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3. Ankyrin-B dysfunction predisposes to arrhythmogenic cardiomyopathy and is amenable to therapy

Author

Roberts, Jason D, Murphy, Nathaniel P, Hamilton, Robert M, Lubbers, Ellen R, James, Cynthia A, Kline, Crystal F, Gollob, Michael H, Krahn, Andrew D, Sturm, Amy C, Musa, Hassan, El-Refaey, Mona, Koenig, Sara, Aneq, Meriam Åström, Hoorntje, Edgar T, Graw, Sharon L, Davies, Robert W, Rafiq, Muhammad Arshad, Koopmann, Tamara T, Aafaqi, Shabana, Fatah, Meena, Chiasson, David A, Taylor, Matthew RG, Simmons, Samantha L, Han, Mei, van Opbergen, Chantal JM, Wold, Loren E, Sinagra, Gianfranco, Mittal, Kirti, Tichnell, Crystal, Murray, Brittney, Codima, Alberto, Nazer, Babak, Nguyen, Duy T, Marcus, Frank I, Sobriera, Nara, Lodder, Elisabeth M, van den Berg, Maarten P, Spears, Danna A, Robinson, John F, Ursell, Philip C, Green, Anna K, Skanes, Allan C, Tang, Anthony S, Gardner, Martin J, Hegele, Robert A, van Veen, Toon AB, Wilde, Arthur AM, Healey, Jeff S, Janssen, Paul ML, Mestroni, Luisa, van Tintelen, J Peter, Calkins, Hugh, Judge, Daniel P, Hund, Thomas J, Scheinman, Melvin M, and Mohler, Peter J

Subjects
Heart Disease, Cardiovascular, Clinical Research, Rare Diseases, 2.1 Biological and endogenous factors, Aetiology, Animals, Ankyrins, Arrhythmogenic Right Ventricular Dysplasia, Disease Models, Animal, Female, Humans, Indoles, Male, Maleimides, Mice, Mice, Knockout, Myocardium, Wnt Signaling Pathway, beta Catenin, Arrhythmias, Cardiology, Cardiovascular disease, Cell Biology, Genetic diseases, Medical and Health Sciences, Immunology
Abstract

Arrhythmogenic cardiomyopathy (ACM) is an inherited arrhythmia syndrome characterized by severe structural and electrical cardiac phenotypes, including myocardial fibrofatty replacement and sudden cardiac death. Clinical management of ACM is largely palliative, owing to an absence of therapies that target its underlying pathophysiology, which stems partially from our limited insight into the condition. Following identification of deceased ACM probands possessing ANK2 rare variants and evidence of ankyrin-B loss of function on cardiac tissue analysis, an ANK2 mouse model was found to develop dramatic structural abnormalities reflective of human ACM, including biventricular dilation, reduced ejection fraction, cardiac fibrosis, and premature death. Desmosomal structure and function appeared preserved in diseased human and murine specimens in the presence of markedly abnormal β-catenin expression and patterning, leading to identification of a previously unknown interaction between ankyrin-B and β-catenin. A pharmacological activator of the WNT/β-catenin pathway, SB-216763, successfully prevented and partially reversed the murine ACM phenotypes. Our findings introduce what we believe to be a new pathway for ACM, a role of ankyrin-B in cardiac structure and signaling, a molecular link between ankyrin-B and β-catenin, and evidence for targeted activation of the WNT/β-catenin pathway as a potential treatment for this disease.

Published
2019

8. Arabidopsis CML13 and CML14 Have Essential and Overlapping Roles in Plant Development.

Author

Symonds, Kyle, Teresinski, Howard, Hau, Bryan, Chiasson, David, Benidickson, Kirsten, Plaxton, William, and Snedden, Wayne A

Subjects
PLANT development, CALCIUM-binding proteins, PLANT proteins, ARABIDOPSIS, PLANT RNA, GERMINATION, CALCIUM-dependent potassium channels
Abstract

Calmodulin (CaM)-like proteins (CMLs) are the largest family of calcium-binding proteins in plants, yet the functions of most CMLs are unknown. Arabidopsis CML13 and CML14 are closely related paralogs that interact with the isoleucine–glutamine (IQ) domains of myosins, IQ-domain proteins and CaM-binding transcription activators (CAMTAs). Here, we explored the physiological roles of CML13 and CML14 during development by using dexamethasone (Dex)-inducible RNA silencing to suppress either CML13 or CML14 transcript levels. In the absence of inducible suppression, CML13 - and CML14 -RNA-interference lines were indistinguishable from wild-type (WT) plants throughout development. In contrast, induction of silencing treatment led to rapid increases in RNA-hairpin production that correlated with a targeted reduction in CML13 or CML14 transcript levels and a range of developmental and morphological effects. RNA-suppression treatment did not impair the germination of CML13- or 14 -RNA-interference lines, but these seedlings were chlorotic, displayed high mortality and failed to achieve seedling establishment. Under Dex treatment, seeds of CML13- and CML14 -RNA-interference lines exhibited differential sensitivity to exogenous ABA compared to WT seeds. Induced RNA suppression of mature plants led to reduced silique length, shorter roots and rapid leaf senescence in CML13- and 14 -RNA-interference plants, which correlated with increased gene expression of the senescence marker Senescence-Associated Gene13 (SAG13). Plants induced for RNA suppression at 2 weeks post-germination exhibited a much stronger phenotype than treatment of 3-, 4- or 5-week-old plants. Collectively, our data indicate that both CML13 and CML14 are essential for normal development and function across a broad range of tissues and developmental stages. [ABSTRACT FROM AUTHOR]

Published
2024
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9. Asynchronous Hyperbolic UWB Source-Localization and Self-Localization for Indoor Tracking and Navigation

Author

Chiasson, David (author), Lin, Yuan (author), Kok, M. (author), Shull, Peter (author), Chiasson, David (author), Lin, Yuan (author), Kok, M. (author), and Shull, Peter (author)

Abstract

Hyperbolic localization measures the time difference of arrivals (TDOAs) of signals to determine the location of a wireless source or receiver. Traditional methods depend on precise clock synchronization between nodes so that time measurements from independent devices can be meaningfully compared. Imperfect synchronization is often the dominant source of error. We propose two new message based TDOA equations for hyperbolic localization which require no synchronization and meet or exceed state-of-the-art accuracy. Our approaches leverage anchor nodes that observe each other’s packet arrival times and a novel reformulation of the TDOA equation to reduce the effect of clock drift error. Closed-form equations are derived for computing TDOA in both self-localization and source-localization modes of operation along with bounds on maximum clock drift error. Three experiments are performed including a clock drift simulation, a non-line-of-sight (NLOS) simulation, and an indoor validation experiment on custom ultra wideband (UWB) hardware all of which involved eight anchor nodes and one localizing node in a 128m3 capture volume. Our source-localization approach achieved unprecedented accuracy with lower cost equipment and trivial setup. Our self-localization matched state-of-the art accuracy but with infinite scalability and high privacy. These results could enable economical and infinite density indoor navigation and dramatically reduce the economic cost and increase the accuracy of implementing industrial and commercial tracking applications., Green Open Access added to TU Delft Institutional Repository 'You share, we take care!' - Taverne project https://www.openaccess.nl/en/you-share-we-take-care Otherwise as indicated in the copyright section: the publisher is the copyright holder of this work and the author uses the Dutch legislation to make this work public., Team Manon Kok

Published
2023
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41. Ankyrin-B dysfunction predisposes to arrhythmogenic cardiomyopathy and is amenable to therapy

Author

Roberts, Jason D., Murphy, Nathaniel P., Hamilton, Robert M., Lubbers, Ellen R., James, Cynthia A., Kline, Crystal F., Gollob, Michael H., Krahn, Andrew D., Sturm, Amy C., Musa, Hassan, El-Refaey, Mona, Koenig, Sara, Åström, Meriam, Hoorntje, Edgar T., Graw, Sharon L., Davies, Robert W., Rafiq, Muhammad Arshad, Koopmann, Tamara T., Aafaqi, Shabana, Fatah, Meena, Chiasson, David A., Taylor, Matthew R. G., Simmons, Samantha L., Han, Mei, van Opbergen, Chantal J. M., Wold, Loren E., Sinagra, Gianfranco, Mittal, Kirti, Tichnell, Crystal, Murray, Brittney, Codima, Alberto, Nazer, Babak, Nguyen, Duy T., Marcus, Frank I., Sobriera, Nara, Lodder, Elisabeth M., van den Berg, Maarten P., Spears, Danna A., Robinson, John F., Ursell, Philip C., Gréen, Anna, Skanes, Allan C., Tang, Anthony S., Gardner, Martin J., Hegele, Robert A., van Veen, Toon A. B., Wilde, Arthur A. M., Healey, Jeff S., Janssen, Paul M. L., Mestroni, Luisa, van Tintelen, J. Peter, Calkins, Hugh, Judge, Daniel P., Hund, Thomas J., Scheinman, Melvin M., Mohler, Peter J., Roberts, Jason D., Murphy, Nathaniel P., Hamilton, Robert M., Lubbers, Ellen R., James, Cynthia A., Kline, Crystal F., Gollob, Michael H., Krahn, Andrew D., Sturm, Amy C., Musa, Hassan, El-Refaey, Mona, Koenig, Sara, Åström, Meriam, Hoorntje, Edgar T., Graw, Sharon L., Davies, Robert W., Rafiq, Muhammad Arshad, Koopmann, Tamara T., Aafaqi, Shabana, Fatah, Meena, Chiasson, David A., Taylor, Matthew R. G., Simmons, Samantha L., Han, Mei, van Opbergen, Chantal J. M., Wold, Loren E., Sinagra, Gianfranco, Mittal, Kirti, Tichnell, Crystal, Murray, Brittney, Codima, Alberto, Nazer, Babak, Nguyen, Duy T., Marcus, Frank I., Sobriera, Nara, Lodder, Elisabeth M., van den Berg, Maarten P., Spears, Danna A., Robinson, John F., Ursell, Philip C., Gréen, Anna, Skanes, Allan C., Tang, Anthony S., Gardner, Martin J., Hegele, Robert A., van Veen, Toon A. B., Wilde, Arthur A. M., Healey, Jeff S., Janssen, Paul M. L., Mestroni, Luisa, van Tintelen, J. Peter, Calkins, Hugh, Judge, Daniel P., Hund, Thomas J., Scheinman, Melvin M., and Mohler, Peter J.

Abstract

Arrhythmogenic cardiomyopathy (ACM) is an inherited arrhythmia syndrome characterized by severe structural and electrical cardiac phenotypes, including myocardial fibrofatty replacement and sudden cardiac death. Clinical management of ACM is largely palliative, owing to an absence of therapies that target its underlying pathophysiology, which stems partially from our limited insight into the condition. Following identification of deceased ACM probands possessing ANK2 rare variants and evidence of ankyrin-B loss of function on cardiac tissue analysis, an ANK2 mouse model was found to develop dramatic structural abnormalities reflective of human ACM, including biventricular dilation, reduced ejection fraction, cardiac fibrosis, and premature death. Desmosomal structure and function appeared preserved in diseased human and murine specimens in the presence of markedly abnormal beta-catenin expression and patterning, leading to identification of a previously unknown interaction between ankyrin-B and beta-catenin. A pharmacological activator of the WNT/beta-catenin pathway, SB-216763, successfully prevented and partially reversed the murine ACM phenotypes. Our findings introduce what we believe to be a new pathway for ACM, a role of ankyrin-B in cardiac structure and signaling, a molecular link between ankyrin-B and beta-catenin, and evidence for targeted activation of the WNT/beta-catenin pathway as a potential treatment for this disease., Funding Agencies|Marianne Barrie Philanthropic Fund; Canadian Institutes of Health Research [RN332805]; Netherlands CardioVascular Research Initiative: the Dutch Heart Foundation; Dutch Federation of University Medical Centers; Netherlands Organisation for Health Research and Development; Royal Netherlands Academy of Sciences [CVON-PREDICT 2012-10]; Netherlands Cardiovascular Research Initiative - Dutch Heart Foundation [CVON2012-10 PREDICT CVON2018-30 PREDICT2, CVON2015-12 eDETECT]; Netherlands Organization for Scientific Research (NWO) [040.11.586]; Fondation Leducq [16 CVD 02]; Dr. Francis P. Chiramonte Private Foundation; Leyla Erkan Family Fund for ARVD Research; Robin Shah ARVD Fund at Johns Hopkins; Bogle Foundation; Healing Hearts Foundation; Campanella Family; Patrick J. Harrison Family; Peter French Memorial Foundation; Wilmerding Endowments; NIH [HL135754, HL134824, HL139348, HL135096, HL114383, HL114893, HL137331, HL137325, 2UM1HG006542, UL1 TR 001079]; Ohio State Frick Center; JB Project

Published
2019
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49. Acute heart failure in an 8-year-old diabetic girl

Author

Chiasson, David A., Ipp, Moshe, Benson, Lee, and Silver, Meredith M.

Subjects
Takayasu's arteritis -- Complications, Diabetes in children -- Complications, Heart failure -- Causes of, Health
Abstract

An eight-year old girl with insulin-dependent-diabetes mellitus was admitted to the hospital with breathing difficulties, rapid heart beat, sweating, and vomiting. Examination revealed high blood sugar, no fever, and a blood pH of 7.35 (7.0 is neutral). A chest X-ray showed fluid in the right lobe of the lung and a normal heart size. Electrocardiogram and arterial catheterization of the heart revealed heart failure. Despite exhaustive cardiopulmonary support, the child died a few days later. At autopsy, the patient had a narrowing of the aorta, the main artery of the heart. Although vascular disease is a known complication of diabetes mellitus, large vessel disease does not usually occur, and has not been reported in diabetic patients before the third decade of life. In this case, the underlying disease was not the result of diabetes mellitus. Takayasu disease, a disease that affects the aorta, was identified. In addition to aortic damage, involvement of the coronary arteries and other branches of the aorta was found. This was thought to be responsible for the severe stenosis that caused a heart attack, congestive heart failure, and the death of the patient. Characteristics of Takayasu disease include a lack of pulse in the upper extremities caused by the narrowing and blockage of large arteries. This is the first report of Takayasu disease affecting smaller coronary arteries resulting in a massive heart attack. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1990

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