Littérature scientifique sur le sujet « Non-syndromic thoracic aneurysm »
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Articles de revues sur le sujet "Non-syndromic thoracic aneurysm"
Martin‐Blazquez, Ariadna, Angeles Heredero, Gonzalo Aldamiz‐Echevarria, Marta Martin‐Lorenzo et Gloria Alvarez‐Llamas. « Non‐syndromic thoracic aortic aneurysm : cellular and molecular insights ». Journal of Pathology 254, no 3 (24 mai 2021) : 229–38. http://dx.doi.org/10.1002/path.5683.
Texte intégralLuyckx, Ilse, et Bart L. Loeys. « The genetic architecture of non-syndromic thoracic aortic aneurysm ». Heart 101, no 20 (9 septembre 2015) : 1678–84. http://dx.doi.org/10.1136/heartjnl-2014-306381.
Texte intégralArroyave, Jose, Juan Manuel Carretero et Domenico Gruosso. « Isolated aortic dilation without osteoarthritis : a case of SMAD3 mutation ». Cardiology in the Young 28, no 5 (15 février 2018) : 765–67. http://dx.doi.org/10.1017/s1047951118000082.
Texte intégralOstberg, Nicolai P., Mohammad A. Zafar, Bulat A. Ziganshin et John A. Elefteriades. « The Genetics of Thoracic Aortic Aneurysms and Dissection : A Clinical Perspective ». Biomolecules 10, no 2 (24 janvier 2020) : 182. http://dx.doi.org/10.3390/biom10020182.
Texte intégralMonda, Emanuele, Michele Lioncino, Federica Verrillo, Marta Rubino, Martina Caiazza, Alfredo Mauriello, Natale Guarnaccia et al. « The Role of Genetic Testing in Patients with Heritable Thoracic Aortic Diseases ». Diagnostics 13, no 4 (17 février 2023) : 772. http://dx.doi.org/10.3390/diagnostics13040772.
Texte intégralDe Cario, Rosina, Marco Giannini, Giulia Cassioli, Ada Kura, Anna Maria Gori, Rossella Marcucci, Stefano Nistri, Guglielmina Pepe, Betti Giusti et Elena Sticchi. « Tracking an Elusive Killer : State of the Art of Molecular-Genetic Knowledge and Laboratory Role in Diagnosis and Risk Stratification of Thoracic Aortic Aneurysm and Dissection ». Diagnostics 12, no 8 (22 juillet 2022) : 1785. http://dx.doi.org/10.3390/diagnostics12081785.
Texte intégralGasiulė, Stankevičius, Patamsytė, Ražanskas, Žukovas, Kapustina, Žaliaduonytė, Benetis, Lesauskaitė et Vilkaitis. « Tissue-Specific miRNAs Regulate the Development of Thoracic Aortic Aneurysm : the Emerging Role of KLF4 Network ». Journal of Clinical Medicine 8, no 10 (3 octobre 2019) : 1609. http://dx.doi.org/10.3390/jcm8101609.
Texte intégralHolt, Margrethe, Bjørn E. Seim, Jonas Øgaard, Maria B. Olsen, Per R. Woldbæk, John-Peder Escobar Kvitting, Pål Aukrust et al. « Selective and marked decrease of complement receptor C5aR2 in human thoracic aortic aneurysms : a dysregulation with potential inflammatory effects ». Open Heart 6, no 2 (novembre 2019) : e001098. http://dx.doi.org/10.1136/openhrt-2019-001098.
Texte intégralPatuzzo, Cristina, A. Pasquali, E. Trabetti, G. Malerba, PF Pignatii, M. Tessari et G. Faggian. « A Preliminary microRNA Analysis of non Syndromic Thoracic Aortic Aneurysms ». Balkan Journal of Medical Genetics 15, Supplement (1 décembre 2012) : 51–55. http://dx.doi.org/10.2478/v10034-012-0019-6.
Texte intégralZhang, Eryong. « Non-syndromic thoracic aortic aneurysms and dissections-a genetic review ». Frontiers in Bioscience 18, no 1 (2013) : 305. http://dx.doi.org/10.2741/4101.
Texte intégralThèses sur le sujet "Non-syndromic thoracic aneurysm"
MARCONI, Maddalena. « A proteomic approach to the study of human thoracic aorta aneurysms ». Doctoral thesis, 2011. http://hdl.handle.net/11562/350598.
Texte intégralCardiovascular disease is the leading cause of illness and death in the whole world. In the United States, for example, there are an estimated 62 million people with cardiovascular disease. In 2000, approximately 946,000 deaths were attributed to cardiovascular disease, accounting for 39% of all deaths in the USA. Among these causes of death thoracic aorta aneurysms (TAAs) can be found. Both familial and nonfamilial nonsyndromic thoracic aortic aneurysms (NSTAAs) are less well characterized than syndromic ones. This is the aim of my thesis: increasing our knowledge about the specific morphological and molecular characteristics that underlie NSTAAs. Tunica media samples taken from nine selected nonfamilial NSTAAs and nine reference patients were investigated via proteomics-bioinformatics, immunoblotting, quantitative histology (QH), and immunohistochemistry (IHC)/immunofluorescence (IF). The first characteristic I observed is a deep disorganization at extracellular matrix (ECM) level. I found a distorted elastic fiber network partnered with an increase in collagen fibers. The vascular smooth cells (VSMCs) decreased in number due to a proapoptotic increase in Caspase-3 activity. In the same media samples cystathionine gamma-lyase (CTH) was diffusely upregulated, and by producing H2S might be responsible for both the apoptosis and a hindered cell proliferation. VSMCs presented even a change in their phenotype, switching from a contractile to synthetic/secretory one. At the ECM level I found an increase in Paxillin (PXN) holoprotein, and in its cleaved form. Expression of the Testican-2 proteoglycan was also boosted. Conversely, the microfibrillar-associated glycoprotein-1 (MAGP-1) was found decreased. Alterations at the cytoskeletal level were also present; in fact there was a significant down-regulation in Vimentin (VIM) expression. Moreover, I found deeply altered even two important cell signaling systems in NSTAAs. On the one hand, an upregulation of Jagged1 (JAG1) holoprotein and its receptor, Notch1, whose signal was hindered by an accumulation of extracellular soluble JAG1 fragments. On the other hand, I observed an upregulated ectodysplasin (EDA) protein combined with a downregulation of its receptor (EDAR). In conclusion, I found a weakening of the aortic wall caused by an imbalance between elastic and fibrosis components in NSTAAs. This imbalance is coupled with a perturbed ratio between dying and proliferating cell fractions. In NSTAAs I found even deep alterations in ECM, cytoskeleton, and cell signaling. All together these changes concur to aneurysm progression.