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  • 1
    Publication Date: 2011-02-26
    Description: Many successful vaccines induce persistent antibody responses that can last a lifetime. The mechanisms by which they do so remain unclear, but emerging evidence indicates that they activate dendritic cells via Toll-like receptors (TLRs). For example, the yellow fever vaccine YF-17D, one of the most successful empiric vaccines ever developed, activates dendritic cells via multiple TLRs to stimulate proinflammatory cytokines. Triggering specific combinations of TLRs in dendritic cells can induce synergistic production of cytokines, which results in enhanced T-cell responses, but its impact on antibody responses remain unknown. Learning the critical parameters of innate immunity that program such antibody responses remains a major challenge in vaccinology. Here we demonstrate that immunization of mice with synthetic nanoparticles containing antigens plus ligands that signal through TLR4 and TLR7 induces synergistic increases in antigen-specific, neutralizing antibodies compared to immunization with nanoparticles containing antigens plus a single TLR ligand. Consistent with this there was enhanced persistence of germinal centres and of plasma-cell responses, which persisted in the lymph nodes for 〉1.5 years. Surprisingly, there was no enhancement of the early short-lived plasma-cell response relative to that observed with single TLR ligands. Molecular profiling of activated B cells, isolated 7 days after immunization, indicated that there was early programming towards B-cell memory. Antibody responses were dependent on direct triggering of both TLRs on B cells and dendritic cells, as well as on T-cell help. Immunization protected completely against lethal avian and swine influenza virus strains in mice, and induced robust immunity against pandemic H1N1 influenza in rhesus macaques.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3057367/" 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/PMC3057367/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kasturi, Sudhir Pai -- Skountzou, Ioanna -- Albrecht, Randy A -- Koutsonanos, Dimitrios -- Hua, Tang -- Nakaya, Helder I -- Ravindran, Rajesh -- Stewart, Shelley -- Alam, Munir -- Kwissa, Marcin -- Villinger, Francois -- Murthy, Niren -- Steel, John -- Jacob, Joshy -- Hogan, Robert J -- Garcia-Sastre, Adolfo -- Compans, Richard -- Pulendran, Bali -- HHSN266200700006C/PHS HHS/ -- HHSN266200700010C/PHS HHS/ -- N01 AI50025/AI/NIAID NIH HHS/ -- R01 AI048638/AI/NIAID NIH HHS/ -- R01 AI048638-07/AI/NIAID NIH HHS/ -- R01 AI048638-08/AI/NIAID NIH HHS/ -- R01 DK057665/DK/NIDDK NIH HHS/ -- R01 DK057665-09/DK/NIDDK NIH HHS/ -- R01 DK057665-10/DK/NIDDK NIH HHS/ -- R01 DK057665-11/DK/NIDDK NIH HHS/ -- R01 DK057665-12/DK/NIDDK NIH HHS/ -- R01 DK057665-13/DK/NIDDK NIH HHS/ -- R01DK057665/DK/NIDDK NIH HHS/ -- R37 AI048638/AI/NIAID NIH HHS/ -- R37 AI048638-09A1/AI/NIAID NIH HHS/ -- R37 AI048638-10/AI/NIAID NIH HHS/ -- R37 AI048638-11/AI/NIAID NIH HHS/ -- R37AI48638/AI/NIAID NIH HHS/ -- R56 AI048638/AI/NIAID NIH HHS/ -- R56 AI048638-09/AI/NIAID NIH HHS/ -- U01AI070469/AI/NIAID NIH HHS/ -- U19AI057266/AI/NIAID NIH HHS/ -- U19AI090023/AI/NIAID NIH HHS/ -- U54AI057157/AI/NIAID NIH HHS/ -- U54AI57158/AI/NIAID NIH HHS/ -- England -- Nature. 2011 Feb 24;470(7335):543-7. doi: 10.1038/nature09737.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Emory Vaccine Center, Emory University, Atlanta, Georgia 30329, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21350488" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Neutralizing/biosynthesis/*immunology ; Antibodies, Viral/biosynthesis/*immunology ; Antibody Formation/*immunology ; Dendritic Cells/cytology/immunology ; Hemagglutinin Glycoproteins, Influenza Virus/immunology ; Immunity, Innate/*immunology ; Immunologic Memory/*immunology ; Influenza A Virus, H1N1 Subtype/immunology ; Influenza A Virus, H5N1 Subtype/immunology ; Influenza Vaccines/administration & dosage/*immunology ; Lactic Acid ; Ligands ; Lymph Nodes/cytology/immunology ; Lymphocyte Activation ; Macaca mulatta/immunology/virology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Nanoparticles/administration & dosage ; Plasma Cells/cytology/immunology/metabolism ; Polyglycolic Acid ; T-Lymphocytes/immunology ; Toll-Like Receptors/immunology/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2016-03-24
    Description: Endoplasmic reticulum (ER) stress is a major contributor to inflammatory diseases, such as Crohn disease and type 2 diabetes. ER stress induces the unfolded protein response, which involves activation of three transmembrane receptors, ATF6, PERK and IRE1alpha. Once activated, IRE1alpha recruits TRAF2 to the ER membrane to initiate inflammatory responses via the NF-kappaB pathway. Inflammation is commonly triggered when pattern recognition receptors (PRRs), such as Toll-like receptors or nucleotide-binding oligomerization domain (NOD)-like receptors, detect tissue damage or microbial infection. However, it is not clear which PRRs have a major role in inducing inflammation during ER stress. Here we show that NOD1 and NOD2, two members of the NOD-like receptor family of PRRs, are important mediators of ER-stress-induced inflammation in mouse and human cells. The ER stress inducers thapsigargin and dithiothreitol trigger production of the pro-inflammatory cytokine IL-6 in a NOD1/2-dependent fashion. Inflammation and IL-6 production triggered by infection with Brucella abortus, which induces ER stress by injecting the type IV secretion system effector protein VceC into host cells, is TRAF2, NOD1/2 and RIP2-dependent and can be reduced by treatment with the ER stress inhibitor tauroursodeoxycholate or an IRE1alpha kinase inhibitor. The association of NOD1 and NOD2 with pro-inflammatory responses induced by the IRE1alpha/TRAF2 signalling pathway provides a novel link between innate immunity and ER-stress-induced inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4869892/" 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/PMC4869892/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keestra-Gounder, A Marijke -- Byndloss, Mariana X -- Seyffert, Nubia -- Young, Briana M -- Chavez-Arroyo, Alfredo -- Tsai, April Y -- Cevallos, Stephanie A -- Winter, Maria G -- Pham, Oanh H -- Tiffany, Connor R -- de Jong, Maarten F -- Kerrinnes, Tobias -- Ravindran, Resmi -- Luciw, Paul A -- McSorley, Stephen J -- Baumler, Andreas J -- Tsolis, Renee M -- AI044170/AI/NIAID NIH HHS/ -- AI076246/AI/NIAID NIH HHS/ -- AI076278/AI/NIAID NIH HHS/ -- AI096528/AI/NIAID NIH HHS/ -- AI109799/AI/NIAID NIH HHS/ -- AI112258/AI/NIAID NIH HHS/ -- AI117303/AI/NIAID NIH HHS/ -- GM056765/GM/NIGMS NIH HHS/ -- R01 AI044170/AI/NIAID NIH HHS/ -- R01 AI076246/AI/NIAID NIH HHS/ -- R01 AI076278/AI/NIAID NIH HHS/ -- R01 AI096528/AI/NIAID NIH HHS/ -- R01 AI109799/AI/NIAID NIH HHS/ -- R21 AI112258/AI/NIAID NIH HHS/ -- R21 AI117303/AI/NIAID NIH HHS/ -- R25 GM056765/GM/NIGMS NIH HHS/ -- England -- Nature. 2016 Apr 21;532(7599):394-7. doi: 10.1038/nature17631. Epub 2016 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Microbiology and Immunology, School of Medicine, University of California at Davis, One Shields Ave, Davis, California 95616, USA. ; Center for Comparative Medicine, Schools of Medicine and Veterinary Medicine, University of California at Davis, One Shields Ave, Davis, California 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27007849" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Outer Membrane Proteins/metabolism ; Brucella abortus/immunology/pathogenicity ; Cell Line ; Dithiothreitol/pharmacology ; Endoplasmic Reticulum/drug effects/pathology ; *Endoplasmic Reticulum Stress/drug effects ; Endoribonucleases/antagonists & inhibitors ; Female ; Humans ; Immunity, Innate ; Inflammation/chemically induced/*metabolism ; Interleukin-6/biosynthesis ; Male ; Mice ; Mice, Inbred C57BL ; NF-kappa B/metabolism ; Nod1 Signaling Adaptor Protein/immunology/*metabolism ; Nod2 Signaling Adaptor Protein/immunology/*metabolism ; Protein-Serine-Threonine Kinases/antagonists & inhibitors ; Receptors, Pattern Recognition/metabolism ; *Signal Transduction/drug effects ; TNF Receptor-Associated Factor 2/metabolism ; Taurochenodeoxycholic Acid/pharmacology ; Thapsigargin/pharmacology ; Unfolded Protein Response/drug effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2016-03-17
    Description: The integrated stress response (ISR) is a homeostatic mechanism by which eukaryotic cells sense and respond to stress-inducing signals, such as amino acid starvation. General controlled non-repressed (GCN2) kinase is a key orchestrator of the ISR, and modulates protein synthesis in response to amino acid starvation. Here we demonstrate in mice that GCN2 controls intestinal inflammation by suppressing inflammasome activation. Enhanced activation of ISR was observed in intestinal antigen presenting cells (APCs) and epithelial cells during amino acid starvation, or intestinal inflammation. Genetic deletion of Gcn2 (also known as Eif2ka4) in CD11c(+) APCs or intestinal epithelial cells resulted in enhanced intestinal inflammation and T helper 17 cell (TH17) responses, owing to enhanced inflammasome activation and interleukin (IL)-1beta production. This was caused by reduced autophagy in Gcn2(-/-) intestinal APCs and epithelial cells, leading to increased reactive oxygen species (ROS), a potent activator of inflammasomes. Thus, conditional ablation of Atg5 or Atg7 in intestinal APCs resulted in enhanced ROS and TH17 responses. Furthermore, in vivo blockade of ROS and IL-1beta resulted in inhibition of TH17 responses and reduced inflammation in Gcn2(-/-) mice. Importantly, acute amino acid starvation suppressed intestinal inflammation via a mechanism dependent on GCN2. These results reveal a mechanism that couples amino acid sensing with control of intestinal inflammation via GCN2.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4854628/" 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/PMC4854628/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ravindran, Rajesh -- Loebbermann, Jens -- Nakaya, Helder I -- Khan, Nooruddin -- Ma, Hualing -- Gama, Leonardo -- Machiah, Deepa K -- Lawson, Benton -- Hakimpour, Paul -- Wang, Yi-chong -- Li, Shuzhao -- Sharma, Prachi -- Kaufman, Randal J -- Martinez, Jennifer -- Pulendran, Bali -- R01 DK088227/DK/NIDDK NIH HHS/ -- R01 DK103185/DK/NIDDK NIH HHS/ -- R37 AI048638/AI/NIAID NIH HHS/ -- R37 DK042394/DK/NIDDK NIH HHS/ -- R37 DK057665/DK/NIDDK NIH HHS/ -- U19 AI057266/AI/NIAID NIH HHS/ -- U19 AI090023/AI/NIAID NIH HHS/ -- ZIA ES103286-01/Intramural NIH HHS/ -- England -- Nature. 2016 Mar 24;531(7595):523-7. doi: 10.1038/nature17186. Epub 2016 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Emory Vaccine Center, Yerkes National Primate Research Center, 954 Gatewood Road, Atlanta, Georgia 30329, USA. ; School of Pharmaceutical Sciences, University of Sao Paulo, Sao Paulo 05508, Brazil. ; Department of Biotechnology and Bioinformatics, School of Life Sciences, University of Hyderabad, Hyderabad 500 046, India. ; Division of Pathology, Yerkes National Primate Research Center, 954 Gatewood Road, Atlanta, Georgia 30329, USA. ; Virology Core, Emory Vaccine Center and Yerkes National Primate Research Center, 954 Gatewood Road, Atlanta, Georgia 30329, USA. ; Degenerative Disease Program, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, California 92037 USA. ; National Institute of Environmental Health Sciences, Mail Drop D2-01 Research Triangle Park, North Carolina 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26982722" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/administration & dosage/deficiency/*metabolism/pharmacology ; Animals ; Antigen-Presenting Cells/immunology/metabolism ; Autophagy ; Colitis/etiology/*metabolism/pathology/prevention & control ; Disease Models, Animal ; Epithelial Cells/metabolism ; Female ; Humans ; Inflammasomes/*antagonists & inhibitors/metabolism ; Inflammation/etiology/*metabolism/pathology/prevention & control ; Interleukin-1beta/immunology ; Intestines/*metabolism/*pathology ; Male ; Mice ; Microtubule-Associated Proteins/deficiency/metabolism ; Protein-Serine-Threonine Kinases/deficiency/genetics/*metabolism ; Reactive Oxygen Species/metabolism ; Stress, Physiological ; Th17 Cells/immunology ; Ubiquitin-Activating Enzymes/deficiency/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2013-12-07
    Description: The yellow fever vaccine YF-17D is one of the most successful vaccines ever developed in humans. Despite its efficacy and widespread use in more than 600 million people, the mechanisms by which it stimulates protective immunity remain poorly understood. Recent studies using systems biology approaches in humans have revealed that YF-17D-induced early expression of general control nonderepressible 2 kinase (GCN2) in the blood strongly correlates with the magnitude of the later CD8(+) T cell response. We demonstrate a key role for virus-induced GCN2 activation in programming dendritic cells to initiate autophagy and enhanced antigen presentation to both CD4(+) and CD8(+) T cells. These results reveal an unappreciated link between virus-induced integrated stress response in dendritic cells and the adaptive immune response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4048998/" 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/PMC4048998/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ravindran, Rajesh -- Khan, Nooruddin -- Nakaya, Helder I -- Li, Shuzhao -- Loebbermann, Jens -- Maddur, Mohan S -- Park, Youngja -- Jones, Dean P -- Chappert, Pascal -- Davoust, Jean -- Weiss, David S -- Virgin, Herbert W -- Ron, David -- Pulendran, Bali -- 084812/Wellcome Trust/United Kingdom -- 084812/Z/08/Z/Wellcome Trust/United Kingdom -- N01 AI50019/AI/NIAID NIH HHS/ -- N01 AI50025/AI/NIAID NIH HHS/ -- P51 OD011132/OD/NIH HHS/ -- R37 AI048638/AI/NIAID NIH HHS/ -- R37 DK057665/DK/NIDDK NIH HHS/ -- R56 AI048638/AI/NIAID NIH HHS/ -- U19 AI057266/AI/NIAID NIH HHS/ -- U19 AI090023/AI/NIAID NIH HHS/ -- U54 AI057157/AI/NIAID NIH HHS/ -- U54 AI057160/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2014 Jan 17;343(6168):313-7. doi: 10.1126/science.1246829. Epub 2013 Dec 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Emory Vaccine Center, Yerkes National Primate Research Center, Emory University, 954 Gatewood Road, Atlanta, GA 30329, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24310610" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigen Presentation ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/immunology ; Cell Line ; Cricetinae ; Dendritic Cells/enzymology/*immunology ; Enzyme Activation ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Microtubule-Associated Proteins/genetics ; Protein-Serine-Threonine Kinases/*biosynthesis/genetics ; Yellow Fever Vaccine/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Acta mechanica 31 (1979), S. 253-280 
    ISSN: 1619-6937
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics , Physics
    Description / Table of Contents: Zusammenfassung Die vorliegenden Untersuchungen beziehen sich auf die mathematische Behandlung des „Modalwellen”-Problems. Die achsensymmetrische Strömung einer nichtviskosen Flüssigkeit in einem dünnwandigen viskoelastischen Rohr, unter bestimmten vereinfachenden Annahmen, wird betrachtet. Zuerst werden die Gleichungen des Ausbreitungsraumes im Langwellenbereich abgeleitet und eine allgemeine Methode zur Herleitung dieser Gleichungen für beliebige Wellenlängen bei nichtrotierender Strömung angegeben. Eine Operatorenmethode mit multiplem Maßstab wird verwendet zur Herleitung der nichtlinearen Schrödinger-Gleichung für die Modulation der periodischen Wellen, und die „langmodulierten Wellen” sowie die „modulierten Langwellen” werden aufgezeigt. Weiters wird die Existenz und die Stabilität der Stokes-Wellen im System untersucht. Anschließend werden die progressiven Wellenlösungen der Langwellengleichungen diskutiert. Eines der wichtigsten Ergebnisse dieser Arbeit ist, daß die Gleichungen des Ausbreitungsraumes keine partiellen Differentialgleichungen mehr sind, sondern Ausdrücke von Pseudo-Differentialoperatoren.
    Notes: Summary Our investigations in this paper are centred around the mathematical analysis of a “modal wave” problem. We have considered the axisymmetric flow of an inviscid liquid in a thinwalled viscoelastic tube under certain simplifying assumptions. We have first derived the propagation space equations in the long wave limit and also given a general procedure to derive these equations for arbitrary wave length, when the flow is irrotational. We have used the method of operators of multiple scales to derive the nonlinear Schrödinger equation governing the modulation of periodic waves and we have elaborated on the “long modulated waves” and the “modulated long waves”. We have also examined the existence and stability of Stokes waves in this system. This is followed by a discussion of the progressive wave solutions of the long wave equations. One of the most important results of our paper is that the propagation space equations are no longer partial differential equations but they are in terms of pseudo-differential operators.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Acta mechanica 40 (1981), S. 1-10 
    ISSN: 1619-6937
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics , Physics
    Description / Table of Contents: Zusammenfassung In der vorliegenden Arbeit wird das Charakteristikenverfahren für zweidimensionale instationäre Strömungen auf ein Problem der Axialturbinen angewandt. Das System besteht aus zwei Gitterreihen, den feststehenden Leitschaufeln und den hierzu senkrecht bewegten Laufschaufeln. Die anfangs ungestörte konstante Strömung wird gestört, indem den Laufschaufeln eine geringe Normalgeschwindigkeit erteilt wird, um eine konstante Anstellung zu simulieren. Die gestörte Strömung ist periodisch nach den ersten drei Perioden. Berechnet wurde das gestörte Dichtefeld während einer Periode.
    Notes: Summary In this paper we have used the method of characteristics developed for two dimensional unsteady flow problems to study a simplified axial turbine problem. The system consists of two sets of blades —the guiding vanes which are fixed and the rotor blades which move perpendicular to these vanes. The initial undisturbed constant flow in the system is perturbed by introducing a small velocity normal to the rotor blades to simulate a slight constant inclination. The resulting perturbed flow is periodic after the first three cycles. We have studied the perturbed density distribution throughout the system during a period.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Acta mechanica 73 (1988), S. 239-244 
    ISSN: 1619-6937
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics , Physics
    Notes: Summary The shock manifold equation is a first order nonlinear partial differential equation, which describes the kinematics of a shockfront in an ideal gas with constant specific heats. However, it was found that there was more than one of these shock manifold equations, and the shock surface could be embedded in a one parameter family of surfaces, obtained as a solution of any of these shock manifold equations. Associated with each shock manifold equation is a set of characteristic curves called ‘shock rays’. This paper investigates the nature of various associated shock ray equations.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1619-6937
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics , Physics
    Notes: Summary With the use of tensor analysis and the method of singular surfaces, an infinite system of equations can be derived to study the propagation of curved shocks of arbitrary strength in gas dynamics. The first three of these have been explicitly given here. This system is further reduced to one involving scalars only. The choice of dependent variables in the infinite system is quite important, it leads to coefficients free from singularities for all values of the shock strength.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1619-6937
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics , Physics
    Notes: Summary In this paper the kinematics of a weak shock front governed by a hyperbolic system of conservation laws is studied. This is used to develop a method for solving problems, involving the propagation of nonlinear unimodal waves. It consists of first solving the nonlinear wave problem by moving along the bicharacteristics of the system and then fitting the shock into this solution field, so that it satisfies the necessary jump conditions. The kinematics of the shock leads in a natural way to the definition of “shock-rays”, which play the same role as the “rays” in a continuous flow. A special case of a circular cylinder introduced suddenly in a constant streaming flow is studied in detail. The shock fitted in the upstream region propagates with a velocity which is the mean of the velocities of the linear and the nonlinear wave fronts. In the downstream the solution is given by an expansion wave.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 0022-328X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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