Literatura científica selecionada sobre o tema "Ventricular chambers expansion"
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Artigos de revistas sobre o assunto "Ventricular chambers expansion"
Creswell, L. L., M. J. Moulton, S. G. Wyers, J. S. Pirolo, D. S. Fishman, W. H. Perman, K. W. Myers et al. "An experimental method for evaluating constitutive models of myocardium in in vivo hearts". American Journal of Physiology-Heart and Circulatory Physiology 267, n.º 2 (1 de agosto de 1994): H853—H863. http://dx.doi.org/10.1152/ajpheart.1994.267.2.h853.
Texto completo da fonteTodo, Tomoki, Masaaki Usui e Kintomo Takakura. "Treatment of severe intraventricular hemorrhage by intraventricular infusion of urokinase". Journal of Neurosurgery 74, n.º 1 (janeiro de 1991): 81–86. http://dx.doi.org/10.3171/jns.1991.74.1.0081.
Texto completo da fonteSagitova, G. R., I. V. Tkachev, O. V. Antonova e O. V. Davydova. "A clinical case of aortic coarctation in combination with a septal defect in a newborn child". Meditsinskiy sovet = Medical Council, n.º 17 (2 de novembro de 2023): 220–24. http://dx.doi.org/10.21518/ms2023-254.
Texto completo da fontePfefferbaum, Adolf, Natalie M. Zahr, Dirk Mayer, Shara Vinco, Juan Orduna, Torsten Rohlfing e Edith V. Sullivan. "Ventricular Expansion in Wild-Type Wistar Rats After Alcohol Exposure by Vapor Chamber". Alcoholism: Clinical and Experimental Research 32, n.º 8 (agosto de 2008): 1459–67. http://dx.doi.org/10.1111/j.1530-0277.2008.00721.x.
Texto completo da fonteLaurindo, F. R., R. E. Goldstein, N. J. Davenport, D. Ezra e G. Z. Feuerstein. "Mechanisms of hypotension produced by platelet-activating factor". Journal of Applied Physiology 66, n.º 6 (1 de junho de 1989): 2681–90. http://dx.doi.org/10.1152/jappl.1989.66.6.2681.
Texto completo da fonteGalli, Alessio, e Federico Lombardi. "Postinfarct Left Ventricular Remodelling: A Prevailing Cause of Heart Failure". Cardiology Research and Practice 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/2579832.
Texto completo da fonteMicheletti, R., E. D. Di Paola, A. Schiavone, E. English, P. Benatti, J. M. Capasso, P. Anversa e G. Bianchi. "Propionyl-L-carnitine limits chronic ventricular dilation after myocardial infarction in rats". American Journal of Physiology-Heart and Circulatory Physiology 264, n.º 4 (1 de abril de 1993): H1111—H1117. http://dx.doi.org/10.1152/ajpheart.1993.264.4.h1111.
Texto completo da fonteLi, Baosheng, Qiong Li, Xiaowei Wang, Kumar P. Jana, Giorgio Redaelli, Jan Kajstura e Piero Anversa. "Coronary constriction impairs cardiac function and induces myocardial damage and ventricular remodeling in mice". American Journal of Physiology-Heart and Circulatory Physiology 273, n.º 5 (1 de novembro de 1997): H2508—H2519. http://dx.doi.org/10.1152/ajpheart.1997.273.5.h2508.
Texto completo da fonteLee, Da Young. "Obesity and heart failure with preserved ejection fraction: pathophysiology and clinical significance". Cardiovascular Prevention and Pharmacotherapy 4, n.º 2 (30 de abril de 2022): 70–74. http://dx.doi.org/10.36011/cpp.2022.4.e10.
Texto completo da fonteMorton, Sarah U., Paul J. Scherz, Kimberly R. Cordes, Kathryn N. Ivey, Didier Y. R. Stainier e Deepak Srivastava. "microRNA-138 modulates cardiac patterning during embryonic development". Proceedings of the National Academy of Sciences 105, n.º 46 (12 de novembro de 2008): 17830–35. http://dx.doi.org/10.1073/pnas.0804673105.
Texto completo da fonteTeses / dissertações sobre o assunto "Ventricular chambers expansion"
Darby, Daniel. "A mechanism of oriented cell division underlying cardiac chamber expansion". Electronic Thesis or Diss., Sorbonne université, 2019. http://www.theses.fr/2019SORUS666.
Texto completo da fonteThe development of the heart is an intricate process both physically and genetically which requires regulation on many levels. Perturbations of this cardiogenic programme often has potent consequence on the organ and this is evident from the 1% incidence in births which are affected by a congenital heart disease (CHD). CHDs, such as cardiomyopathies, affect the architecture of the cardiac muscle, which is vital to the heartsfunction. The shape of the ventricular walls is particularly important to their function in terms of both defining the shape of the ventricular chambers and in establishing an appropriate myofiber architecture for efficient contractions (Meilhac et al., 2003). Previous work in the lab has provided insight into how this is achieved in the ventricles. It was found, through clonal analysis, that oriented tissue growth underlies cardiac chamber expansion (Meilhac et al., 2004). Analysis of earlier stages of the embryonic heart found regional coordination of cell divisions which preconfigured the myofiber architecture of the adult heart (Le Garrec et al., 2013). These studies suggest that oriented cell division plays an important role in sculpting the heart. However a mechanism by which this is regulated has yet to be established in the expanding ventricular chambers. In this project we use a combination of transcriptomic analysis, 3D cell segmentation, embryo culture experiments and molecular interference to investigate a mechanism for oriented cell division. Using bulk RNAseq we identified the NuMA:GPSM apparatus, the Planar Cell Polarity pathway and the integrin mechano-sensing pathway as candidates for further analysis. In combination with the transcriptomic analysis we wanted to identify if cells in the expanding ventricles were behaving according to Hertwig’s rule. To do this we have established CUBIC clearing and three dimensional lightsheet microscopy along with an automatic cell segmentation method to quantify cell elongations in the cardiac chambers. By comparing the elongation ratio of the cell to the detected axes of division the tools and approaches described above will enable us to identify if coordination existed between the two and if this was regionally specific. To analyse the impact of cardiac contractions on oriented cell division we established embryo culture experiment conditions paired with pharmaceutical interference of contractions. Preliminary results indicate that both an increase and decrease of contraction rate affects the shape of the heart. Finally, we will target the three pathways mentioned above with dominant negative proteins in chimeric hearts to dissect the molecular pathways. The outcome of this research will have potential applications in tissue engineering therapies targeting the heart