Relevant bibliographies by topics / Atrial differentiation

Academic literature on the topic 'Atrial differentiation'

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Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Atrial differentiation"

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Mesquita, Fernanda C. P., Jacquelynn Morrissey, Po-Feng Lee, Gustavo Monnerat, Yutao Xi, Helen Andersson, Fabio C. S. Nogueira, et al. "Cues from human atrial extracellular matrix enrich the atrial differentiation of human induced pluripotent stem cell-derived cardiomyocytes." Biomaterials Science 9, no. 10 (2021): 3737–49. http://dx.doi.org/10.1039/d0bm01686a.

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Decellularized extracellular matrix (dECM) from human atria preserves key native components that directed the cardiac differentiation of hiPSCs to an atrial-like phenotype, yielding a twofold increase of functional atrial-like cells.
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Rautaharju, Pentti M. "Differentiation of atrial flutter from atrial fibrillation." Journal of Electrocardiology 33, no. 2 (April 2000): 203. http://dx.doi.org/10.1016/s0022-0736(00)80078-3.

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Davies, M. J., J. Rode, N. Woolf, and D. M. Krikler. "NEUROENDOCRINE DIFFERENTIATION IN ATRIAL MYXOMAS." Lancet 330, no. 8562 (October 1987): 800. http://dx.doi.org/10.1016/s0140-6736(87)92533-5.

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Knight, Bradley P., Gregory F. Michaud, S. Adam Strickberger, and Fred Morady. "Electrocardiographic differentiation of atrial flutter from atrial fibrillation by physicians." Journal of Electrocardiology 32, no. 4 (October 1999): 315–19. http://dx.doi.org/10.1016/s0022-0736(99)90002-x.

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Muir, T. M., J. Hair, G. C. Inglis, J. W. Dow, G. B. Lindop, and B. J. Leckie. "Dexamethasone-induced differentiation of atrial myocytes in culture." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 3 (September 1, 1992): H722—H729. http://dx.doi.org/10.1152/ajpheart.1992.263.3.h722.

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Atrial and ventricular myocytes from fetal and newborn rats were cultured in medium supplemented with fetal or newborn calf serum with and without glucocorticoid. Myocyte morphology was examined by light and electron microscopy, and the amount of stored and secreted atrial natriuretic peptide (ANP) was measured. Without dexamethasone, neonatal atrial myocytes cultured for 7 days contained myofibrils organized into sarcomeres and numerous endocrine granules containing immunostainable ANP. Secretion of immunoreactive ANP reached a peak between days 7 and 9 of culture. Myocytes from fetal rats secreted ANP but contained few endocrine granules, and myofilaments were poorly organized. By contrast, the addition of dexamethasone (1 nM-1 microM) to the culture medium of newborn myocytes promoted development of numerous endocrine storage granules, mitochondria, and myofibrils with prominent Z-bands. Dexamethasone also increased the cellular content of ANP and ANP-specific mRNA in both atrial and ventricular myocytes. In the presence of dexamethasone myocytes maintained their structural integrity for periods of at least 45 days.
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Schwach, Verena, Carla Cofiño-Fabres, Simone A. ten Den, and Robert Passier. "Improved Atrial Differentiation of Human Pluripotent Stem Cells by Activation of Retinoic Acid Receptor Alpha (RARα)." Journal of Personalized Medicine 12, no. 4 (April 13, 2022): 628. http://dx.doi.org/10.3390/jpm12040628.

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Human pluripotent stem cell (hPSC)-derived cardiomyocytes have proven valuable for modeling disease and as a drug screening platform. Here, we depict an optimized protocol for the directed differentiation of hPSCs toward cardiomyocytes with an atrial identity by modulating the retinoic acid signaling cascade in spin embryoid bodies. The crucial steps of the protocol, including hPSC maintenance, embryoid body (EB) differentiation, the induction of cardiac mesoderm, direction toward the atrial phenotype, as well as molecular and functional characterization of the cardiomyocytes, are described. Atrial cardiomyocytes (AMs) can be generated within 14 days. Most importantly, we show that induction of the specific retinoic acid receptor alpha (RARα) increased the efficiency of atrial differentiation to 72% compared with 45% after modulating the retinoic acid (RA) pathway with all-trans RA (atRA). In contrast, the induction of RARβ signaling only had a minor impact on the efficiency of atrial differentiation (from about 45% to 50%). Similarly, the total yield of AM per EB of 5000 hPSCs was increased from 10,350 (2.07 per hPSC) to 16,120 (3.22 per hPSC) while selectively modulating RARα signaling. For further purification of the AMs, we describe a metabolic selection procedure that enhanced the AM percentage to more than 90% without compromising the AM yield (15,542 per EB, equal to 3.11 per hPSC) or functionality of the AMs as evaluated by RNAseq, immunostaining, and optical action potential measurement. Cardiomyocytes with distinct atrial and ventricular properties can be applied for selective pharmacology, such as the development of novel atrial-specific anti-arrhythmic agents, and disease modeling, including atrial fibrillation, which is the most common heart rhythm disorder. Moreover, fully characterized and defined cardiac subtype populations are of the utmost importance for potential cell-based therapeutic approaches.
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Kallstrom, Eric, Elizabeth Kallus, Krista Erbe, Michael Rampoldi, Don Le, and Neeley Bryan. "Differentiation of Left Atrial Myxomas by Multimodality Imaging." Journal of Diagnostic Medical Sonography 36, no. 1 (August 27, 2019): 52–63. http://dx.doi.org/10.1177/8756479319872153.

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A tumor is an excessive growth of cells that results from the body’s inability to balance the growth of new cells and the destruction of old cells. Tumors can occur throughout the body and are classified as either benign or malignant. However, cardiac tumors are a rare occurrence. When present, several imaging modalities are available to illustrate their presence and characteristics. Not all cardiac masses look similar and, depending on their size and location, may pose different health risks to the patient. This case series introduces six left atrial myxomas with dissimilar appearances initially detected by transthoracic echocardiography, along with cross-correlation by transesophageal echocardiography, computed tomography, and mechanical resonance imaging.
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Wolke, Carmen, Elmer Antileo, and Uwe Lendeckel. "WNT signaling in atrial fibrillation." Experimental Biology and Medicine 246, no. 9 (February 27, 2021): 1112–20. http://dx.doi.org/10.1177/1535370221994086.

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The Wnt signaling pathway regulates physiological processes such as cell proliferation and differentiation, cell fate decisions, and stem cell maintenance and, thus, plays essential roles in embryonic development, but also in adult tissue homeostasis and repair. The Wnt signaling pathway has been associated with heart development and repair and has been shown to be crucially involved in proliferation and differentiation of progenitor cells into cardiomyocytes. The investigation of the role of the Wnt signaling pathway and the regulation of its expression/activity in atrial fibrillation has only just begun. The present minireview (I) provides original data regarding the expression of Wnt signaling components in atrial tissue of patients with atrial fibrillation or sinus rhythm and (II) summarizes the current state of knowledge of the regulation of Wnt signaling components’ expression/activity and the contribution of the various levels of the Wnt signal transduction pathway to the processes of the development, maintenance, and progression of atrial fibrillation.
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Yao, Yao, Amanda N. Marra, and Deborah Yelon. "Pathways Regulating Establishment and Maintenance of Cardiac Chamber Identity in Zebrafish." Journal of Cardiovascular Development and Disease 8, no. 2 (January 29, 2021): 13. http://dx.doi.org/10.3390/jcdd8020013.

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The vertebrate heart is comprised of two types of chambers—ventricles and atria—that have unique morphological and physiological properties. Effective cardiac function depends upon the distinct characteristics of ventricular and atrial cardiomyocytes, raising interest in the genetic pathways that regulate chamber-specific traits. Chamber identity seems to be specified in the early embryo by signals that establish ventricular and atrial progenitor populations and trigger distinct differentiation pathways. Intriguingly, chamber-specific features appear to require active reinforcement, even after myocardial differentiation is underway, suggesting plasticity of chamber identity within the developing heart. Here, we review the utility of the zebrafish as a model organism for studying the mechanisms that establish and maintain cardiac chamber identity. By combining genetic and embryological approaches, work in zebrafish has revealed multiple players with potent influences on chamber fate specification and commitment. Going forward, analysis of cardiomyocyte identity at the single-cell level is likely to yield a high-resolution understanding of the pathways that link the relevant players together, and these insights will have the potential to inform future strategies in cardiac tissue engineering.
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Hotchkiss, Adam, Tiam Feridooni, Mark Baguma-Nibasheka, Kathleen McNeil, Sarita Chinni, and Kishore B. S. Pasumarthi. "Atrial natriuretic peptide inhibits cell cycle activity of embryonic cardiac progenitor cells via its NPRA receptor signaling axis." American Journal of Physiology-Cell Physiology 308, no. 7 (April 1, 2015): C557—C569. http://dx.doi.org/10.1152/ajpcell.00323.2014.

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The biological effects of atrial natriuretic peptide (ANP) are mediated by natriuretic peptide receptors (NPRs), which can either activate guanylyl cyclase (NPRA and NPRB) or inhibit adenylyl cyclase (NPRC) to modulate intracellular cGMP or cAMP, respectively. During cardiac development, ANP serves as an early maker of differentiating atrial and ventricular chamber myocardium. As development proceeds, expression of ANP persists in the atria but declines in the ventricles. Currently, it is not known whether ANP is secreted or the ANP-NPR signaling system plays any active role in the developing ventricles. Thus the primary aims of this study were to 1) examine biological activity of ANP signaling systems in embryonic ventricular myocardium, and 2) determine whether ANP signaling modulates proliferation/differentiation of undifferentiated cardiac progenitor cells (CPCs) and/or cardiomyocytes. Here, we provide evidence that ANP synthesized in embryonic day (E)11.5 ventricular myocytes is actively secreted and processed to its biologically active form. Notably, NPRA and NPRC were detected in E11.5 ventricles and exogenous ANP stimulated production of cGMP in ventricular cell cultures. Furthermore, we showed that exogenous ANP significantly decreased cell number and DNA synthesis of CPCs but not cardiomyocytes and this effect could be reversed by pretreatment with the NPRA receptor-specific inhibitor A71915. ANP treatment also led to a robust increase in nuclear p27 levels in CPCs compared with cardiomyocytes. Collectively, these data provide evidence that in the developing mammalian ventricles ANP plays a local paracrine role in regulating the balance between CPC proliferation and differentiation via NPRA/cGMP-mediated signaling pathways.
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Dissertations / Theses on the topic "Atrial differentiation"

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Jambi, Majed. "Differentiation of Human Atrial Myocytes from Endothelial Progenitor Cell-Derived Induced Pluripotent Stem Cells." Thèse, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/31158.

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Recent advances in cellular reprogramming have enabled the generation of embryoniclike cells from virtually any cell of the body. These inducible pluripotent stem cells (iPSCs) are capable of indefinite self-renewal while maintaining the ability to differentiate into all cell types. Nowhere will this technology have a greater impact than in the ability to generate disease and patient-specific cell lines. Here we explore the capacity of human iPSCs reprogrammed from peripheral blood endothelial progenitor cells lines to differentiate into atrial myocytes for the study of patient specific atrial physiology. Methods and Results: Late outgrowth endothelial progenitor cells (EPCs) cultured from clinical blood samples provided a robust cell source for genetic reprogramming. Transcriptome analysis hinted that EPCs would be comparatively more amenable to pluripotent reprogramming than the traditional dermal fibroblast. After 6 passages, EPCs were transduced with a doxycycline inducible lentivirus system encoding human transcription factors OCT4, SOX2, KLF4 and Nanog to permit differentiation after removal of doxycycline. The high endogenous expression of key pluripotency transcripts enhanced the ease of iPSC generation as demonstrated by the rapid emergence of typical iPSC colonies. Following removal of doxycycline, genetically reprogrammed EPC-iPSC colonies displayed phenotypic characteristics identical to human embryonic stem cells and expressed high levels of the pluripotent markers SSEA-4, TRA1-60 and TRA1-81. After exposure to conditions known to favor atrial identity, EPC- iPSC differentiating into sheets of beating cardiomyocytes that expressed high levels of several atrial-specific expressed genes (CACNA1H, KCNA5, and MYL4). Conclusions: EPCs provide a stable platform for genetic reprogramming into a pluripotent state using a doxycycline conditional expression system that avoids reexpression of oncogenic/pluripotent factors. Human EPC-derived iPSC can be differentiated into functional cardiomyocytes that express characteristic markers of atrial identity.
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GIANNETTI, FEDERICA. "HIPS AND MES AS A CELLULAR MODEL TO STUDY THE MECHANISMS BEHIND ARRHYTHMIAS." Doctoral thesis, Università degli Studi di Milano, 2022. http://hdl.handle.net/2434/903405.

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Mouse embryonic stem cells (mESc) and human induced pluripotent stem cells (hiPSc) are commonly exploited in research for their ability to potentially differentiate into any cell subtype. Regarding cardiac differentiation, today's existing protocols are well advanced in recapitulating and promoting cardiomyocytes (CMs) differentiation, making CMs derived from mESc and hiPSc a good in vitro model for analyzing heart pathologies. In this thesis, these models have been used to characterize and better comprehend the functional output caused by genetic alterations. In the first part, mESc-derived cardiomyocytes help to elucidate the electrical dysregulation produced by the knock-out of Striatin (STRN), a scaffold protein with a role in organizing subcellular multiprotein complexes. STRN loss has been found in patients with dilated cardiomyopathy (DCM) and its mutation linked to DCM and ARVC in dogs. However, STRN physiological role in the cardiac context is not yet clear, for this reason the electrical characterization, by patch-clamp analysis, of mouse embryonic stem cells mESc-derived cardiomyocytes (mCMs) knock out for the STRN gene (STRN-KO) may help elucidating STRN role and its pathological implications. In this context, action potential (AP) analysis showed a higher rate and upstroke velocity of STRN-KO mCMs compared to its isogenic WT control. Accordingly, a significantly larger INa current density, responsible of the phase 0, was found in STRN-KO than in WT mCMs, while the other currents analyzed (If, ICaL and IKr) were similar. Literature data show that downregulation of STRN destabilize microtubules, and their disassembling increases sodium current in neonatal cardiomyocytes. Here is shown that treating STRN-KO mCMs with the microtubule stabilizer Taxol (10 μM) reverted INa density to values similar to WT cells. These data lead to the conclusion that STRN loss affects the electrical properties of mCMs likely acting on cytoskeleton stability and consequently on sodium channels trafficking and/or activity, creating a substrate more prone to develop arrhythmias. In the second part of the thesis, hiPSc-derived cardiomyocytes, obtained from a patient with atrial fibrillation (AF)carrying a heterozygous GOF point mutation in the PITX2 gene, are used to distinguish if this genetic condition predispose or AF. In GWAS studies, PITX2 is the genetic locus most associated with AF, it is often dysregulated in AF patients and its presence or absence correlates with electrical alterations. Moreover, PITX2 loss of function in zebrafish has been linked to perturbations of metabolic pathways forerunning AF-like phenotypes. APs recorded from small hiPSc-derived CMs (hpCMs) clusters reveals that PITX2-hpCMs are bradycardic, with a larger action potential amplitude and a shorter action potential duration than to three unrelated controls. Moreover, preliminary data obtained from atrial hiPSc-derived CMs, used to further elucidate the consequence of this mutation in the atrial background, showed no differences in ICaL and If densities; however, activation curve of If is negatively shifted with a higher inverse slope factor in PITX2 atrial hiPSc-derived CMs, implying a minor contribution of this current during the slow diastolic depolarization. Seahorse metabolic analysis indicates that PITX2-haCMs generates more ATP compared to isogenic control, and this difference is due to increased oxidative phosphorylation in mitochondria. In conclusion, although a more detailed characterization will be required, the PITX2 GOF mutation seems to enhance oxidative phosphorylation and a slower beating rate, altering not only the electrical activity but also the metabolism of cardiomyocytes. Overall, these in vitro models of cardiomyocytes were ideal to identify the functional outcome of genetic alteration, either to investigate the electrical mechanism behind arrhythmias or to characterize the role of a specific protein in the specific cardiac context.
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Huber, Adrian Thomas. "Multi-organ non-invasive tissue characterization of fibrosis, adipose tissue, edema and inflammation with magnetic resonance (MR) imaging : applications to myocardium, skeletal muscle and liver interactions Cardiac MR strain: a noninvasive biomarker of fibro-fatty remodeling of the left atrial myocardium Comparison of MR T1 and T2 mapping parameters to characterize myocardial and skeletal muscle involvement in systemic Idiopathic Inflammatory Myopathy (IIM) Non-invasive differentiation of acute viral myocarditis and idiopathic inflammatory myopathy with cardiac involvement using magnetic resonance imaging T1 and T2 mapping CT predicts liver fibrosis: Prospective evaluation of morphology- and attenuationbased quantitative scores in routine portal venous abdominal scans." Thesis, Sorbonne université, 2019. http://www.theses.fr/2019SORUS135.

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Cette thèse réalise une preuve de concept pour quantifier la déformation de l’oreillette gauche (OG) en IRM, ainsi que la relaxométrie IRM dans le myocarde, dans les muscles squelettiques et dans le foie. Grâce à l’interaction entre radiologues et ingénieurs, deux logiciels différents ont été développés, appliqués et validés pour l'analyse de la déformation myocardique multi-chambre et pour la cartographie quantitative du T1 multi-organes. La première publication a montré une forte corrélation de la déformation de l’OG, avec le degré de remplacement fibro-graisseux en histologie. Ce biomarqueur d'imagerie fonctionnelle est prometteur, puisque le remodelage structurel du myocarde est un substrat morphologique connu du dysfonctionnement électro-physiologique et de la fibrillation atriale. La deuxième publication a démontré l'influence de la composition et de la vascularisation de différents tissus sur les paramètres cartographiques T1. ΔT1 (prise de contraste musculaire relative) et EHF (prise de contraste musculaire normalisée par la prise de contraste dans le sang) ont été introduits comme alternatives simples au volume extracellulaire (ECV). Dans la troisième publication, les paramètres de relaxométrie appliqués aux muscles squelettiques ont permis une discrimination entre patients avec myocardite aiguë et patients avec des myosites systémiques. La quatrième publication a introduit le T1 du foie pour quantifier l’insuffisance cardiaque chez des patients avec des cardiomyopathies idiopathiques dilatées, montrant de meilleures performances que les paramètres fonctionnels établis tels que les volumes, la fraction d'éjection ou la déformation myocardique
This thesis provides a proof of concept for MR atrial strain, as well as MR relaxometry in the myocardium, in skeletal muscles and in the liver. Thanks to a close interaction between radiologist and software engineers, two different softwares were developed, applied and validated: one for multiorgan T1 mapping in the myocardium, skeletal muscle and liver, another one for cardiac four-chamber strain analysis and volumetry. The first publication showed a strong correlation of LA strain with the degree of fibro-fatty replacement in histology. Such functional imaging biomarker in combination with LA volumetry could help to guide clinical decisions, since myocardial structural remodeling is a known morphologic substrate of LA dysfunction, atrial fibrillation and adverse outcome. In the second publication, MR relaxometry parameters applied to the myocardium and skeletal muscles in IIM patients and healthy volunteers were used as a model to demonstrate influences of different tissue composition and vascularization on T1 mapping parameters. ΔT1 and EHF were introduced as simple alternatives to ECV in highly vascularized tissues such as the myocardium. In the third publication, MR relaxometry parameters applied to the skeletal muscls allowed for an accurate discrimination of AVM and IIM with cardiac involvement. However, when applied to the myocardium, parametric mapping did not separate between the two groups. The fourth publication introduced native T1 of the liver an easily accessible and accurate non-invasive imaging associate of congestive HF in IDCM patients with better performance than established functional parameters such as LV volumes, ejection fraction or strain
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Baik, Hayeon. "Role of the SUMO pathway in Acute Myeloid Leukemias response to treatments." Thesis, Montpellier, 2017. http://www.theses.fr/2017MONTT016/document.

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Les thérapies de différenciation sont une alternative prometteuse aux drogues génotoxiques utilisées en chimiothérapie pour le traitement de nombreux cancers. En particulier, l’acide tout-trans rétinoïque (ATRA) est utilisé avec succès pour traiter la leucémie aiguë promyélocytaire, un sous-type des leucémies aiguës myéloïdes (LAM). Malheureusement, son efficacité clinique est limitée dans les autres sous-types des LAM. Cela est en particulier du à une répression épigénétique des gènes de réponse à l’ATRA. Les SUMO constituent une famille de modificateurs post-traductionnels apparentés à l’ubiquitine dont la conjugaison sur de nombreuses protéines, appelée sumoylation, est impliquée dans la régulation de nombreux processus cellulaires, dont la transcription. Dans ce contexte, l’objective de ma thèse a été de comprendre le rôle de la sumoylation dans la réponse des LAM aux thérapies de différenciation. Nous avons pu montrer que la sumoylation réprime la différenciation induite par ATRA dans plusieurs lignées cellulaires, des cellules primaires de patients y compris celles résistantes à la chimiothérapie. L’inhibition de la sumoylation par les inhibiteurs pharmacologiques ou la surexpression des désumoylases augmente de façon remarquable la différenciation par ATRA et, à l’inverse l’augmentation de la sumoylation suite à une surexpression de SUMO ou son enzyme de conjugaison Ubc9 réduit fortement l’efficacité d’ATRA. L’ATRA synergise avec l’inhibition de la sumoylation pour limiter la prolifération des cellules de LAM in vitro et in vivo. D’un point de vue mécanistique, l’inhibition de la sumoylation favorise la différenciation des cellules de LAM en facilitant l’expression des gènes responsables de la différenciation myéloïde. Ainsi, cibler la sumoylation constitue une approche prometteuse pour sensibiliser la LAM aux thérapies de différenciation
Differentiation therapies are a promising alternative to genotoxic-based chemotherapies in the treatment of many cancers. In particular, All-trans-retinoic acid (ATRA) is successfully used for Acute Promyelocytic Leukemias, a subtype of Acute Myeloid Leukemias. However, its clinical efficiency is very limited in the other AML subtypes, in particular because of epigenetic repression of ATRA-responsive genes. SUMOs are a family of post-translational modifiers related to ubiquitin and their conjugation, sumoylation, to their substrate proteins regulate many processes including gene transcription. The aim of my thesis was to understand the role of sumoylation in AML responses to treatments. I showed that sumoylation represses ATRA-induced differentiation in many AML cell lines and primary patient samples, including those resistant to chemotherapies. Inhibition of sumoylation with pharmacological inhibitors or overexpression of desumoylases markedly increased their differentiation by ATRA and increasing sumoylation by overexpression of SUMO or its conjugating enzyme Ubc9 strongly reduce ATRA efficiency. Inhibition of sumoylation synergize with ATRA to arrest AML cells proliferation both in vitro and in vivo. Mechanistically, inhibition of sumoylation primes AML cells for differentiation by facilitating the expression of master genes of the myeloid differentiation. Targeting the SUMO pathway thus constitute a promising approach to sensitize AML to differentiation therapies
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Salvatico, Jose. "The Expression of MKRN1, an E3 Ubiquitin Ligase for Telomerase Reverse Transcriptase, Is Induced with Differentiation Therapy in Leukemia." Master's thesis, University of Central Florida, 2009. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/3744.

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Telomeres are important structural and functional components of chromosomes, serving to provide stability and enabling full replication of the chromosomes. However, a shortening of the telomeres occurs with each cell division that can be fixed by a polymerase activity provided by telomerase, preventing this loss which would otherwise eventually lead to chromosome end-to-end fusions, senescence and cell death. The telomerase activity is present in stem cells and germ line cells, but absent or barely noticeable in adult somatic cells. However, in approximately 80-90% of transformed somatic cells the telomerase activity is recovered, resulting in a "telomerase positive phenotype". This phenotype has been a prime target in cancer research, and recently a novel mechanism for regulating telomerase levels has been uncovered. Makorin 1 RING finger protein (MKRN1) was found to be an E3 ubiquitin ligase for hTERT, the rate-limiting catalytic component of telomerase, leading to the ubiqutin-mediated 26s proteasomal degradation of hTERT and reduced telomerase activity. So, MKRN1 plays a role in telomere homeostasis. In this study we looked at the expression of MKRN1 in numerous tumor cell lines (Hela, HCT116, HL60) and the normal diploid fibroblasts (WI-38). In the latter cell line, basal levels of MKRN1 were found to increase 6-fold when the cells were serum starved and arrested in G1/G0. In contrast, the cancer cell lines expressed MKRN1 at low levels or undetectable. This would indicate that MKRN1 is up-regulated in resting or G1 arrested cells.In one cell line the promyelocytic leukemia, HL-60, showed no protein levels of MKRN1. This cell line is able to be terminally differentiated upon ATRA treatment, when cells are arrested at G1. In this model system of cellular differentiation hTERT mRNA levels and telomerase activity decrease drastically and quickly. We hypothesized that the differentiation of HL-60 induced by ATRA would be accompanied by an increase in MKRN1 levels. MKRN1 mRNA and protein levels were strongly up-regulated during the ATRA-mediated differentiation of HL-60 cells. Although, a decrease in hTERT mRNA is a contributor to telomerase inhibition during cellular differentiation; our data indicate that the up-regulation of MKRN1 ensures the effective removal of residual telomerase activity by the ubiquitin-mediated degradation pathway at the proteasome.
M.S.
Department of Molecular Biology and Microbiology
Burnett College of Biomedical Sciences
Molecular and Microbiology MS
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Kårehed, Karin. "Signal Transduction in Malignant Cells – Transformation, Activation and Differentiation." Doctoral thesis, Uppsala University, Department of Genetics and Pathology, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6346.

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All aspects of cell life are regulated by signal transduction mechanisms. This thesis describes the regulatory roles of a few key signal transduction molecules involved in three major biological responses. The studied pathways include platelet derived growth factor (PDGF)-BB induced transformation of murine fibroblasts, interferon (IFN)-γ stimulated monocyte activation and all-trans retinoic acid (ATRA) induced myeloid differentiation.

We found that intact phosphoinositide 3OH-kinase (PI3K) activity is essential in the signaling pathway that leads to the morphological alterations and migration pattern characteristic of PDGF-BB transformed NIH/sis and NIH/COL1A1 fibroblasts. Furthermore, our data indicated that the small Rho-GTPase, Rac1 is the predominant mediator of these signals downstream of PI3K.

The study of the IFN-γ induced activation of monocytic U-937 cells showed that upregulation of the high affinity receptor for IgG (FcγRI) is dependent on the coordination of several regulatory events: the PKR-mediated serine 727 phosphorylation of Stat1, the expression of the hematopoietic lineage specific transcription factor PU.I, and the activation of the NFκB pathway.

ATRA-induced differentiation and cell cycle arrest are impaired in U-937 sublines expressing phosphorylation deficient Stat1 (Stat1Y701F and Stat1S727A). The findings in paper III indicated that the expression pattern of the myeloid specific transcription factors Stat2, ICSBP and c/EBPε was altered in the sublines and that intact Stat1 activation is critical for maintaining the balance of the transcriptional network during ATRA induced terminal differentiation.

Finally, ATRA-induced differentiation and growth arrest were blocked by treatment with the IKKα/β inhibitor BMS345541 or by ectopic expression of the NFκB super repressor IκBα (S32A/S36A). The fact that IκB(AA) sublines differentiated normally in response to vitamin D3, showed that NFκB inhibition specifically affected ATRA induced responses. Notably we suggest that the activity of the NFκB pathway may interfere with the differentiation process via a direct effect on the RAR/RXR mediated transcription.

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Dimberg, Anna. "The Role of Stat1 in Retinoic Acid-induced Myelomonocytic Differentiation of Human Leukemia Cells." Doctoral thesis, Uppsala University, Department of Genetics and Pathology, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-1669.

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All-trans retinoic acid (ATRA), a biologically active metabolite of vitamin A, is a powerful inducer of terminal differentiation and growth arrest of several myeloid cell lines in vitro. Although the efficacy of ATRA as an anti-cancer drug has been demonstrated by the successful treatment of acute promyelocytic leukemia (APL), knowledge concerning the molecular mechanisms directing ATRA-induced differentiation and cell cycle arrest of myeloid cells is lacking. Our results show, for the first time, that the complex regulation of cell cycle proteins and myeloid-specific transcription factors induced by ATRA relies on functional Stat1. We found that Stat1 is activated by both tyrosine-701 and serine-727 phosphorylation upon ATRA-induced differentiation of the human monoblastic cell line U-937. Expression of phosphorylation deficient mutants of Stat1 (Stat1Y701F or Stat1S727A) inhibited both ATRA-induced differentiation and cell cycle arrest of U-937 cells, pointing to a requirement of active Stat1 in these processes.

Detailed analysis of the molecular mechanism of ATRA-induced cell cycle arrest and differentiation showed that the onset of cell cycle arrest was associated with a decrease in c-Myc and cyclin E levels and upregulation of p27Kip1 and p21WAF1/CIP1. This was followed by a rapid fall in cyclin A and B and a coordinate dephosphorylation of the retinoblastoma protein (pRb). The inhibition of ATRA-induced cell-cycle arrest by constitutive expression of Stat1Y701F or Stat1S727A was associated with impaired regulation of these cyclins and p27Kip1, positioning Stat1 activation upstream of these events. To further understand the process of ATRA-induced differentiation, the regulation of myeloid-specific transcription factors was investigated during ATRA-treatment. Notably, ATRA-induced upregulation of Stat2, ICSBP and C/EBP-ε was selectively impaired in sublines expressing Stat1Y701F or Stat1S727A, suggesting an important function of these factors downstream Stat1. Taken together, the work in this thesis clearly demonstrates that Stat1 plays a key role in ATRA-induced terminal differentiation of myeloid cells, through regulation of cell cycle proteins and myeloid-specific transcription factors.

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Hotchkiss, Adam Gordon. "The Effects of Calcium Channel Blockade and Atrial Natriuretic Peptide Signalling on Proliferation and Differentiation of Cardiac Progenitor Cells." 2013. http://hdl.handle.net/10222/36236.

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Cardiac progenitor cells (CPCs) are abundant in the embryonic heart and have hallmark features which include a rapid rate of cell division and the ability to differentiate into mature heart muscle cells (cardiomyocytes). Based on these features, CPCs are considered an attractive candidate cell type for transplantation therapies which aim to replenish the diseased heart muscle tissue (myocardium) with new muscle forming cells. A better understanding of how pharmacological drugs and endogenous hormones/signalling molecules modulate the balance between proliferation and differentiation of CPCs could be used to develop more effective cell based therapies for myocardial repair. Furthermore, this information could provide valuable new insight into molecular mechanisms regulating normal cardiogenesis during the embryonic period. The specific aims of the present study were to characterize the effects of the Ca2+ channel blocking drug nifedipine and the endogenous hormone/paracrine factor atrial natriuretic peptide (ANP) on CPC proliferation and differentiation. Results showed that primary cultured CPCs, isolated from the ventricles of embryonic day (E) 11.5 mouse embryos, underwent a reduction in cell cycle activity following exposure to nifedipine. Furthermore, systemic administration of nifedipine to adult mice receiving transplanted E11.5 ventricular cells (containing CPCs) was associated with smaller graft sizes compared to control animals that did not receive the drug. Results from the present study also demonstrated that ANP receptor mediated signalling systems are biologically active in E11.5 ventricular cells and have an antiproliferative effect on cultured E11.5 CPCs. Moreover, preliminary data provided evidence that genetic ablation of the ANP high affinity receptor (NPRA) may be associated with impaired development of the ventricular cardiac conduction system. Collectively, work from this thesis provides evidence that interactions between transplanted cells and pharmacological drugs could have a significant impact on the effectiveness of cell based therapies and that ANP signalling systems may play a critical role in cardiac ontogeny by regulating the balance between CPC proliferation and differentiation.
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Li, I.-Ting, and 李伊婷. "The anti-inflammatory role of apoptotic ATRA-NB4 cells in the resolution of differentiation syndrome." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/12833815224409163853.

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碩士
國立陽明大學
生理學研究所
100
All- trans retinoic acid (ATRA) has been used successfully in the treatment of acute promyelocytic leukemia (APL). However, this treatment may complicate with differentiation syndrome (DS) in 30% of patients, which manifests with clinical picture of acute lung injury and massive infiltration of ATRA-treated APL (ATRA-APL) cells into alveolar spaces. It is not clear how these ATRA-APL cells were cleared during resolution phase of DS. Previous studies have reported that cross-talk between apoptotic ATRA-APL cells and alveolar macrophage is crucial during the resolution phase of DS. In this study, we investigated the mechanism underlying the interaction between apoptotic ATRA-APL (NB4) cells and alveolar macrophages (NR8383). Different stages of apoptotic cells were determined by flowcytometry by using antibodies specific to annexin V and 7-AAD. Condition medium (CM) derived from apoptotic ATRA-NB4 cells was harvested to determine its biological activity by transmigration assay and adhesion assay. Our results indicated that NR8383 cells were able to engulf apoptotic ATRA-NB4 cells. Furthermore, the CM derived from apoptotic ATRA-NB4 cells had anti-inflammatory activity as evidenced by inhibiting the recipient cells migration and adhesion to human umbilical vein endothelial cells (HUVEC). Further studies we focused on investigating the mediators responsible for the anti-inflammatory activities in the CM which facilitate the phagocytosis activity of alveolar macrophage. Annexin A1 is a mediator that regulates the immune response of glucocorticoids. We found that apoptotic ATRA-NB4 cells would release Annexin A1 via microparticle (MP). On the other hand, the release of the pro-inflammatory cytokine: IL-8 will diminish as well. Based on these finding, we conclude that the CM collected from apoptotic ATRA-NB4 cells has anti-inflammatory activities by releasing AnxA1(+) MP and reducing the release of IL-8. During the resolution stage of DS, these apoptotic cells could increase clearance of dying cells and prevent further infiltration in alveolar. Thus, these findings would suggest the potential therapeutic strategies to modulate the resolution of acute lung injury in DS.
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MURAKAMI, Masashi, and 真史 村上. "ATRA inhibits ceramide kinase transcription through an ATRA-related transcription factor, COUP-TFI, in a human neuroblastoma cell line, SH-SY5Y." Thesis, 2010. http://hdl.handle.net/2237/14433.

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Books on the topic "Atrial differentiation"

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Jones, Michael, Norman Qureshi, and Kim Rajappan. Multifocal atrial tachycardia. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0113.

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Multifocal atrial tachycardia (MAT) is an atrial arrhythmia arising in the left or right atrium, or both, with multiple different P wave morphologies (at least three), with an atrial rate usually faster than 100 min−1. The atrial rhythm may be irregular; however, the defining difference between MAT and atrial fibrillation is the presence of a P wave prior to each QRS complex in MAT (but the absence of P waves in atrial fibrillation). MAT may be compared to sinus rhythm with very frequent polymorphic atrial ectopic beats, and in fact similar pathophysiologic mechanisms underlie both conditions; thus, differentiating one from the other may be difficult—the principle difference is the lack of a single dominant sinus pacemaker in MAT.
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Banerjee, Ashis, and Clara Oliver. Cardiac emergencies. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198786870.003.0009.

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Chest pain is a common presenting complaint for patients in the emergency department. This chapter focuses on the management and recent changes to non-ST-segment elevation myocardial infarction (NSTEMI) and STEMI pathways, in keeping with national guidance. Arrhythmia management including atrial fibrillation as well as the use of scoring systems as the CHADVASC score also commonly appears in the short-answer question (SAQ) paper, which is covered in this chapter in line with current NICE guidance. In addition, there is also a section on the diagnosis and differentiation on managing a patient with a transient loss of consciousness and the associated risk factors of sudden cardiac death. This chapter also includes sections on hypertensive emergencies and the management of heart failure.
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Campione, Marina, Amelia Aranega, and Diego Franco. Cardiac looping and laterality. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0014.

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Dextral looping is a complex process which progresses concomitantly with cardiac chamber differentiation and ultimately leads to the final alignment of the cardiac regions. Generation of cardiac asymmetry is crucial to ensure the proper form and consequent function of the heart and thus is a highly regulated process. Molecular signals originate long before morphological asymmetry and therefore can direct it; a complex regulatory network has been characterized which invariably converges on the Tgf-β‎ signalling molecule Nodal and its downstream target, the homeobox transcription factor Pitx2. We review current data regarding the cellular and molecular bases of cardiac looping and laterality, and describe current understaning of the role of Nodal and Pitx2. The morphogenetic role of the Pitx2 gene and its modulation of transcription and function, which have recently linked laterality to atrial fibrillation, are emphasized.
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Heidbuchel, Hein, Mattias Duytschaever, and Haran Burri. LAA or LSPV? Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198766377.003.0034.

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D’Andrea, Antonello, André La Gerche, and Christine Selton-Suty. Systemic disease and other conditions: athlete’s heart. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0055.

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The term ‘athlete’s heart’ refers to the structural, functional, and electrical adaptations that occur as a result of habitual exercise training. It is characterized by an increase of the internal chamber dimensions and wall thickness of both atria and ventricles. The athlete’s right ventricle also undergoes structural, functional, and electrical remodelling as a result of intense exercise training. Some research suggests that the haemodynamic stress of intense exercise is greater for the right heart and, as a result, right heart remodelling is slightly more profound when compared with the left heart. Echocardiography is the primary tool for the assessment of morphological and functional features of athlete’s heart and facilitates differentiation between physiological and pathological LV hypertrophy. Doppler myocardial and strain imaging can give additional information to the standard indices of global systolic and diastolic function and in selected cases cardiac magnetic resonance imaging may help in the diagnosis of specific myocardial diseases among athletes such as hypertrophic cardiomyopathy, dilated cardiomyopathy, or arrhythmogenic right ventricular cardiomyopathy.
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Karatasakis, G., and G. D. Athanassopoulos. Cardiomyopathies. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199599639.003.0019.

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Echocardiography is a key diagnostic method in the management of patients with cardiomyopathies.The main echocardiographic findings of hypertrophic cardiomyopathy are asymmetric hypertrophy of the septum, increased echogenicity of the myocardium, systolic anterior motion, turbulent left ventricular (LV) outflow tract blood flow, intracavitary gradient of dynamic nature, mid-systolic closure of the aortic valve and mitral regurgitation. The degree of hypertrophy and the magnitude of the obstruction have prognostic meaning. Echocardiography plays a fundamental role not only in diagnostic process, but also in management of patients, prognostic stratification, and evaluation of therapeutic intervention effects.In idiopathic dilated cardiomyopathy, echocardiography reveals dilation and impaired contraction of the LV or both ventricles. The biplane Simpson’s method incorporates much of the shape of the LV in calculation of volume; currently, three-dimensional echocardiography accurately evaluates LV volumes. Deformation parameters might be used for detection of early ventricular involvement. Stress echocardiography using dobutamine or dipyridamole may contribute to risk stratification, evaluating contractile reserve and left anterior descending flow reserve. LV dyssynchrony assessment is challenging and in patients with biventricular pacing already applied, optimization of atrio-interventricular delays should be done. Specific characteristics of right ventricular dysplasia and isolated LV non-compaction can be recognized, resulting in an increasing frequency of their prevalence. Rare forms of cardiomyopathy related with neuromuscular disorders can be studied at an earlier stage of ventricular involvement.Restrictive and infiltrative cardiomyopathies are characterized by an increase in ventricular stiffness with ensuing diastolic dysfunction and heart failure. A variety of entities may produce this pathological disturbance with amyloidosis being the most prevalent. Storage diseases (Fabry, Gaucher, Hurler) are currently treatable and early detection of ventricular involvement is of paramount importance for successful treatment. Traditional differentiation between constrictive pericarditis (surgically manageable) and the rare cases of restrictive cardiomyopathy should be properly performed.
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Book chapters on the topic "Atrial differentiation"

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Degos, Laurent. "ATRA Therapy in Acute Promyelocytic Leukemia a Model for Differentiation Therapy." In Cancer Therapy, 99–108. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84613-7_8.

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Nalliah, Chrishan, and Jonathan Kalman. "Focal Atrial Tachycardia and its Differentiation from Macroreentrant Atrial Tachycardia." In Practical Cardiac Electrophysiology, 341. Jaypee Brothers Medical Publishers (P) Ltd., 2017. http://dx.doi.org/10.5005/jp/books/13028_22.

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Lip, Gregory Y. H. "Epidemiology of supraventricular tachycardias." In ESC CardioMed, 2050. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0476.

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The precise description of the epidemiology of supraventricular tachycardias is difficult as the published data often has poor differentiation between atrial fibrillation, atrial flutter, and other supraventricular arrhythmias. In contrast to the extensive epidemiology on atrial fibrillation, a specific focus on supraventricular tachycardia population epidemiology is sparse, especially in the general population (rather than observational cohorts from specialized centres).
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Rudya, A., A. Kibarskis, and V. Shlleikis. "Differentiation of atrial rhythms by differentially amplified ECG." In Electrocardiology ’87, 533–36. De Gruyter, 1988. http://dx.doi.org/10.1515/9783112484289-116.

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Rudys, A., A. Kibarskis, and V. Shileikis. "Differentiation of atrial rhythms by differentially amplified ECG." In Electrocardiology ’87, 533–36. De Gruyter, 1988. http://dx.doi.org/10.1515/9783112542385-116.

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Kelly, Robert G. "Cardiac embryogenesis." In ESC CardioMed, edited by Miguel Torres, 33–36. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0004.

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The embryonic heart forms in anterior lateral splanchnic mesoderm and is derived from Mesp1-expressing progenitor cells. During embryonic folding, the earliest differentiating progenitor cells form the linear heart tube in the ventral midline. The heart tube extends in length and loops to the right as new myocardium is progressively added at the venous and arterial poles from multipotent second heart field cardiovascular progenitor cells in contiguous pharyngeal mesoderm. While the linear heart tube gives rise to the left ventricle, the right ventricle, outflow tract, and a large part of atrial myocardium are derived from the second heart field. Progressive myocardial differentiation is controlled by intercellular signals within the progenitor cell niche. The embryonic heart is the template for septation and growth of the four-chambered definitive heart and defects in progenitor cell deployment result in a spectrum of common forms of congenital heart defects.
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Kelly, Robert G. "Cardiac embryogenesis." In ESC CardioMed, edited by Miguel Torres, 33–36. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0004_update_001.

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The embryonic heart forms in anterior lateral splanchnic mesoderm and is derived from Mesp1-expressing progenitor cells. During embryonic folding, the earliest differentiating progenitor cells form the linear heart tube in the ventral midline. The heart tube extends in length and loops to the right as new myocardium is progressively added at the venous and arterial poles from multipotent second heart field cardiovascular progenitor cells in contiguous pharyngeal mesoderm. While the linear heart tube gives rise to the left ventricle, the right ventricle, outflow tract, and a large part of atrial myocardium are derived from the second heart field. Progressive myocardial differentiation is controlled by intercellular signals within the progenitor cell niche. The embryonic heart is the template for septation and growth of the four-chambered definitive heart and defects in progenitor cell deployment result in a spectrum of common forms of congenital heart defects.
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Kelly, Robert G. "Cardiac embryogenesis." In ESC CardioMed, edited by Miguel Torres, 33–36. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0004_update_002.

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The embryonic heart forms in anterior lateral splanchnic mesoderm and is derived from Mesp1-expressing progenitor cells. During embryonic folding, the earliest differentiating progenitor cells form the linear heart tube in the ventral midline. The heart tube extends in length and loops to the right as new myocardium is progressively added at the venous and arterial poles from multipotent second heart field cardiovascular progenitor cells in contiguous pharyngeal mesoderm. While the linear heart tube gives rise to the left ventricle, the right ventricle, outflow tract, and a large part of atrial myocardium are derived from the second heart field. Progressive myocardial differentiation is controlled by intercellular signals within the progenitor cell niche. The embryonic heart is the template for septation and growth of the four-chambered definitive heart and defects in progenitor cell deployment result in a spectrum of common forms of congenital heart defects.
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Tardos, Jonathan, Nawal Aamir, Dhaval Desai, Amanda Chajkowski, and Amit H. Patel. "Frozen Hearts: The Emerging Role of Cryoablation for Pulmonary Vein Isolation." In Atrial Fibrillation - Diagnosis and Management in the 21st Century [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.105885.

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The cornerstone for the modern treatment of paroxysmal atrial fibrillation (AF) is pulmonary vein isolation, also called an AF ablation. Various ablation technologies exist to accomplish this goal with specific advantages. This chapter will focus on the unique attributes of cryoablation for pulmonary vein isolation. Specifically, we will summarize the trial data and outcomes of cryoablation in patients with paroxysmal and persistent AF from the initial FDA approval studies to novel uses beyond the pulmonary veins. Readers will have an appreciation of the unique characteristics differentiating cryoablation from radiofrequency (RF) catheter ablation and other techniques such as surgical MAZE. Clinical trial data show both noninferiority, and in some cases, superior outcomes of cryoablation to antiarrhythmic drug therapy and other ablation techniques.
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Sareban, Mahdi, and Josef Niebauer. "Ambulatory (24-hour Holter monitoring, event recorders) and signal-averaged ECG for arrhythmia registration in the athlete’s heart." In The ESC Textbook of Sports Cardiology, edited by Antonio Pelliccia, Hein Heidbuchel, Domenico Corrado, Mats Börjesson, and Sanjay Sharma, 107–14. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198779742.003.0012.

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Systematic physical exercise leads to structural, functional, and electrical cardiovascular changes summarized in the term ‘athlete’s heart’. Arrhythmias that are common features in the resting ECG of otherwise healthy athletes may be an expression of the athlete’s heart, but on the other hand may be caused by underlying cardiac pathology, opening up a grey zone of diagnostic uncertainty. Differentiating adaptive changes from pathological cardiac conditions is of great clinical importance because some cardiomyopathies are leading causes of sudden cardiac death in athletes. In addition, there is increasing evidence that excessive endurance training may induce intermittent atrial arrhythmias, which can be hard to detect by resting ECG. Therefore this chapter will highlight 24-hour Holter monitoring, event recorders, and signal-averaged ECGs in the emerging field of ambulatory arrhythmia registration as part of the diagnostic work-up of athlete’s heart.
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Conference papers on the topic "Atrial differentiation"

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Razzaq, Nauman, Shafa-at Ali Sheikh, Tahir Zaidi, Imran Akhtar, and Syed Hassaan Ahmed. "Automated Differentiation between Normal Sinus Rhythm, Atrial Tachycardia, Atrial Flutter and Atrial Fibrillation during Electrophysiology." In 2017 IEEE 17th International Conference on Bioinformatics and Bioengineering (BIBE). IEEE, 2017. http://dx.doi.org/10.1109/bibe.2017.00-43.

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Zaidi, Syed Hassan, Shafa-at Ali Sheikh, Imran Akhtar, and Tahir Zaidi. "Differentiation between Atrial Fibrillation and Atrial Flutter using 1D Poincare maps based on endocardial bipolar intracardiac electrograms extracted from the Right Atria." In 2016 13th International Bhurban Conference on Applied Sciences and Technology (IBCAST). IEEE, 2016. http://dx.doi.org/10.1109/ibcast.2016.7429858.

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Byram, Brett, Lauren Oliveri, Patrick Wolf, and Gregg Trahey. "Acute and chronic myocardial infarct differentiation using atrial kick induced strain (AKIS) imaging." In 2013 IEEE International Ultrasonics Symposium (IUS). IEEE, 2013. http://dx.doi.org/10.1109/ultsym.2013.0027.

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Nopp, S., O. Königsbrügge, D. Kraemmer, I. Pabinger, and C. Ay. "Growth differentiation factor-15 predicts major cardiac adverse events and all-cause mortality in patients with atrial fibrillation." In 65th Annual Meeting of the Society of Thrombosis and Haemostasis Research. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1728087.

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Yang, Guang, Xiahai Zhuang, Habib Khan, Shouvik Haldar, Eva Nyktari, Lei Li, Xujiong Ye, et al. "Differentiation of pre-ablation and post-ablation late gadolinium-enhanced cardiac MRI scans of longstanding persistent atrial fibrillation patients." In SPIE Medical Imaging, edited by Samuel G. Armato and Nicholas A. Petrick. SPIE, 2017. http://dx.doi.org/10.1117/12.2250910.

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Liu, Yingjuan, Mun-kit Choy, Gennadiy Tenin, Sabu Abraham, Graeme Black, and Bernard Keavney. "BS2 STX18-AS1 is a long noncoding rna governing in vitro cardiomyocyte differentiation and predisposing to atrial septal defect via downregulation of NKX2-5." In British Cardiovascular Society Annual Conference ‘Digital Health Revolution’ 3–5 June 2019. BMJ Publishing Group Ltd and British Cardiovascular Society, 2019. http://dx.doi.org/10.1136/heartjnl-2019-bcs.166.

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Maji, U., M. Mitra, and S. Pal. "Differentiating normal sinus rhythm and atrial fibrillation in ECG signal: A phase rectified signal averaging based approach." In 2014 International Conference on Control, Instrumentation, Energy and Communication (CIEC). IEEE, 2014. http://dx.doi.org/10.1109/ciec.2014.6959073.

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Watters, Karen M., Kenneth R. Bryan, Nimah H. Foley, and Raymond L. Stallings. "Abstract 202: Expressional alterations in functional ultra-conserved non-coding RNAs in response to ATRA-induced differentiation and changes in MYCN levels in neuroblastoma cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-202.

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