Relevant bibliographies by topics / AUTOANTIGENS OF HUMANS

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

Academic literature on the topic 'AUTOANTIGENS OF HUMANS'

Author: Grafiati
Published: 11 September 2023

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Journal articles on the topic "AUTOANTIGENS OF HUMANS"

1

Ludewig, Burkhard, Philippe Krebs, Helen Metters, Jutta Tatzel, Özlem Türeci, and Ugur Sahin. "Molecular Characterization of Virus-induced Autoantibody Responses." Journal of Experimental Medicine 200, no. 5 (September 6, 2004): 637–46. http://dx.doi.org/10.1084/jem.20040358.

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Here we present a comprehensive molecular mapping of virus-induced autoimmune B cell responses obtained by serological identification of antigens by recombinant expression cloning analysis. Immunoscreening of cDNA expression libraries of various organs (lung, liver, and spleen) using sera from mice infected with cytopathic (vaccinia virus [VV]) or noncytopathic (lymphocytic choriomeningitis virus [LCMV]) viruses revealed a broad specificity of the elicited autoantibody response. Interestingly, the majority of the identified autoantigens have been previously described as autoantigens in humans. We found that induction of virus-induced autoantibodies of the immunoglobulin G class largely depends on the CD40–CD40L-mediated interaction between T and B cells. Furthermore, antibody titers against a number of autoantigens were comparable to the concomitantly induced antiviral antibody response. Comparison of serum reactivity against a selected panel of autoantigens after infection with VV, LCMV, or vesicular stomatitis virus showed that the different virus infections triggered distinct autoantibody responses, suggesting that virus infections may leave specific “autoantibody fingerprints” in the infected host.
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Mikecz, K., T. T. Glant, E. Buzás, and A. R. Poole. "Cartilage proteoglycans as potential autoantigens in humans and in experimental animals." Agents and Actions 23, no. 1-2 (February 1988): 63–66. http://dx.doi.org/10.1007/bf01967190.

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Francoeur, A. M., C. L. Peebles, K. J. Heckman, J. C. Lee, and E. M. Tan. "Identification of ribosomal protein autoantigens." Journal of Immunology 135, no. 4 (October 1, 1985): 2378–84. http://dx.doi.org/10.4049/jimmunol.135.4.2378.

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Abstract Approximately 20% of patients with systemic lupus erythematosus and with anti-Sm autoantibodies synthesize autoantibodies, called anti-rRNP, to components of the ribosome. We found that anti-rRNP sera reacted predominantly with three ribosomal phosphoproteins of approximate Mr = 38,000, 16,000 and 15,000, both by immunoprecipitation and by immunoblotting. The human autoantibodies cross-reacted with similar antigens present in rodent, brine shrimp, and yeast cells but reacted weakly if at all with proteins of bacteria. Thus the human autoantibodies recognize epitopes that are widely conserved in evolution. Purified ribosomal proteins together with specific rabbit antisera were used to identify the two smaller rRNP antigens as the acidic phosphoproteins of the large ribosomal subunit, designated P1/P2(L40/L41) (rat), eL7/eL12 (Artemia, brine shrimp), and A1/A2 (yeast). These proteins function in the elongation step of protein synthesis in an analogous fashion to the L7/L12 ribosomal proteins of E. coli. The 38,000-dalton rRNP antigen corresponds to a nonacidic protein also associated with the large ribosomal subunit. The human autoantibodies appear to have a specificity similar to that of a previously described mouse monoclonal antibody obtained from mice injected with heterologous (chick) ribosomes, suggesting that both the human polyclonal autoantibodies and the mouse monoclonal recognize a class of epitope(s) that is common in all three ribosomal proteins. In addition, we found that many of the anti-ribosomal sera contained a further class of autoantibodies reactive with naked RNA. These may be similar to the anti-RNA antibodies previously described in both humans and mice with autoimmune disease.
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Harrison, Leonard C., Majella Dempsey-Collier, David R. Kramer, and Kazuma Takahashi. "Aerosol Insulin Induces Regulatory CD8 γδ T Cells That Prevent Murine Insulin-dependent Diabetes." Journal of Experimental Medicine 184, no. 6 (December 1, 1996): 2167–74. http://dx.doi.org/10.1084/jem.184.6.2167.

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Cellular immune hyporesponsiveness can be induced by the presentation of soluble protein antigens to mucosal surfaces. Most studies of mucosa-mediated tolerance have used the oral route of antigen delivery and few have examined autoantigens in natural models of autoimmune disease. Insulin is an autoantigen in humans and nonobese diabetic (NOD) mice with insulindependent diabetes mellitus (IDDM). When we administered insulin aerosol to NOD mice after the onset of subclinical disease, pancreatic islet pathology and diabetes incidence were both significantly reduced. Insulin-treated mice had increased circulating antibodies to insulin, absent splenocyte proliferation to the major epitope, insulin B chain amino acids 9–23, which was associated with increased IL-4 and particularly IL-10 secretion, and reduced proliferation to glutamic acid decarboxylase, another islet autoantigen. The ability of splenocytes from insulin-treated mice to suppress the adoptive transfer of diabetes to nondiabetic mice by T cells of diabetic mice was shown to be caused by small numbers of CD8 γδ T cells. These findings reveal a novel mechanism for suppressing cell-mediated autoimmune disease. Induction of regulatory CD8 γδ T cells by aerosol insulin is a therapeutic strategy with implications for the prevention of human IDDM.
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Vaughan, Kerrie, Yohan Kim, and Alessandro Sette. "A Comparison of Epitope Repertoires Associated with Myasthenia Gravis in Humans and Nonhuman Hosts." Autoimmune Diseases 2012 (2012): 1–16. http://dx.doi.org/10.1155/2012/403915.

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Here we analyzed the molecular targets associated with myasthenia gravis (MG) immune responses, enabled by an immune epitope database (IEDB) inventory of approximately 600 MG-related epitopes derived from 175 references. The vast majority of epitopes were derived from theα-subunit of human AChR suggesting that other MG-associated autoantigens should be investigated further. Humanα-AChR was mostly characterized in humans, whereas reactivity primarily toT. californicaAChR was examined in animal models. While the fine specificity of T-cell response was similar in the two systems, substantial antibody reactivity to the C-terminus was detected in the nonhuman system, but not in humans. Further analysis showed that the reactivity of nonhuman hosts to the C-terminus was eliminated when data were restricted to hosts tested in the context of autoimmune disease (spontaneous or induced), demonstrating that the epitopes recognized in humans and animals were shared when disease was present. Finally, we provided data subsets relevant to particular applications, including those associated with HLA typing or restriction, sets of epitopes recognized by monoclonal antibodies, and epitopes associated with modulation of immunity or disease. In conclusion, this analysis highlights gaps, differences, and similarities in the epitope repertoires of humans and animal models.
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Misharin, Alexander V., Yuji Nagayama, Holly A. Aliesky, Basil Rapoport, and Sandra M. McLachlan. "Studies in Mice Deficient for the Autoimmune Regulator (Aire) and Transgenic for the Thyrotropin Receptor Reveal a Role for Aire in Tolerance for Thyroid Autoantigens." Endocrinology 150, no. 6 (March 5, 2009): 2948–56. http://dx.doi.org/10.1210/en.2008-1690.

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The autoimmune regulator (Aire) mediates central tolerance for many autoantigens, and autoimmunity occurs spontaneously in Aire-deficient humans and mice. Using a mouse model of Graves’ disease, we investigated the role of Aire in tolerance to the TSH receptor (TSHR) in Aire-deficient and wild-type mice (hyperthyroid-susceptible BALB/c background). Mice were immunized three times with TSHR A-subunit expressing adenovirus. The lack of Aire did not influence T-cell responses to TSHR protein or TSHR peptides. However, antibody levels were higher in Aire-deficient than wild-type mice after the second (but not the third) immunization. After the third immunization, hyperthyroidism persisted in a higher proportion of Aire-deficient than wild-type mice. Aire-deficient mice were crossed with transgenic strains expressing high or low-intrathyroidal levels of human TSHR A subunits. In the low-expressor transgenics, Aire deficiency had the same effect on the pattern of the TSHR antibody response to immunization as in nontransgenics, although the amplitude of the response was lower in the transgenics. High-expressor A-subunit transgenics were unresponsive to immunization. We examined intrathymic expression of murine TSHR, thyroglobulin, and thyroid peroxidase (TPO), the latter two being the dominant autoantigens in Hashimoto’s thyroiditis (particularly TPO). Expression of the TSHR and thyroglobulin were reduced in the absence of Aire. Dramatically, thymic expression of TPO was nearly abolished. In contrast, the human A-subunit transgene, lacking a potential Aire-binding motif, was unaffected. Our findings provide insight into how varying intrathymic autoantigen expression may modulate thyroid autoimmunity and suggest that Aire deficiency may contribute more to developing Hashimoto’s thyroiditis than Graves’ disease.
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Liminet, Christelle, Julien Vouillarmet, Karim Chikh, and Emmanuel Disse. "Antibody-Mediated Insulin Resistance: When Insulin and Insulin Receptor Act as Autoantigens in Humans." Canadian Journal of Diabetes 40, no. 5 (October 2016): 462–65. http://dx.doi.org/10.1016/j.jcjd.2016.02.007.

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Härkönen, Taina, Anja Paananen, Hilkka Lankinen, Tapani Hovi, Outi Vaarala, and Merja Roivainen. "Enterovirus infection may induce humoral immune response reacting with islet cell autoantigens in humans." Journal of Medical Virology 69, no. 3 (January 13, 2003): 426–40. http://dx.doi.org/10.1002/jmv.10306.

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Chen, Xin, Venkata Mallajosyula, Mustafa Ghanizada, Elsa Sola, Lei Chen, Lilit Kamalyan, Jing Li, and Mark M. Davis. "Distinct roles of CD4 +and CD8 +Tregs in regulating human autoreactive T cells, B cells, and antibodies in genetically engineered tonsil organoid system." Journal of Immunology 210, no. 1_Supplement (May 1, 2023): 247.20. http://dx.doi.org/10.4049/jimmunol.210.supp.247.20.

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Abstract CD4 +and CD8 +regulatory T cells (Treg) are critical for maintaining immune tolerance, and alternations in number and function are associated with detrimental outcomes in infectious and autoimmune diseases. Despite their importance, their distinct roles and mechanisms in regulating self-tolerance need to be better characterized in humans. Here we analyzed the relative contribution of CD4 +and CD8 +Tregs to control autoreactive T cells, B cells, and antibodies in an entirely human tonsil organoid system in vitro. We disrupted their suppressive functions by knocking out FOXP3 and GZMB genes using CRISPR/Cas9 technology. Normally tonsil organoids make robust antibody and cellular responses to live attenuated flu vaccine, but not to autoantigens. In contrast, FOXP3 KO tonsil organoids produced autoantibodies when stimulated with a panel of classical autoantigens, including double-stranded DNA and others. We also detected increased CD8 +T cells specific for autoantigens, including SMCY antigen. With the GZMB KO, we found a marked increase in follicular helper T cells and autoreactive CD4 +and CD8 +T cells. Interestingly the GZMB KO tonsils showed an expansion of plasmablasts, but only a low level of autoantibodies and autoreactive B cells was detected. This indicates that CD8 +Tregs control the early T and B cell activation but not autoantibody production. Moreover, knocking out FOXP3 generated high-affinity HA-specific antibodies in tonsil organoids compared to control, indicating that CD4 +Tregs are a key checkpoint for high-affinity antibodies and the production of autoantibodies. We conclude that CD8 +and CD4 +Tregs have distinct and complementary roles in regulating cellular and humoral responses and preventing autoimmunity.
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Mamula, M. J., S. Fatenejad, and J. Craft. "B cells process and present lupus autoantigens that initiate autoimmune T cell responses." Journal of Immunology 152, no. 3 (February 1, 1994): 1453–61. http://dx.doi.org/10.4049/jimmunol.152.3.1453.

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Abstract Antibodies against U small nuclear ribonucleoprotein (snRNP) particles are a common finding in the sera of humans with SLE and in certain strains of mice with murine lupus. It is likely that Th cells are important in amplifying this autoantibody response. The focus of this work was to investigate events that might initiate autoimmune B and T cell response in non-autoimmune mice to native snRNP particles. Mice that were immunized and boosted with native mouse snRNPs failed to produce any detectable specific anti-snRNP antibody or T cell responses, suggesting that these autoreactive cells were deleted from the repertoire or were anergic to stimulation with this self Ag. In contrast, immunization with native foreign (human) snRNPs elicited both T cells and cross-reactive anti-snRNP antibodies; the latter predominantly were directed toward the A protein of the U1 snRNP. When mice were immunized with human and mouse snRNPs together in adjuvant, T cells specific for mouse snRNPs could be elicited. The results of these experiments suggested that the mechanism of breaking T cell tolerance to self snRNPs was dependent on the ability of cross-reactive B cells to process and present these autoantigens. To address this hypothesis, B cells purified from mice immunized with recombinant human A protein were transferred into naive mice. Upon boosting with native mouse snRNPs, autoreactive CD4+ T cells specific for mouse Ags, and not cross-reactive with human snRNPs, were observed. These studies support a model of molecular mimicry whereby autoantigen-presenting B cells are generated by foreign cross-reactive determinants that can, in turn, elicit an autoimmune T cell response.
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Dissertations / Theses on the topic "AUTOANTIGENS OF HUMANS"

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KOTHARI, VANSHIKA. "IN SILICO PREDICTION OF EPITOPES OF COMMENSAL VIRUS THAT CROSS-REACT WITH HUMAN AUTOANTIGENS." Thesis, DELHI TECHNOLOGICAL UNIVERSITY, 2021. http://dspace.dtu.ac.in:8080/jspui/handle/repository/18394.

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The prevalence and epidemiology of autoimmune diseases in developed, as well as in developing countries have increased over the past decade. The human body consists of trillions of microorganisms and the composition is unique to each individual. It consists of commensal as well as pathogenic viruses. The interactions between host-microbiota helps to regulate immune system. However, there are many factors that can alter the interactions which ultimately leads to dysbiosis. Dysbiosis can lead to development of autoimmune diseases along with other complex diseases. Viruses are obligate intracellular parasites. Commensal viruses is a new concept because there can be some viruses which may not be detrimental to human body. However, sometimes autoimmune reactions are generated as a result of cross-reactivity of epitopes of virus with autoantigens of humans. This study aims, to find various commensal viruses found in human body, to predict potential epitopes in viruses, sequence homology with autoantigens of humans and to check binding energy of viral epitopes with MHC class I and T-cell receptor. This will help us to develop new preventive and therapeutic strategies.
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Iwobi, Mabel Uzoamaka. "Salivary autoantigens in human rheumatic diseases." Thesis, University of Sussex, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260048.

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Zhu, Jianhui. "Induction of the cellular expression of human Ro autoantigens." Thesis, McGill University, 1995. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=39900.

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Ro autoantigens are intracellular ribonucleoproteins of unknown function. Autoantibodies to these antigens are detected frequently in patients with systemic lupus erythematosus (SLE) and involved in the pathogenesis of lupus skin lesions. Although the mechanisms responsible for the induction of these autoantibodies and immunologic tissue damage are unclear, one possibility is that Ro autoantigens are expressed on the cell surface and induce an immune response. Cell surface expression of Ro antigens has been reported previously following ultraviolet B (UVB) irradiation or estrogen stimulation of human keratinocytes. In this thesis, the effect of human cytomegalovirus (CMV) infection on the surface expression of Ro antigens and calreticulin on human fibroblasts and keratinocytes was investigated using a fixed cell enzyme-linked immunoassay (ELISA), immunofluorescence, flow cytometry (FACS) analysis and immunoblotting. CMV infection of cultured human fibroblast cells was found to increase the cell surface expression of calreticulin, but not 60kD/Ro antigen. However, CMV infection, in combination with UVB irradiation, synergistically induced the expression of 52kD/Ro antigen, but not 60kD/Ro or calreticulin, on the surface of these cells. This enhanced expression of 52kD/Ro autoantigen on CMV and UVB treated cells was significant and specific, compared with untreated cells, cells infected with CMV or irradiated with UVB only, and cells subjected to other treatments including low pH. These studies were then extended to human keratinocytes, which are relevant to the skin disease associated with the presence of anti-Ro antibodies in SLE. Human CMV was demonstrated to be capable of infecting keratinocytes in vitro and induced the surface expression of 60kD/Ro antigen, but not 52kD/Ro and calreticulin, on human keratinocytes. As there was no increase in total cellular expression of 60kD/Ro antigen after viral infection, 60kD/Ro antigen appears to be redistributed from the
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Whitehead, Clark Merrill. "The identification and characterization of two human autoantigens, HsEg5 and ASE-1." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0027/NQ49554.pdf.

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Schirmer, Jan Henrik [Verfasser], and Friedrich [Akademischer Betreuer] Haag. "Charakterisierung putativer humaner Autoantigene / Jan Henrik Schirmer. Betreuer: Friedrich Haag." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2012. http://d-nb.info/1025150910/34.

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Purdy, Lisa Eileen. "Establishing a framework for mapping DQ8 restricted T cell epitopes for human diabetes autoantigens." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/mq22657.pdf.

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Barbar, Élie. "Caractérisation de RoBP1, nouveau partenaire cellulaire des ribonucléprotéines Ro humaines et autoantigène potentiel dans des maladies autoimmune." Sherbrooke : Université de Sherbrooke, 2000.

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Yaciuk, Jane Cherie. "Mechanisms of T cell tolerance to the RNA-binding nuclear autoantigen human La/SS-B." Oklahoma City : [s.n.], 2008.

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Hasler, Daniele [Verfasser], and Gunter [Akademischer Betreuer] Meister. "The Role of the Lupus Autoantigen La in the Human MicroRNA Pathway / Daniele Hasler ; Betreuer: Gunter Meister." Regensburg : Universitätsbibliothek Regensburg, 2019. http://d-nb.info/1180719557/34.

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Koelsch, Kristi Ann. "Insights into the regulation of human B cell tolerance by analysis of the immunoglobulin repertroire." Oklahoma City : [s.n.], 2009.

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Books on the topic "AUTOANTIGENS OF HUMANS"

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Martin, Alberto. Epitope studies on the human autoantigen, histidyl-tRNA synthetase. Ottawa: National Library of Canada, 1994.

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2

Cattran, Daniel C., and Heather N. Reich. Membranous glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0064_update_001.

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It has been clear for several decades from comparison with the rodent model disease Heymann nephritis that membranous glomerulonephritis (MGN) is an immune condition in which antibodies, usually autoantibodies, bind to targets on the surface of podocytes. However, the antigen in Heymann nephritis, megalin, is not present on human podocytes. The first potential antigen was identified by studying rare examples of maternal alloimmunization, leading to congenital membranous nephropathy in the infant caused by antibodies to neutral endopeptidase. More recently, the target of autoantibody formation in most patients with primary MGN has been identified to be the phospholipase A2 receptor, PLA2R. Genome-wide association studies identify predisposing genetic loci at HLADQ and at the locus encoding the autoantigen itself. So antibodies to at least two different molecular targets can cause MGN, and it seems likely that there may be other targets in secondary types of MGN, and possibly haptenized or otherwise modified molecules are implicated in drug- and toxin-induced MGN. Once antibodies are fixed, animal models and human observations suggest that complement is involved in mediating tissue damage. However, immunoglobulin G4, not thought to fix complement, is the predominant isotype in human MGN, and the mechanisms are not fully unravelled. Podocyte injury is known to cause proteinuria. In MGN, antibody fixation or cell damage may stimulate production of extracellular matrix to account for the increased GBM thickness with ‘podocyte type’ basement membrane collagen isoforms, and ultimately cell death and glomerulosclerosis.
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Book chapters on the topic "AUTOANTIGENS OF HUMANS"

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Takeda, Hiroyuki. "Autoantibody Profiling Using Human Autoantigen Protein Array and AlphaScreen." In Methods in Molecular Biology, 93–112. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8802-0_10.

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Wang, Dan, Yupeng Zhang, Qing Meng, and Xiaobo Yu. "AAgAtlas 1.0: A Database of Human Autoantigens Extracted from Biomedical Literature." In Methods in Molecular Biology, 365–74. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0389-5_21.

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Ganesan, Vinitha, and Dana P. Ascherman. "Citrullinated Autoantigen Targets as Markers of Extra-Articular Disease in Rheumatoid Arthritis." In Protein Deimination in Human Health and Disease, 191–203. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-58244-3_11.

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Ma, S., and A. M. Jevnikar. "Suppression of Autoimmune Diabetes by the Use of Transgenic Plants Expressing Autoantigens to Induce Oral Tolerance." In Molecular Farming of Plants and Animals for Human and Veterinary Medicine, 179–96. Dordrecht: Springer Netherlands, 2002. http://dx.doi.org/10.1007/978-94-017-2317-6_8.

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Kenan, D. J., and J. D. Keene. "The Human La Autoantigen Contains an RNA Binding Domain and an ATP Binding Domain." In Molecular and Cell Biology of Autoantibodies and Autoimmunity. Abstracts, 35–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-46681-6_29.

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Mimori, T., N. Hama, A. Suwa, Y. Ohsone, M. Akizuki, M. Homma, A. J. Griffith, and J. A. Hardin. "Molecular Cloning of the Human Autoantigen KU (p70/p80), a DNA-Terminal-Binding Protein Complex." In Molecular and Cell Biology of Autoantibodies and Autoimmunity. Abstracts, 53. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-46681-6_45.

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Netter, H. J., H. H. Guldner, C. Szostecki, H. J. Lakomek, and H. Will. "Identification of Several Independent Autoreactive Epitopes of the Human 68 kDa (U 1) snRNP-Autoantigen." In Molecular and Cell Biology of Autoantibodies and Autoimmunity. Abstracts, 60–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-46681-6_53.

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Earnshaw, W. C., H. Saitoh, J. E. Tomkiel, C. A. Cooke, R. L. Bernat, H. Ratrie, M. Maurer, and N. F. Rothfield. "Molecular cloning and characterization of human centromeric autoantigen CENP-C: a component of the inner kinetochore plate." In Chromosomes Today, 23–34. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1510-0_2.

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Guldner, H. H., H. J. Netter, C. Szostecki, E. Jäger, and H. Will. "Molecular Mimicry: A Common Epitope of the (U1) snRNP Associated p68 Autoantigen and a Protein of a Human Pathogenic Virus." In Molecular and Cell Biology of Autoantibodies and Autoimmunity. Abstracts, 22–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-46681-6_20.

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Christen, U., and J. Gut. "Molecular Mimicry of CF3CO-Lysine by Lipoic Acid I: The Dihydrolipoamide Acetyltransferase Subunit of the Human Pyruvate Dehydrogenase as Autoantigen in Halothane Hepatitis." In Archives of Toxicology, 565. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79451-3_50.

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Conference papers on the topic "AUTOANTIGENS OF HUMANS"

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PEZZOTTI, MARIO, and ALBERTO FALORNI. "TRANSGENIC PLANTS EXPRESSING HUMAN GLUTAMIC ACID DECARBOXYLASE (GAD65), A MAJOR AUTOANTIGEN IN TYPE 1 DIABETES MELLITUS." In International Seminar on Nuclear War and Planetary Emergencies 25th Session. Singapore: World Scientific Publishing Co. Pte. Ltd., 2001. http://dx.doi.org/10.1142/9789812797001_0061.

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