| 1. |
- Adcox, K, et al.
(författare)
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PHENIX detector overview
- 2003
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Ingår i: Nuclear Instruments & Methods in Physics Research. Section A: Accelerators, Spectrometers, Detectors, and Associated Equipment. - 0167-5087. ; 499:2-3, s. 469-479
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Tidskriftsartikel (refereegranskat)abstract
- The PHENIX detector is designed to perform a broad study of A-A, p-A, and p-p collisions to investigate nuclear matter under extreme conditions. A wide variety of probes, sensitive to all timescales, are used to study systematic variations with species and energy as well as to measure the spin structure of the nucleon. Designing for the needs of the heavy-ion and polarized-proton programs has produced a detector with unparalleled capabilities. PHENIX measures electron and muon pairs, photons, and hadrons with excellent energy and momentum resolution. The detector consists of a large number of subsystems that are discussed in other papers in this volume. The overall design parameters of the detector are presented. (C) 2002 Elsevier Science B.V. All rights reserved.
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| 2. |
- Burova, L, et al.
(författare)
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Role of group A streptococcal IgG-binding proteins in triggering experimental glomerulonephritis in the rabbit
- 2003
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Ingår i: APMIS : acta pathologica, microbiologica, et immunologica Scandinavica. - : Wiley. - 1600-0463. ; 111:10, s. 955-962
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Tidskriftsartikel (refereegranskat)abstract
- Our previous studies have indicated that the IgG-binding M-family proteins (IgGBP) of group A streptococci may be involved in eliciting experimental acute poststreptococcal glomerulonephritis (APSGN) in the rabbit. These surface proteins were also found to trigger production of anti-IgG, which might conceivably act to enhance renal deposition of immune complexes (IC). In the present study, a clinical isolate of serotype M22 (strain AL168), an isogenic double mutant deficient for both the IgGBPs Mrp and Emm, as well as mutants deficient in only one of the proteins were tested for capacity to induce glomerulonephritis. Streptococci to be used for injecting rabbits were heat-killed. Surface-bound IgG was removed by 1 M KSCN and cells were then repeatedly washed in PBS before use. Rabbits were injected intravenously with 10(9) cells three times a week for 8 weeks and, following one month of rest, for another 6 weeks. Deposits of IgG and C3 as well as induced chemokines TNF-alpha, IL-1beta and IL-6 were traced in cryostat sections using specific antibodies and appropriate peroxidase-labelled anti-antibodies. In four rabbits immunized with the double mutant strain, no deposits were found, and as examined by TEM, only subtle and transient renal changes were observed. In contrast, the original strain AL168 induced pronounced inflammatory and degenerative glomerular changes in all four rabbits injected, and deposits of TNF-alpha, IL-1beta and IL-6 were found in mesangial and endothelial cells. Similar deposits and glomerular changes were seen in all eight rabbits injected with the mrp-emm+ mutant and in four out of seven animals receiving the mrp+emm- mutant. There was a highly significant correlation between high levels of circulating anti-IgG and development of APSGN. These results confirm an important role of streptococcal IgGBP in triggering experimental APSGN as earlier proposed by our group.
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| 3. |
- Hillarp, A, et al.
(författare)
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Molecular cloning of rat C4b binding protein alpha- and beta-chains : structural and functional relationships among human, bovine, rabbit, mouse, and rat proteins
- 1997
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Ingår i: Journal of immunology. - 0022-1767. ; 158:3, s. 23-1315
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Tidskriftsartikel (refereegranskat)abstract
- The C4b binding protein (C4BP) functions as a regulator of the complement system by interacting with the activated form of the fourth complement component, C4b. Human C4BP also interacts with the anticoagulant protein S and the serum amyloid P component (SAP). It is composed of seven identical 70-kDa alpha-chains and one 45-kDa beta-chain. The alpha-chain contains a binding site for C4b, whereas the beta-chain contains the protein S binding site. Recent studies have shown rabbit and bovine plasma to lack a C4BP-protein S complex, and the mouse beta-chain gene to have evolved into a pseudogene. Using a gel filtration chromatography system in combination with Western blotting, we detected a complex between C4BP and protein S in rat plasma, similar to the complex known in human plasma. Using purified rat C4BP and SAP we were unable to detect any complex between the two proteins, but rat C4BP was able to form a complex with human SAP. Rat cDNA clones encoding the C4BP alpha- and beta-chains were isolated from a rat liver cDNA library. The rat alpha-chain cDNA predicted a mature polypeptide chain of 545 amino acid residues, whereas the beta-chain cDNA predicted a mature polypeptide of 243 amino acid residues. The overall amino acid sequence identities between the rat alpha-chain and the mouse, human, rabbit, and bovine alpha-chains were 64, 60, 59, and 52%, respectively. The identities between the rat beta-chain and the human and bovine beta-chains were 68 and 57%, respectively. The rat represents the first non-primate species in which the C4BP-protein S interaction has been found to be conserved.
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| 4. |
- Burova, LA, et al.
(författare)
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Induction of myocarditis in rabbits injected with group A streptococci
- 2004
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Ingår i: Indian Journal of Medical Research. - 0971-5916. ; 119, s. 183-185
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Tidskriftsartikel (refereegranskat)abstract
- Background & objectives: We have earlier proposed that group A streptococcal (GAS) immunoglobulin binding surface proteins (IgGBPs) might trigger anti-IgG production and immune complex formation leading to glomerulonephritis. In the present study, cardiac tissue material from rabbits injected with heat-killed GAS was investigated. Methods: Rabbits were injected intravenously with 10(9) colony forming units of streptococci three times weekly for 8 wk. Cardiac tissue samples were obtained at different times and deposition of IgG, C3, TNF-alpha and IL-6 was studied. Results: After 8 or more weeks of intravenous (iv) injections, minimal changes were seen in animals receiving an IgG non-binding GAS strain, type T27, whereas in those animals receiving either of two IgG binding GAS strains, types M1 or M22, strong inflammatory and degenerative myocardial changes accompanied by deposition of IgG and C3 were noted. Furthermore, on injecting rabbits with defined mutants of a type M22 strain, the development of myocardial tissue damage proved to. be dependent on the presence streptococcal IgGBPs. Interpretation & conclusion: The present data supported a role of streptococcal IgGBPs in the induction of myocardial tissue injury by GAS.
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| 5. |
- Burova, LA, et al.
(författare)
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Myocardial tissue damage in rabbits injected with group A streptococci, types M1 and M22. Role of bacterial immunoglobuhn G-binding surface proteins
- 2005
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Ingår i: APMIS : acta pathologica, microbiologica, et immunologica Scandinavica. - : Wiley. - 1600-0463. ; 113:1, s. 21-30
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Tidskriftsartikel (refereegranskat)abstract
- Acute rheumatic fever (ARF) and acute poststreptococcal glomerulonephritis (APSGN), two important sequelae of streptococcal throat or skin infections, according to current concepts may be elicited by autoimmune mechanisms due to molecular mimicry between group A streptococci (GAS) and human tissue. In the case of APSGN, however, Our experimental data have indicated that GAS immunoglobulin-binding surface proteins (IgG Bps) might be of pathogenic significance by triggering anti-IgG production and immune complex formation leading to renal damage. Thus, rabbits injected with IEG-binding, as opposed to non-binding, GAS strains were found to develop renal deposition of IgG and complement factor C3 and inflammatory and degenerative glomerular changes resembling the picture seen in APSGN. In the present study, cardiac tissue material from rabbits injected with GAS was investigated. After 8 or more weeks of intravenous (i.v.) injections, minimal changes were seen in those animals receiving an IgG non-binding GAS strain, type T27, whereas those animals receiving either of two IgG-binding GAS strains, types M1 or M22, developed strong inflammatory and degenerative myocardial changes accompanied by deposition of IgG and C3. Furthermore, on injecting rabbits with defined mutants of a type M22 strain, the development of myocardial tissue damage proved to be dependent on the presence of streptococcal IgG-binding activity. Our results demonstrate that myocardial tissue changes may be induced in the rabbit by i.v. injection of whole heat-killed GAS of at least two M serotypes. Conceivably, induction of immune complexes by bacterial IqG BPs may lead to myocardial deposition of IgG, in turn triggering a series of events, involving the complement system and proinflammatory cytokines, with resulting tissue damage. Though many virulence factors may be involved in the development of ARF and APSGN, and a given GAS strain will never cause both, our results may suggest a new pathogenetic mechanism common to these two major non-suppurative complications.
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| 6. |
- Deshpande, Srikanth, et al.
(författare)
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Effect of spanwise variation of chord on the performance of a turbine cascade
- 2017
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Ingår i: Turbomachinery. - 9780791850787 ; 2A-2017
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Konferensbidrag (refereegranskat)abstract
- This paper compares the aerodynamic performance of two cascade designs, viz.: -constant-chord and varying-chord. The varying-chord design is typical of industrial gas turbines and steam turbine stators in order to reduce manufacturing costs. The present study aims to increase the understanding of the implications of this manufacturing constraint on the aerodynamics of the stator. Experiments are carried out in a linear cascade wind tunnel. Numerical simulations are performed using commercial code CFX. The profile losses and secondary losses in the two designs are compared. The overall total pressure losses indicate better aerodynamic performance of a turbine cascade with constant chord as compared to a turbine cascade of varying-chord design
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