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Relevant bibliographies by topics / Surfactant/Lipids

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Journal articles

Academic literature on the topic 'Surfactant/Lipids'

Author: Grafiati

Published: 7 September 2023

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Journal articles on the topic "Surfactant/Lipids"

1

SHIMIZU, Takao. "Biologically Active Lipids: From Prostaglandins to Surfactant Lipids." Journal of the Mass Spectrometry Society of Japan 57, no. 3 (2009): 153–55. http://dx.doi.org/10.5702/massspec.57.153.

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2

Wright, J. R. "Clearance and recycling of pulmonary surfactant." American Journal of Physiology-Lung Cellular and Molecular Physiology 259, no. 2 (1990): L1—L12. http://dx.doi.org/10.1152/ajplung.1990.259.2.l1.

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In a steady state the rate of secretion of pulmonary surfactant lipids and proteins into the alveolar airspace must be balanced by the rate of removal. Several potential pathways for clearance have been identified including uptake by alveolar type II cells, which also synthesize and secrete surfactant components, uptake by other epithelial cells, and internalization by alveolar macrophages. A small amount of surfactant moves up the airways and through the epithelium-endothelium barrier into the blood. Some of the surfactant lipids and proteins that are cleared from the alveolar airspace appear

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3

KEOUGH, KEVIN M. W. "Physicochemical properties of surfactant lipids." Biochemical Society Transactions 13, no. 6 (1985): 1081–84. http://dx.doi.org/10.1042/bst0131081.

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4

Batenburg, J. J. "Surfactant phospholipids: synthesis and storage." American Journal of Physiology-Lung Cellular and Molecular Physiology 262, no. 4 (1992): L367—L385. http://dx.doi.org/10.1152/ajplung.1992.262.4.l367.

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Pulmonary surfactant, a complex consisting of 90% lipids and 10% specific proteins, lines the alveoli of the lung and prevents alveolar collapse and transudation by lowering the surface tension at the air-liquid interface. Dipalmitoylphosphatidylcholine constitutes approximately 50% of the surfactant lipids and is primarily responsible for the surface tension-lowering property of the surfactant mixture. This phospholipid, together with the other surfactant phospholipids, is produced at the endoplasmic reticulum of the alveolar type II epithelial cells. The characteristic lamellar bodies in the

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5

Casals, Cristina, Belen García-Fojeda, Paula Tenreiro, and Carlos M. Minutti. "Surfactant lipids inhibit PI3K-dependent signaling pathways induced by IL-4 in alveolar macrophages." Journal of Immunology 210, no. 1_Supplement (2023): 72.32. http://dx.doi.org/10.4049/jimmunol.210.supp.72.32.

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Abstract Alveolar macrophages (AMs) are less able to respond to IL-4 in vivo than macrophages from the peritoneal cavity, due to a still-unknown factor of the lung environment. The aim of this study is to investigate whether surfactant lipids, which are continuously endocytosed by AMs, could influence IL-4-mediated alternative activation and proliferation of AMs. To that end, AMs were preincubated with surfactant lipids and stimulated with IL-4 in the presence or absence of surfactant protein SP-A, an amplifier of IL-4 actions. We found that alveolar lipids reduced IL-4- and IL-4+SP-A-dependen

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6

Mudgil, Poonam, and Thomas J. Millar. "Surfactant Properties of Human Meibomian Lipids." Investigative Opthalmology & Visual Science 52, no. 3 (2011): 1661. http://dx.doi.org/10.1167/iovs.10-5445.

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7

Van Iwaarden, J. F., H. Shimizu, P. H. M. Van Golde, D. R. Voelker, and L. M. G. Van Golde. "Rat surfactant protein D enhances the production of oxygen radicals by rat alveolar macrophages." Biochemical Journal 286, no. 1 (1992): 5–8. http://dx.doi.org/10.1042/bj2860005.

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Rat surfactant protein D (SP-D) was shown to enhance the production of oxygen radicals by rat alveolar macrophages. This enhancement, which was determined by a lucigenin-dependent chemiluminescence assay, was maximal after 18 min at an SP-D concentration of 0.2 micrograms/ml. Surfactant lipids did not influence the stimulation of alveolar macrophages by SP-D, whereas the oxygen-radical production of these cells induced by surfactant protein A was inhibited by the lipids in a concentration-dependent manner.

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8

Kremlev, S. G., and D. S. Phelps. "Effect of SP-A and surfactant lipids on expression of cell surface markers in the THP-1 monocytic cell line." American Journal of Physiology-Lung Cellular and Molecular Physiology 272, no. 6 (1997): L1070—L1077. http://dx.doi.org/10.1152/ajplung.1997.272.6.l1070.

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Pulmonary surfactant and its lipid components inhibit cell proliferation and cytokine expression. Surfactant protein A (SP-A) can stimulate these same functions. We assessed the impact of SP-A and surfactant lipids on the expression of the cell surface markers, CD14, CD54 (intercellular adhesion molecule-1), and CD11b, by the human monocytic cell line THP-1 using fluorescent antibody staining and fluorescence-activated cell sorting. Under basal conditions CD14 and CD54 were undetectable, and CD11b was expressed at low levels. Incubation of the cells in 1,25(OH)2D3 alone, or with low doses of s

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9

Soll, Roger F., and Jerold F. Lucey. "Surfactant Replacement Therapy." Pediatrics In Review 12, no. 9 (1991): 261–67. http://dx.doi.org/10.1542/pir.12.9.261.

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Despite medical and technological advances, respiratory distress syndrome (RDS) remains a major cause of morbidity and mortality in premature infants. Thirty years have passed since Avery and Mead demonstrated that infants dying of RDS were deficient in pulmonary surfactant. In those three decades, advances in our understanding of the composition, function, and metabolism of pulmonary surfactant have finally led to clinical trials of surfactant replacement therapy in thousands of premature infants. This article reviews the current status of surfactant replacement therapy. BACKGROUND Pulmonary

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10

Kremlev, S. G., T. M. Umstead, and D. S. Phelps. "Surfactant protein A regulates cytokine production in the monocytic cell line THP-1." American Journal of Physiology-Lung Cellular and Molecular Physiology 272, no. 5 (1997): L996—L1004. http://dx.doi.org/10.1152/ajplung.1997.272.5.l996.

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Surfactant lipids inhibit cytokine production by immune cells, and surfactant protein A (SP-A) stimulates it. By enzyme-linked immunosorbent assay and mRNA blotting, we studied proinflammatory cytokine production by the monocytic cell line THP-1. SP-A caused increases in tumor necrosis factor (TNF)-alpha within 1 h, peaking at 4 h and then declining. Interleukin (IL)-1 beta increased and stayed elevated for 24 h. SP-A stimulated IL-8 also, peaking at 4 h, rapidly declining, and peaking again at 24 h. SP-A-dependent changes were detected for IL-6, but at higher SP-A doses. mRNA levels for TNF-a

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