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José M. Icardo

Bio: José M. Icardo is an academic researcher from University of Cantabria. The author has contributed to research in topics: Bulbus arteriosus & Sinus venosus. The author has an hindex of 28, co-authored 96 publications receiving 2341 citations.


Papers
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Journal ArticleDOI
07 Aug 1998-Cell
TL;DR: Pitx2, a member of the bicoid-related family of homeobox-containing genes, is asymmetrically expressed in the left lateral plate mesoderm and derived tissues during chick and mouse development and experiments demonstrate that Shh and nodal positively regulate Pitx2 expression.

324 citations

Journal ArticleDOI
TL;DR: The data reveal the existence of molecular isomerism not only in the atrial, but also in the ventricular compartment of the heart.

144 citations

Journal ArticleDOI
TL;DR: A morphologic study of ventricular trabeculation in chick embryo hearts between days 2 and 5 of incubation is presented, suggesting that the continuous synthesis of extracellular material by the myocytes may increase the hydrostatic pressure within the myocardium, inducing the formation and the enlargement of these intercellular spaces.
Abstract: This paper presents a morphologic study of ventricular trabeculation in chick embryo hearts between days 2 and 5 of incubation. Trabeculation appears to be the expression of three closely interrelated events: the formation of endocardial outgrowths that eventually invade the myocardium; the development of large intercellular spaces between the myocytes, and the decrease in thickness of the cardiac jelly. Endocardial cells present morphologic differences between trabeculated and nontrabeculated areas of the ventricular region. The elongation of the endocardial cells in the endocardial outgrowths and the presence of mitoses suggest that the endocardium grows out by means of an increase in cell number and by redistribution and elongation of the preexisting endocardial cells. The intercellular spaces of the myocardium appear filled with abundant extracellular material. It is suggested that the continuous synthesis of extracellular material by the myocytes may increase the hydrostatic pressure within the myocardium, inducing the formation and the enlargement of these intercellular spaces. The development and later rupture of endocardium-covered cords is described here. These cords are made up of a core of cardiac jelly material revested by endocardium. The cords may be engaged in the removal of substantial amounts of cardiac jelly during the formation of the trabeculae.

78 citations

Journal ArticleDOI
22 Aug 2018-PLOS ONE
TL;DR: Acinetobacter baumannii can undergo a rapid adaptation to both the temperature shift and nutrients availability, conditions that can be easily found by bacteria in a new patient in the hospital setting, and is considered a substantial factor in infection control practices.
Abstract: Acinetobacter baumannii is a cause of healthcare-associated infections. Although A. baumannii is an opportunistic pathogen, its infections are notoriously difficult to treat due to intrinsic and acquired antimicrobial resistance, often limiting effective therapeutic options. A. baumannii can survive for long periods in the hospital environment, particularly on inanimate surfaces. Such environments may act as a reservoir for cross-colonization and infection outbreaks and should be considered a substantial factor in infection control practices. Moreover, clothing of healthcare personnel and gadgets may play a role in the spread of nosocomial bacteria. A link between contamination of hospital surfaces and A. baumannii infections or between its persistence in the environment and its virulence has not yet been established. Bacteria under stress (i.e., long-term desiccation in hospital setting) could conserve factors that favor infection. To investigate whether desiccation and/or starvation may be involved in the ability of certain strains of A. baumannii to retain virulence factors, we have studied five well-characterized clinical isolates of A. baumannii for which survival times were determined under simulated hospital conditions. Despite a considerable reduction in the culturability over time (up to 88% depending on strain and the condition tested), some A. baumannii strains were able to maintain their ability to form biofilms after rehydration, addition of nutrients, and changing temperature. Also, after long-term desiccation, several clinical strains were able to grow in the presence of non-immune human serum as fine as their non-stressed homologs. Furthermore, we also show that the ability of bacterial strains to kill Galleria mellonella larvae does not change although A. baumannii cells were stressed by long-term starvation (up to 60 days). This means that A. baumannii can undergo a rapid adaptation to both the temperature shift and nutrients availability, conditions that can be easily found by bacteria in a new patient in the hospital setting.

72 citations

Journal ArticleDOI
TL;DR: The development of the heart from the formation of theHeart mesoderm to cardiac septation is summarized, and a brief account of morphological changes is provided, but attention is focused on mechanisms rather than on morphologic descriptions.
Abstract: This paper summarizes the development of the heart from the formation of the heart mesoderm to cardiac septation. A brief account of morphological changes is provided, but attention is focused on mechanisms rather than on morphologic descriptions. Heart induction and differentiation, and the expression of cardiac specific proteins, are reviewed. New developments in these areas include the possible role of cell surface proteins and peptide growth factors in the segregation of the splanchnic mesoderm and in cardiac commitment. Past and recent experiments indicate that the heart morphogenetic information is engraved in the precardiac mesoderm. In spite of this, specific differentiative signals can be overriden experimentally demonstrating the unstability of the cardiac phenotype at the early heart tube stage. The relationship between differentiation and morphogenesis is analyzed. While cardiac differentiation appears to be a prerequisite for morphogenesis, a number of experiments indicate that differentiation can proceed in the absence of any morphogenesis. Formation of the heart loop is separated into two different components; looping itself and the acquisition of handedness. Late heart morphogenesis is explained in terms of differential tissue growth and tissue remodeling. This not only includes morphogenetic changes intrinsic to the heart but the addition of new cell types (neural crest, epicardium, vessels, nerves) that become integrated into the developing heart. The contribution of specific mechanisms to our understanding of heart development, such as cell death and hemodynamics is also analyzed.

67 citations


Cited by
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Journal ArticleDOI
TL;DR: Two sets of cardiogenic precursors are defined, one of which expresses and requires Isl1 and the other of which does not, which have implications for the development of specific cardiac lineages, left-right asymmetry, cardiac evolution, and isolation of cardiac progenitor cells.

1,550 citations

Journal ArticleDOI
TL;DR: Mice generated in which the fibronectin gene is inactivated display shortened anterior-posterior axes, deformed neural tubes and severe defects in mesodermally derived tissues, proving that fibronECTin is required for embryogenesis.
Abstract: To examine the role of fibronectin in vivo, we have generated mice in which the fibronectin gene is inactivated. Heterozygotes have one half normal levels of plasma fibronectin, yet appear normal. When homozygous, the mutant allele causes early embryonic lethality, proving that fibronectin is required for embryogenesis. However, homozygous mutant embryos implant and initiate gastrulation normally including extensive mesodermal movement. Neural folds also form but the mutant embryos subsequently display shortened anterior-posterior axes, deformed neural tubes and severe defects in mesodermally derived tissues. Notochord and somites are absent; the heart and embryonic vessels are variable and deformed, and the yolk sac, extraembryonic vasculature and amnion are also defective. These abnormalities can be interpreted as arising from fundamental deficits in mesodermal migration, adhesion, proliferation or differentiation as a result of the absence of fibronectin. The nature of these embryonic defects leads to reevaluation of suggested roles for fibronectin during early development based on results obtained in vitro and in embryos of other species.

1,310 citations

Journal ArticleDOI
23 Nov 1995-Nature
TL;DR: It is shown that neUREgulin -/ - embryos die during embryogenesis and display heart malformations, and the phenotype demonstrates that in vivo neuregulin acts locally and frequently in a paracrine manner.
Abstract: Neuregulin (also called NDF, heregulin, GGF and ARIA) is a member of the EGF family which induces growth and differentiation of epithelial, glial and muscle cells in culture. The biological effects of the factor are mediated by tyrosine kinase receptors. Neuregulin can bind directly to erbB3 and erbB4 and receptor heterodimerization allows neuregulin-dependent activation of erbB2 (refs 1, 2, 5). A targeted mutation in mice reveals multiple essential roles of neuregulin in development. Here we show that neuregulin -/- embryos die during embryogenesis and display heart malformations. In addition, Schwann cell precursors and cranial ganglia fail to develop normally. The phenotype demonstrates that in vivo neuregulin acts locally and frequently in a paracrine manner. All cell types affected by the mutation express either erbB3 or erbB4, indicating that either of these tyrosine kinase receptors can be a component in recognition and transmission of essential neuregulin signals.

1,208 citations

Journal ArticleDOI
09 Jan 2003-Nature
TL;DR: In vivo imaging is shown to show the presence of high-shear, vortical flow at two key stages in the developing heart, and predict flow-induced forces much greater than might have been expected for micro-scale structures at low Reynolds numbers.
Abstract: The pattern of blood flow in the developing heart has long been proposed to play a significant role in cardiac morphogenesis. In response to flow-induced forces, cultured cardiac endothelial cells rearrange their cytoskeletal structure and change their gene expression profiles. To link such in vitro data to the intact heart, we performed quantitative in vivo analyses of intracardiac flow forces in zebrafish embryos. Using in vivo imaging, here we show the presence of high-shear, vortical flow at two key stages in the developing heart, and predict flow-induced forces much greater than might have been expected for micro-scale structures at low Reynolds numbers. To test the relevance of these shear forces in vivo, flow was occluded at either the cardiac inflow or outflow tracts, resulting in hearts with an abnormal third chamber, diminished looping and impaired valve formation. The similarity of these defects to those observed in some congenital heart diseases argues for the importance of intracardiac haemodynamics as a key epigenetic factor in embryonic cardiogenesis.

989 citations

Journal ArticleDOI
05 Dec 1980-JAMA
TL;DR: This third edition of what has now become a well-established textbook in cardiovascular medicine is again edited by Dr Eugene Braunwald with the assistance of 65 other authors who read like a Who's Who of American Cardiology.
Abstract: This third edition of what has now become a well-established textbook in cardiovascular medicine is again edited by Dr Eugene Braunwald with the assistance of 65 other authors who read like a Who's Who of American Cardiology. Since the second edition, 12 new chapters have been added or substituted and others have been significantly revised. The first volume includes Part I on "Examination of the Patient" and Part II on "Normal and Abnormal Circulatory Function." The second volume deals with specific diseases. Part III, "Diseases of the Heart, Pericardium and Vascular System," includes new sections on "Risk Factors for Coronary Artery Disease," "The Pathogenesis of Atherosclerosis," and "Interventional Catheterization Techniques." Part IV, "Broader Perspectives on Heart Disease and Cardiologic Practice," includes new chapters on "Genetics and Cardiovascular Disease," "Aging in Cardiac Disease," and "Cost Effective Strategies in Cardiology." The last 200 pages of the book (Part V) are devoted to

927 citations