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  1. Book ; Online ; E-Book: Osteocardiology

    Rajamannan, Nalini M.

    cardiac bone formation

    2018  

    Author's details Nalini M. Rajamannan
    Keywords Calcification ; Osteogenesis ; Chondrogenesis ; Calcific aortic valve disease ; Coronary Calcification ; Cardiac Fibrosis
    Subject code 610
    Language English
    Size 1 Online-Ressource (xiv, 99 Seiten), Illustrationen
    Publisher Springer
    Publishing place Cham
    Publishing country Germany
    Document type Book ; Online ; E-Book
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    HBZ-ID HT019536797
    ISBN 978-3-319-64994-8 ; 9783319649931 ; 3-319-64994-9 ; 3319649930
    DOI 10.1007/978-3-319-64994-8
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Book: Molecular biology of valvular heart disease

    Rajamannan, Nalini M.

    2014  

    Author's details Nalini M. Rajamannan ed
    Keywords Heart valves/Diseases/Molecular aspects ; Cellular therapy
    Subject code 616.125
    Language English
    Size XVII, 150 S., illustrations (black and white, and colour), 26 cm
    Publisher Springer
    Publishing place London u.a.
    Publishing country Great Britain
    Document type Book
    Note Includes bibliographical references
    HBZ-ID HT018274161
    ISBN 978-1-4471-6349-7 ; 9781447163503 ; 1-4471-6349-4 ; 1447163508
    Database Catalogue ZB MED Medicine, Health

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  3. Book: Cardiac valvular medicine

    Rajamannan, Nalini M.

    2013  

    Author's details Nalini M. Rajamannan ed
    Keywords Heart valves/Diseases
    Language English
    Size XIII, 254 S. : zahlr. Ill., graph. Darst., 26 cm
    Publisher Springer
    Publishing place Dordrecht u.a.
    Publishing country Netherlands
    Document type Book
    Note Includes bibliographical references and index
    HBZ-ID HT017532822
    ISBN 978-1-4471-4131-0 ; 1-4471-4131-8 ; 9781447141327 ; 1447141326
    Database Catalogue ZB MED Medicine, Health

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  4. Article ; Online: The Lp(a)/BMI Gradient in Osteocardiology: The Copenhagen Connection.

    Rajamannan, Nalini M

    Journal of the American College of Cardiology

    2022  Volume 79, Issue 6, Page(s) 559–561

    MeSH term(s) Atherosclerosis ; Body Mass Index ; Humans ; Lipoproteins
    Chemical Substances Lipoproteins
    Language English
    Publishing date 2022-02-10
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 605507-2
    ISSN 1558-3597 ; 0735-1097
    ISSN (online) 1558-3597
    ISSN 0735-1097
    DOI 10.1016/j.jacc.2021.11.044
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Aortic Valve Disease Is Not a Monogenetic Disorder.

    Rajamannan, Nalini M

    JACC. Basic to translational science

    2017  Volume 2, Issue 5, Page(s) 626

    Language English
    Publishing date 2017-10-30
    Publishing country United States
    Document type Journal Article
    ISSN 2452-302X
    ISSN (online) 2452-302X
    DOI 10.1016/j.jacbts.2017.09.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Osteocardiology: Defining the Go/No-Go Time Point for Therapy.

    Rajamannan, Nalini M

    Cardiology

    2018  Volume 139, Issue 3, Page(s) 175–183

    Abstract: Recent epidemiological studies have revealed that the risk factors associated with coronary artery calcification (CAC), including male gender, smoking, hypertension, and elevated serum cholesterol, are similar to the risk factors associated with the ... ...

    Abstract Recent epidemiological studies have revealed that the risk factors associated with coronary artery calcification (CAC), including male gender, smoking, hypertension, and elevated serum cholesterol, are similar to the risk factors associated with the development of calcific aortic valve disease (CAVD). The results of the experimental and clinical studies demonstrate that traditional risk factors initiate early atherosclerosis which over time differentiates to form bone in the heart causing clinical CAC and CAVD. Understanding the cellular mechanisms of cardiovascular calcification, the end-stage process of the atherosclerosis will help define the specific time point to modify this cellular process of bone formation in the heart termed osteocardiology. This time point between subclinical atherosclerosis and clinical calcification is the go/no-go time point, or the point of no return with severe clinical calcification in the heart. This review will summarize the development of bone formation in the heart termed osteocardiology, to define the go/no-go time point for therapy initiation to slow the progression of cardiovascular calcification.
    MeSH term(s) Atherosclerosis/physiopathology ; Atherosclerosis/therapy ; Coronary Artery Disease/physiopathology ; Coronary Artery Disease/therapy ; Disease Progression ; Humans ; Osteogenesis ; Risk Factors ; Vascular Calcification/diagnostic imaging ; Vascular Calcification/etiology ; Vascular Calcification/therapy
    Language English
    Publishing date 2018-01-27
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 80092-2
    ISSN 1421-9751 ; 0008-6312
    ISSN (online) 1421-9751
    ISSN 0008-6312
    DOI 10.1159/000485074
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: TIEG1 is upregulated in Lrp5/6-mediated valve osteogenesis.

    Rajamannan, Nalini M

    Journal of cellular biochemistry

    2018  Volume 120, Issue 3, Page(s) 3362–3366

    Abstract: We have previously demonstrated that Lrp5/6/β-catenin plays an important role in valve calcification with a specific osteogenic phenotype defined by increased bone mineral content and overall valve thickening. Recent studies indicate that TIEG1 may be ... ...

    Abstract We have previously demonstrated that Lrp5/6/β-catenin plays an important role in valve calcification with a specific osteogenic phenotype defined by increased bone mineral content and overall valve thickening. Recent studies indicate that TIEG1 may be involved in mediating the Wnt signaling pathway in bone, which is known to play critical roles in osteoblast differentiation and bone mineralization. Therefore, we sought to test the role of TIEG1 in mediating Wnt signaling, in an established model of hypercholesterolemic valve disease. Our previous model treated null mice with cholesterol diets: Lrp5
    MeSH term(s) Animals ; Aortic Valve Stenosis/genetics ; Aortic Valve Stenosis/metabolism ; Aortic Valve Stenosis/pathology ; Calcinosis/genetics ; Calcinosis/metabolism ; Calcinosis/pathology ; Cell Differentiation ; Core Binding Factor Alpha 1 Subunit/genetics ; Core Binding Factor Alpha 1 Subunit/metabolism ; DNA-Binding Proteins/physiology ; Female ; Hypercholesterolemia/genetics ; Hypercholesterolemia/metabolism ; Hypercholesterolemia/pathology ; Low Density Lipoprotein Receptor-Related Protein-5/physiology ; Low Density Lipoprotein Receptor-Related Protein-6/genetics ; Low Density Lipoprotein Receptor-Related Protein-6/metabolism ; Male ; Mice ; Mice, Knockout ; Mice, Knockout, ApoE/physiology ; Osteoblasts/metabolism ; Osteoblasts/pathology ; Osteogenesis ; Transcription Factors/physiology
    Chemical Substances Core Binding Factor Alpha 1 Subunit ; DNA-Binding Proteins ; Low Density Lipoprotein Receptor-Related Protein-5 ; Low Density Lipoprotein Receptor-Related Protein-6 ; Lrp5 protein, mouse ; Lrp6 protein, mouse ; Runx2 protein, mouse ; Tieg1 protein, mouse ; Transcription Factors
    Language English
    Publishing date 2018-09-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 392402-6
    ISSN 1097-4644 ; 0730-2312
    ISSN (online) 1097-4644
    ISSN 0730-2312
    DOI 10.1002/jcb.27606
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Role of Oxidative Stress Markers in Left-Sided Valve Disease: The LDL-Density-Pressure Theory.

    Rajamannan, Nalini M

    Cardiology

    2016  Volume 134, Issue 1, Page(s) 54–56

    MeSH term(s) Biomarkers ; Humans ; Lipoproteins, LDL ; Oxidative Stress ; Pressure
    Chemical Substances Biomarkers ; Lipoproteins, LDL
    Language English
    Publishing date 2016
    Publishing country Switzerland
    Document type Comment ; Journal Article
    ZDB-ID 80092-2
    ISSN 1421-9751 ; 0008-6312
    ISSN (online) 1421-9751
    ISSN 0008-6312
    DOI 10.1159/000444183
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Fenfluramine-Phentermine is Associated with an Increase in Cellular Proliferation Ex Vivo and In Vitro.

    Rajamannan, Nalini M

    The Journal of heart valve disease

    2017  Volume 26, Issue 4, Page(s) 467–471

    Abstract: ... 10-7 and 10-8 M) on porcine aortic valve subendothelial cells, using a [3H]-thymidine incorporation ...

    Abstract Background and aim of the study: Fenfluraminephentermine (FenPhen) has been implicated in accelerated valvular heart disease, characterized by valvular regurgitation and thickening, and resembling the histopathologic lesions found in carcinoid. The study aim was to determine whether cellular proliferation is present in FenPhen-exposed valves, by utilizing an in-vitro model to test whether FenPhen has a direct mitogenic effect on cardiac valvular cells, as compared to serotonin.
    Methods: Ex-vivo valves were tested for proliferation in surgically removed FenPhen-exposed valves (n = 10) and compared to proliferation levels in normal human cardiac valves removed at autopsy (n = 10). Immunostaining for a DNA polymerase, proliferating cell nuclear antigen (PCNA), was performed and quantified using digital imaging analysis. In-vitro assays were performed for direct proliferative effects of serotonin and FenPhen (10-6, 10-7 and 10-8 M) on porcine aortic valve subendothelial cells, using a [3H]-thymidine incorporation assay.
    Results: Ex-vivo PCNA levels in human FenPhenexposed valves were elevated compared to controls (22.8 ± 4.54 versus 1.26 ± 0.47; p <0.001). In vivo, serotonin and FenPhen markedly increased (10-fold) cell proliferation (as measured by [3H]-thymidine incorporation) in subendothelial cells in vitro (p <0.001). This proliferative response was demonstrated by PCNA staining in carcinoid heart valves and FenPhen-exposed valves. Mechanistically, plateletderived growth factor increased cell proliferation in a dose-related manner (p <0.001), the response being inhibited by a MAP kinase inhibitor (determined by monitoring p42/44 levels).
    Conclusions: In vitro, FenPhen acts as a powerful mitogen on subendothelial myofibroblast valve cells. Ex vivo, cellular proliferation was significantly elevated in human FenPhen-exposed cells.
    MeSH term(s) Animals ; Anti-Obesity Agents/toxicity ; Aortic Valve/drug effects ; Aortic Valve/metabolism ; Aortic Valve/pathology ; Cardiotoxicity ; Case-Control Studies ; Cell Proliferation/drug effects ; Cells, Cultured ; Dose-Response Relationship, Drug ; Drug Combinations ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Fenfluramine/chemistry ; Fenfluramine/toxicity ; Heart Valve Diseases/chemically induced ; Heart Valve Diseases/metabolism ; Heart Valve Diseases/pathology ; Humans ; Myofibroblasts/drug effects ; Myofibroblasts/metabolism ; Myofibroblasts/pathology ; Phentermine/chemistry ; Phentermine/toxicity ; Proliferating Cell Nuclear Antigen/metabolism ; Serotonin/toxicity ; Signal Transduction/drug effects
    Chemical Substances Anti-Obesity Agents ; Drug Combinations ; Proliferating Cell Nuclear Antigen ; Fenfluramine (2DS058H2CF) ; Serotonin (333DO1RDJY) ; Phentermine (C045TQL4WP) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2017
    Publishing country England
    Document type Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1205265-6
    ISSN 2053-2644 ; 0966-8519
    ISSN (online) 2053-2644
    ISSN 0966-8519
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Calcific Aortic Valve Disease in Familial Hypercholesterolemia: The LDL-Density-Gene Effect.

    Rajamannan, Nalini M

    Journal of the American College of Cardiology

    2015  Volume 66, Issue 24, Page(s) 2696–2698

    MeSH term(s) Aortic Valve/pathology ; Aortic Valve Stenosis/etiology ; Calcinosis/etiology ; Female ; Humans ; Hyperlipoproteinemia Type II/complications ; Male
    Language English
    Publishing date 2015-12-22
    Publishing country United States
    Document type Comment ; Editorial
    ZDB-ID 605507-2
    ISSN 1558-3597 ; 0735-1097
    ISSN (online) 1558-3597
    ISSN 0735-1097
    DOI 10.1016/j.jacc.2015.10.011
    Database MEDical Literature Analysis and Retrieval System OnLINE

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