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  1. Article ; Online: Are Senolytic Agents Guilty of Overkill or Inappropriate Age Discrimination?

    Rabinovitch, Marlene

    Circulation

    2023  Volume 147, Issue 8, Page(s) 667–668

    MeSH term(s) Humans ; Senotherapeutics ; Ageism ; Cellular Senescence
    Chemical Substances Senotherapeutics
    Language English
    Publishing date 2023-02-20
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.122.060247
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ui IV Zs.60: Show issues Location:
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  2. Article ; Online: Life-saving effect of pulmonary surfactant in premature babies.

    Raj, J Usha / Bland, Richard D / Bhattacharya, Jahar / Rabinovitch, Marlene / Matthay, Michael A

    The Journal of clinical investigation

    2024  Volume 134, Issue 9

    Abstract: The discovery and replacement of lung surfactant have helped increase survival rates for neonatal respiratory distress syndrome in extremely premature infants. ...

    Abstract The discovery and replacement of lung surfactant have helped increase survival rates for neonatal respiratory distress syndrome in extremely premature infants.
    MeSH term(s) Humans ; Infant, Newborn ; Pulmonary Surfactants/metabolism ; Respiratory Distress Syndrome, Newborn ; Infant, Premature ; Infant, Extremely Premature
    Chemical Substances Pulmonary Surfactants
    Language English
    Publishing date 2024-05-01
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI179948
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: NETs Activate Pulmonary Arterial Endothelial Cells.

    Rabinovitch, Marlene

    Arteriosclerosis, thrombosis, and vascular biology

    2016  Volume 36, Issue 10, Page(s) 2035–2037

    MeSH term(s) Endothelial Cells ; Extracellular Traps ; Neutrophils ; Pulmonary Artery
    Language English
    Publishing date 2016
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 1221433-4
    ISSN 1524-4636 ; 1079-5642
    ISSN (online) 1524-4636
    ISSN 1079-5642
    DOI 10.1161/ATVBAHA.116.308206
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Combining induced pluripotent stem cell with next generation sequencing technology to gain new insights into pathobiology and treatment of pulmonary arterial hypertension.

    Rabinovitch, Marlene

    Pulmonary circulation

    2013  Volume 3, Issue 1, Page(s) 153–155

    Language English
    Publishing date 2013-04-02
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2638089-4
    ISSN 2045-8940 ; 2045-8932
    ISSN (online) 2045-8940
    ISSN 2045-8932
    DOI 10.4103/2045-8932.109963
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  5. Article: A Computational Growth and Remodeling Framework for Adaptive and Maladaptive Pulmonary Arterial Hemodynamics.

    Szafron, Jason M / Yang, Weiguang / Feinstein, Jeffrey A / Rabinovitch, Marlene / Marsden, Alison L

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Hemodynamic loading is known to contribute to the development and progression of pulmonary arterial hypertension (PAH). This loading drives changes in mechanobiological stimuli that affect cellular phenotypes and lead to pulmonary vascular remodeling. ... ...

    Abstract Hemodynamic loading is known to contribute to the development and progression of pulmonary arterial hypertension (PAH). This loading drives changes in mechanobiological stimuli that affect cellular phenotypes and lead to pulmonary vascular remodeling. Computational models have been used to simulate mechanobiological metrics of interest, such as wall shear stress, at single time points for PAH patients. However, there is a need for new approaches that simulate disease evolution to allow for prediction of long-term outcomes. In this work, we develop a framework that models the pulmonary arterial tree through adaptive and maladaptive responses to mechanical and biological perturbations. We coupled a constrained mixture theory-based growth and remodeling framework for the vessel wall with a morphometric tree representation of the pulmonary arterial vasculature. We show that non-uniform mechanical behavior is important to establish the homeostatic state of the pulmonary arterial tree, and that hemodynamic feedback is essential for simulating disease time courses. We also employed a series of maladaptive constitutive models, such as smooth muscle hyperproliferation and stiffening, to identify critical contributors to development of PAH phenotypes. Together, these simulations demonstrate an important step towards predicting changes in metrics of clinical interest for PAH patients and simulating potential treatment approaches.
    Language English
    Publishing date 2023-04-21
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.04.20.537714
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: A computational growth and remodeling framework for adaptive and maladaptive pulmonary arterial hemodynamics.

    Szafron, Jason M / Yang, Weiguang / Feinstein, Jeffrey A / Rabinovitch, Marlene / Marsden, Alison L

    Biomechanics and modeling in mechanobiology

    2023  Volume 22, Issue 6, Page(s) 1935–1951

    Abstract: Hemodynamic loading is known to contribute to the development and progression of pulmonary arterial hypertension (PAH). This loading drives changes in mechanobiological stimuli that affect cellular phenotypes and lead to pulmonary vascular remodeling. ... ...

    Abstract Hemodynamic loading is known to contribute to the development and progression of pulmonary arterial hypertension (PAH). This loading drives changes in mechanobiological stimuli that affect cellular phenotypes and lead to pulmonary vascular remodeling. Computational models have been used to simulate mechanobiological metrics of interest, such as wall shear stress, at single time points for PAH patients. However, there is a need for new approaches that simulate disease evolution to allow for prediction of long-term outcomes. In this work, we develop a framework that models the pulmonary arterial tree through adaptive and maladaptive responses to mechanical and biological perturbations. We coupled a constrained mixture theory-based growth and remodeling framework for the vessel wall with a morphometric tree representation of the pulmonary arterial vasculature. We show that non-uniform mechanical behavior is important to establish the homeostatic state of the pulmonary arterial tree, and that hemodynamic feedback is essential for simulating disease time courses. We also employed a series of maladaptive constitutive models, such as smooth muscle hyperproliferation and stiffening, to identify critical contributors to development of PAH phenotypes. Together, these simulations demonstrate an important step toward predicting changes in metrics of clinical interest for PAH patients and simulating potential treatment approaches.
    MeSH term(s) Humans ; Hypertension, Pulmonary ; Pulmonary Artery ; Lung ; Hemodynamics ; Stress, Mechanical ; Vascular Remodeling
    Language English
    Publishing date 2023-09-02
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 2093052-5
    ISSN 1617-7940 ; 1617-7959
    ISSN (online) 1617-7940
    ISSN 1617-7959
    DOI 10.1007/s10237-023-01744-z
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5966: Show issues Location:
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  7. Article ; Online: Molecular pathogenesis of pulmonary arterial hypertension.

    Rabinovitch, Marlene

    The Journal of clinical investigation

    2012  Volume 122, Issue 12, Page(s) 4306–4313

    Abstract: Recent clinical and experimental studies are redefining the cellular and molecular bases of pulmonary arterial hypertension (PAH). The genetic abnormalities first identified in association with the idiopathic form of PAH--together with a vast increase in ...

    Abstract Recent clinical and experimental studies are redefining the cellular and molecular bases of pulmonary arterial hypertension (PAH). The genetic abnormalities first identified in association with the idiopathic form of PAH--together with a vast increase in our understanding of cell signaling, cell transformation, and cell-cell interactions; gene expression; microRNA processing; and mitochondrial and ion channel function--have helped explain the abnormal response of vascular cells to injury. Experimental and clinical studies now converge on the intersection and interactions between a genetic predisposition involving the BMPR2 signaling pathway and an impaired metabolic and chronic inflammatory state in the vessel wall. These deranged processes culminate in an exuberant proliferative response that occludes the pulmonary arterial (PA) lumen and obliterates the most distal intraacinar vessels. Here, we describe emerging therapies based on preclinical studies that address these converging pathways.
    MeSH term(s) Animals ; Bone Morphogenetic Protein Receptors, Type II/genetics ; Bone Morphogenetic Protein Receptors, Type II/physiology ; Estrogens/metabolism ; Glycolysis ; Humans ; Hypertension, Pulmonary/genetics ; Hypertension, Pulmonary/metabolism ; Hypertension, Pulmonary/physiopathology ; Mutation ; Pancreatic Elastase/metabolism ; Receptors, Serotonin/metabolism ; Serotonin Plasma Membrane Transport Proteins/metabolism ; Signal Transduction ; Stem Cells/metabolism
    Chemical Substances Estrogens ; Receptors, Serotonin ; Serotonin Plasma Membrane Transport Proteins ; BMPR2 protein, human (EC 2.7.11.30) ; Bone Morphogenetic Protein Receptors, Type II (EC 2.7.11.30) ; Pancreatic Elastase (EC 3.4.21.36)
    Language English
    Publishing date 2012-12-03
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI60658
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Inflammatory Basis of Pulmonary Arterial Hypertension: Implications for Perioperative and Critical Care Medicine.

    Goldenberg, Neil M / Rabinovitch, Marlene / Steinberg, Benjamin E

    Anesthesiology

    2019  Volume 131, Issue 4, Page(s) 898–907

    MeSH term(s) Critical Care/methods ; Humans ; Inflammation/complications ; Perioperative Care/methods ; Pulmonary Arterial Hypertension/complications ; Pulmonary Arterial Hypertension/surgery
    Language English
    Publishing date 2019-05-16
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 269-0
    ISSN 1528-1175 ; 0003-3022
    ISSN (online) 1528-1175
    ISSN 0003-3022
    DOI 10.1097/ALN.0000000000002740
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  9. Article: PPARgamma and the pathobiology of pulmonary arterial hypertension.

    Rabinovitch, Marlene

    Advances in experimental medicine and biology

    2010  Volume 661, Page(s) 447–458

    Abstract: Peroxisome proliferator-activated receptor gamma (PPARgamma) is a nuclear receptor that functions as a transcription factor to regulate adipogenesis and metabolism by binding to PPAR response elements (PPAREs) in the promoter region of various target ... ...

    Abstract Peroxisome proliferator-activated receptor gamma (PPARgamma) is a nuclear receptor that functions as a transcription factor to regulate adipogenesis and metabolism by binding to PPAR response elements (PPAREs) in the promoter region of various target genes. Activation of PPARgamma suppresses smooth muscle cell proliferation and migration. This chapter discusses the potential protective role of PPARgamma and its downstream signaling cascades in the development of pulmonary arterial hypertension. Furthermore, the chapter also provides an overview on the cellular and molecular mechanisms involved in PPARgamma-mediated inhibitory effect on pulmonary vascular remodeling, a major contributor to the elevated pulmonary vascular resistance in patients with pulmonary arterial hypertension.
    MeSH term(s) Animals ; Bone Morphogenetic Protein 2/metabolism ; Humans ; Hypertension, Pulmonary/drug therapy ; Hypertension, Pulmonary/pathology ; Hypertension, Pulmonary/physiopathology ; Insulin Resistance ; Myocytes, Smooth Muscle/cytology ; Myocytes, Smooth Muscle/physiology ; PPAR gamma/agonists ; PPAR gamma/genetics ; PPAR gamma/metabolism ; Signal Transduction/physiology
    Chemical Substances Bone Morphogenetic Protein 2 ; PPAR gamma
    Language English
    Publishing date 2010
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2214-8019 ; 0065-2598
    ISSN (online) 2214-8019
    ISSN 0065-2598
    DOI 10.1007/978-1-60761-500-2_29
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Computational simulation-derived hemodynamic and biomechanical properties of the pulmonary arterial tree early in the course of ventricular septal defects.

    Dong, Melody L / Lan, Ingrid S / Yang, Weiguang / Rabinovitch, Marlene / Feinstein, Jeffrey A / Marsden, Alison L

    Biomechanics and modeling in mechanobiology

    2021  Volume 20, Issue 6, Page(s) 2471–2489

    Abstract: Untreated ventricular septal defects (VSDs) can lead to pulmonary arterial hypertension (PAH) characterized by elevated pulmonary artery (PA) pressure and vascular remodeling, known as PAH associated with congenital heart disease (PAH-CHD). Though ... ...

    Abstract Untreated ventricular septal defects (VSDs) can lead to pulmonary arterial hypertension (PAH) characterized by elevated pulmonary artery (PA) pressure and vascular remodeling, known as PAH associated with congenital heart disease (PAH-CHD). Though previous studies have investigated hemodynamic effects on vascular mechanobiology in late-stage PAH, hemodynamics leading to PAH-CHD initiation have not been fully quantified. We hypothesize that abnormal hemodynamics from left-to-right shunting in early stage VSDs affects PA biomechanical properties leading to PAH initiation. To model PA hemodynamics in healthy, small, moderate, and large VSD conditions prior to the onset of vascular remodeling, computational fluid dynamics simulations were performed using a 3D finite element model of a healthy 1-year-old's proximal PAs and a body-surface-area-scaled 0D distal PA tree. VSD conditions were modeled with increased pulmonary blood flow to represent degrees of left-to-right shunting. In the proximal PAs, pressure, flow, strain, and wall shear stress (WSS) increased with increasing VSD size; oscillatory shear index decreased with increasing VSD size in the larger PA vessels. WSS was higher in smaller diameter vessels and increased with VSD size, with the large VSD condition exhibiting WSS >100 dyn/cm[Formula: see text], well above values typically used to study dysfunctional mechanotransduction pathways in PAH. This study is the first to estimate hemodynamic and biomechanical metrics in the entire pediatric PA tree with VSD severity at the stage leading to PAH initiation and has implications for future studies assessing effects of abnormal mechanical stimuli on endothelial cells and vascular wall mechanics that occur during PAH-CHD initiation and progression.
    MeSH term(s) Biomechanical Phenomena ; Computer Simulation ; Heart Septal Defects, Ventricular/physiopathology ; Hemodynamics/physiology ; Humans ; Infant ; Male ; Models, Biological ; Pulmonary Artery/physiopathology
    Language English
    Publishing date 2021-09-28
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 2093052-5
    ISSN 1617-7940 ; 1617-7959
    ISSN (online) 1617-7940
    ISSN 1617-7959
    DOI 10.1007/s10237-021-01519-4
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