Relevant bibliographies by topics / Autoimmune diseases – Animal models

Contents

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

Academic literature on the topic 'Autoimmune diseases – Animal models'

Author: Grafiati
Published: 4 June 2021
Last updated: 31 January 2023

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Journal articles on the topic "Autoimmune diseases – Animal models"

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Burkhardt, H., and J. R. Kalden. "Animal models of autoimmune diseases." Rheumatology International 17, no. 3 (September 1997): 91–99. http://dx.doi.org/10.1007/s002960050015.

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Gregersen, J. W., S. Holmes, and L. Fugger. "Humanized animal models for autoimmune diseases." Tissue Antigens 63, no. 5 (May 2004): 383–94. http://dx.doi.org/10.1111/j.0001-2815.2004.00243.x.

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Ludewig, Burkhard, Rolf M. Zinkernagel, and Hans Hengartner. "Transgenic Animal Models for Virus-Induced Autoimmune Diseases." Experimental Physiology 85, no. 6 (November 2000): 653–59. http://dx.doi.org/10.1111/j.1469-445x.2000.02093.x.

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Rose, Noel R. "Autoimmune diseases in animal models and human patients." Pathophysiology 5 (June 1998): 261. http://dx.doi.org/10.1016/s0928-4680(98)81315-1.

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Taneja, Veena, and Chella S. David. "Lessons from animal models for human autoimmune diseases." Nature Immunology 2, no. 9 (September 2001): 781–84. http://dx.doi.org/10.1038/ni0901-781.

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Zhan, Xianbao, Fan Wang, Yan Bi, and Baoan Ji. "Animal models of gastrointestinal and liver diseases. Animal models of acute and chronic pancreatitis." American Journal of Physiology-Gastrointestinal and Liver Physiology 311, no. 3 (September 1, 2016): G343—G355. http://dx.doi.org/10.1152/ajpgi.00372.2015.

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Animal models of pancreatitis are useful for elucidating the pathogenesis of pancreatitis and developing and testing novel interventions. In this review, we aim to summarize the most commonly used animal models, overview their pathophysiology, and discuss their strengths and limitations. We will also briefly describe common animal study procedures and refer readers to more detailed protocols in the literature. Although animal models include pigs, dogs, opossums, and other animals, we will mainly focus on rodent models because of their popularity. Autoimmune pancreatitis and genetically engineered animal models will be reviewed elsewhere.
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Tian, David H., Chamini J. Perera, and Gila Moalem-Taylor. "Neuropathic Pain in Animal Models of Nervous System Autoimmune Diseases." Mediators of Inflammation 2013 (2013): 1–13. http://dx.doi.org/10.1155/2013/298326.

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Neuropathic pain is a frequent chronic presentation in autoimmune diseases of the nervous system, such as multiple sclerosis (MS) and Guillain-Barre syndrome (GBS), causing significant individual disablement and suffering. Animal models of experimental autoimmune encephalomyelitis (EAE) and experimental autoimmune neuritis (EAN) mimic many aspects of MS and GBS, respectively, and are well suited to study the pathophysiology of these autoimmune diseases. However, while much attention has been devoted to curative options, research into neuropathic pain mechanisms and relief has been somewhat lacking. Recent studies have demonstrated a variety of sensory abnormalities in different EAE and EAN models, which enable investigations of behavioural changes, underlying mechanisms, and potential pharmacotherapies for neuropathic pain associated with these diseases. This review examines the symptoms, mechanisms, and clinical therapeutic options in these conditions and highlights the value of EAE and EAN animal models for the study of neuropathic pain in MS and GBS.
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Liu, Shou-Pei, Zhen-Hua Bian, Zhi-Bin Zhao, Jinjun Wang, Weici Zhang, Patrick S. C. Leung, Liang Li, and Zhe-Xiong Lian. "Animal Models of Autoimmune Liver Diseases: a Comprehensive Review." Clinical Reviews in Allergy & Immunology 58, no. 2 (February 19, 2020): 252–71. http://dx.doi.org/10.1007/s12016-020-08778-6.

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Liu, Yan, Christoph Meyer, Chengfu Xu, Honglei Weng, Claus Hellerbrand, Peter ten Dijke, and Steven Dooley. "Animal models of chronic liver diseases." American Journal of Physiology-Gastrointestinal and Liver Physiology 304, no. 5 (March 1, 2013): G449—G468. http://dx.doi.org/10.1152/ajpgi.00199.2012.

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Chronic liver diseases are frequent and potentially life threatening for humans. The underlying etiologies are diverse, ranging from viral infections, autoimmune disorders, and intoxications (including alcohol abuse) to imbalanced diets. Although at early stages of disease the liver regenerates in the absence of the insult, advanced stages cannot be healed and may require organ transplantation. A better understanding of underlying mechanisms is mandatory for the design of new drugs to be used in clinic. Therefore, rodent models are being developed to mimic human liver disease. However, no model to date can completely recapitulate the “corresponding” human disorder. Limiting factors are the time frame required in humans to establish a certain liver disease and the fact that rodents possess a distinct immune system compared with humans and have different metabolic rates affecting liver homeostasis. These features account for the difficulties in developing adequate rodent models for studying disease progression and for testing new pharmaceuticals to be translated into the clinic. Nevertheless, traditional and new promising animal models that mimic certain attributes of chronic liver diseases are established and being used to deepen our understanding in the underlying mechanisms of distinct liver diseases. This review aims at providing a comprehensive overview of recent advances in animal models recapitulating different features and etiologies of human liver diseases.
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Morahan, Grant, and Laurence Morel. "Genetics of autoimmune diseases in humans and in animal models." Current Opinion in Immunology 14, no. 6 (December 2002): 803–11. http://dx.doi.org/10.1016/s0952-7915(02)00401-6.

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Dissertations / Theses on the topic "Autoimmune diseases – Animal models"

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Li, Jinan. "Multifunctional roles of plasmin in inflammation : Studies of animal models on rheumatoid arthritis, multiple sclerosis, wound healing and infection." Doctoral thesis, Umeå : Dept. of medical biochemistry and biophysics, Univ, 2005. http://www.diva-portal.org/umu/theses/abstract.xsql?dbid=422.

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Ma, Liang, and 馬亮. "Induction and regulation of autoimmune responses by dendritic cells upon interaction with dying cells in murine models." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B3554756X.

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Kezic, Jelena Marie. "A study of the monocyte-derived cell populations of the uveal tract and retina in homeostatic conditions and during the early stages of ocular autoimmune disease." University of Western Australia. School of Anatomy and Human Biology, 2008. http://theses.library.uwa.edu.au/adt-WU2009.0084.

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The eye contains closely related but widely different tissues, offering a unique opportunity to investigate the phenotype and function of monocyte-derived cell populations within functionally unique microenvironments in a single complex organ. The uveal tract and retina contain rich networks of immune cells that reside and traffic through the eye, these cells having been implicated in various ocular inflammatory processes and immune-mediated diseases. One such inflammatory condition is human posterior uveitis, an autoimmune disease mainly affecting the retina. As current treatments for posterior uveitis only serve to slow down disease progression, studies using animal models, namely, experimental autoimmune uveoretinitis (EAU), have focused on determining the key cellular and molecular mediators involved in disease initiation in order to expand the potential for novel therapeutic applications. The overall purpose of experiments in this thesis was to explore monocyte-derived cell populations of the uveal tract and retina, this being achieved by utilising a novel transgenic mouse model. Cx3cr1gfp/gfp transgenic mice on both BALB/c and C57Bl/6 backgrounds contain an enhanced green fluorescent protein (eGFP) encoding cassette knocked into the Cx3cr1 gene, disrupting its expression but facilitating GFP expression under the control of the Cx3cr1 promoter. Heterozygous (Cx3cr1+/gfp) mice were generated by crossing Cx3cr1gfp/gfp mice to wild-type (WT) mice. This transgenic model allowed for the exquisite visualisation of Cx3cr1-bearing monocyte-derived dendritic cells (DC) and macrophages in ocular tissues, whilst also enabling the investigation of a potential role for Cx3cr1 in recruiting monocyte-derived cells to the eye in steady-state and inflammatory conditions.
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Marshall, Aiden Christopher James 1976. "The role of Fas and TNFα in experimental autoimmune gastritis." Monash University, Dept. of Pathology and Immunology, 2003. http://arrow.monash.edu.au/hdl/1959.1/9413.

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Eppert, Bryan L. "Autoimmune Mechanisms in Cigarette Smoke-Induced Inflammation and Pathology." University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1382950967.

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Stromnes, Ingunn Margarete. "T cell determinants of central nervous system autoimmune disease /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8333.

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Nordquist, Niklas. "Genetic Studies of Rheumatoid Arthritis using Animal Models." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-5117-9/.

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Raza, Abbas. "Genetic And Functional Approaches To Understanding Autoimmune And Inflammatory Pathologies." ScholarWorks @ UVM, 2020. https://scholarworks.uvm.edu/graddis/1175.

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Our understanding of genetic predisposition to inflammatory and autoimmune diseases has been enhanced by large scale quantitative trait loci (QTL) linkage mapping and genome-wide association studies (GWAS). However, the resolution and interpretation of QTL linkage mapping or GWAS findings are limited. In this work, we complement genetic predictions for several human diseases including multiple sclerosis (MS) and systemic capillary leakage syndrome (SCLS) with genetic and functional data in model organisms to associate genes with phenotypes and diseases. Focusing on MS, an autoimmune inflammatory disease of the central nervous system (CNS), we experimentally tested the effect of three of the GWAS candidate genes (SLAMF1, SLAMF2 and SLAMF7) in the experimental autoimmune encephalomyelitis (EAE) mouse model and found a male-specific locus distal to these loci regulating CNS autoimmune disease. Functional data in mouse suggests this male-specific locus modulates the frequency of immune cells including CD11b+, TCRαβ+CD4+Foxp3+, and TCRαβ+CD8+IL-17+ cells during EAE disease. Orchiectomy experiments demonstrate that this male specific phenotype is dependent on testis but not testosterone (T) or 5α-dihydrotestosterone (DHT). Using a bioinformatic approach, we identified SLAMF8 and SLAMF9 along with other differentially expressed genes in linkage with MS-GWAS predictions whose expression is testis-dependent, but not directly regulated by T or DHT, as potential positional candidates regulating CNS autoimmune disease. Further refinement of this locus is required to identify the causal gene(s) that may be targeted for prevention and/or treatment of MS in men. Using SCLS, an extremely rare disorder of unknown etiology characterized by recurrent episodes of vascular leakage, we identified and modeled this disease in an inbred mouse strain, SJL, using susceptibility to histamine- and infection-triggered vascular leak as the major phenotypic readout. This trait “Histamine hypersensitivity” (Histh/Histh) was mapped to a region on Chr 6. Remarkably, Histh is syntenic to the genomic locus most strongly associated with SCLS in humans (3p25.3). Subsequent studies found that the Histh locus is not unique to SJL but additional mouse strains also exhibit Histh phenotype. Considering GWAS studies in SCLS are limited by the small number of patients, we utilized interval-specific SNP-based association testing among Histh phenotyped mouse strains to predict Histh candidates. Furthermore, to dissect the complexity of Histh QTL, we developed network-based functional prediction methods to rank genes in this locus by predicting functional association with multiple Histh-related processes. The top-ranked genes include Cxcl12, Ret, Cacna1c, and Cntn3, all of which have strong functional associations and are proximal to SNPs segregating with Histh. Lastly, we utilized the power of integrating genetic and functional approaches to understand susceptibility to Bordetella pertussis and pertussis toxin (PTX) induced histamine sensitization (Bphs/Bphs), a sub-phenotype with an established role in autoimmunity. Congenic mapping in mice had earlier linked Bphs to histamine H1 receptor gene (Hrh1/H1R) and demonstrated that H1R differs at three amino acid residues in Bphs-susceptible and -resistant mice. Our subsequent studies identified eight inbred mouse strains that were susceptible to Bphs despite carrying a resistant H1R allele. Genetic analyses mapped the locus complementing Bphs to mouse Chr 6, in linkage disequilibrium with Hrh1; we have designated this Bphs-enhancer (Bphse). Similar to the approaches used for Histh, we utilized interval-specific SNP based association testing and network-based functional enrichment to predict nine candidate loci for Bphse including Atp2b2, Atg7, Pparg, Syn2, Ift122, Raf1, Mkrn2, Timp4 and Gt(ROSA)26Sor. Overall, these studies demonstrate the power of integrating genetic and functional methods in humans and animal models to predict highly plausible loci underlying QTL/GWAS data.
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Todd, Derrick James. "Role of the Intestinal Immune System in the Pathogenesis of Autoimmune Diabetes in the BB Rat Model of Type 1 Diabetes Mellitus." eScholarship@UMMS, 2001. https://escholarship.umassmed.edu/gsbs_diss/138.

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The intestine is the largest lymphoid organ in the body, challenged constantly by an enonnous quantity and diversity of antigens. Distinct from peripheral lymphocytes, intestinal lymphocytes have evolved unique mechanisms of tolerance and appear to govern mucosal processes such as "chronic physiologic inflammation" and oral tolerance. Failure of mucosal tolerance has been implicated in the pathogenesis of several diseases, including inflammatory bowel disease, celiac disease, and even autoimmune diabetes. One population of intestinal lymphocytes, intraepithelial lymphocytes (IELs), exists within the intestinal epithelium itself and remains poorly characterized. IELs respond to unique activation signals and appear to be in part responsible for the maintenance of epithelial integrity and mucosal tolerance. Type 1 diabetes is one of the most common chronic childhood illnesses and causes significant morbidity and mortality. Type 1 diabetes mellitus is an autoimmune disease that results from immune-mediated destruction of insulin-producing pancreatic beta cells and is characterized by an absolute insulin deficiency. Several animal models are used to study the immunopathogenesis of type 1 diabetes, including the BB rat and NOD mouse. BBDP rats spontaneously develop autoimmune diabetes mellitus and are severely deficient in peripheral T cells. BBDR rats do not spontaneously develop autoimmune diabetes, have nonnal numbers of peripheral T cells, and can be induced to become diabetic by injections of a cytotoxic anti-ART2a mAb and low doses of poly I:C. The cause of autoimmune diabetes in BB rats and humans is still unknown, but both genetic and environmental factors appear to participate. I hypothesize that one important class of environmental factors--diet and enteromicrobial agents--participates in this pathogenic process through the mediation of the gut immune system. In this dissertation, I report a new method for the isolation of rat IELs that is based on the selective removal of intestinal epithelial cells under conditions that leave the basement membrane undisturbed. The yield of rat IELs using this method is 5-10 fold greater than that reported for other methods. Morphological and phenotypic analyses demonstrate that the purified cell population is comprised of IELs and is not contaminated with lamina propria or Peyer's patch lymphocytes. Phenotypic analysis reveals 5 major subsets of IELs, including populations of γδ T and natural killer (NK) cells present at levels not previously detected. I also report that rat intraepithelial NK (IENK) and peripheral NK cells are similar in morphology, in their ability to lyse NK-sensitive targets, and in their ability to suppress a one-way mixed lymphocyte culture. In contrast, IENK cells differ from splenic NK cells phenotypically, and a substantial fraction of IENK cells appear to spontaneously secrete IL-4 and/or IFN-γ. I conclude that rat IELs harbor a large population of NKR-P1A+ CD3-cells that function as NK cells but display an activated phenotype and unusual cytokine profile that clearly distinguish them from splenic NK cells. Their phenotypic and functional characteristics suggest that these distinctive intraepithelial NK cells may participate in the regulation of mucosal immunity. I next demonstrate that, prior to diabetes, both BBDP and ART2a-depleted BBDR rats have a reduced total number of IELs and exhibit a selective deficiency of IENK cell number and function as compared to control BBDR rats. The deficiency of BBDP rat IELs can be corrected by engraftment of bone marrow from histocompatible WF donors. These results suggest 1) that the peripheral lymphopenia in BBDP rats extends to the IEL compartment, particularly to IENK cells, 2) that in BBDR rats the diabetes-inducing treatment depletes IELs, particularly IENK cells, and 3) that the defect in BBDP rat IELs is intrinsic to hematopoietic cells, not intestinal stromal cells. I also establish that, unlike BBDR and WF rats, BBDP rats are also deficient in γδTCR+IELs, a population of T cells that may play a role in normal mucosal tolerance. In addition, I report preliminary data supporting the hypothesis that systemic autoreactivity may be initiated in the intestine; peripheral autoreactive lymphocyte populations appear to emanate first from mesenteric lymph nodes that drain the intestine, and such cells may initiate a type 2 autoimmune phenomenon driven by IL-4. Collectively, my findings support the hypothesis that a failure of mucosal tolerance in BBDP rats, perhaps secondary to deficiencies in one or more IEL subpopulations, participates in the pathogenesis of autoimmune diabetes in these animals by activating peripheral autoreactive T cells. The nature of the autoimmune response in BB rats (driven by IL-4) appears to be distinct from that of NOD mice. Despite the differences between these two well-accepted animal models of autoimmune diabetes, until more is known about the pathogenesis of type 1 DM in humans, lessons learned from both the BB rat and NOD mouse continue to be of tremendous benefit to our understanding of human disease.
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Gómez, Morago Alba. "Estudio de los mecanismos terapéuticos en la inducción de tolerancia inmunológica en un modelo animal de esclerosis múltiple." Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/386466.

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La terapia génica puede ser una herramienta para inducir tolerancia inmunológica de forma experimental. Nuestro trabajo anterior mostró que la transferencia de células de médula ósea que habían sido transducidas con un autoantígeno (MOG40-55) en ratones con encefalomielitis autoinmune experimental (EAE) mejoró el pronóstico de los animales. En este trabajo, hemos tratado de identificar la subpoblación de células de médula ósea transducidas que fue la principal responsable del efecto terapéutico observado. Se encontró que en los cultivos de transducción de células de médula ósea se generaban células mieloides supresoras de los dos subtipos descritos, tanto granulocíticos (CD11b+ Gr-1high) como monocíticos (CD11b+ Gr-1low), y que las células transducidas con mayor eficacia consistieron en gran medida de estos tipos de células. Tanto las células de médula ósea como las dos subpoblaciones de células mieloides supresoras presentaron una capacidad de inhibir la proliferación de células T inducidas por un antígeno in vitro. Curiosamente, a pesar de la constatación de que células CD11b+ Gr-1low transducidas fueron inmunosupresora in vitro y tenían actividades de la arginasa y de la óxido nítrico sintasa, sólo la subpoblación de células CD11b+ Gr-1high transducidas con el antígeno tenía un efecto terapéutico en ratones con EAE establecida. Por último, se observó un mayor porcentaje de células T reguladoras en los bazos de ratones tratados con la población de médula ósea total transducida con MOG y las células CD11b+ Gr-1high lo que sugiere un papel para las células T reguladoras en la mediación del efecto terapéutico.
Gene therapy can be used to experimentally induce immune tolerance. Our previous work showed that transferring bone marrow cells that had been transduced with an autoantigen (MOG40-55) into mice with experimental autoinmune encephalomyelitis improved the animals’ prognosis. In this work, we sought to identify the cell subpopulation in the transduced bone marrow that was primarily responsible for the observed therapeutic effect. We found that both granulocyte-like (CD11b+ Gr-1hi) and monocyte-like (CD11b+ Gr-1lo) myeloid-derived suppressor cells were generated during the standard 4-day retroviral transduction of bone marrow cultures and that the effectively transduced cells largely consisted of these cell types. Both of the myeloid cell subtypes inhibited antigen-induced T cell proliferation in vitro, and they were significantly more suppressive than their sham-transduced controls. Interestingly, despite the finding that transduced CD11b+ Gr-1lo cells were immunosuppressive in vitro and exhibited arginase and nitric oxide synthase activities, only the antigen-transduced CD11b+ Gr-1hi cell subpopulation had a therapeutic effect in mice with the experimentally induced disease. Finally, we observed higher percentages of T regulatory cells in the spleens of mice treated with MOG-expressing total bone marrow population and CD11b+ Gr-1hi cells, which suggests a role for these T regulatory cells in mediating the therapeutic effect.
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Books on the topic "Autoimmune diseases – Animal models"

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The use of SCID mice in the investigation of human autoimmune disease. Austin: R.G. Landes, 1994.

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Animal models for retinal diseases. [Totowa, N.J.]: Humana Press, 2010.

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Chan, Chi-Chao, ed. Animal Models of Ophthalmic Diseases. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-19434-9.

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Pang, Iok-Hou, and Abbot F. Clark, eds. Animal Models for Retinal Diseases. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-541-5.

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J, Pfeiffer Carl, ed. Animal models for intestinal disease. Boca Raton, Fla: CRC Press, 1985.

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Animal models of human disease. Amsterdam: Elsevier/AP, 2011.

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Gross, David R. Animal models in cardiovascular research. 3rd ed. Dordrecht: Springer, 2009.

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S, Chan Lawrence, ed. Animal models of human inflammatory skin diseases. Boca Raton: CRC Press, 2004.

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Animal models in cardiovascular research. Boston: Nijhoff, 1985.

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Animal models in cardiovascular research. 2nd ed. Dordrecht: Kluwer Academic, 1994.

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Book chapters on the topic "Autoimmune diseases – Animal models"

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Moritoki, Yuki, and Yoshiyuki Ueno. "Animal Models for Primary Biliary Cirrhosis." In Autoimmune Liver Diseases, 171–99. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54789-1_14.

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Kielczewski, Jennifer L., and Rachel R. Caspi. "Animal Models of Autoimmune Uveitis." In Animal Models of Ophthalmic Diseases, 85–100. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19434-9_6.

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Germolec, Dori, Sheetal Thakur, and Jean Pfau. "Autoimmune Disease, Animal Models." In Encyclopedia of Immunotoxicology, 93–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-54596-2_140.

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Germolec, Dori, Sheetal Thakur, and Jean Pfau. "Autoimmune Disease, Animal Models." In Encyclopedia of Immunotoxicology, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27786-3_140-2.

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Eriksson, Urs. "Autoimmune Heart Disease: Animal Models." In Encyclopedia of Medical Immunology, 104–11. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-0-387-84828-0_190.

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Soos, Jeanne M. "Rheumatoid Arthritis and Related Autoimmune Diseases, Animal Models." In Encyclopedia of Immunotoxicology, 781–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-54596-2_1291.

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Giarratana, Nadia, Giuseppe Penna, and Luciano Adorini. "Animal Models of Spontaneous Autoimmune Disease." In Immunological Tolerance, 285–311. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-395-0_17.

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Nagayama, Yuji, and Norio Abiru. "Animal Models of Autoimmune Thyroid Disease." In Immunoendocrinology: Scientific and Clinical Aspects, 415–26. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-478-4_25.

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Adachi, Yasushi, Ming Li, Richard K. Burt, Naoki Hosaka, and Susumu Ikehara. "Animal Models of Bone Marrow Transplantation for Autoimmune Diseases." In Hematopoietic Stem Cell Transplantation and Cellular Therapies for Autoimmune Diseases, 190–203. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9781315151366-23.

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McDevitt, H. O., R. Perry, and L. A. Steinman. "Monoclonal Anti-La Antibody Therapy in Animal Models of Autoimmune Disease." In Ciba Foundation Symposium 129 - Autoimmunity and Autoimmune Disease, 184–93. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470513484.ch12.

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Conference papers on the topic "Autoimmune diseases – Animal models"

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Kamaruddin, A. "Animal Models of Diseases." In 2nd International University of Malaya Research Imaging Symposium (UMRIS) 2005: Fundamentals of Molecular Imaging. Kuala Lumpur, Malaysia: Department of Biomedical Imaging, University of Malaya, 2005. http://dx.doi.org/10.2349/biij.1.1.e7-46.

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Stemeier, K., J. Mertin, J. Pill, and F. Hartig. "EFFECTS OF THROMBOXANE RECEPTOR BLOCKER BM 13.505 ON THE DEVELOPMENT OF PROTEINURIA IN AUTOIMMUNE NZB/W MICE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643757.

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Female F1 hybrid of New Zealand black and white mice(NZB/W) spontaneouslydevelop an autoimmune disease characterize by afatal immune complex glomerulonephritis.Theyare considered to be a relevant model of human systemic lupus erythematosus. We observeda doubling of the concentration of TXB2 in urine at the same time when onset of proteinuria was noticed. This suggests that TXA2 synthetized by mesangial and epithelial cells of the glomeruli as well as by some inflammatory cells and platelets might be an important mediator in the pathogenesis of thi auto immune-mediated glomerular disease. Weused BM 13.505 as an long-acting TX receptor blocker for evaluating the importance of TXA2 on the development of proteinuria and compared its effects with that of the immunsuppressive agent cyclophosphamide.NZB/W mice were distributed to vehicle-treated (V-)group 20 mg/kg BM 13.505 (BM-) group and 20 mg/kgcyclophosphamide (C-) group( = 13 -14).Daily dosing by gavage was startedat the age of12 weeks. Every fourth week theurinary concentrations of proteins were measured by th biuret method and TXB2by a RIA. An increasein TXB2 was seen in the V- and BM-group, while in the C-group TXB2 was lowered. At 36 weeks of age 8of 14 animals of the V-group were proteinuria positive (>100 mg/100 ml). The study was finished at 44 weeks because more than 2/3 of the animals of the V-group haddeveloped a proteinuria. Previously four animals died and in most of other the disease was faradvanced. In the BM-group no animal had diedor showed signs of illness. However seven ofthe animals had slightly elevated protein concentrations in urine and two moderate elevated values. In the C-group no proteinuria was detected. Histological examinations of thekidneys showed a correlation in individualanimals of the V-group between the duration and extent of proteinuria and changes in the morphology of the glomeruli. In the BM-treated animals slight to moderate protein deposits were detectable, while in cyclophosphamide-treated animals glomeruli were of normal structure. This study presents someevidence that TXA2 may be an important mediator in the pathogenesis of this immune-mediated renal disease. Manifestation of this disease is delayed by the administration of thespecific TX receptor blocker BM 13.505.
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3

"Structure Prediction with FAMS for Proteins Screened Critically to Autoimmune Diseases based upon Bioinformatics." In International Conference on Bioinformatics Models, Methods and Algorithms. SciTePress - Science and and Technology Publications, 2013. http://dx.doi.org/10.5220/0004188802610267.

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Gudasheva, T., T. Antipova, P. Povarnina, and S. Seredenin. "NGF Loop 4 Dimeric Dipeptide Mimetic Active on Animal Models of Parkinson’s, Alzheimer’s Diseases and Stroke." In The Twenty-Third American and the Sixth International Peptide Symposium. Prompt Scientific Publishing, 2013. http://dx.doi.org/10.17952/23aps.2013.194.

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Siczek, Krzysztof, Przemyslaw Kubiak, and Justyn Ochocki. "Prevention of the probe hole clogging up during administration of nano Ag preparations in animal models of gastrointestinal diseases." In 6th International Electronic Conference on Medicinal Chemistry. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/ecmc2020-07463.

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Yoshimoto, K., K. Suzuki, K. Sugahara, and T. Takeuchi. "THU0055 Low molecular weight baff signaling inhibitors ameliorate IL-6, IL-10 and IGG production in vitro and in vivo models of autoimmune diseases." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.4176.

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7

Koff, Matthew F., Thomas R. Gardner, Eric Balaguer, Chris Kawcak, C. Wayne McIlwraith, and Van C. Mow. "Precise Quantitative Models of the Equine Articular Carpus Anatomy and Contact Areas." In ASME 2001 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2001. http://dx.doi.org/10.1115/imece2001/bed-23054.

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Abstract Osteochondral diseases occur within ail bones and cartilages of the equine carpus and can lead to loss of athletic use and occasionally catastrophic injury that necessitate euthanasia. The intensity and direction of stresses that lead to such injuries are unknown. Joint modeling is a commonly used technique in human orthopaedic research that allows investigators to determine the internal stresses of joints. Through the use of computer models, various scenarios, such as ligament damage, can be simulated and changes in the resulting joint surface stresses determined [1]. The purpose of this study was to experimentally obtain precise quantitative contact area data of the articular surfaces of the distal radius, the proximal and distal aspects of the radial carpal bone and the proximal aspect of the 3rd carpal bone of the equine carpus. These data provide normative contact and cartilage thickness values for the equine carpus that will facilitate the use of this joint as a large animal model for osteoarthritis studies. Furthermore, these experimental data will serve as the basis for the development and calibration of an equine carpus whole joint computer model.
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Oliveira, Kathllyn Joyce De Jesus, and João Ronaldo Tavares De Vasconcellos Neto. "A INSERÇÃO DE VITAMINA D NO TRATAMENTO DE DOENÇAS AUTOIMUNES." In I Congresso Brasileiro de Imunologia On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/1001.

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INTRODUÇÃO: As doenças autoimunes representam reações imunes exacerbadas direcionadas a autoantígenos, devido à ausência de mecanismos destinados a autotolerância. Ao longo das últimas décadas, a prevalência destas patologias apresenta elevadas proporções principalmente em mulheres, devido a condições hormonais. OBJETIVOS: Determinar a relação entre a concentração de vitamina D e o desenvolvimento de doenças autoimunes. MATERIAIS E MÉTODOS: Trata-se de uma revisão de literatura realizada a partir do banco de dados PubMed, entre os anos de 2019 e 2021, através dos descritores Vitamin D Deficiency e Autoimmune Diseases. RESULTADO: Os pacientes com doenças autoimunes geralmente possuem a hipovitaminose D. As células do sistema imunológico expressam o receptor de vitamina D, desse modo, o composto lipossolúvel descrito exerce a modulação do sistema imune, possui ação antiinflamatória e contribui para o aumento de linfócitos T regulatórios, capazes de limitar a resposta imune. A vitamina D quando introduzida via ingestão de alimentos de origem animal, torna-se susceptível a consecutivas reações químicas de hidroxilação no organismo humano, presentes tanto a nível renal como hepático. Cabe ressaltar também, que a forma ativa designada como calcitriol, suprime a ação da resposta Th1, associada a interferon gama e interleucinas, induz a ação de linfócitos auxiliares 2, além disso, contempla características antioxidante, assim como antifibrótica. CONCLUSÃO: Estudos estabelecem relação direta entre insuficiência de vitamina D e progressão de doenças autoimunes. A adesão de níveis séricos adequados desta substância através da suplementação ou exposição solar, consiste em um recurso com baixo custo de saúde pública e acessível para tratar ou prevenir as doenças autoimunes.
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Jo-Avila, Miguel, Kevin Roos, Ahmed Al-Jumaily, and Jun Lu. "Super Imposed Length Oscillations (SILO) and Their Effect on Asthmatic Models (Acute and Chronic) During an Asthmatic Attack." In ASME 2014 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/imece2014-37633.

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The main driving mechanism during an asthmatic attack is the hyperconstriction of airway smooth muscle (ASM), which reduces the airway lumen and makes normal breathing difficult. The contraction can be relieved using bronchodilator drugs such as Isoproterenol, which induce temporary relaxation of the constricted airways. Pharmacological treatments are widely used in asthma, but their effectiveness varies from one subject to another, as do their side effects. Studies have shown that mechanical oscillations equivalent to physiological patterns such as breathing and deep inspiration in healthy airways can induce airway relaxation, but this type of response is not observed in asthmatics. Length oscillations seem to be a non-medicinal approach to treat ASM hyperconstriction present in many respiratory diseases such as asthma. Currently little is known about the effect of other oscillations’ patterns and their combination with breathing and deep inspiration on healthy and asthmatic airways during an asthmatic attack. Preliminary results obtained from in vitro and in vivo experiments in our laboratory indicate that the use of super imposed length oscillations (SILO) over normal breathing patterns can induce relaxation during an induced asthmatic attack on healthy and asthmatic subjects. These tests have been carried out using animal models which have been prepared under an acute protocol for the disease (new asthmatics), but these oscillations still remain to be tested in chronic asthmatic models (chronic asthmatics).
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Guarino, Maria, Marlene Lages, Ipek Suluova, Rui Fonseca Pinto, and Nuno Lopes. "The CBmeter: designing innovative strategies for early diagnosis of metabolic diseases." In 13th International Conference on Applied Human Factors and Ergonomics (AHFE 2022). AHFE International, 2022. http://dx.doi.org/10.54941/ahfe1001410.

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Diabetes is a disease with high prevalence worldwide, however, about 44% of patients are asymptomatic, which leads to a later diagnosis of the disease and, consequently, increases the risk of developing complications. The development of new approaches for early diagnosis is imperative to allow proper adoption of preventive measures. From a motivational point of view, it is easier for patients to adopt healthy eating habits and lifestyles when there is an altered marker that indicates subclinical disease, particularly in a pathology that remains asymptomatic until advanced stages. Thus, timely diagnosis based on a measurable and monitorable indicator is extremely important so that such behaviors are implemented as early as possible, increasing effective health gains and reducing the costs related to this pathology. Pre-clinical studies in animal models have shown that the etiology of type 2 diabetes mellitus (T2DM) is related to alterations in the carotid bodies (CB), chemosensory organs located in the bifurcation of the carotid arteries. In animals with T2DM it has been observed that the CBs are overactivated causing an increased heart rate, respiratory rate, and blood glucose levels. In humans, this mechanism has been confirmed but is not yet well-characterized. This paper highlights the importance of developing a device that allows early detection of changes in CB activity correlating it with emerging diabetes. The design strategies to prototype the CBmeter were to model and characterize the features of interest for the diagnosis- respiratory rate, heart rate, peripheral oxygen saturation and glucose - in healthy people and people with diabetes using a combination of set commercial sensors pre-existent in the market that were integrated to collect real-time data. After determining health and disease patterns, the CBmeter development pipeline includes a co-design approach in which physiologists, endocrinologists, nurses, computer and electrical engineers, designers and patients are collaborating to develop an easy-to-use, portable, and minimally invasive medical device that associates CB function with endocrine dysregulation, with very small discomfort and risk for users. The definition and specification of the most appropriate architecture for the CBmeter, in order to allow its modularity, signal acquisition and consequently the communication between the sensor/device and the receiver/backend in the most efficient way is being allied to the selection of materials, tools and steps to create an innovative product, that will fill a technical gap in the market, designed for the early diagnosis of metabolic diseases, in a subclinical phase, with the potential to contribute with significant gains for public health in the medium/long term.
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