Relevant bibliographies by topics / Surfactant/Lipids

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Surfactant/Lipids'

Author: Grafiati
Published: 7 September 2023

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Journal articles on the topic "Surfactant/Lipids"

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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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Wright, J. R. "Clearance and recycling of pulmonary surfactant." American Journal of Physiology-Lung Cellular and Molecular Physiology 259, no. 2 (August 1, 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 to be “recycled” in that they appear in the lamellar body, a surfactant secretory granule found in the type II cell. Some surfactant lipids are degraded, probably intracellularly, and the degradation products are reutilized to synthesize new lipids. Several factors have been shown to affect internalization by the type II cell and/or alveolar clearance including the surfactant proteins, lipids, and known stimuli of surfactant secretion. Surfactant proteins may be involved in regulating pool size by modulating both secretion rates and uptake rates, possibly by a receptor-mediated process, although such receptors have not yet been identified or isolated. Clearance of surfactant lipids from the alveolar airspace is more rapid than clearance from the whole lung, and these two processes may be regulated by different factors. Elucidation of the factors that fine tune the balance between synthesis, secretion, and clearance of the lipid and protein components of surfactant awaits further investigation
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KEOUGH, KEVIN M. W. "Physicochemical properties of surfactant lipids." Biochemical Society Transactions 13, no. 6 (December 1, 1985): 1081–84. http://dx.doi.org/10.1042/bst0131081.

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Batenburg, J. J. "Surfactant phospholipids: synthesis and storage." American Journal of Physiology-Lung Cellular and Molecular Physiology 262, no. 4 (April 1, 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 these cells serve as storage depot for the surfactant before this is secreted onto the alveolar surface. This article reviews the pathways via which the surfactant lipids are synthesized, our current knowledge of the regulation of these pathways, and what is known about intracellular traffic of phospholipids from their site of synthesis to the lamellar bodies.
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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 (May 1, 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-dependent arginase activity, the expression of genes associated with alternative activation, and proliferation of AMs. Mechanistically, endocytosed lipids decreased IL-4- and IL-4+SP-A-induced activation of the PI3K-Akt-mTORC1 signaling axis, but not the IL-4-dependent STAT6 axis. Lipid-dependent inhibition of the Akt/mTORC1 signaling axis is consistent with reduced IL-4+SP-A-driven glycolysis and mitochondrial respiration as well as decreased ATP citrate lyase expression and histone acetylation stimulated by IL-4. We conclude that surfactant lipids inhibit PI3K-dependent signaling pathways and suggest that decrease of surfactant lipids in chronic lung diseases might augment IL-4-dependent fibrotic responses. This research is funded by the Spanish Ministry of Science and Innovation through Grant PID2021-123044OB-I00 to C. Casals
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Mudgil, Poonam, and Thomas J. Millar. "Surfactant Properties of Human Meibomian Lipids." Investigative Opthalmology & Visual Science 52, no. 3 (March 24, 2011): 1661. http://dx.doi.org/10.1167/iovs.10-5445.

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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 (August 15, 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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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 (June 1, 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 surfactant lipids, increased CD14, CD54, and CD11b. Expression was increased further by SP-A. However, the SP-A-induced increases in cell markers were blocked by simultaneous treatment with lipid. The results suggest that the ability of the macrophage to participate in an inflammatory response is enhanced by SP-A alone or by surfactant containing a higher than normal proportion of SP-A. They further suggest that the addition of lipids results in a phenotype less prone to initiate an inflammatory reaction.
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Soll, Roger F., and Jerold F. Lucey. "Surfactant Replacement Therapy." Pediatrics In Review 12, no. 9 (March 1, 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 surfactant is essential for normal lung function. Surfactant forms a film at the alveolar surface, which prevents the lung from collapsing at the end of expiration. Surfactant may have other functions as well, including the prevention of pulmonary edema, the prevention of infection, and the prevention of lung injury from toxic substances, such as oxygen (Table 1) CHEMICAL MAKEUP The chemical makeup of pulmonary surfactant has been well defined (Table 2). Lipids are the major component, comprising up to 80% to 90% of surfactant by weight. The majority of the lipids in pulmonary surfactant are highly polar phospholipids, predominantly phosphatidylcholine. Three proteins associated with surfactant have been these surfactant proteins may play a critical role in surfactant function by improving the adsorption of surfactant at the alveolar surface and by aiding in surfactant re-uptake and metabolism.
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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 (May 1, 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-alpha and IL-1 beta increased in response to SP-A, peaking within 2 h. The increases in TNF-alpha mRNA and protein induced by SP-A were inhibited by surfactant lipids. For IL-1 beta and IL-8, the lipids either had no inhibitory influence or inhibited less than for TNF-alpha. This suggests that the ability of macrophages to participate in inflammatory reactions is enhanced by SP-A alone or by mixtures of lipids and SP-A containing more SP-A than in normal surfactant, as occurs in many conditions leading to inflammation.
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Dissertations / Theses on the topic "Surfactant/Lipids"

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Nag, Kaushik. "Association and interactions of pulmonary surfactant lipids and proteins in model membranes at the air-water interface." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1996. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ56665.pdf.

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Alghaithy, Abdulaziz. "Induction of interleukin-8 in lung epithelial cells by Gram negative bacteria and its modulation by pulmonary surfactant lipids." Thesis, Cardiff University, 2006. http://orca.cf.ac.uk/54104/.

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The surfactants did not inhibit IL-8 induced by IL-1[Special character omitted.] in A549 cells suggesting that they act at the level of the LPS receptor complex. Disruption of membrane micro-domains ('rafts') with methyl-[Special character omitted.]-cyclodextrin significantly inhibited bacteria and LPS induced IL-8 in A549 cells. Isolation of membrane raft containing fractions by sucrose density gradient ultra-centrifugation showed that TLR4 is recruited into membrane lipid rafts on cell stimulation with the bacteria or LPS. The surfactants inhibited the bacterial and LPS mediated translocation of TLR4 into raft domains suggesting that their mechanism of action involves inhibition of LPS receptor complex formation in lipid raft domains.
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Ocampo, Minette C. "Protein-Lipid Interactions with Pulmonary Surfactant Using Atomic Force Microscopy." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1395050693.

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Schief, William R. "Phase transitions in two-dimensional model systems /." Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/9806.

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Hajhassan, Houssein. "Synthese et etude de la structure et de proprietes de lipopeptides amphipatiques." Orléans, 1987. http://www.theses.fr/1987ORLE2007.

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Des lipopeptides amphipathes ont ete synthetises : suivant la methode utilisee. On obtient des lipsamino-acides ou des lipopeptides ; etude par diffraction x, proprietes tensio-actives, pouvoir emulsifiant. Par le test d'hemolyse, il a ete montre que certains lipopeptides ont une hemocompatibilite similaire a celles des meilleurs tensio-actifs bicatenaires
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Book chapters on the topic "Surfactant/Lipids"

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Haagsman, Henk P., Joseph J. Batenburg, Cecile Clercx, Math J. H. Geelen, and Lambert M. G. van Golde. "Surfactant Lipids and Proteins in the Perinatal and Adult Lung." In Endocrine and Biochemical Development of the Fetus and Neonate, 231–50. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4615-9567-0_24.

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Al-Saiedy, Mustafa, Francis Green, and Matthias Amrein. "The Effects of Free Radicals on Pulmonary Surfactant Lipids and Proteins." In Oxidative Stress in Lung Diseases, 3–24. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-32-9366-3_1.

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Kim, Hyungjun. "Interfacial Reactions of Ozone with Lipids and Proteins in a Model Lung Surfactant System." In Springer Theses, 107–23. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-7601-7_7.

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Beattie, J. Renwick, and Bettina C. Schock. "Identifying the Spatial Distribution of Vitamin E, Pulmonary Surfactant and Membrane Lipids in Cells and Tissue by Confocal Raman Microscopy." In Methods in Molecular Biology, 513–35. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-322-0_26.

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Shinoda, Wataru, and Masakatsu Hato. "Molecular Dynamics Study of Isoprenoid-Chained Lipids: Salient Features of Isoprenoid Chains As Compared with Ordinary Alkyl Chains." In Self-Organized Surfactant Structures, 175–94. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2010. http://dx.doi.org/10.1002/9783527632633.ch9.

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Whitsett, Jeffrey A. "Composition of Pulmonary Surfactant Lipids and Proteins." In Fetal and Neonatal Physiology, 1084–93. Elsevier, 2011. http://dx.doi.org/10.1016/b978-1-4160-3479-7.10100-4.

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Bourbon, Jacques R. "Nature, Function, and Biosynthesis of Surfactant Lipids." In Pulmonary Surfactant: Biochemical, Functional, Regulatory, and Clinical Concepts, 37–76. CRC Press, 2019. http://dx.doi.org/10.1201/9780367812812-3.

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KALYANASUNDARAM, K. "Photoprocesses in Lipids, Surfactant Vesicles, and Liposomes." In Photochemistry in Microheterogeneous Systems, 173–220. Elsevier, 1987. http://dx.doi.org/10.1016/b978-0-12-394995-0.50010-8.

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Whitsett, Jeffrey A. "Composition of Pulmonary Surfactant Lipids and Proteins." In Fetal and Neonatal Physiology, 1005–13. Elsevier, 2004. http://dx.doi.org/10.1016/b978-0-7216-9654-6.50103-x.

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Bourke, S. J. "Lipoid (lipid) pneumonia." In Oxford Textbook of Medicine, edited by Pallav L. Shah, 4263–65. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0429.

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Lipoid pneumonia is an unusual form of lung disease resulting from the accumulation of lipids in the alveoli, where they provoke a foreign body reaction with associated inflammation and sometimes local fibrosis. The lipids may be endogenous or exogenous in origin, and the clinical mechanisms and circumstances differ accordingly. Exogenous lipoid pneumonia occurs when animal, vegetable, or mineral oils are aspirated or inhaled into the lungs, provoking a foreign body reaction with chronic inflammation. Typical symptoms are cough and breathlessness. The chest radiograph and CT may show interstitial thickening, with areas of consolidation that may coalesce into a mass (paraffinoma) which simulates carcinoma. Bronchoalveolar lavage and biopsy show lipid-laden macrophages. In endogenous lipoid pneumonia the lipids are derived from surfactant and cholesterol released from decaying cells distal to bronchial obstruction.
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Conference papers on the topic "Surfactant/Lipids"

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Numata-Nakamura, M., H. Lee, H. W. Chu, M. A. Seibold, and D. R. Voelker. "Pulmonary Surfactant Lipids Antagonize Human Rhinovirus Infections." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5757.

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Numata-Nakamura, M., Y. A. Bochkov, H. Ruder, M. A. Seibold, A. H. Liu, and D. R. Voelker. "Pulmonary Surfactant Lipids as Novel Lipids Antivirals Against Human Rhinovirus-C Infection." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7428.

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Hall, S. B., R. Loney, M. Dagan, and S. Rananavare. "An Alkane Promotes Rapid Adsorption by the Surfactant Lipids." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a4052.

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MISRA, MANOJ, and K. ANANTHAPADMANABHAN. "QUANTITATIVE ANALYSIS OF SURFACTANT INDUCED ULTRASTRUCTURAL CHANGES IN SKIN LIPIDS." In Proceedings of the Fifth Royal Society–Unilever Indo-UK Forum in Materials Science and Engineering. A CO-PUBLICATION OF IMPERIAL COLLEGE PRESS AND THE ROYAL SOCIETY, 2000. http://dx.doi.org/10.1142/9781848160163_0012.

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Nakamura, Mari, Yoji Nagashima, Pitchaimani Kandasamy, Kevan L. Hartshorn, and Dennis R. Voelker. "Anionic Pulmonary Surfactant Lipids Inhibit Influenza A Virus Induced Inflammation And Infection." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1047.

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Nishitani, Chiaki, Shigeru Ariki, Motoko Takahashi, Yuichiro Kurimura, Atsushi Saito, Takeyuki Shimizu, and Yoshio Kuroki. "Oxidized Surfactant Lipids And Oxidized PAPC Attenuate LPS-Induced Inflammatory Responses By Different Mechanisms." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1098.

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García-Fojeda, Belén, Carlos Minutti, Marianela Landoni, Paula Tenreiro, and Cristina Casals. "Lung surfactant lipids reduce the alternative activation and proliferation of alveolar macrophages induced by IL-4." In ERS Lung Science Conference 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/23120541.lsc-2022.251.

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Villeneuve, Pierre, Claire Bourlieu-Lacanal, David McClements, Eric Decker, and Erwann Durand. "Lipid oxidation in emulsions and bulk oils: A review of the importance of micelles." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/lzak8107.

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Lipid oxidation is a major cause of quality deterioration in food or cosmetic products. In these matrices, lipids are often present in a bulk or in emulsified forms. In both systems, the rate, extent and pathway of oxidation are highly dependent on the presence of colloidal structures and interfaces because these are the locations where oxidation normally occurs. In bulk oils, reverse micelles (association colloids) are present and are believed to play a crucial role on lipid oxidation. Conversely, in emulsions, surfactant micelles are present that also play a major role in lipid oxidation pathways. This review discusses the current understanding of the influence of micellar structures on lipid oxidation. In particular, is discussed the major impact of the presence of micelles in emulsions, or reverse micelles (association colloids) in bulk oil on the oxidative stability of both systems. Indeed, both micelles in emulsions and associate colloids in bulk oil are discussed as nanoscale structures that can serve as reservoirs of antioxidants and pro-oxidants and are involved in their transport within the concerned system. Their role as nanoreactors where lipid oxidation reactions occur is also commented. Significance of your research to the AOCS membership? The results underline the importance of a better understanding of the role of micelles in the control of lipid oxidation in food or cosmetic products.
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Tamaddoni, Nima, Graham J. Taylor, and Stephen A. Sarles. "Robust Sensing and Reversible Actuation Using Triblock Copolymer Stabilized Intradroplet Interfaces." In ASME 2015 Conference on Smart Materials, Adaptive Structures and Intelligent Systems. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/smasis2015-8840.

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In this work, a recently developed method for forming copolymer-stabilized interfaces (CSI) between aqueous droplets is pursued to as a means to construct smart materials and systems. The ABA type copolymer employed consists of two hydrophilic (PEO) groups sandwiching a hydrophobic PDMS core. Aqueous droplets submerged in triblock copolymer (PEO-PDMS-PEO)-oil mixtures are rapidly coated in copolymer monolayers, however, unlike phospholipid-stabilized droplet interface bilayers (DIBs), electrical measurements reveal that there is no spontaneous formation of a “thinned” interface with droplet contact alone. The capacitance of the interface begins increasing significantly only upon application of sufficient voltage (>100mV), and capacitance then stabilizes within minutes. Further, the interfacial capacitance and area decreases when applied voltage is reduced back to 0mV, and droplets eventually return to their initial separated state. The fact that droplet adhesion and formation of the interface is voltage dependent and completely reversible clearly distinguishes a CSI from a DIB, and the novel polymer based interface is significantly more robust with average rupture potential of ≥ 800mV compared to 200–300mV with DIBs. Durable and stable CSIs could feasibly be used in applications ranging from sensing and energy harvesting to mechanical actuation. To demonstrate, this work introduces a new version of the DIB based hair cell sensor, now replacing lipids with block copolymers to provide greater durability, stability, and resistance to rupture when subjected to airflow. We calculate the current generated by the vibrating membranes in DIBs and CSIs to study the influence of surfactant selection on the hair cell durability and the related airflow operation range. We conclude that the hair cell constructed using triblock copolymer, as opposed to a DIB, withstands higher nominal airflow speeds (45m/s) and higher applied bias voltages (i.e. 0.1–1V) without rupturing. The ability to apply higher voltages provides a means of tuning the hair-cell sensitivity. Separately, the results of initial trials demonstrate the possibility for voltage-controlled shape change using networks of droplets and CSIs. The ability to apply large voltages and induce change in interfacial area leads to rearrangement of the droplet networks due to conservation of volume. Several embodiments of possible actuators based on this mechanism are discussed. In concert, the various aspects of this work highlight the potential use of CSIs in developing novel, reliable smart materials for sensing and actuation.
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