrast to WT mice, white adipocytes did not increase their expression of Ucp1 nor of other markers of browning adipocytes. Interestingly, Glut4 expression was already enhanced in the WAT of young Panx1−/− mice kept at 22 °C as compared to WT mice. Thus, Panx1 deletion exerts overall beneficial metabolic effects in mice that are pre-adapted to chronic cold exposure. Panx1−/− mice show morphological characteristics of WAT browning, which are exacerbated upon cold exposure, an effect that appears to be associated with Ucp1-independent thermogenesis. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

16. Pannexin1 deletion in lymphatic endothelium affects lymphatic function in a sex‐dependent manner.

Author

Ehrlich, Avigail, Pelli, Graziano, Pick, Robert, Clochard, Linda, Molica, Filippo, and Kwak, Brenda R.

Subjects
FREE fatty acids, ENDOTHELIUM, DIETARY fats, EXTRACELLULAR fluid, LYMPHATICS, DELETION mutation
Abstract

The lymphatic network of capillaries and collecting vessels ensures tissue fluid homeostasis, absorption of dietary fats and trafficking of immune cells. Pannexin1 (Panx1) channels allow for the passage of ions and small metabolites between the cytosol and extracellular environment. Panx1 channels regulate the pathophysiological function of several tissues in a sex‐dependent manner. Here, we studied the role of Panx1 in lymphatic function, and potential sex‐dependent differences therein, in Prox1‐CreERT2Panx1fl/fl and Panx1fl/fl control mice. Panx1 expression was higher in lymphatic endothelial cells (LECs) of male mice. Lymphatic vessel morphology was not affected in Prox1‐CreERT2Panx1fl/fl male and female mice. Lymphatic drainage was decreased by 25% in male Prox1‐CreERT2Panx1fl/fl mice, but was similar in females of both genotypes. Accordingly, only male Prox1‐CreERT2Panx1fl/fl mice exhibited tail swelling, pointing to interstitial fluid accumulation in males upon Panx1 deletion in LECs. Moreover, serum triglyceride and free fatty acid levels raised less in Prox1‐CreERT2Panx1fl/fl mice of both sexes in an oral lipid tolerance test. Finally, the percentage of migratory dendritic cells arriving in draining lymph nodes was increased in Prox1‐CreERT2Panx1fl/fl female mice, but was comparable between male mice of both genotypes. Our results point to a LEC‐specific role for Panx1 in the functions of the lymphatic system. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

18. Structure-Based Design and Synthesis of Stapled 10Panx1 Analogues for Use in Cardiovascular Inflammatory Diseases

Author

Lamouroux, Arthur, primary, Tournier, Malaury, additional, Iaculli, Debora, additional, Caufriez, Anne, additional, Rusiecka, Olga M., additional, Martin, Charlotte, additional, Bes, Viviane, additional, Carpio, Laureano E., additional, Girardin, Yana, additional, Loris, Remy, additional, Tabernilla, Andrés, additional, Molica, Filippo, additional, Gozalbes, Rafael, additional, Mayán, María D., additional, Vinken, Mathieu, additional, Kwak, Brenda R., additional, and Ballet, Steven, additional

Published
2023
Full Text
View/download PDF

21. Interplay of Connexins and Pannexins in Tissue Function and Disease

Author

Martin, Patricia and Kwak, Brenda R.

Abstract

This Special Issue is related to the 18th biannual International Gap Junction Conference (IGJC2017), which has been held at the Crowne Plaza Hotel, Glasgow and hosted by Glasgow Caledonian University, 29 July–3 August, 2017. This Special Issue, entitled “Interplay of Connexins and Pannexins in Tissue Function and Disease”, focuses on six key state-of-the-art reviews, written by leads in the field on cutting edge topics and the latest developments in clinical trials in diverse organ systems. A further 14 original articles contributed by delegates attending the meeting are also included and celebrate 50 years of Gap Junction Research. Topics: Connexins and Pannexins: Trafficking, Assembly, Gating, and Protein–Protein Interactions Roles in the Cardiovascular System Roles in Tumorigenesis Roles in Epithelial Tissue and Wound Healing Connexin Therapy Translated to Clinic

Published
2018

22. Artery-Associated Sympathetic Innervation Drives Rhythmic Vascular Inflammation of Arteries and Veins

Author

de Juan, Alba, Ince, Louise Madeleine, Pick, Robert, Chen, Chien-Sin, Molica, Filippo, Zuchtriegel, Gabriele, Wang, Chen, Zhang, Dachuan, Druzd, David, Hessenauer, Maximilian E.T., Pelli, Graziano, Kolbe, Isa, Oster, Henrik, Prophete, Colette, Hergenhan, Sophia Martina, Albrecht, Urs, Ripperger, Jürgen, Montanez, Eloi, Reichel, Christoph A., Soehnlein, Oliver, Kwak, Brenda R., Frenette, Paul S., and Scheiermann, Christoph

Published
2019
Full Text
View/download PDF

24. Mitochondrial pannexin1 controls cardiac sensitivity to ischaemia/reperfusion injury

Author

Rusiecka, Olga M, Molica, Filippo, Nielsen, Morten S, Tollance, Axel, Morel, Sandrine, Frieden, Maud, Chanson, Marc, Boengler, Kerstin, Kwak, Brenda R, Rusiecka, Olga M, Molica, Filippo, Nielsen, Morten S, Tollance, Axel, Morel, Sandrine, Frieden, Maud, Chanson, Marc, Boengler, Kerstin, and Kwak, Brenda R

Abstract

AIMS: No effective therapy is available in clinics to protect the heart from ischaemia/reperfusion (I/R) injury. Endothelial cells are activated after I/R, which may drive the inflammatory response by releasing ATP through pannexin1 (Panx1) channels. Here, we investigated the role of Panx1 in cardiac I/R.METHODS AND RESULTS: Panx1 was found in cardiac endothelial cells, neutrophils, and cardiomyocytes. After in vivo I/R, serum Troponin-I, and infarct size were less pronounced in Panx1-/- mice, but leukocyte infiltration in the infarct area was similar between Panx1-/- and wild-type mice. Serum Troponin-I and infarct size were not different between mice with neutrophil-specific deletion of Panx1 and Panx1fl/fl mice, suggesting that cardioprotection by Panx1 deletion rather involved cardiomyocytes than the inflammatory response. Physiological cardiac function in wild-type and Panx1-/- hearts was similar. The time to onset of contracture and time to maximal contracture were delayed in Panx1-/- hearts, suggesting reduced sensitivity of these hearts to ischaemic injury. Moreover, Panx1-/- hearts showed better recovery of left ventricle developed pressure, cardiac contractility, and relaxation after I/R. Ischaemic preconditioning failed to confer further protection in Panx1-/- hearts. Panx1 was found in subsarcolemmal mitochondria (SSM). SSM in WT or Panx1-/- hearts showed no differences in morphology. The function of the mitochondrial permeability transition pore and production of reactive oxygen species in SSM was not affected, but mitochondrial respiration was reduced in Panx1-/- SSM. Finally, Panx1-/- cardiomyocytes had a decreased mitochondrial membrane potential and an increased mitochondrial ATP content.CONCLUSION: Panx1-/- mice display decreased sensitivity to cardiac I/R injury, resulting in smaller infarcts and improved recovery of left ventricular function. This cardioprotective effect of Panx1 deletion seems to involve cardiac mitochondria rat

Published
2023

30. Exosomes secreted by cardiomyocytes subjected to ischaemia promote cardiac angiogenesis

Author

Ribeiro-Rodrigues, Teresa M., Laundos, Tiago L., Pereira-Carvalho, Rita, Batista-Almeida, Daniela, Pereira, Ricardo, Coelho-Santos, Vanessa, Silva, Ana P., Fernandes, Rosa, Zuzarte, Monica, Enguita, Francisco J., Costa, Marina C., Pinto-do-Ó, Perpetua, Pinto, Marta T., Gouveia, Pedro, Ferreira, Lino, Mason, Justin C., Pereira, Paulo, Kwak, Brenda R., Nascimento, Diana S., and Girão, Henrique

Published
2017
Full Text
View/download PDF

31. FOXC2 and fluid shear stress stabilize postnatal lymphatic vasculature

Author

Sabine, Amelie, Bovay, Esther, Demir, Cansaran Saygili, Kimura, Wataru, Jaquet, Muriel, Agalarov, Yan, Zangger, Nadine, Scallan, Joshua P., Graber, Werner, Gulpinar, Elgin, Kwak, Brenda R., Makinen, Taija, Martinez-Corral, Ines, Ortega, Sagrario, Delorenzi, Mauro, Kiefer, Friedemann, Davis, Michael J., Djonov, Valentin, Miura, Naoyuki, and Petrova, Tatiana V.

Subjects
Physiological aspects, Health aspects, Lymphatic vessels -- Physiological aspects, Shear (Mechanics) -- Physiological aspects, Transcription factors -- Health aspects
Abstract

Introduction Active and complex signaling is involved both in the growth of new vessels and their stabilization and maintenance. Blood vessel stabilization encompasses proliferation arrest, restoration of the vascular barrier [...], Biomechanical forces, such as fluid shear stress, govern multiple aspects of endothelial cell biology. In blood vessels, disturbed flow is associated with vascular diseases, such as atherosclerosis, and promotes endothelial cell proliferation and apoptosis. Here, we identified an important role for disturbed flow in lymphatic vessels, in which it cooperates with the transcription factor FOXC2 to ensure lifelong stability of the lymphatic vasculature. In cultured lymphatic endothelial cells, FOXC2 inactivation conferred abnormal shear stress sensing, promoting junction disassembly and entry into the cell cycle. Loss of FOXC2-dependent quiescence was mediated by the Hippo pathway transcriptional coactivator TAZ and, ultimately, led to cell death. In murine models, inducible deletion of Foxc2 within the lymphatic vasculature led to cell-cell junction defects, regression of valves, and focal vascular lumen collapse, which triggered generalized lymphatic vascular dysfunction and lethality. Together, our work describes a fundamental mechanism by which FOXC2 and oscillatory shear stress maintain lymphatic endothelial cell quiescence through intercellular junction and cytoskeleton stabilization and provides an essential link between biomechanical forces and endothelial cell identity that is necessary for postnatal vessel homeostasis. As FOXC2 is mutated in lymphedema-distichiasis syndrome, our data also underscore the role of impaired mechanotransduction in the pathology of this hereditary human disease.

Published
2015
Full Text
View/download PDF

38. Exploring intracranial aneurysm instability markers to improve disease modeling

Author

Dupuy, Nicolas, Juchler, Norman, Morel, Sandrine, Kwak, Brenda R., Hirsch, Sven, Bijlenga, Philippe, Dupuy, Nicolas, Juchler, Norman, Morel, Sandrine, Kwak, Brenda R., Hirsch, Sven, and Bijlenga, Philippe

Abstract

Intracranial aneurysm (IA) shape is proposed to be a predicting factor of rupture. In this study, using 3D-angiographies, surgical and histological images, we ranked 11 IAs according to different characteristics (homogeneity, aspect and thickness), and correlations between the different ranking systems were investigated. We showed positive correlations between IA morphology (normalized total Gaussian curvature, GLN) and wall aspect ranking, and between GLN and histology ranking. Correlations between increased GLN, inhomogeneity of IA wall aspect and thickness were shown. This exploratory study supports the GLN in its ability to quantify IA shape and to be used as an IA wall feature predictor.

Published
2022

39. Neutralization of S100A4 induces stabilization of atherosclerotic plaques:role of smooth muscle cells

Author

Sakic, Antonija, Chaabane, Chiraz, Ambartsumian, Noona, Klingelhofer, Jörg, Lemeille, Sylvain, Kwak, Brenda R., Grigorian, Mariam, Bochaton-Piallat, Marie-Luce, Sakic, Antonija, Chaabane, Chiraz, Ambartsumian, Noona, Klingelhofer, Jörg, Lemeille, Sylvain, Kwak, Brenda R., Grigorian, Mariam, and Bochaton-Piallat, Marie-Luce

Abstract

Aims During atherosclerosis, smooth muscle cells (SMCs) accumulate in the intima where they switch from a contractile to a synthetic phenotype. From porcine coronary artery, we isolated spindle-shaped (S) SMCs exhibiting features of the contractile phenotype and rhomboid (R) SMCs typical of the synthetic phenotype. S100A4 was identified as a marker of R-SMCs in vitro and intimal SMCs, in pig and man. S100A4 exhibits intra- and extracellular functions. In this study, we investigated the role of extracellular S100A4 in SMC phenotypic transition.Methods and results S-SMCs were treated with oligomeric recombinant S100A4 (oS100A4), which induced nuclear factor (NF)-kappa B activation. Treatment of S-SMCs with oS100A4 in combination with platelet-derived growth factor (PDGF)-BB induced a complete SMC transition towards a pro-inflammatory R-phenotype associated with NF-kappa B activation, through toll-like receptor-4. RNA sequencing of cells treated with oS100A4/PDGF-BB revealed a strong up-regulation of pro-inflammatory genes and enrichment of transcription factor binding sites essential for SMC phenotypic transition. In a mouse model of established atherosclerosis, neutralization of extracellular S100A4 decreased area of atherosclerotic lesions, necrotic core, and CD68 expression and increased alpha-smooth muscle actin and smooth muscle myosin heavy chain expression.Conclusion We suggest that the neutralization of extracellular S100A4 promotes the stabilization of atherosclerotic plaques. Extracellular S100A4 could be a new target to influence the evolution of atherosclerotic plaques.

Published
2022

42. Peptide Inhibitors Based on the C-Terminal Tail of Connexin43

Author

Iaculli, Debora, Lamouroux, Arthur, Montgomery, Jade, Vinken, Mathieu, Kwak, Brenda R., Ballet, Steven, Faculty of Sciences and Bioengineering Sciences, Chemistry, Organic Chemistry, Pharmaceutical and Pharmacological Sciences, and Experimental in vitro toxicology and dermato-cosmetology

Published
2022
Full Text
View/download PDF

45. Novel methodologies for biomarker discovery in atherosclerosis

Author

Hoefer, Imo E., Steffens, Sabine, Ala-Korpela, Mika, Bäck, Magnus, Badimon, Lina, Bochaton-Piallat, Marie-Luce, Boulanger, Chantal M., Caligiuri, Giuseppina, Dimmeler, Stefanie, Egido, Jesus, Evans, Paul C., Guzik, Tomasz, Kwak, Brenda R., Landmesser, Ulf, Mayr, Manuel, Monaco, Claudia, Pasterkamp, Gerard, Tuñón, Jose, and Weber, Christian

Published
2015
Full Text
View/download PDF

48. Activation of the Hypoxia-Inducible Factor Pathway Inhibits Epithelial Sodium Channel–Mediated Sodium Transport in Collecting Duct Principal Cells

Author

Dizin, Eva, primary, Olivier, Valérie, additional, Roth, Isabelle, additional, Sassi, Ali, additional, Arnoux, Grégoire, additional, Ramakrishnan, Suresh, additional, Morel, Sandrine, additional, Kwak, Brenda R., additional, Loffing, Johannes, additional, Hummler, Edith, additional, Wenger, Roland H., additional, Frew, Ian J., additional, and Feraille, Eric, additional

Published
2021
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results