Literatura académica sobre el tema "Ventricular chambers expansion"
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Artículos de revistas sobre el tema "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 completoTodo, Tomoki, Masaaki Usui y Kintomo Takakura. "Treatment of severe intraventricular hemorrhage by intraventricular infusion of urokinase". Journal of Neurosurgery 74, n.º 1 (enero de 1991): 81–86. http://dx.doi.org/10.3171/jns.1991.74.1.0081.
Texto completoSagitova, G. R., I. V. Tkachev, O. V. Antonova y 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 noviembre de 2023): 220–24. http://dx.doi.org/10.21518/ms2023-254.
Texto completoPfefferbaum, Adolf, Natalie M. Zahr, Dirk Mayer, Shara Vinco, Juan Orduna, Torsten Rohlfing y 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 completoLaurindo, F. R., R. E. Goldstein, N. J. Davenport, D. Ezra y G. Z. Feuerstein. "Mechanisms of hypotension produced by platelet-activating factor". Journal of Applied Physiology 66, n.º 6 (1 de junio de 1989): 2681–90. http://dx.doi.org/10.1152/jappl.1989.66.6.2681.
Texto completoGalli, Alessio y 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 completoMicheletti, R., E. D. Di Paola, A. Schiavone, E. English, P. Benatti, J. M. Capasso, P. Anversa y 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 completoLi, Baosheng, Qiong Li, Xiaowei Wang, Kumar P. Jana, Giorgio Redaelli, Jan Kajstura y 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 noviembre de 1997): H2508—H2519. http://dx.doi.org/10.1152/ajpheart.1997.273.5.h2508.
Texto completoLee, 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 completoMorton, Sarah U., Paul J. Scherz, Kimberly R. Cordes, Kathryn N. Ivey, Didier Y. R. Stainier y Deepak Srivastava. "microRNA-138 modulates cardiac patterning during embryonic development". Proceedings of the National Academy of Sciences 105, n.º 46 (12 de noviembre de 2008): 17830–35. http://dx.doi.org/10.1073/pnas.0804673105.
Texto completoTesis sobre el tema "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 completoThe 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