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Takuhiro Sonoyama Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan

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Masakatsu Sone Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan

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Naohisa Tamura Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan

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Kyoko Honda Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan

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Daisuke Taura Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan

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Katsutoshi Kojima Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan

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Yorihide Fukuda Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan

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Naotetsu Kanamoto Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan

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Masako Miura Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan

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Akihiro Yasoda Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan

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Hiroshi Arai Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan

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Hiroshi Itoh Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan

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Kazuwa Nakao Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan

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) plasma renin activity of non-PA group, IHA group, and APA group at 0900, 2300 and after dexamethasone administration. The median of each value is shown. ACTH, adrenocorticotropic hormone; F, cortisol; PRA, plasma renin activity; dex, dexamethasone. PAC

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-14-0086
Volume/Issue:
Volume 3: Issue 4
Open access
Sarah Zaheer Division of Endocrinology, Metabolism, and Nutrition, Duke University Medical Center, Durham, North Carolina, USA

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Kayla Meyer Division of Endocrinology, Diabetes and Hypertension, Brigham and Women’s Hospital, Boston, Massachusetts, USA

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Rebecca Easly Division of Endocrinology, Diabetes and Hypertension, Brigham and Women’s Hospital, Boston, Massachusetts, USA

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Omar Bayomy Department of Medicine, Brigham and Women’s Hospital, Boston, Massachusetts, USA

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Janet Leung Section of Endocrinology, Virginia Mason Medical Center, Seattle, Washington, USA

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Andrew W Koefoed Division of Endocrinology, Diabetes and Hypertension, Brigham and Women’s Hospital, Boston, Massachusetts, USA

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Mahyar Heydarpour Division of Endocrinology, Diabetes and Hypertension, Brigham and Women’s Hospital, Boston, Massachusetts, USA

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Roy Freeman Harvard Medical School, Boston, Massachusetts, USA
Department of Neurology, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA

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Gail K Adler Division of Endocrinology, Diabetes and Hypertension, Brigham and Women’s Hospital, Boston, Massachusetts, USA
Department of Medicine, Brigham and Women’s Hospital, Boston, Massachusetts, USA
Harvard Medical School, Boston, Massachusetts, USA

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Glucocorticoid use is the most common cause of secondary osteoporosis. Poor skeletal health related to glucocorticoid use is thought to involve inhibition of the Wnt/β-catenin signaling pathway, a key pathway in osteoblastogenesis. Sclerostin, a peptide produced primarily by osteocytes, is an antagonist of the Wnt/β-catenin signaling pathway, raising the possibility that sclerostin is involved in glucocorticoids’ adverse effects on bone. The aim of this study was to determine whether an acute infusion of cosyntropin (i.e. ACTH(1–24)), which increases endogenous cortisol, increases serum sclerostin levels as compared to a placebo infusion. This study was performed using blood samples obtained from a previously published, double-blind, placebo-controlled, randomized, cross-over study among healthy men and women who received infusions of placebo or cosyntropin after being supine and fasted overnight (ClinicalTrials.gov NCT02339506). A total of 17 participants were analyzed. There was a strong correlation (R2 = 0.65, P < 0.0001) between the two baseline sclerostin measurements measured at the start of each visit, and men had a significantly higher average baseline sclerostin compared to women. As anticipated, cosyntropin significantly increased serum cortisol levels, whereas cortisol levels fell during placebo infusion, consistent with the diurnal variation in cortisol. There was no significant effect of cosyntropin as compared to placebo infusions on serum sclerostin over 6–24 h (P = 0.10). In conclusion, this randomized, placebo-controlled study was unable to detect a significant effect of a cosyntropin infusion on serum sclerostin levels in healthy men and women.

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-21-0263
Volume/Issue:
Volume 10: Issue 12
Open access
Arno Téblick Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium

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Ilse Vanhorebeek Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium

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Inge Derese Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium

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An Jacobs Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium

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Renata Haghedooren Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium

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Sofie Maebe Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium

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Gerdien A Zeilmaker-Roest Department of Neonatal & Pediatric Intensive Care, Division of Pediatric Intensive Care, Erasmus MC – Sophia Children’s Hospital, Rotterdam, the Netherlands

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Enno D Wildschut Department of Neonatal & Pediatric Intensive Care, Division of Pediatric Intensive Care, Erasmus MC – Sophia Children’s Hospital, Rotterdam, the Netherlands

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Lies Langouche Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium

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Greet Van den Berghe Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium

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In critically ill adults, high plasma cortisol in the face of low ACTH coincides with high pro-opiomelanocortin (POMC) levels. Glucocorticoids further lower ACTH without affecting POMC. We hypothesized that in pediatric cardiac surgery-induced critical illness, plasma POMC is elevated, plasma ACTH transiently rises intraoperatively but becomes suppressed post-operatively, and glucocorticoid administration amplifies this phenotype. From 53 patients (0–36 months), plasma was obtained pre-operatively, intraoperatively, and on post-operative days 1 and 2. Plasma was also collected from 24 healthy children. In patients, POMC was supra-normal pre-operatively (P < 0.0001) but no longer thereafter (P > 0.05). ACTH was never high in patients. While in glucocorticoid-naive patients ACTH became suppressed by post-operative day 1 (P < 0.0001), glucocorticoid-treated patients had already suppressed ACTH intraoperatively (P ≤ 0.0001). Pre-operatively high POMC, not accompanied by increased plasma ACTH, suggests a centrally activated HPA axis with reduced pituitary processing of POMC into ACTH. Increasing systemic glucocorticoid availability with glucocorticoid treatment accelerated the suppression of plasma ACTH.

Significance statement

Glucocorticoids are often administered during pediatric cardiac surgery. In critically ill children, endogenous systemic glucocorticoid availability is elevated already upon ICU admission while ACTH levels are normal. This hormonal constellation suggests the presence of active feedback inhibition of ACTH. In this study, we have documented that intraoperative administration of glucocorticoids accelerates the suppression of ACTH, resulting in low plasma ACTH already upon ICU admission. Pre-operative plasma POMC, the ACTH precursor, but not ACTH, was increased. This is compatible with a centrally activated HPA axis prior to surgery in young children but reduced processing of POMC into ACTH within the pituitary. These findings suggest that glucocorticoid treatment in the context of pediatric cardiac surgery may amplify pre-existing impaired pituitary processing of the prohormone POMC.

Article Type:
Research Article
Collections:
Adrenal
DOI:
https://doi.org/10.1530/EC-24-0078
Volume/Issue:
Volume 13: Issue 6
Open access
Giovanni Fanni Department of Medical Sciences, Clinical Diabetes and Metabolism, Uppsala University, Uppsala, Sweden

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Petros Katsogiannos Department of Medical Sciences, Clinical Diabetes and Metabolism, Uppsala University, Uppsala, Sweden

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Bipasha Nandi Jui Department of Medical Sciences, Clinical Diabetes and Metabolism, Uppsala University, Uppsala, Sweden

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Magnus Sundbom Department of Surgical Sciences, Uppsala University, Uppsala, Sweden

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Susanne Hetty Department of Medical Sciences, Clinical Diabetes and Metabolism, Uppsala University, Uppsala, Sweden

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Maria J Pereira Department of Medical Sciences, Clinical Diabetes and Metabolism, Uppsala University, Uppsala, Sweden

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Jan W Eriksson Department of Medical Sciences, Clinical Diabetes and Metabolism, Uppsala University, Uppsala, Sweden

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-effects models for differences in hormone levels or AUC OGTT across visits: * P  < 0.05; ** P  < 0.01; *** P  < 0.001. N = 13 (except for glucagon, N = 7). ACTH, adrenocorticotropic hormone; GH, growth hormone; GLP-1, glucagon-like peptide 1; GIP, glucose

Article Type:
Research Article
Collections:
Metabolic Syndrome and Diabetes
DOI:
https://doi.org/10.1530/EC-22-0172
Volume/Issue:
Volume 11: Issue 8
Open access
Janko Sattler Adrenal Steroid Group, ANZAC Research Institute, University of Sydney, Sydney, NSW, Australia
Department of Rheumatology and Clinical Immunology, Charité-University Medicine, Berlin, Germany

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Jinwen Tu Adrenal Steroid Group, ANZAC Research Institute, University of Sydney, Sydney, NSW, Australia
Bone Research Program, ANZAC Research Institute, University of Sydney, Sydney, NSW, Australia
Concord Clinical School, The University of Sydney, Sydney, Australia

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Shihani Stoner Bone Research Program, ANZAC Research Institute, University of Sydney, Sydney, NSW, Australia

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Jingbao Li Bone Research Program, ANZAC Research Institute, University of Sydney, Sydney, NSW, Australia
Key Laboratory for Space Bioscience and Biotechnology, Institute of Special Environmental Biophysics, School of Life Sciences, Northwestern Polytechnical University, Shaanxi, China

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Frank Buttgereit Department of Rheumatology and Clinical Immunology, Charité-University Medicine, Berlin, Germany

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Markus J Seibel Bone Research Program, ANZAC Research Institute, University of Sydney, Sydney, NSW, Australia
Concord Clinical School, The University of Sydney, Sydney, Australia
Department of Endocrinology & Metabolism, Concord Hospital, Sydney, Australia

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Hong Zhou Bone Research Program, ANZAC Research Institute, University of Sydney, Sydney, NSW, Australia
Concord Clinical School, The University of Sydney, Sydney, Australia

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Mark S Cooper Adrenal Steroid Group, ANZAC Research Institute, University of Sydney, Sydney, NSW, Australia
Concord Clinical School, The University of Sydney, Sydney, Australia
Department of Endocrinology & Metabolism, Concord Hospital, Sydney, Australia

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on a joint inflammation intensity scale from 0 to 12 points. Serum assays for corticosterone and adrenocorticotropic hormone Serum samples were collected at 12:00 h, before animals were killed and stored at −80°C until further examination

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-17-0361
Volume/Issue:
Volume 7: Issue 2
Open access
Rachel Forfar Centre for Therapeutics Discovery, LifeArc, Accelerator Building, Open Innovation Campus, Stevenage, UK

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Mashal Hussain Centre for Endocrinology, William Harvey Research Institute, Queen Mary University of London, London, UK

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Puneet Khurana Centre for Therapeutics Discovery, LifeArc, Accelerator Building, Open Innovation Campus, Stevenage, UK

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Jennifer Cook Centre for Therapeutics Discovery, LifeArc, Accelerator Building, Open Innovation Campus, Stevenage, UK

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Steve Lewis Centre for Therapeutics Discovery, LifeArc, Accelerator Building, Open Innovation Campus, Stevenage, UK

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Dillon Popat Centre for Endocrinology, William Harvey Research Institute, Queen Mary University of London, London, UK

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David Jackson Centre for Endocrinology, William Harvey Research Institute, Queen Mary University of London, London, UK

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Ed McIver Centre for Therapeutics Discovery, LifeArc, Accelerator Building, Open Innovation Campus, Stevenage, UK

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Jeff Jerman Centre for Therapeutics Discovery, LifeArc, Accelerator Building, Open Innovation Campus, Stevenage, UK

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Debra Taylor Centre for Therapeutics Discovery, LifeArc, Accelerator Building, Open Innovation Campus, Stevenage, UK

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Adrian JL Clark Centre for Endocrinology, William Harvey Research Institute, Queen Mary University of London, London, UK

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Li F Chan Centre for Endocrinology, William Harvey Research Institute, Queen Mary University of London, London, UK

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Introduction The melanocortins, comprising the α-, β-, and γ-melanocyte-stimulating hormones (MSHs) and adrenocorticotropic hormone (ACTH), are a family of peptide hormones cleaved from the prohormone pro-opiomelanocortin that have a diverse

Article Type:
Research Article
Collections:
Adrenal
DOI:
https://doi.org/10.1530/EC-22-0338
Volume/Issue:
Volume 11: Issue 12
Open access
Amit Kumar Department of Medicine, Christian Medical College and Hospital, Ludhiana, Punjab, India

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Maria Ghosh Department of Biochemistry, Christian Medical College and Hospital, Ludhiana, Punjab, India

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Jubbin Jagan Jacob Department of Endocrinology, Christian Medical College and Hospital, Ludhiana, Punjab, India

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tests and an Acton Prolongatum® (adrenocorticotropic hormone(1–34) (ACTH(1–34)) stimulation test (APST). Inclusion and exclusion criteria Adult patients (≥18 years) with EuVHNa who provided consent were included. Patients were considered to have

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-21-0500
Volume/Issue:
Volume 10: Issue 12
Open access
Nathalia G B P Ferreira Unidade de Endocrinologia do Desenvolvimento, Laboratório de Hormônios e Genética Molecular LIM42, Disciplina de Endocrinologia, Faculdade de Medicina da Universidade de São Paulo (FMUSP), São Paulo, Brazil

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Joao L O Madeira Unidade de Endocrinologia do Desenvolvimento, Laboratório de Hormônios e Genética Molecular LIM42, Disciplina de Endocrinologia, Faculdade de Medicina da Universidade de São Paulo (FMUSP), São Paulo, Brazil

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Peter Gergics Laboratório de Sequenciamento em Larga Escala (SELA), Faculdade de Medicina FMUSP, Universidade de São Paulo, São Paulo, Brazil

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Renata Kertsz Unidade de Endocrinologia do Desenvolvimento, Laboratório de Hormônios e Genética Molecular LIM42, Disciplina de Endocrinologia, Faculdade de Medicina da Universidade de São Paulo (FMUSP), São Paulo, Brazil

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Juliana M Marques Unidade de Endocrinologia do Desenvolvimento, Laboratório de Hormônios e Genética Molecular LIM42, Disciplina de Endocrinologia, Faculdade de Medicina da Universidade de São Paulo (FMUSP), São Paulo, Brazil

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Nicholas S S Trigueiro Unidade de Endocrinologia do Desenvolvimento, Laboratório de Hormônios e Genética Molecular LIM42, Disciplina de Endocrinologia, Faculdade de Medicina da Universidade de São Paulo (FMUSP), São Paulo, Brazil

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Anna Flavia Figueredo Benedetti University of Michigan Medical School, Department of Human Genetics, Ann Arbor, Michigan, United States

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Bruna V Azevedo Unidade de Endocrinologia do Desenvolvimento, Laboratório de Hormônios e Genética Molecular LIM42, Disciplina de Endocrinologia, Faculdade de Medicina da Universidade de São Paulo (FMUSP), São Paulo, Brazil

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Bianca H V Fernandes Unidade de Endocrinologia do Desenvolvimento, Laboratório de Hormônios e Genética Molecular LIM42, Disciplina de Endocrinologia, Faculdade de Medicina da Universidade de São Paulo (FMUSP), São Paulo, Brazil
Universidade de São Paulo, Zebrafish Facility, São Paulo, São Paulo, Brazil

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Debora D Bissegatto Unidade de Endocrinologia do Desenvolvimento, Laboratório de Hormônios e Genética Molecular LIM42, Disciplina de Endocrinologia, Faculdade de Medicina da Universidade de São Paulo (FMUSP), São Paulo, Brazil

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Isabela P Biscotto Unidade de Endocrinologia do Desenvolvimento, Laboratório de Hormônios e Genética Molecular LIM42, Disciplina de Endocrinologia, Faculdade de Medicina da Universidade de São Paulo (FMUSP), São Paulo, Brazil

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Qing Fang Laboratório de Sequenciamento em Larga Escala (SELA), Faculdade de Medicina FMUSP, Universidade de São Paulo, São Paulo, Brazil

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Qianyi Ma Laboratório de Sequenciamento em Larga Escala (SELA), Faculdade de Medicina FMUSP, Universidade de São Paulo, São Paulo, Brazil

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Asye B Ozel Laboratório de Sequenciamento em Larga Escala (SELA), Faculdade de Medicina FMUSP, Universidade de São Paulo, São Paulo, Brazil

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Jun Li Laboratório de Sequenciamento em Larga Escala (SELA), Faculdade de Medicina FMUSP, Universidade de São Paulo, São Paulo, Brazil

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Sally A Camper Laboratório de Sequenciamento em Larga Escala (SELA), Faculdade de Medicina FMUSP, Universidade de São Paulo, São Paulo, Brazil

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Alexander A L Jorge Unidade de Endocrinologia Genética, Laboratório de Endocrinologia Celular e Molecular LIM25, Disciplina de Endocrinologia da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil

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Berenice B Mendonça Unidade de Endocrinologia do Desenvolvimento, Laboratório de Hormônios e Genética Molecular LIM42, Disciplina de Endocrinologia, Faculdade de Medicina da Universidade de São Paulo (FMUSP), São Paulo, Brazil

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Ivo J P Arnhold Unidade de Endocrinologia do Desenvolvimento, Laboratório de Hormônios e Genética Molecular LIM42, Disciplina de Endocrinologia, Faculdade de Medicina da Universidade de São Paulo (FMUSP), São Paulo, Brazil

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Luciani R Carvalho Unidade de Endocrinologia do Desenvolvimento, Laboratório de Hormônios e Genética Molecular LIM42, Disciplina de Endocrinologia, Faculdade de Medicina da Universidade de São Paulo (FMUSP), São Paulo, Brazil

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committee under the number CAAE 0642812.4.0000.0068 Proband A female patient was born from consanguineous parents and presented with CPHD (growth hormone (GH), thyroid-stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), prolactin (PRL

Article Type:
Research Article
Collections:
Paediatric Endocrinology
DOI:
https://doi.org/10.1530/EC-22-0473
Volume/Issue:
Volume 12: Issue 8
Open access
Jan W Eriksson Department of Medical Sciences, Uppsala University, Uppsala, Sweden

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Reem A Emad Department of Pharmacy, Uppsala University, Uppsala, Sweden

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Martin H Lundqvist Department of Medical Sciences, Uppsala University, Uppsala, Sweden

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Niclas Abrahamsson Department of Medical Sciences, Uppsala University, Uppsala, Sweden

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Maria C Kjellsson Department of Pharmacy, Uppsala University, Uppsala, Sweden

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(GH) ( 10 ). Cortisol secretion is primarily regulated by adrenocorticotropic hormone (ACTH), which, in turn, is stimulated by corticotrophin-releasing hormone (CRH) via the hypothalamic–pituitary–adrenal (HPA) axis. A major physiological effect of

Article Type:
Research Article
Collections:
Metabolic Syndrome and Diabetes
DOI:
https://doi.org/10.1530/EC-22-0506
Volume/Issue:
Volume 12: Issue 4
Open access
Fidéline Bonnet-Serrano Université Paris Cité, Paris, France
Inserm U1016-CNRS UMR8104, Paris, France
Hormonology Department, Cochin Hospital, Paris, France

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Maxime Barat Université Paris Cité, Paris, France
Inserm U1016-CNRS UMR8104, Paris, France
Radiology Department, Cochin Hospital, Paris, France

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Anna Vaczlavik Université Paris Cité, Paris, France
Inserm U1016-CNRS UMR8104, Paris, France
Reference Center for Rare Adrenal Diseases, Endocrinology Department, Cochin Hospital, Paris, France

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Anne Jouinot Inserm U1016-CNRS UMR8104, Paris, France

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Lucas Bouys Université Paris Cité, Paris, France
Inserm U1016-CNRS UMR8104, Paris, France
Reference Center for Rare Adrenal Diseases, Endocrinology Department, Cochin Hospital, Paris, France

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Christelle Laguillier-Morizot Université Paris Cité, Paris, France
Hormonology Department, Cochin Hospital, Paris, France
INSERM, Physiopathologie et Pharmacotoxicologie Placentaire Humaine : Microbiote Pré & Post natal, Paris, France

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Corinne Zientek Hormonology Department, Cochin Hospital, Paris, France

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Catherine Simonneau Hormonology Department, Cochin Hospital, Paris, France

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Etienne Larger Université Paris Cité, Paris, France
Inserm U1016-CNRS UMR8104, Paris, France
Diabetology Department, Cochin Hospital, Paris, France

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Laurence Guignat Reference Center for Rare Adrenal Diseases, Endocrinology Department, Cochin Hospital, Paris, France

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Lionel Groussin Université Paris Cité, Paris, France
Inserm U1016-CNRS UMR8104, Paris, France
Reference Center for Rare Adrenal Diseases, Endocrinology Department, Cochin Hospital, Paris, France

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Guillaume Assié Université Paris Cité, Paris, France
Inserm U1016-CNRS UMR8104, Paris, France
Reference Center for Rare Adrenal Diseases, Endocrinology Department, Cochin Hospital, Paris, France

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Jean Guibourdenche Université Paris Cité, Paris, France
Hormonology Department, Cochin Hospital, Paris, France
INSERM, Physiopathologie et Pharmacotoxicologie Placentaire Humaine : Microbiote Pré & Post natal, Paris, France

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Ioannis Nicolis Université Paris Cité, Paris, France
UR 7537 BioSTM, Paris, France

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Marie-Claude Menet Institut de Chimie Physique, Université Paris-Saclay-CNRS, UMR8000, Orsay, France

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Jérôme Bertherat Université Paris Cité, Paris, France
Inserm U1016-CNRS UMR8104, Paris, France
Reference Center for Rare Adrenal Diseases, Endocrinology Department, Cochin Hospital, Paris, France

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G-protein coupled membrane receptors, responsible for a cortisol response to non-physiological stimuli ( 8 , 9 , 10 ). The second one is the secretion of an ectopic intra-adrenal adrenocorticotropic hormone (ACTH) by clusters of adrenocortical

Article Type:
Research Article
Collections:
Adrenal
DOI:
https://doi.org/10.1530/EC-22-0063
Volume/Issue:
Volume 11: Issue 8
Open access