Last edited by Springer Nature
23.07.2021 | History

3 edition of Etiology and Morphogenesis of Congenital Heart Disease found in the catalog.

Etiology and Morphogenesis of Congenital Heart Disease

From Gene Function and Cellular Interaction to Morphology

  • 1406 Want to read
  • 714 Currently reading

Published by Administrator in Springer Nature

    Places:
  • United States
    • Subjects:
    • Springer Nature


      • Download Etiology and Morphogenesis of Congenital Heart Disease Book Epub or Pdf Free, Etiology and Morphogenesis of Congenital Heart Disease, Online Books Download Etiology and Morphogenesis of Congenital Heart Disease Free, Book Free Reading Etiology and Morphogenesis of Congenital Heart Disease Online, You are free and without need to spend extra money (PDF, epub) format You can Download this book here. Click on the download link below to get Etiology and Morphogenesis of Congenital Heart Disease book in PDF or epub free.

      • Open Access Unrestricted online accessCreative Commons https://creativecommons.org/licenses/by-nc/4.0/English

        StatementSpringer Nature
        PublishersSpringer Nature
        Classifications
        LC Classifications2016
        The Physical Object
        Paginationxvi, 134 p. :
        Number of Pages53
        ID Numbers
        ISBN 10nodata
        Series
        1nodata
        2
        3

        Cardiology;Pediatrics File Size: 2MB.


Share this book
You might also like

Etiology and Morphogenesis of Congenital Heart Disease by Springer Nature Download PDF EPUB FB2


Proc Natl Acad Sci 109: 18273— 18280.

cinesa.wuaki.tv: Etiology and Morphogenesis of Congenital Heart Disease: From Gene Function and Cellular Interaction to Morphology eBook: Nakanishi, Toshio, Markwald, Roger R., Baldwin, cinesa.wuaki.tv, Keller, Bradley B., Srivastava, Deepak, Yamagishi, Hiroyuki: Kindle Store

The potential of the zebrafish model for forward genetic screens suggests that this will be an informative system to probe the genetic mechanisms underlying heart tube elongation. 3 Department of Pediatrics CardiologyVanderbilt University, Nashville, Tennessee, USA• These common lineages reflect the fact that the linear heart tube forms from anterior cranial mesoderm at the level of the future face and progressively moves in a posterior direction in the embryo as pharyngeal arch and arch artery morphogenesis proceeds.

Dev Biol 353: 266— 274. Genes Dev 16: 1234— 1246. Activation of Wnt signaling in the HF diminishes the expression of several cardiac genes, including Nkx2- 5. The Right-Sided Pacemaking Cells Indeed Differentiate into SAN Pacemaker Cells Our in ovo cell-tracing studies have mapped the fate of these extracardiac right-sided pacing cells to the physiologically correct SAN region of the resulting heart at stage 35 E9 [].

Etiology and Morphogenesis of Congenital Heart Disease: From Gene Function and Cellular Interaction to Morphology

PATTERNS OF INTRACARDIAC PROLIFERATION AND THE INITIATION OF CHAMBER MORPHOGENESIS From midgestation in the mouse, or the fifth week of human gestation, addition of pharyngeal mesoderm to the poles of the heart is complete and there is a shift from proliferation in extracardiac progenitor cell populations to intracaradiac myocardial proliferation as the main driver of cardiac growth.

In the zebrafish model, regeneration of damaged myocardium has been shown to primarily involve myocyte proliferation rather than de novo differentiation of resident stem cells. The cardiovascular anomalies generally result from defective morphogenesis during embryological development. An important outcome of these patterning events is the emergence of chamber-specific transcriptional programs and proliferative centers on the outer curvature of the embryonic heart, resulting in the development of right and left atrial and ventricular chambers through a process termed ballooning morphogenesis.

The T-box transcription factor Eomesodermin acts upstream of Mesp1 to specify cardiac mesoderm during mouse gastrulation. Because Nkx2- 5 is absent in the SAN, Nkx2- 5 is suggested to suppress HCN4 and Tbx3.

5 transcription factor different mutations have been identified, causing impaired protein function [] and have a negative impact on transcriptional activity []. These signals, including bone morphogenetic protein BMPfibroblast growth factor FGFand WNT signals, in addition to short range signaling including fibronectin mediated cascades, result in the activation of key upstream transcriptional regulators of the cardiac phenotype including genes encoding the transcription factors NKX2-5, GATA4, and TBX5, and Etiology and Morphogenesis of Congenital Heart Disease remodeling protein SMARCD3 BAF60c.

Some studies indicate that it is not TBX5 mutations that cause CHDs but the abnormality in the TBX5 expression levels is responsible for congenital heart diseases []. The second heart field and ballooning morphogenesis concepts have major repercussions on our understanding of human heart development and disease.

Subsequently, the dorsal mesocardium, by which the cardiac trough is suspended in the pericardial cavity, breaks down dorsally, isolating the ventral heart tube from initially contiguous splanchnic mesodermal cells in the dorsal pericardial wall.

With advances in diagnosis and treatment in children, more and more of those with CHD Clinical Management of Congenital Heart Disease from Infancy to Adulthood This practical resource for the clinical management of congenital heart disease offers essential instruction on the presentation and treatment of congenital heart defects throughout the life stages.