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Journal articles on the topic 'Foam cells'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 March 2023

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1

Damiani, Stefania, Maria Grazia Cattani, Laura Buonamici, and V. Eusebi. "Mammary foam cells." Virchows Archiv 432, no. 5 (May 19, 1998): 433–40. http://dx.doi.org/10.1007/s004280050187.

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2

FOWLER, STANLEY D., EUGENE P. MAYER, and PHILLIP GREENSPAN. "Foam Cells and Atherogenesisa." Annals of the New York Academy of Sciences 454, no. 1 (October 1985): 79–90. http://dx.doi.org/10.1111/j.1749-6632.1985.tb11846.x.

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3

Yu, Xiao-Hua, Yu-Chang Fu, Da-Wei Zhang, Kai Yin, and Chao-Ke Tang. "Foam cells in atherosclerosis." Clinica Chimica Acta 424 (September 2013): 245–52. http://dx.doi.org/10.1016/j.cca.2013.06.006.

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4

Kraynik, Andrew M. "Foam Structure: From Soap Froth to Solid Foams." MRS Bulletin 28, no. 4 (April 2003): 275–78. http://dx.doi.org/10.1557/mrs2003.80.

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AbstractThe properties of solid foams depend on their structure, which usually evolves in the fluid state as gas bubbles expand to form polyhedral cells. The characteristic feature of foam structure—randomly packed cells of different sizes and shapes—is examined in this article by considering soap froth. This material can be modeled as a network of minimal surfaces that divide space into polyhedral cells. The cell-level geometry of random soap froth is calculated with Brakke's Surface Evolver software. The distribution of cell volumes ranges from monodisperse to highly polydisperse. Topological and geometric properties, such as surface area and edge length, of the entire foam and individual cells, are discussed. The shape of struts in solid foams is related to Plateau borders in liquid foams and calculated for different volume fractions of material. The models of soap froth are used as templates to produce finite element models of open-cell foams. Three-dimensional images of open-cell foams obtained with x-ray microtomography allow virtual reconstruction of skeletal structures that compare well with the Surface Evolver simulations of soap-froth geometry.
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5

Shashkin, P., B. Dragulev, and K. Ley. "Macrophage Differentiation to Foam Cells." Current Pharmaceutical Design 11, no. 23 (September 1, 2005): 3061–72. http://dx.doi.org/10.2174/1381612054865064.

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6

Kruth, Howard, S. "Macrophage foam cells and atherosclerosis." Frontiers in Bioscience 6, no. 1 (2001): d429. http://dx.doi.org/10.2741/kruth.

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7

Kruth, Howard S. "Macrophage foam cells and atherosclerosis." Frontiers in Bioscience 6, no. 3 (2001): d429–455. http://dx.doi.org/10.2741/a620.

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8

Parthasarathy, S., T. R. Das, R. Kumar, and K. S. Gopalakrishnan. "Foam separation of microbial cells." Biotechnology and Bioengineering 32, no. 2 (July 5, 1988): 174–83. http://dx.doi.org/10.1002/bit.260320207.

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9

Beranek, J. T. "Histogenesis of foam cells in xanthomas." Clinical and Experimental Dermatology 16, no. 5 (September 1991): 402. http://dx.doi.org/10.1111/j.1365-2230.1991.tb00414.x.

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10

Reiss, Allison B., and Bruce N. Cronstein. "Regulation of Foam Cells by Adenosine." Arteriosclerosis, Thrombosis, and Vascular Biology 32, no. 4 (April 2012): 879–86. http://dx.doi.org/10.1161/atvbaha.111.226878.

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11

FRANCO, M., F. SCHMITT, W. A. REJAILI, R. M. VIERO, and C. E. BACCHI. "Renal interstitial foam cells are macrophages." Histopathology 20, no. 2 (February 1992): 173–76. http://dx.doi.org/10.1111/j.1365-2559.1992.tb00949.x.

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12

Dabbs, David J. "Mammary ductal foam cells: Macrophage immunophenotype." Human Pathology 24, no. 9 (September 1993): 977–81. http://dx.doi.org/10.1016/0046-8177(93)90111-s.

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13

Krishnamurthy, S., and H. M. Kuerer. "FOAM CELLS IN NIPPLE ASPIRATION FLUID." Cytopathology 13, no. 1 (February 2002): 64. http://dx.doi.org/10.1046/j.1365-2303.2002.0362a.x.

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14

Zakaria, Zunaida, Zulkifli Mohamad Ariff, and Azhar Abu Bakar. "Monitoring deformation mechanism of foam cells in polyethylene foams via optical microscopy: Effect of density and microstructure." Journal of Cellular Plastics 54, no. 6 (August 27, 2018): 957–76. http://dx.doi.org/10.1177/0021955x18795035.

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The effect of cellular microstructure and density of low-density polyethylene (LDPE) foam during the compressive deformation were evaluated. Progressive foam cell structure deformation at crosshead speed of 10 mm/min was closely monitored and captured using a portable digital microscope with the assistance of a proposed coating technique to enhance contrast of the foam cells. Results revealed that higher density foam, LDPE1.0, experienced higher compressive stress than the LDPE0.5 foam. It was believed that thicker cell walls in the LDPE1.0 foam contributed to the foam stiffness and higher stress was required to impose cell bending, buckling, and collapse. It was also discovered that the existence of larger cells within a group or cluster of small cells in the LDPE1.0 foam acted as stress concentration points and initiated the formation of shear bands in the foam cells deformation mechanism. The extent of compressive strain on the foam cells were also investigated, and results showed that cells undergo lower compressive strain compared to the actual deformation level given directly by the machine crosshead. Cells located in the middle section of the foam recorded a strain of about 13% when the bulk foam was deformed at 20% strain. The success in capturing the actual cell strain using the proposed coating technique proved that with the right improvisation, the micromechanical deformation of optically challenged white polyethylene foam samples can be monitored effectively using optical microscopy.
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15

Claudy, A. L., L. Misery, D. Serre, and S. Boucheron. "Multiple Juvenile Xanthogranulomas Without Foam Cells and Giant Cells." Pediatric Dermatology 10, no. 1 (March 1993): 61–63. http://dx.doi.org/10.1111/j.1525-1470.1993.tb00017.x.

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16

TANZ, WARREN S., Y. ALYSSA KIM, ROBERT A. SCHWARTZ, THOMAS WALTERS, CAMILA K. JANNIGER, and W. CLARK LAMBERT. "JUVENILE XANTHOGRANULOMA WITH INCONSPICUOUS FOAM CELLS AND GIANT CELLS." International Journal of Dermatology 34, no. 9 (September 1995): 653–55. http://dx.doi.org/10.1111/j.1365-4362.1995.tb01104.x.

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17

Davies, J. D. "Mammary ductal foam cells: Macrophage immunophenotype for further cells?" Human Pathology 25, no. 2 (February 1994): 214. http://dx.doi.org/10.1016/0046-8177(94)90282-8.

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18

Kloc, Malgorzata, Jacek Z. Kubiak, and Rafik M. Ghobrial. "Macrophage-, Dendritic-, Smooth Muscle-, Endothelium-, and Stem Cells-Derived Foam Cells in Atherosclerosis." International Journal of Molecular Sciences 23, no. 22 (November 16, 2022): 14154. http://dx.doi.org/10.3390/ijms232214154.

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Atherosclerosis is an inflammatory disease depending on the buildup, called plaque, of lipoproteins, cholesterol, extracellular matrix elements, and various types of immune and non-immune cells on the artery walls. Plaque development and growth lead to the narrowing of the blood vessel lumen, blocking blood flow, and eventually may lead to plaque burst and a blood clot. The prominent cellular components of atherosclerotic plaque are the foam cells, which, by trying to remove lipoprotein and cholesterol surplus, also participate in plaque development and rupture. Although the common knowledge is that the foam cells derive from macrophages, studies of the last decade clearly showed that macrophages are not the only cells able to form foam cells in atherosclerotic plaque. These findings give a new perspective on atherosclerotic plaque formation and composition and define new targets for anti-foam cell therapies for atherosclerosis prevention. This review gives a concise description of foam cells of different pedigrees and describes the main mechanisms participating in their formation and function.
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19

Banka, CL, AS Black, CA Dyer, and LK Curtiss. "THP-1 cells form foam cells in response to coculture with lipoproteins but not platelets." Journal of Lipid Research 32, no. 1 (January 1991): 35–43. http://dx.doi.org/10.1016/s0022-2275(20)42241-2.

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20

Ravnskov, Uffe, and Kilmer S. McCully. "How Macrophages are Converted to Foam Cells." Journal of Atherosclerosis and Thrombosis 19, no. 10 (2012): 949–50. http://dx.doi.org/10.5551/jat.13979.

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21

Agren, M. S., and L. Franzen. "Foam cells after treatment with hydrocolloid dressings." British Journal of Dermatology 125, no. 2 (August 1991): 193. http://dx.doi.org/10.1111/j.1365-2133.1991.tb06076.x.

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22

Fowler, Stanley. "Characterization of Foam Cells in Experimental Atherosclerosis." Acta Medica Scandinavica 208, S642 (April 24, 2009): 151–58. http://dx.doi.org/10.1111/j.0954-6820.1980.tb10947.x.

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23

Schönholzer, Karl W., Mary Waldron, and Alex B. Magil. "Intraglomerular Foam Cells and Human Focal Glomerulosclerosis." Nephron 62, no. 2 (1992): 130–36. http://dx.doi.org/10.1159/000187020.

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24

Guerrini, Valentina, and Maria Laura Gennaro. "Foam Cells: One Size Doesn’t Fit All." Trends in Immunology 40, no. 12 (December 2019): 1163–79. http://dx.doi.org/10.1016/j.it.2019.10.002.

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25

Yang, Si Yi, Er Tuan Zhao, and Yu Kun An. "Research on Manufacturing the Metal Foams with Regular Cells by 3D Printing." Advanced Materials Research 1120-1121 (July 2015): 1233–37. http://dx.doi.org/10.4028/www.scientific.net/amr.1120-1121.1233.

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In the paper the methods of designing and manufacturing of the metals foam with regular cells are researched. The software models of metals foam are designed by CAD. The models are transmitted into 3D printing machine to manufacture foam framework. The metal foams with regular cells and fixed porosities are manufactured by chemical plating, electric plating and investment cast. According to the applications the structures of metal foams can be designed to control sizes, shapes and distribution of pores, porosities, density and to control the properties of metals foam, which can satisfy various demands of applications. Nickel foam with regular cells is designed and manufactured by this method.
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26

Somodi, Laura, Emőke Horváth, Helga Bárdos, Barbara Baráth, Dávid Pethő, Éva Katona, József Balla, Nicola J. Mutch, and László Muszbek. "Cellular FXIII in Human Macrophage-Derived Foam Cells." International Journal of Molecular Sciences 24, no. 5 (March 2, 2023): 4802. http://dx.doi.org/10.3390/ijms24054802.

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Macrophages express the A subunit of coagulation factor XIII (FXIII-A), a transglutaminase which cross-links proteins through Nε-(γ-L-glutamyl)-L-lysyl iso-peptide bonds. Macrophages are major cellular constituents of the atherosclerotic plaque; they may stabilize the plaque by cross-linking structural proteins and they may become transformed into foam cells by accumulating oxidized LDL (oxLDL). The combination of oxLDL staining by Oil Red O and immunofluorescent staining for FXIII-A demonstrated that FXIII-A is retained during the transformation of cultured human macrophages into foam cells. ELISA and Western blotting techniques revealed that the transformation of macrophages into foam cells elevated the intracellular FXIII-A content. This phenomenon seems specific for macrophage-derived foam cells; the transformation of vascular smooth muscle cells into foam cells fails to induce a similar effect. FXIII-A containing macrophages are abundant in the atherosclerotic plaque and FXIII-A is also present in the extracellular compartment. The protein cross-linking activity of FXIII-A in the plaque was demonstrated using an antibody labeling the iso-peptide bonds. Cells showing combined staining for FXIII-A and oxLDL in tissue sections demonstrated that FXIII-A-containing macrophages within the atherosclerotic plaque are also transformed into foam cells. Such cells may contribute to the formation of lipid core and the plaque structurization.
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27

Roveillo, Quentin, Julien Dervaux, Yuxuan Wang, Florence Rouyer, Drazen Zanchi, Laurent Seuront, and Florence Elias. "Trapping of swimming microalgae in foam." Journal of The Royal Society Interface 17, no. 168 (July 2020): 20200077. http://dx.doi.org/10.1098/rsif.2020.0077.

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Massive foam formation in aquatic environments is a seasonal event that has a significant impact on the stability of marine ecosystems. Liquid foams are known to filter passive solid particles, with large particles remaining trapped by confinement in the network of liquid channels and small particles being freely advected by the gravity-driven flow. By contrast, the potential role of a similar retention effect on biologically active particles such as phytoplankton cells is still relatively unknown. To assess if phytoplankton cells are passively advected through a foam, the model unicellular motile alga Chlamydomonas reinhardtii (CR) was incorporated in a bio-compatible foam, and the number of cells escaping the foam at the bottom was measured in time. Comparing the escape dynamics of living and dead CR cells, we found that dead cells are totally advected by the liquid flow towards the bottom of the foam, as expected since the diameter of CR remains smaller than the typical foam channel diameter. By contrast, living motile CR cells escape the foam at a significantly lower rate: after 2 hours, up to 60% of the injected cells may remain blocked in the foam, while 95% of the initial liquid volume in the foam has been drained out of the foam. Microscopic observation of the swimming CR cells in a chamber mimicking the cross-section of foam internal channels revealed that swimming CR cells accumulate near channels corners. A theoretical analysis based on the probability density measurements in the micro chambers has shown that this trapping at the microscopic scale contributes to explain the macroscopic retention of the microswimmers in the foam. At the crossroads of distinct fields including marine ecology of planktonic organisms, fluid dynamics of active particles in a confined environment and the physics of foam, this work represents a significant step in the fundamental understanding of the ecological consequences of aquatic foams in water bodies.
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28

Busam, Klaus J., Juan Rosai, Kristin Iversen, and Achim A. Jungbluth. "Xanthogranulomas With Inconspicuous Foam Cells and Giant Cells Mimicking Malignant Melanoma." American Journal of Surgical Pathology 24, no. 6 (June 2000): 864–69. http://dx.doi.org/10.1097/00000478-200006000-00013.

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29

Shapiro, Philip E., David N. Silvers, Ruth K. Treiber, Philip H. Cooper, Lawrence D. True, and Raffaele Lattes. "Juvenile xanthogranulomas with inconspicuous or absent foam cells and giant cells." Journal of the American Academy of Dermatology 24, no. 6 (June 1991): 1005–9. http://dx.doi.org/10.1016/s0190-9622(08)80116-8.

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30

Shapiro, P. E., D. N. Silvers, R. K. Treiber, and R. Lattes. "Juvenile Xanthogranulomas with Inconspicuous or Absent Foam Cells and Giant Cells." American Journal of Dermatopathology 13, no. 2 (April 1991): 198. http://dx.doi.org/10.1097/00000372-199104000-00026.

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31

Tong, M., K. Cole, and S. J. Neethling. "Drainage and stability of 2D foams: Foam behaviour in vertical Hele-Shaw cells." Colloids and Surfaces A: Physicochemical and Engineering Aspects 382, no. 1-3 (June 2011): 42–49. http://dx.doi.org/10.1016/j.colsurfa.2010.11.007.

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32

Paul, Antoni, Todd A. Lydic, Ryan Hogan, and Young-Hwa Goo. "Cholesterol Acceptors Regulate the Lipidome of Macrophage Foam Cells." International Journal of Molecular Sciences 20, no. 15 (August 2, 2019): 3784. http://dx.doi.org/10.3390/ijms20153784.

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Arterial foam cells are central players of atherogenesis. Cholesterol acceptors, apolipoprotein A-I (apoA-I) and high-density lipoprotein (HDL), take up cholesterol and phospholipids effluxed from foam cells into the circulation. Due to the high abundance of cholesterol in foam cells, most previous studies focused on apoA-I/HDL-mediated free cholesterol (FC) transport. However, recent lipidomics of human atherosclerotic plaques also identified that oxidized sterols (oxysterols) and non-sterol lipid species accumulate as atherogenesis progresses. While it is known that these lipids regulate expression of pro-inflammatory genes linked to plaque instability, how cholesterol acceptors impact the foam cell lipidome, particularly oxysterols and non-sterol lipids, remains unexplored. Using lipidomics analyses, we found cholesterol acceptors remodel foam cell lipidomes. Lipid subclass analyses revealed various oxysterols, sphingomyelins, and ceramides, species uniquely enriched in human plaques were significantly reduced by cholesterol acceptors, especially by apoA-I. These results indicate that the function of lipid-poor apoA-I is not limited to the efflux of cholesterol and phospholipids but suggest that apoA-I serves as a major regulator of the foam cell lipidome and might play an important role in reducing multiple lipid species involved in the pathogenesis of atherosclerosis.
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33

Ivan, Luminita, and Felicia Antohe. "Hyperlipidemia induces endothelial-derived foam cells in culture." Journal of Receptors and Signal Transduction 30, no. 2 (March 2, 2010): 106–14. http://dx.doi.org/10.3109/10799891003630606.

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34

Rolschau, J., F. Hassing Nielsen, and B. Brock Jacobsen. "FOAM CELLS IN THE PLACENTA IN EXTREME HYPERLIPAEMIA." Acta Pathologica Microbiologica Scandinavica Section A Pathology 80A, no. 6 (August 15, 2009): 751–55. http://dx.doi.org/10.1111/j.1699-0463.1972.tb00346.x.

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35

Wu, Min, Meixia Liu, Gang Guo, Wengao Zhang, and Longtao Liu. "Polydatin Inhibits Formation of Macrophage-Derived Foam Cells." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/729017.

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Rhizoma Polygoni Cuspidati, a Chinese herbal medicine, has been widely used in traditional Chinese medicine for a long time. Polydatin, one of the major active ingredients inRhizoma Polygoni Cuspidati, has been recently shown to possess extensive cardiovascular pharmacological activities. In present study, we examined the effects of Polydatin on the formation of peritoneal macrophage-derived foam cells in Apolipoprotein E gene knockout mice (ApoE−/−) and explored the potential underlying mechanisms. Peritoneal macrophages were collected from ApoE−/−mice and culturedin vitro. These cells sequentially were divided into four groups: Control group, Model group, Lovastatin group, and Polydatin group. Our results demonstrated that Polydatin significantly inhibits the formation of foam cells derived from peritoneal macrophages. Further studies indicated that Polydatin regulates the metabolism of intracellular lipid and possesses anti-inflammatory effects, which may be regulated through the PPAR-γsignaling pathways.
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36

Vilela, D. suarez, and F. M. izquierdo Garcia. "Foam cells and histiocytes in endometrial stromal tumours." Histopathology 32, no. 6 (June 1998): 568–69. http://dx.doi.org/10.1046/j.1365-2559.1998.0434a.x.

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37

Cox, Brian E., Evelyn E. Griffin, J. Erin Tillman, and W. Gray (Jay) Jerome. "Lysosomal Cholesterol Accumulation in Model Atherosclerotic Foam Cells." Microscopy and Microanalysis 9, S02 (July 31, 2003): 1360–61. http://dx.doi.org/10.1017/s1431927603446801.

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38

Howell, Kenneth W., and Joseph C. Cleveland. "Purinergic Signaling Promotes Macrophage Differentiation to Foam Cells." Journal of the American College of Surgeons 221, no. 4 (October 2015): S182. http://dx.doi.org/10.1016/j.jamcollsurg.2015.07.433.

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39

Bobryshev, Yu V., R. S. A. Lord, N. K. Golovanova, N. D. Zvezdina, and N. V. Prokazova. "Role of ganglioside GM3 in foam cells formation." Atherosclerosis 151, no. 1 (July 2000): 289. http://dx.doi.org/10.1016/s0021-9150(00)81312-x.

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40

Lu, Kuo-Yun, Li-Chieh Ching, Kuo-Hui Su, Yuan-Bin Yu, Yu Ru Kou, Sheng-Huang Hsiao, Yu-Chu Huang, et al. "Erythropoietin Suppresses the Formation of Macrophage Foam Cells." Circulation 121, no. 16 (April 27, 2010): 1828–37. http://dx.doi.org/10.1161/circulationaha.109.876839.

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41

Hilgenfeldt, S., A. M. Kraynik, D. A. Reinelt, and J. M. Sullivan. "The structure of foam cells: Isotropic Plateau polyhedra." Europhysics Letters (EPL) 67, no. 3 (August 2004): 484–90. http://dx.doi.org/10.1209/epl/i2003-10295-7.

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42

Tian, Ling, Nanlan Luo, Richard L. Klein, B. Hong Chung, W. Timothy Garvey, and Yuchang Fu. "Adiponectin reduces lipid accumulation in macrophage foam cells." Atherosclerosis 202, no. 1 (January 2009): 152–61. http://dx.doi.org/10.1016/j.atherosclerosis.2008.04.011.

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43

Tashiro, Takashi, Mitsuyoshi Hirokawa, and Toshiaki Sano. "Are mammary pagetoid foam cells histiocytic or epithelial?" Virchows Archiv 439, no. 1 (February 8, 2001): 102–3. http://dx.doi.org/10.1007/s004280000345.

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44

Krishnamurthy, S., N. Sneige, N. G. Ordóñez, K. K. Hunt, and H. M. Kuerer. "Characterization of foam cells in nipple aspirate fluid." Diagnostic Cytopathology 27, no. 5 (October 29, 2002): 261–64. http://dx.doi.org/10.1002/dc.10155.

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45

Evdokymov, Nikolai, Holm Altenbach, and Victor A. Eremeyev. "Collapse criteria of foam cells under various loading." PAMM 11, no. 1 (December 2011): 365–66. http://dx.doi.org/10.1002/pamm.201110174.

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46

Daub, Karin, Harald Langer, Peter Seizer, Konstantinos Stellos, Andreas E. May, Pankaj Goyal, Boris Bigalke, et al. "Platelets induce differentiation of human CD34 + progenitor cells into foam cells and endothelial cells." FASEB Journal 20, no. 14 (October 31, 2006): 2559–61. http://dx.doi.org/10.1096/fj.06-6265fje.

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47

Robichaud, Sabrina, Adil Rasheed, Antonietta Pietrangelo, Anne Doyoung Kim, Dominique M. Boucher, Christina Emerton, Viyashini Vijithakumar, et al. "Autophagy Is Differentially Regulated in Leukocyte and Nonleukocyte Foam Cells During Atherosclerosis." Circulation Research 130, no. 6 (March 18, 2022): 831–47. http://dx.doi.org/10.1161/circresaha.121.320047.

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Rationale: Atherosclerosis is characterized by an accumulation of foam cells within the arterial wall, resulting from excess cholesterol uptake and buildup of cytosolic lipid droplets (LDs). Autophagy promotes LD clearance by freeing stored cholesterol for efflux, a process that has been shown to be atheroprotective. While the role of autophagy in LD catabolism has been studied in macrophage-derived foam cells, this has remained unexplored in vascular smooth muscle cell (VSMC)-derived foam cells that constitute a large fraction of foam cells within atherosclerotic lesions. Objective: We performed a comparative analysis of autophagy flux in lipid-rich aortic intimal populations to determine whether VSMC-derived foam cells metabolize LDs similarly to their macrophage counterparts. Methods and Results: Atherosclerosis was induced in GFP-LC3 (microtubule-associated proteins 1A/1B light chain 3) transgenic mice by PCSK9 (proprotein convertase subtilisin/kexin type 9)-adeno-associated viral injection and Western diet feeding. Using flow cytometry of aortic digests, we observed a significant increase in dysfunctional autophagy of VSMC-derived foam cells during atherogenesis relative to macrophage-derived foam cells. Using cell culture models of lipid-loaded VSMCs and macrophages, we show that autophagy-mediated cholesterol efflux from VSMC foam cells was poor relative to macrophage foam cells, and largely occurs when HDL (high-density lipoprotein) was used as a cholesterol acceptor, as opposed to apoA-1 (apolipoproteinA-1). This was associated with the predominant expression of ABCG1 in VSMC foam cells. Using metformin, an autophagy activator, cholesterol efflux to HDL was significantly increased in VSMC, but not in macrophage, foam cells. Conclusions: These data demonstrate that VSMC and macrophage foam cells perform cholesterol efflux by distinct mechanisms, and that autophagy flux is highly impaired in VSMC foam cells, but can be induced by pharmacological means. Further investigation is warranted into targeting autophagy specifically in VSMC foam cells, the predominant foam cell subtype of advanced atherosclerotic plaques, to promote reverse cholesterol transport and resolution of the atherosclerotic plaque.
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48

Lawrence, E., D. Wulfsohn, and R. Pyrz. "Microstructural Characterisation of a Syntactic Foam." Polymers and Polymer Composites 9, no. 7 (October 2001): 449–58. http://dx.doi.org/10.1177/096739110100900702.

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Stereological sampling procedures were used to characterize the geometry of the cells of a syntactic foam. The foam, formed by extrusion, consisted of hollow polymeric microballoons in a low-density polyethylene matrix. Estimates of cell volume fraction, number density and the mean and standard deviation of volumes of cells were made using design-based methods, which are generally valid without any assumptions about cell shape. Additionally, the distribution of cell aspect ratio was estimated, assuming ellipsoidal cells with the major axis in the direction of extrusion. In addition to describing the stereological methods used, this paper illustrates how the results of a pilot study can be used to design an efficient sampling protocol.
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49

Ji, Xiang, Dan Liu, Feng Wu, Yu Cen, and Lan Ma. "Phage Display Preparation of Specific Polypeptides in Atherosclerotic Foam Cells." Applied Sciences 12, no. 2 (January 6, 2022): 562. http://dx.doi.org/10.3390/app12020562.

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Abstract:
Atherosclerosis and related complications are the most common causes of death in modern societies. Macrophage-derived foam cells play critical roles in the initiation and progression of atherosclerosis. Effective, rapid, and instrument-independent detection in the early stage of chronic atherosclerosis progression could provide an opportunity for early intervention and treatment. Therefore, as a starting point, in this study, we aimed to isolate and prepare foam cell-specific polypeptides using a phage display platform. The six target polypeptides, which were acquired in this study, were evaluated by ELISA and showed strong specificity with foam cells. Streptavidin coupled quantum dots (QDs) were used as fluorescence developing agents, and images of biotin-modified polypeptides specifically binding with foam cells were clearly observed. The polypeptides obtained in this study could lay the foundation for developing a rapid detection kit for early atherosclerosis lesions and could provide new materials for research on the mechanisms of foam cell formation and the development of blocking drugs.
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50

Yakushin, Vladimir, Ugis Cabulis, Velta Fridrihsone, Sergey Kravchenko, and Romass Pauliks. "Properties of polyurethane foam with fourth-generation blowing agent." e-Polymers 21, no. 1 (January 1, 2021): 763–69. http://dx.doi.org/10.1515/epoly-2021-0081.

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Abstract Climate change makes it imperative to use materials with minimum global warming potential. The fourth-generation blowing agent HCFO-1233zd-E is one of them. The use of HCFO allows the production of polyurethane foam with low thermal conductivity. Thermal conductivity, like other foam properties, depends not only on the density but also on the cellular structure of the foam. The cellular structure, in turn, depends on the technological parameters of foam production. A comparison of pouring and spray foams of the same low density has shown that the cellular structure of spray foam consists of cells with much less sizes than pouring foam. Due to the small size of cells, spray foam has a lower radiative constituent in the foam conductivity and, as a result, a lower overall thermal conductivity than pouring foam. The water absorption of spray foam, due to the fine cellular structure, also is lower than that of pouring foam. Pouring foam with bigger cells has higher compressive strength and modulus of elasticity in the foam rise direction. On the contrary, spray foam with a fine cellular structure has higher strength and modulus in the perpendicular direction. The effect of foam aging on thermal conductivity was also studied.
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