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  • 1
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    NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-04-30
    Description: The inflammatory nature of atherosclerosis is well established but the agent(s) that incite inflammation in the artery wall remain largely unknown. Germ-free animals are susceptible to atherosclerosis, suggesting that endogenous substances initiate the inflammation. Mature atherosclerotic lesions contain macroscopic deposits of cholesterol crystals in the necrotic core, but their appearance late in atherogenesis had been thought to disqualify them as primary inflammatory stimuli. However, using a new microscopic technique, we revealed that minute cholesterol crystals are present in early diet-induced atherosclerotic lesions and that their appearance in mice coincides with the first appearance of inflammatory cells. Other crystalline substances can induce inflammation by stimulating the caspase-1-activating NLRP3 (NALP3 or cryopyrin) inflammasome, which results in cleavage and secretion of interleukin (IL)-1 family cytokines. Here we show that cholesterol crystals activate the NLRP3 inflammasome in phagocytes in vitro in a process that involves phagolysosomal damage. Similarly, when injected intraperitoneally, cholesterol crystals induce acute inflammation, which is impaired in mice deficient in components of the NLRP3 inflammasome, cathepsin B, cathepsin L or IL-1 molecules. Moreover, when mice deficient in low-density lipoprotein receptor (LDLR) were bone-marrow transplanted with NLRP3-deficient, ASC (also known as PYCARD)-deficient or IL-1alpha/beta-deficient bone marrow and fed on a high-cholesterol diet, they had markedly decreased early atherosclerosis and inflammasome-dependent IL-18 levels. Minimally modified LDL can lead to cholesterol crystallization concomitant with NLRP3 inflammasome priming and activation in macrophages. Although there is the possibility that oxidized LDL activates the NLRP3 inflammasome in vivo, our results demonstrate that crystalline cholesterol acts as an endogenous danger signal and its deposition in arteries or elsewhere is an early cause rather than a late consequence of inflammation. These findings provide new insights into the pathogenesis of atherosclerosis and indicate new potential molecular targets for the therapy of this disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2946640/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2946640/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duewell, Peter -- Kono, Hajime -- Rayner, Katey J -- Sirois, Cherilyn M -- Vladimer, Gregory -- Bauernfeind, Franz G -- Abela, George S -- Franchi, Luigi -- Nunez, Gabriel -- Schnurr, Max -- Espevik, Terje -- Lien, Egil -- Fitzgerald, Katherine A -- Rock, Kenneth L -- Moore, Kathryn J -- Wright, Samuel D -- Hornung, Veit -- Latz, Eicke -- R01 AI075318/AI/NIAID NIH HHS/ -- R01 AI083713/AI/NIAID NIH HHS/ -- R01 AI083713-01/AI/NIAID NIH HHS/ -- R01 HL093262/HL/NHLBI NIH HHS/ -- R01 HL093262-01A1/HL/NHLBI NIH HHS/ -- England -- Nature. 2010 Apr 29;464(7293):1357-61. doi: 10.1038/nature08938.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20428172" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis Regulatory Proteins ; Atherosclerosis/chemically induced/*metabolism/*pathology ; Bone Marrow Transplantation ; Carrier Proteins/genetics/*metabolism ; Cathepsin B/metabolism ; Cathepsin L/metabolism ; Cholesterol/*chemistry/*metabolism/pharmacology ; Crystallization ; Cytoskeletal Proteins/deficiency ; Diet, Atherogenic ; Female ; Humans ; Inflammation/chemically induced/metabolism/pathology ; Interleukin-1/deficiency ; Interleukin-18/metabolism ; Lysosomes/drug effects/pathology ; Mice ; Mice, Inbred C57BL ; Peritoneal Cavity/pathology ; Phagocytes/drug effects/pathology/physiology ; Receptors, LDL/deficiency ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Requirement of JNK2 for scavenger receptor A-mediated foam cell formation in atherogenesis (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-30
    Description: In vitro studies suggest a role for c-Jun N-terminal kinases (JNKs) in proatherogenic cellular processes. We show that atherosclerosis-prone ApoE-/- mice simultaneously lacking JNK2 (ApoE-/- JNK2-/- mice), but not ApoE-/- JNK1-/- mice, developed less atherosclerosis than do ApoE-/- mice. Pharmacological inhibition of JNK activity efficiently reduced plaque formation. Macrophages lacking JNK2 displayed suppressed foam cell formation caused by defective uptake and degradation of modified lipoproteins and showed increased amounts of the modified lipoprotein-binding and -internalizing scavenger receptor A (SR-A), whose phosphorylation was markedly decreased. Macrophage-restricted deletion of JNK2 was sufficient to decrease atherogenesis. Thus, JNK2-dependent phosphorylation of SR-A promotes uptake of lipids in macrophages, thereby regulating foam cell formation, a critical step in atherogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ricci, Romeo -- Sumara, Grzegorz -- Sumara, Izabela -- Rozenberg, Izabela -- Kurrer, Michael -- Akhmedov, Alexander -- Hersberger, Martin -- Eriksson, Urs -- Eberli, Franz R -- Becher, Burkhard -- Boren, Jan -- Chen, Mian -- Cybulsky, Myron I -- Moore, Kathryn J -- Freeman, Mason W -- Wagner, Erwin F -- Matter, Christian M -- Luscher, Thomas F -- New York, N.Y. -- Science. 2004 Nov 26;306(5701):1558-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Research, Institute of Physiology, and Division of Cardiology, University Hospital Zurich, CH-8057 Zurich, Switzerland. romeo.ricci@cell.biol.ethz.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15567863" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD36/metabolism ; Aorta/chemistry/pathology ; Apolipoproteins E/genetics ; Arteriosclerosis/*metabolism/pathology ; Bone Marrow Transplantation ; Cells, Cultured ; Cholesterol/metabolism ; Cholesterol, Dietary/administration & dosage ; Diet, Atherogenic ; Endothelial Cells/physiology ; Foam Cells/*metabolism ; Lipoproteins, LDL/metabolism ; Macrophages/*metabolism ; Macrophages, Peritoneal/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitogen-Activated Protein Kinase 8/metabolism ; Mitogen-Activated Protein Kinase 9/genetics/*metabolism ; Muscle, Smooth, Vascular/cytology ; Myocytes, Smooth Muscle/physiology ; Phosphorylation ; Receptors, Immunologic/genetics/*metabolism ; Receptors, Scavenger ; Scavenger Receptors, Class A ; T-Lymphocytes/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Inhibition of miR-33a/b in non-human primates raises plasma HDL and lowers VLDL triglycerides (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-10-21
    Description: Cardiovascular disease remains the leading cause of mortality in westernized countries, despite optimum medical therapy to reduce the levels of low-density lipoprotein (LDL)-associated cholesterol. The pursuit of novel therapies to target the residual risk has focused on raising the levels of high-density lipoprotein (HDL)-associated cholesterol in order to exploit its atheroprotective effects. MicroRNAs (miRNAs) have emerged as important post-transcriptional regulators of lipid metabolism and are thus a new class of target for therapeutic intervention. MicroRNA-33a and microRNA-33b (miR-33a/b) are intronic miRNAs whose encoding regions are embedded in the sterol-response-element-binding protein genes SREBF2 and SREBF1 (refs 3-5), respectively. These miRNAs repress expression of the cholesterol transporter ABCA1, which is a key regulator of HDL biogenesis. Recent studies in mice suggest that antagonizing miR-33a may be an effective strategy for raising plasma HDL levels and providing protection against atherosclerosis; however, extrapolating these findings to humans is complicated by the fact that mice lack miR-33b, which is present only in the SREBF1 gene of medium and large mammals. Here we show in African green monkeys that systemic delivery of an anti-miRNA oligonucleotide that targets both miR-33a and miR-33b increased hepatic expression of ABCA1 and induced a sustained increase in plasma HDL levels over 12 weeks. Notably, miR-33 antagonism in this non-human primate model also increased the expression of miR-33 target genes involved in fatty acid oxidation (CROT, CPT1A, HADHB and PRKAA1) and reduced the expression of genes involved in fatty acid synthesis (SREBF1, FASN, ACLY and ACACA), resulting in a marked suppression of the plasma levels of very-low-density lipoprotein (VLDL)-associated triglycerides, a finding that has not previously been observed in mice. These data establish, in a model that is highly relevant to humans, that pharmacological inhibition of miR-33a and miR-33b is a promising therapeutic strategy to raise plasma HDL and lower VLDL triglyceride levels for the treatment of dyslipidaemias that increase cardiovascular disease risk.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3235584/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3235584/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rayner, Katey J -- Esau, Christine C -- Hussain, Farah N -- McDaniel, Allison L -- Marshall, Stephanie M -- van Gils, Janine M -- Ray, Tathagat D -- Sheedy, Frederick J -- Goedeke, Leigh -- Liu, Xueqing -- Khatsenko, Oleg G -- Kaimal, Vivek -- Lees, Cynthia J -- Fernandez-Hernando, Carlos -- Fisher, Edward A -- Temel, Ryan E -- Moore, Kathryn J -- 1P30HL101270/HL/NHLBI NIH HHS/ -- P01HL098055/HL/NHLBI NIH HHS/ -- R00 HL088528/HL/NHLBI NIH HHS/ -- R00 HL088528-04/HL/NHLBI NIH HHS/ -- R00 HL088528-05/HL/NHLBI NIH HHS/ -- R00HL088528/HL/NHLBI NIH HHS/ -- R01AG02055/AG/NIA NIH HHS/ -- R01HL084312/HL/NHLBI NIH HHS/ -- R01HL107953/HL/NHLBI NIH HHS/ -- R01HL108182/HL/NHLBI NIH HHS/ -- R01HL58541/HL/NHLBI NIH HHS/ -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2011 Oct 19;478(7369):404-7. doi: 10.1038/nature10486.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Marc and Ruti Bell Vascular Biology and Disease Program, Leon H. Charney Division of Cardiology, Department of Medicine, New York University School of Medicine, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22012398" target="_blank"〉PubMed〈/a〉
    Keywords: ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters/metabolism ; Animals ; Cells, Cultured ; *Cercopithecus aethiops/blood/genetics/metabolism ; Cholesterol, LDL/blood ; Gene Expression Regulation/*drug effects ; Gene Silencing ; HEK293 Cells ; Humans ; Lipoproteins, HDL/*blood ; Lipoproteins, VLDL/*blood ; Liver/*drug effects/metabolism ; Male ; MicroRNAs/*antagonists & inhibitors/metabolism ; Oligoribonucleotides, Antisense/*pharmacology ; Time Factors ; Triglycerides/*blood
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Food security: focus on agriculture (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-04-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Porter, John R -- Challinor, Andrew -- Ewert, Frank -- Falloon, Pete -- Fischer, Tony -- Gregory, Peter -- Van Ittersum, Martin K -- Olesen, Jorgen E -- Moore, Kenneth J -- Rosenzweig, Cynthia -- Smith, Pete -- New York, N.Y. -- Science. 2010 Apr 9;328(5975):172-3. doi: 10.1126/science.328.5975.172.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20378800" target="_blank"〉PubMed〈/a〉
    Keywords: *Agriculture/methods ; *Crops, Agricultural ; Environment ; *Food Supply
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    MiR-33 contributes to the regulation of cholesterol homeostasis (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-15
    Description: Cholesterol metabolism is tightly regulated at the cellular level. Here we show that miR-33, an intronic microRNA (miRNA) located within the gene encoding sterol-regulatory element-binding factor-2 (SREBF-2), a transcriptional regulator of cholesterol synthesis, modulates the expression of genes involved in cellular cholesterol transport. In mouse and human cells, miR-33 inhibits the expression of the adenosine triphosphate-binding cassette (ABC) transporter, ABCA1, thereby attenuating cholesterol efflux to apolipoprotein A1. In mouse macrophages, miR-33 also targets ABCG1, reducing cholesterol efflux to nascent high-density lipoprotein (HDL). Lentiviral delivery of miR-33 to mice represses ABCA1 expression in the liver, reducing circulating HDL levels. Conversely, silencing of miR-33 in vivo increases hepatic expression of ABCA1 and plasma HDL levels. Thus, miR-33 appears to regulate both HDL biogenesis in the liver and cellular cholesterol efflux.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3114628/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3114628/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rayner, Katey J -- Suarez, Yajaira -- Davalos, Alberto -- Parathath, Saj -- Fitzgerald, Michael L -- Tamehiro, Norimasa -- Fisher, Edward A -- Moore, Kathryn J -- Fernandez-Hernando, Carlos -- 1P30HL101270-01/HL/NHLBI NIH HHS/ -- P30 HL101270/HL/NHLBI NIH HHS/ -- R01 AG020255/AG/NIA NIH HHS/ -- R01 AG020255-09/AG/NIA NIH HHS/ -- R01AG02055/AG/NIA NIH HHS/ -- R01HL074136/HL/NHLBI NIH HHS/ -- R01HL084312/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2010 Jun 18;328(5985):1570-3. doi: 10.1126/science.1189862. Epub 2010 May 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Leon H. Charney Division of Cardiology and the Marc and Ruti Bell Vascular Biology and Disease Program, New York University School of Medicine, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20466885" target="_blank"〉PubMed〈/a〉
    Keywords: ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters/genetics/metabolism ; Animals ; Apolipoprotein A-I/metabolism ; Carrier Proteins/genetics/metabolism ; Cell Line ; Cholesterol/*metabolism ; Cholesterol, Dietary/administration & dosage ; Dietary Fats/administration & dosage ; Gene Expression Regulation ; Homeostasis ; Humans ; Hypercholesterolemia/genetics/metabolism ; Introns ; Lipoproteins/genetics/metabolism ; Lipoproteins, HDL/blood/*metabolism ; Liver/*metabolism ; Macrophages/metabolism ; Macrophages, Peritoneal/metabolism ; Membrane Glycoproteins/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; MicroRNAs/genetics/*metabolism ; Proteins/genetics/metabolism ; Sterol Regulatory Element Binding Protein 2/genetics/metabolism ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 6
    Electronic Resource
    Electronic Resource
    Test of a two-dimensionally focusing quasi-optical antenna using a gyrotron (1989)
    Woodbury, NY : American Institute of Physics (AIP)
    Applied Physics Letters 54 (1989), S. 1740-1741 
    Details
    ISSN: 1077-3118
    Source: AIP Digital Archive
    Topics: Physics
    Notes: A quasi-optical antenna having one elliptical reflector and one parabolic reflector has been built for millimeter wave scattering measurements on the TORTUS tokamak plasma at the University of Sydney. This letter reports the first demonstration of the properties of such an antenna using a gyrotron millimeter wave source. Its advantages are (1) good two-dimensional focusing (along the major radius and the toroidal directions) and (2) easy movement of the focus across the diameter of the plasma by changing the orientation of the parabolic reflector.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.101276
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  • 7
    Electronic Resource
    Electronic Resource
    Photoluminescence decay time studies of type II GaAs/AlAs quantum-well structures (1989)
    [S.l.] : American Institute of Physics (AIP)
    Journal of Applied Physics 65 (1989), S. 3606-3609 
    Details
    ISSN: 1089-7550
    Source: AIP Digital Archive
    Topics: Physics
    Notes: We have investigated the temperature dependence of the photoluminescence (PL) decay kinetics of a series of GaAs/AlAs quantum-well structures where the GaAs thickness was kept constant at 25 A(ring) and the AlAs was varied between 41 and 19 A(ring). In these structures the band alignment is type II and the dominant photoluminescence process at 4 K is due to recombination of excitons involving electrons confined at the AlAs X point and holes in the GaAs. At 4 K on the low-energy side of the zero-phonon type II transition the PL decay is a single exponential over at least two decades. The time constant of this decay is a strong function of the AlAs layer thickness. The variation of this decay time is described by a change in the oscillator strength of the type II process due to the change in the mixing between the Xz (AlAs) electron states and the Γ (GaAs) electron states. At higher temperatures (T〉15 K) the photoluminescence intensity and the decay time decrease very rapidly with increasing temperature. This is due to the increased influence of nonradiative processes as the type II excitons become delocalized.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.342640
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  • 8
    Electronic Resource
    Electronic Resource
    Drag Reduction in Nature (1991)
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Fluid Mechanics 23 (1991), S. 65-79 
    Details
    ISSN: 0066-4189
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1146/annurev.fl.23.010191.000433
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  • 9
    Electronic Resource
    Electronic Resource
    Barrier thickness dependence of the photoscreening of the piezoelectric field in (111) orientated GaAs–InxGa1−xAs double quantum wells (1998)
    [S.l.] : American Institute of Physics (AIP)
    Journal of Applied Physics 84 (1998), S. 3349-3353 
    Details
    ISSN: 1089-7550
    Source: AIP Digital Archive
    Topics: Physics
    Notes: In this article we present low temperature photoluminescence spectra from a series of (111) orientated GaAs–InxGa1−xAs double quantum well structures with differing barrier thicknesses. We demonstrate an enhancement in the carrier screening of the strain induced internal piezoelectric field by photocreated electrons and holes as the barrier thickness is increased. The enhanced screening arises from an increase in the spatial separation of the electron and hole populations. Additionally, we observed a photoinduced spatial transfer of the second lowest lying heavy hole level. This spatial transfer is a strong function of the electron and hole separation and limits the amount of the optically pumped "blue" shift of the lowest energy intersubband transition. © 1998 American Institute of Physics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.368491
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  • 10
    Electronic Resource
    Electronic Resource
    A two-dimensionally focusing, quasi-optical antenna for millimeter-wave scattering in plasmas (1990)
    [S.l.] : American Institute of Physics (AIP)
    Journal of Applied Physics 67 (1990), S. 7086-7091 
    Details
    ISSN: 1089-7550
    Source: AIP Digital Archive
    Topics: Physics
    Notes: A two-dimensionally focusing, quasi-optical antenna having one elliptical reflector and one parabolic reflector has been built for use with a tunable gyrotron in order to carry out millimeter-wave scattering measurements on the TORTUS tokamak plasma at the University of Sydney. The advantages of this antenna are the following: (1) The elliptical reflector focuses the radiation beam in the toroidal direction, while the parabolic reflector focuses in the direction of major radius. This gives excellent two-dimensional focusing in the plasma region, and consequently excellent spatial resolution. (2) The focal point can be easily swept along the direction of major radius in the whole plasma region, simply by changing the angle of the parabolic reflector by a small amount. These features have been demonstrated experimentally using the tunable gyrotron source, GYROTRON III, and in computations of the radiated fields.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.345058
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