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Pulmonary surfactants and their role in pathophysiology of lung disorders

TLDR
The biochemical, physiological, developmental and clinical aspects of pulmonary surfactant are presented in this article to understand the pathophysiological mechanisms of these diseases.
Abstract
Surfactant is an agent that decreases the surface tension between two media. The surface tension between gaseous-aqueous interphase in the lungs is decreased by the presence of a thin layer of fluid known as pulmonary surfactant. The pulmonary surfactant is produced by the alveolar type-II (AT-II) cells of the lungs. It is essential for efficient exchange of gases and for maintaining the structural integrity of alveoli. Surfactant is a secretory product, composed of lipids and proteins. Phosphatidylcholine and phosphatidylglycerol are the major lipid constituents and SP-A, SP-B, SP-C, SP-D are four types of surfactant associated proteins. The lipid and protein components are synthesized separately and are packaged into the lamellar bodies in the AT-II cells. Lamellar bodies are the main organelle for the synthesis and metabolism of surfactants. The synthesis, secretion and recycling of the surfactant lipids and proteins is regulated by complex genetic and metabolic mechanisms. The lipid-protein interaction is very important for the structural organization of surfactant monolayer and its functioning. Alterations in surfactant homeostasis or biophysical properties can result in surfactant insufficiency which may be responsible for diseases like respiratory distress syndrome, lung proteinosis, interstitial lung diseases and chronic lung diseases. The biochemical, physiological, developmental and clinical aspects of pulmonary surfactant are presented in this article to understand the pathophysiological mechanisms of these diseases.

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Effect of particle agglomeration in nanotoxicology.

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The impact of vitamin D on fetal and neonatal lung maturation. A systematic review

TL;DR: The hypothesis of hypovitaminosis D as a frequent, modifiable risk factor of RDS and BPD should be tested in randomized controlled trials on pregnant women, those with threatening preterm delivery, or in the preterm neonates.
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Myc Expression Drives Aberrant Lipid Metabolism in Lung Cancer

TL;DR: A transgenic mouse model of KRAS-driven lung adenocarcinoma that affords reversible activation of MYC is described, showing how MYC drives the production of specific eicosanoids critical for lung cancer cell survival and proliferation, with possible implications for the use of COX and LOX pathway inhibitors for lungcancer therapy.
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Evaluation of the Transwell System for Characterization of Dissolution Behavior of Inhalation Drugs: Effects of Membrane and Surfactant.

TL;DR: The optimized procedure, using membranes with increased permeability and surfactant containing dissolution medium, represents a good starting point to further evaluate in vitro/in vivo correlations.
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Effect of mechanical ventilation on inflammatory mediators in patients with acute respiratory distress syndrome: a randomized controlled trial.

TL;DR: Mechanical ventilation can induce a cytokine response that may be attenuated by a strategy to minimize overdistention and recruitment/derecruitment of the lung, and these physiological improvements are associated with improvements in clinical end points.
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Surface properties in relation to atelectasis and hyaline membrane disease.

TL;DR: Evidence is presented that the material responsible for such a low surface tension is absent in the lungs of infants under 1,100-1,200 gm.
Journal ArticleDOI

Basal cells as stem cells of the mouse trachea and human airway epithelium

TL;DR: The pseudostratified epithelium of the mouse trachea and human airways contains a population of basal cells expressing Trp-63 and cytokeratins 5, which generate differentiated cells during postnatal growth and in the adult during both steady state and epithelial repair.
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Alveolar epithelial type II cell: defender of the alveolus revisited

TL;DR: Controversy about the character of hyperplastic AE2 cells, reported to synthesise profibrotic factors, proscribes drawing a definite conclusion today.
Journal ArticleDOI

Pulmonary Alveolar Proteinosis

TL;DR: In acquired pulmonary alveolar proteinosis, lipids and proteins accumulate within the alveoli becauseAlveolar macrophages cannot catabolize surfactants.
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