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Inflammation, growth factors, and pulmonary vascular remodeling.

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TLDR
An overview of specific inflammatory pathways involving cells, chemokines and cytokines, cellular dysfunctions, growth factors, and viral proteins is provided, highlighting their potential role in pulmonary vascular remodeling and the possibility of future targeted therapy.
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This article is published in Journal of the American College of Cardiology.The article was published on 2009-06-30 and is currently open access. It has received 646 citations till now. The article focuses on the topics: Vascular endothelial growth factor B & Growth factor.

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Special article2015 ESC/ERS Guidelines for the Diagnosis and Treatment of Pulmonary Hypertension

TL;DR: This article is being published concurrently in the European Heart Journal and the European Respiratory Journal and is identical except for minor stylistic and spelling differences in keeping with each journal’s style.
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Mechanisms of disease: pulmonary arterial hypertension

TL;DR: Perturbations of a number of molecular mechanisms have been described, including pathways involving growth factors, cytokines, metabolic signaling, elastases, and proteases, that may underlie the pathogenesis of the disease.
References
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Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia

TL;DR: After 5 years of follow-up, continuous treatment of chronic-phase CML with imatinib as initial therapy was found to induce durable responses in a high proportion of patients.
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NFAT proteins: key regulators of T-cell development and function

TL;DR: This Review focuses on the recent advances in the understanding of the regulation, mechanism of action and functions of NFAT proteins in T cells.
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Reversal of experimental pulmonary hypertension by PDGF inhibition.

TL;DR: STI571 reverses vascular remodeling and cor pulmonale in severe experimental pulmonary hypertension regardless of the initiating stimulus, and offers a unique novel approach for antire-modeling therapy in progressed pulmonary hypertension.
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HIV-1 Nef protein protects infected primary cells against killing by cytotoxic T lymphocytes

TL;DR: It is found that CTLs inefficiently lysed primary cells infected with HIV-1 if the viral nef gene product was expressed and Nef protected infected cells by reducing the epitope density on their surface.
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