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Pulmonary arterial hypertension and nifedipine : pathogenesis and management [E-Book]

Contributor(s): Series: New developments in medical researchPublisher: New York : Nova Biomedical, [2015]Description: 1 online resourceContent type:
  • text
Media type:
  • computer
Carrier type:
  • online resource
ISBN:
  • 9781634826358
  • 1634826353
Subject(s): Online resources:
Contents:
Chapter I: Mechanisms of Vascular Remodeling in Pulmonary Arterial Hypertension; Abstract; Introduction; Classification; Symptoms and Diagnosis; Biomarkers; Pathogenesis of PAH; i) Role of Endothelial Cells and Their Cross Talk with Different Cell Types in Vasculature; Endothelial Response to Injury; Endothelial Dysfunction and Vasoconstriction/Vasodilatation.
Endothelial Dysfunction and Impaired AngiogenesisEndothelial Dysfunction and Plexiform Lesions; ii) Role of Inflammation and Autoimmunity; Inflammatory Cells; Cytokines and Chemokines; Molecular Mechanisms Contributing to PAH-PASMC and PAEC Proliferation and Resistance to Apoptosis; The Src/STAT3 Integrative Hub; Metabolic Switch: The Warburg Effect; Epigenetic Mechanisms of PH; Role for miRNAs; DNA Methylation; Modification of Histone Proteins; Potential Implication of Long Noncoding RNA; Vascular Stiffening in PAH: A Cause; or Consequence?; Treatment.
Basic Measures and Conventional TherapiesApproved PAH Therapies; 1) Prostacyclin Pathway; 2) Endothelin Pathway; 3) Nitric Oxide-cGMP Pathway; New Drugs in Early Phase of Development; i) Newer Agents Targeting Established Vasodilatory Pathways; ii) Tyrosine Kinase Inhibition; iii) Serotonin System; iv) Vasoactive Intestinal Peptide; v) RhoA/Rho-Kinase Signaling Pathway; vi) Statins; vii) Apelin; viii) Anti-inflammatory therapies; ix) Restoration of BMPR-II Signaling Axis; Procedures/Nonmedical Therapies; Expected Novel Drugs in Future/ Therapies under Investigation; Gap in Knowledge.
Iv) Neprilysin Knockout ModelOverexpression Models; i) Interleukin-6 Overexpression Model; ii) S100A4/Mts-1 Overexpression Model; Methods to Study PAH; In-vitro Methods; I. Isolation and Culture of Primary Cells; i) Human pulmonary artery endothelial cells from transplant donors; ii) Isolation of pulmonary artery smooth muscle cells; Method; Histological and Morphological Analysis; 1. Hematoxylin and Eosin (H & E) Staining; H & E Staining of Frozen Sections of Pulmonary Artery; Method; H & E Staining for Parrafin Sections of Pulmonary Artery; Method; 2. Masson's Trichrome Staining; Procedure.
Summary: Pulmonary arterial hypertension (PAH) is a progressive, fatal syndrome characterized by increased vascular resistance that leads to right-ventricular hypertrophy and heart failure, eventually leading to death. The chapters of this book describe the molecular mechanisms and cellular events regulating vascular remodeling in PAH; the various animal models and drugs currently being used in various laboratories to study mechanisms leading to pulmonary arterial hypertension; and nifedipine, its pharmacology and it's role in the management of pulmonary hypertension and some of the drawbacks concernin.
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Includes bibliographical references and index.

Description based on print version record.

Chapter I: Mechanisms of Vascular Remodeling in Pulmonary Arterial Hypertension; Abstract; Introduction; Classification; Symptoms and Diagnosis; Biomarkers; Pathogenesis of PAH; i) Role of Endothelial Cells and Their Cross Talk with Different Cell Types in Vasculature; Endothelial Response to Injury; Endothelial Dysfunction and Vasoconstriction/Vasodilatation.

Endothelial Dysfunction and Impaired AngiogenesisEndothelial Dysfunction and Plexiform Lesions; ii) Role of Inflammation and Autoimmunity; Inflammatory Cells; Cytokines and Chemokines; Molecular Mechanisms Contributing to PAH-PASMC and PAEC Proliferation and Resistance to Apoptosis; The Src/STAT3 Integrative Hub; Metabolic Switch: The Warburg Effect; Epigenetic Mechanisms of PH; Role for miRNAs; DNA Methylation; Modification of Histone Proteins; Potential Implication of Long Noncoding RNA; Vascular Stiffening in PAH: A Cause; or Consequence?; Treatment.

Basic Measures and Conventional TherapiesApproved PAH Therapies; 1) Prostacyclin Pathway; 2) Endothelin Pathway; 3) Nitric Oxide-cGMP Pathway; New Drugs in Early Phase of Development; i) Newer Agents Targeting Established Vasodilatory Pathways; ii) Tyrosine Kinase Inhibition; iii) Serotonin System; iv) Vasoactive Intestinal Peptide; v) RhoA/Rho-Kinase Signaling Pathway; vi) Statins; vii) Apelin; viii) Anti-inflammatory therapies; ix) Restoration of BMPR-II Signaling Axis; Procedures/Nonmedical Therapies; Expected Novel Drugs in Future/ Therapies under Investigation; Gap in Knowledge.

Iv) Neprilysin Knockout ModelOverexpression Models; i) Interleukin-6 Overexpression Model; ii) S100A4/Mts-1 Overexpression Model; Methods to Study PAH; In-vitro Methods; I. Isolation and Culture of Primary Cells; i) Human pulmonary artery endothelial cells from transplant donors; ii) Isolation of pulmonary artery smooth muscle cells; Method; Histological and Morphological Analysis; 1. Hematoxylin and Eosin (H & E) Staining; H & E Staining of Frozen Sections of Pulmonary Artery; Method; H & E Staining for Parrafin Sections of Pulmonary Artery; Method; 2. Masson's Trichrome Staining; Procedure.

Pulmonary arterial hypertension (PAH) is a progressive, fatal syndrome characterized by increased vascular resistance that leads to right-ventricular hypertrophy and heart failure, eventually leading to death. The chapters of this book describe the molecular mechanisms and cellular events regulating vascular remodeling in PAH; the various animal models and drugs currently being used in various laboratories to study mechanisms leading to pulmonary arterial hypertension; and nifedipine, its pharmacology and it's role in the management of pulmonary hypertension and some of the drawbacks concernin.

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