Relevant bibliographies by topics / Experimental arthriti

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Academic literature on the topic 'Experimental arthriti'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Experimental arthriti"

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Gómez-SanMiguel, Ana Belén, Ana Isabel Martín, Maria Paz Nieto-Bona, Carmen Fernández-Galaz, María López-Menduiña, María Ángeles Villanúa, and Asunción López-Calderón. "Systemic α-melanocyte-stimulating hormone administration decreases arthritis-induced anorexia and muscle wasting." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 304, no. 10 (May 15, 2013): R877—R886. http://dx.doi.org/10.1152/ajpregu.00447.2012.

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Rheumatoid cachexia is associated with rheumatoid arthritis and it increases mortality and morbidity. Adjuvant-induced arthritis is an experimental model of rheumatoid arthritis that causes anorexia and muscle wasting. α-Melanocyte-stimulating hormone (α-MSH) has anti-inflammatory actions, and it is able to decrease inflammation in several inflammatory diseases including experimental arthritis. In this study we tested whether systemic α-MSH treatment is able to ameliorate cachexia in arthritic rats. On day 8 after adjuvant injection control and arthritic rats were treated with α-MSH (50 μg/rat ip) twice a day, until day 16 when all rats were euthanized. Arthritis decreased food intake, but it increased hypothalamic expression of neuropeptide Y (NPY) and Agouti-related peptides (AgRP) as well as interleukin-1β (IL-1β) and cyclooxygenase-2 (COX-2) mRNA. In arthritic rats, α-MSH decreased the external signs of arthritis and increased food intake ( P < 0.01). In addition, α-MSH decreased hypothalamic expression of IL-1β, COX-2, proopiomelanocortin, and prohormone-converting (PC) enzymes PC1/3 and PC2 mRNA in arthritic rats. In control rats, α-MSH did not modify food intake or hypothalamic expression of aforementioned mRNA. α-MSH prevented arthritis-induced increase in gastrocnemius COX-2, muscle-specific RING-finger protein-1 (MuRF1), and atrogin-1 expression, and it increased fast myofiber size. In conclusion our data show that in arthritic rats peripheral α-MSH treatment has an anti-cachectic action increasing food intake and decreasing muscle wasting.
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Castillero, Estíbaliz, María Paz Nieto-Bona, Carmen Fernández-Galaz, Ana Isabel Martín, María López-Menduiña, Miriam Granado, María Angeles Villanúa, and Asunción López-Calderón. "Fenofibrate, a PPARα agonist, decreases atrogenes and myostatin expression and improves arthritis-induced skeletal muscle atrophy." American Journal of Physiology-Endocrinology and Metabolism 300, no. 5 (May 2011): E790—E799. http://dx.doi.org/10.1152/ajpendo.00590.2010.

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Arthritis is a chronic inflammatory illness that induces cachexia, which has a direct impact on morbidity and mortality. Fenofibrate, a selective PPARα activator prescribed to treat human dyslipidemia, has been reported to decrease inflammation in rheumatoid arthritis patients. The aim of this study was to elucidate whether fenofibrate is able to ameliorate skeletal muscle wasting in adjuvant-induced arthritis, an experimental model of rheumatoid arthritis. On day 4 after adjuvant injection, control and arthritic rats were treated with 300 mg/kg fenofibrate until day 15, when all rats were euthanized. Fenofibrate decreased external signs of arthritis and liver TNFα and blocked arthritis-induced decreased in PPARα expression in the gastrocnemius muscle. Arthritis decreased gastrocnemius weight, which results from a decrease in cross-section area and myofiber size, whereas fenofibrate administration to arthritic rats attenuated the decrease in both gastrocnemius weight and fast myofiber size. Fenofibrate treatment prevented arthritis-induced increase in atrogin-1 and MuRF1 expression in the gastrocnemius. Neither arthritis nor fenofibrate administration modify Akt-FoxO3 signaling. Myostatin expression was not modified by arthritis, but fenofibrate decreased myostatin expression in the gastrocnemius of arthritic rats. Arthritis increased muscle expression of MyoD, PCNA, and myogenin in the rats treated with vehicle but not in those treated with fenofibrate. The results indicate that, in experimental arthritis, fenofibrate decreases skeletal muscle atrophy through inhibition of the ubiquitin-proteasome system and myostatin.
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Perecko, Tomas, Katarina Drabikova, Antonin Lojek, Milan Ciz, Silvester Ponist, Katarina Bauerova, Radomir Nosal, Juraj Harmatha, and Viera Jancinova. "The Effects of Pterostilbene on Neutrophil Activity in Experimental Model of Arthritis." BioMed Research International 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/106041.

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It has been demonstrated that pterostilbene inhibits reactive oxygen species production in neutrophilsin vitro. However, little is known about its effects on neutrophils during inflammationin vivo. In this study, the effect of pterostilbene on neutrophil activity was investigated in experimental arthritis model. Lewis rats were injected by a single intradermal injection of heat-killedMycobacterium butyricumin Freund’s adjuvant to develop arthritis. Another group of arthritic animals received pterostilbene 30 mg/kg, daily, p.o. The number and activity of neutrophils in blood were measured on a weekly basis during the whole experiment. Moreover, the total radical trapping potential in plasma was measured at the end of the experiment. In the pterostilbene treated arthritic group, the treatment significantly lowered the number of neutrophils in blood on days 14 and 21 without significant downregulation of neutrophil oxidative burst. Pterostilbene nonsignificantly increased total radical trapping potential in arthritic animals. These results indicate that the promising effects of pterostilbene on reactive oxygen species operate by different mechanismsin vitroand in the animal model of inflammation. In conclusion, the positive effects of pterostilbene in the model of arthritis may be attributed to regulation of neutrophil number.
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LIU, XIUPING, ZHENGMING XIONG, SHEEN-WOO LEE, JELENA LEVI, SHAHRIAR YAGHOUBI, SANDIP BISWAL, SANJIV SAM GAMBHIR, and ZHEN CHENG. "A NEAR-INFRARED FLUORESCENT DEOXYGLUCOSE DERIVATIVE FOR OPTICAL IMAGING OF EXPERIMENTAL ARTHRITIS." Journal of Innovative Optical Health Sciences 02, no. 02 (April 2009): 179–87. http://dx.doi.org/10.1142/s1793545809000450.

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The purpose of this study is to investigate whether a near-infrared fluorescence (NIRF) probe, Cy5.5-D-glucosamine (Cy5.5-2DG), can image arthritis in collagen-induced arthritic (CIA) mice. The presence of arthritis was verified by both visual examination and micro-computed tomography (MicroCT) imaging. CIA mice were imaged by a micro-positron emission tomography (MicroPET) scanner one hour after intravenous injection of 2-deoxy-2-[18F]fluoro-D-glucose ([18F]FDG). After radioactivity of [18F]FDG decayed away, Cy5.5-2DG was injected into a lateral tail vein of the mice. Arthritic tissue targeting and retention of Cy5.5-2DG in CIA mice were evaluated and quantified by an optical imaging system. Inflammatory tissue in CIA mice was clearly visualized by [18F]FDG-MicroPET scan. NIRF imaging of Cy5.5-2DG in the same mice revealed that the pattern of localization of Cy5.5-2DG in the arthritic tissue was very similar to that of [18F]FDG. Quantification analysis further showed that [18F]FDG uptake in arthritic tissues at one hour post-injection (p.i.) and Cy5.5-2DG uptakes at different time points p.i. were all well correlated (r2over 0.65). In conclusion, Cy5.5-DG can detect arthritic tissues in living mice. The good correlation between the [18F]FDG uptake and Cy5.5-2DG accumulation in the same arthritic tissue warrants further investigation of Cy5.5-2DG as an approach for assessment of anti-inflammatory treatments.
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Brown, Charles R., and Steven L. Reiner. "Clearance of Borrelia burgdorferi May Not Be Required for Resistance to Experimental Lyme Arthritis." Infection and Immunity 66, no. 5 (May 1, 1998): 2065–71. http://dx.doi.org/10.1128/iai.66.5.2065-2071.1998.

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ABSTRACT Infection of inbred mouse strains with Borrelia burgdorferi results in the development of experimental Lyme arthritis. The degree of arthritic pathology has been suggested to correlate with the level of spirochete burden within tissues. To investigate this further, we infected resistant DBA/2 (DBA) and susceptible C3H/HeJ (C3H) mice in the hind footpads and monitored arthritis development for 21 days. To quantitate levels of spirochetes within tissues, we created a competitive PCR molecule containing modified ospA and fla gene segments. C3H mice developed severe arthritis of the tibiotarsal joints, while DBA mice developed only mild inflammation throughout the experimental period. At day 21, when the gross size and histologic composition of ankles revealed significant differences in arthritis between the strains, there was little difference in levels of spirochete DNA as determined by competitive PCR. Cultures of ankle tissue at day 21 were also uniformly positive in both C3H and DBA animals and contained relatively similar levels of spirochetes. These results indicate that the presence of spirochetes in the ankles of experimental animals is not sufficient for arthritis development. Since arthritic and nonarthritic animals can harbor relatively equal spirochete burdens yet retain their distinct phenotypic outcomes, an aberrant or overly exuberant immune response may be an additional requirement for pathology in arthritis-prone mice.
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Fernandes, E. S., S. Awal, R. Karadaghi, and S. D. Brain. "TRP Receptors in Arthritis, Gaining Knowledge for Translation from Experimental Models." Open Pain Journal 6, no. 1 (March 8, 2013): 50–61. http://dx.doi.org/10.2174/1876386301306010050.

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Arthritis is a condition characterised by mainly pain, reduced joint movement and signs of inflammation, such as swelling. The disorder has many different types, of which osteoarthritis (a degenerative joint disease) and rheumatoid arthritis (a chronic autoimmune disease) are the two most common forms. There are >6 million sufferers in the UK and both conditions have a huge potential to impair capabilities and contribute to social and economic burdens. Whilst there are a wide range of arthritic therapies available, many patients under treatment complain of poor pain relief. Thus there is a need for novel therapeutic approaches, and the transient receptor potential (TRP) family of receptor channels has been investigated. One particular area of recent research has been the ligand-gated transient receptor potential vanilloid 1 (TRPV1) channel. Findings from numerous pre-clinical models and scientific studies have shown that TRPV1 desensitisation, or the use of TRPV1 antagonists alleviates pain and some inflammatory aspects. New findings have started to unveil the potential of other TRP channels in mediating arthritic pain and inflammation. With the understanding that the currently available treatments for arthritis are limited, researchers have looked into the exciting prospect that TRP receptor antagonists may be developed into effective, specific drugs, which would potentially protect against the complications of arthritis. These antagonists are still under development, although only data from studies from pre-clinical models are currently available. This review acts to summarize knowledge of the potential influence of TRP receptors in arthritis to date.
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Gómez-SanMiguel, Ana Belén, Carolina Gomez-Moreira, María Paz Nieto-Bona, Carmen Fernández-Galaz, Maria Ángeles Villanúa, Ana Isabel Martín, and Asunción López-Calderón. "Formoterol decreases muscle wasting as well as inflammation in the rat model of rheumatoid arthritis." American Journal of Physiology-Endocrinology and Metabolism 310, no. 11 (June 1, 2016): E925—E937. http://dx.doi.org/10.1152/ajpendo.00503.2015.

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Adjuvant-induced arthritis is an experimental model of rheumatoid arthritis that is associated with body weight loss and muscle wasting. β2-adrenergic receptor agonists are powerful anabolic agents that trigger skeletal muscle hypertrophy and have been proposed as a promising treatment for muscle wasting in human patients. The aim of this work was to determine whether formoterol, a selective β2-adrenoreceptor agonist, is able to ameliorate muscle wasting in arthritic rats. Arthritis was induced in male Wistar rats by intradermal injection of Freund's adjuvant. Control and arthritic rats were injected daily with 50 μg/kg sc formoterol or saline for 12 days. Body weight change, food intake, and arthritis index were analyzed. After euthanasia, in the gastrocnemius mRNA was analyzed by PCR, and proteins were analyzed by Western blotting. Arthritis decreased gastrocnemius weight, cross-sectional area, and myofiber size, whereas formoterol increased those variables in both arthritic and control rats. Formoterol decreased the external signs of arthritis as well as NF-κB(p65) activation, TNFα, and COX-2 levels in the gastrocnemius of arthritic and control rats. Those effects of formoterol were associated with a decreased expression of myostatin, atrogin-1, and MuRF1 and in LC3b lipidation. Arthritis increased the expression of MyoD, myogenin, IGF-I, and IGFBP-3 and -5 in the gastrocnemius. In control and in arthritic rats, treatment with formoterol increased Akt phosphorylation and myogenin levels, whereas it decreased IGFBP-3 expression in the gastrocnemius. These data suggest that formoterol has an anti-inflammatory effect and decreases muscle wasting in arthritic rats through increasing Akt activity and myogenin and decreasing myostatin, the p-NF-κB(p65)/TNF pathway, and IGFBP-3.
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Granado, Miriam, Ana I. Martín, Mª Ángeles Villanúa, and Asunción López-Calderón. "Experimental arthritis inhibits the insulin-like growth factor-I axis and induces muscle wasting through cyclooxygenase-2 activation." American Journal of Physiology-Endocrinology and Metabolism 292, no. 6 (June 2007): E1656—E1665. http://dx.doi.org/10.1152/ajpendo.00502.2006.

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Chronic arthritis induces cachexia associated with an inhibition of the growth hormone (GH)-insulin-like growth factor-I (IGF-I) system and an activation of the E3 ubiquitin-ligating enzymes muscle atrophy F-box (MAFbx) and muscle Ring finger 1 (MuRF1) in the skeletal muscle. The aim of this work was to study the role of cyclooxygenase (COX)-2 in chronic arthritis-induced cachexia. Arthritis was induced in rats by Freund's adjuvant injection, and the effects of two COX inhibitors (indomethacin, a nonspecific inhibitor, and meloxicam, a selective COX-2 inhibitor on pituitary GH and on liver and serum IGF-I levels) were tested. Arthritis decreased body weight gain and GH and liver IGF-I gene expression. In the arthritic rats, both inhibitors, indomethacin and meloxicam, prevented the inhibitory effect of arthritis on body weight gain. Indomethacin and meloxicam administration to arthritic rats increased pituitary GH and liver IGF-I mRNA as well as serum levels of IGF-I. These data suggest that induction of COX-2 during chronic inflammation is involved in the inhibition of the GH-IGF-I axis and in the body weight loss. In the gastrocnemius muscle, arthritis increased the gene expression of tumor necrosis factor (TNF)-α, the E3 ubiquitin-ligating enzymes MAFbx and MuRF1, as well as of IGF-I and IGF-binding protein-5 (IGFBP-5). Inhibition of COX-2 by meloxicam administration increased gastrocnemius weight and decreased MAFbx, MuRF1, TNF-α, and IGFBP-5 gene expression. In summary, our data indicate that chronic arthritis-induced cachexia and muscle wasting are mediated by the COX-2 pathway resulting in a decreased GH-IGF-I secretion and increased expression of MAFbx and MuRF1 mRNA.
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Dorst, Daphne N., Mark Rijpkema, Marti Boss, Birgitte Walgreen, Monique M. A. Helsen, Desirée L. Bos, Maarten Brom, et al. "Targeted photodynamic therapy selectively kills activated fibroblasts in experimental arthritis." Rheumatology 59, no. 12 (July 30, 2020): 3952–60. http://dx.doi.org/10.1093/rheumatology/keaa295.

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Abstract Objective In RA, synovial fibroblasts become activated. These cells express fibroblast activation protein (FAP) and contribute to the pathogenesis by producing cytokines, chemokines and proteases. Selective depletion in inflamed joints could therefore constitute a viable treatment option. To this end, we developed and tested a new therapeutic strategy based on the selective destruction of FAP-positive cells by targeted photodynamic therapy (tPDT) using the anti-FAP antibody 28H1 coupled to the photosensitizer IRDye700DX. Methods After conjugation of IRDye700DX to 28H1, the immunoreactive binding and specificity of the conjugate were determined. Subsequently, tPDT efficiency was established in vitro using a 3T3 cell line stably transfected with FAP. The biodistribution of [111In]In-DTPA-28H1 with and without IRDye700DX was assessed in healthy C57BL/6N mice and in C57BL/6N mice with antigen-induced arthritis. The potential of FAP-tPDT to induce targeted damage was determined ex vivo by treating knee joints from C57BL/6N mice with antigen-induced arthritis 24 h after injection of the conjugate. Finally, the effect of FAP-tPDT on arthritis development was determined in mice with collagen-induced arthritis. Results 28H1-700DX was able to efficiently induce FAP-specific cell death in vitro. Accumulation of the anti-FAP antibody in arthritic knee joints was not affected by conjugation with the photosensitizer. Arthritis development was moderately delayed in mice with collagen-induced arthritis after FAP-tPDT. Conclusion Here we demonstrate the feasibility of tPDT to selectively target and kill FAP-positive fibroblasts in vitro and modulate arthritis in vivo using a mouse model of RA. This approach may have therapeutic potential in (refractory) arthritis.
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Dorst, Daphne N., Marti Boss, Mark Rijpkema, Birgitte Walgreen, Monique M. A. Helsen, Desirée L. Bos, Louis van Bloois, et al. "Photodynamic Therapy Targeting Macrophages Using IRDye700DX-Liposomes Decreases Experimental Arthritis Development." Pharmaceutics 13, no. 11 (November 5, 2021): 1868. http://dx.doi.org/10.3390/pharmaceutics13111868.

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Macrophages play a crucial role in the initiation and progression of rheumatoid arthritis (RA). Liposomes can be used to deliver therapeutics to macrophages by exploiting their phagocytic ability. However, since macrophages serve as the immune system’s first responders, it is inadvisable to systemically deplete these cells. By loading the liposomes with the photosensitizer IRDye700DX, we have developed and tested a novel way to perform photodynamic therapy (PDT) on macrophages in inflamed joints. PEGylated liposomes were created using the film method and post-inserted with micelles containing IRDye700DX. For radiolabeling, a chelator was also incorporated. RAW 264.7 cells were incubated with liposomes with or without IRDye700DX and exposed to 689 nm light. Viability was determined using CellTiterGlo. Subsequently, biodistribution and PDT studies were performed on mice with collagen-induced arthritis (CIA). PDT using IRDye700DX-loaded liposomes efficiently induced cell death in vitro, whilst no cell death was observed using the control liposomes. Biodistribution of the two compounds in CIA mice was comparable with excellent correlation of the uptake with macroscopic and microscopic arthritis scores. Treatment with 700DX-loaded liposomes significantly delayed arthritis development. Here we have shown the proof-of-principle of performing PDT in arthritic joints using IRDye700DX-loaded liposomes, allowing locoregional treatment of arthritis.
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Dissertations / Theses on the topic "Experimental arthriti"

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Holm, Barbro. "Pathogenetic studies of adjuvant-induced arthritis /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-347-3/.

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Larsson, Esbjörn. "Tissue destruction in arthritis : experimental studies /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-708-8.

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Ragno, Silvia. "Heat shock proteins and experimental arthritis." Thesis, Queen Mary, University of London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.281712.

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Ribbhammar, Ulrica. "Identification of genes that regulate arthritis and IgE production in rat and human /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-421-X/.

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Lundberg, Karin. "Arthritogenic and immunogenic properties of modified autoantigens /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-303-5/.

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Quentin, Julie. "Immunomodulation de l'arthrite expérimentale par les cellules dendritiques tolérogènes." Thesis, Montpellier 1, 2011. http://www.theses.fr/2011MON1T018/document.

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Immunomodulation de l'arthrite expérimentale par les cellules dendritiques tolérogènes. Les cellules dendritiques (DCs) sont des cellules présentatrices d'antigènes jouant un rôle clé dans l'initiation et la modulation des réponses immunitaires. En effet, en parallèle de leur capacité à initier une réponse immunitaire adaptative, les DC sont également impliquées dans les mécanismes de tolérance périphérique. Elles sont utilisées depuis 10 ans maintenant en clinique dans des stratégies thérapeutiques anti-tumorale et leurs propriétés tolérogènes ouvrent aujourd'hui leur champ d'applications à des pathologies autoimmunes, l'asthme et la transplantation afin de restaurer une homéostasie de la réponse immune. Les objectifs de ma thèse ont consisté à :- renforcer le potentiel tolérogène des DCs par manipulation in vitro- tester la capacité de DCs tolérogènes à induire une protection de l'arthrite expérimentale- identifier les mécanismes cellulaires et moléculaires impliqués dans la tolérance induite par les DCs. Mon travail de thèse a permis de montrer l'efficacité de la vaccination de souris arthritiques avec des DCs immatures conservant leurs propriétés tolérogènes in vitro et in vivo, grâce au traitement préalable avec un agent immunosuppresseur, la rapamycine. L'injection répétée de DCs immatures induit la génération de lymphocytes T régulateurs CD4+ CD49b+ sécrétant de l'IL-10 ayant de fortes capacités immunosuppressives. Ce projet a permis de mettre en évidence l'efficacité des DCs dans le traitement d'une pathologie autoimmune déjà établie et l'implication d'une population cellulaire régulatrice originale
Tolerogenic dendritic cells for immumodulation in experimental arthritis.Dendritic cells (DCs) are the most potent antigen-presenting cells that play critical roles in the initiation and regulation of immune responses. Based on their tolerogenic properties, DCs offer potential as therapeutic tools to ameliorate or prevent graft rejection or graft-versus-host disease, or to treat autoimmune disorders.The objectives of my PhD consisted to:- reinforce the tolerogenic potential of DCs by in vitro handling.- assess the capacity of such tolerogenic DCs to induce a protective response in experimental autoimmune arthritis- identify cellular and molecular mechanisms implied in the tolerogenic DCs-induced protectionOur results suggest that, in contrast with conventional DCs, the rapamycin-conditioned iDCs maintain their tolerogenic potential upon injection in inflammatory settings and are able to dampen an already Th1-primed immune response, conferring a protection from arthritis. The protection of the mice was associated with an expansion of the IL-10-secreting CD49b+ Treg in the spleen and liver of the injected mice and a decrease of the Th1 immune response. These results underscore the therapeutic potential of tolerogenic DCs in an established autoimmune disease as well as the anti-inflammatory potential of the CD49b+ Treg cell population induced following DC vaccination
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de, Souza Patricia Regina Soares. "GPR40 expression and function in immune cells and experimental arthritis." Thesis, Queen Mary, University of London, 2017. http://qmro.qmul.ac.uk/xmlui/handle/123456789/25975.

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Omega-3 fatty acids (ω-3 FA, including eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]), are essential polyunsaturated fatty acids which are correlated with lower incidence of chronic diseases. DHA and EPA can be enzymatically converted to resolvins, protectins and maresins, which play important roles in resolution of inflammation. Additionally, ω-3 FA can also directly activate surface receptors, namely the long-chain free fatty acid receptors GPR40 and GPR120, two GPCRs with poorly investigated biology. Using real-time PCR analysis, GPR40 transcript in human neutrophils was detected; the protein expression was also confirmed by flow cytometry and image stream analysis. Expression of GPR40 protein was up-regulated after stimulation with platelet-activating factor (PAF, 10nM) or leukotriene B4 (LTB4, 10nM) for 10 minutes. I utilised the selective agonist GW9508 to investigate the biology of GPR40. Tested on human neutrophils, GW9508 elevated intracellular calcium when applied within the 0.1-10μM range. The up-regulation of GPR40 expression by pro-inflammatory stimuli suggested to us potential regulatory roles for this receptor during inflammation. I then showed that 1 and 10μM GW9508 increased neutrophil chemotaxis in response to the cytokine IL-8 (30ng/ml). In addition, GPR40 activation by GW9508 enhanced phagocytosis of E. coli by human neutrophils by approximately 50% when tested at 0.1 and 1μM. Moreover, GW9508-neutrophil stimulation augmented microvesicle release and delayed apoptosis after stimulation. Finally, I demonstrated that GPR40 is expressed in inflammatory cells isolated from murine arthritic joints, such as neutrophils, macrophages and inflammatory monocytes. KBN-serum induced arthritic mice developed a more severe disease when treated prophylactically with GW9508 (10mg/kg, i.p. treated from day 0, daily), characterized by a higher clinical score and increased oedema when compared to vehicle control mice. Therapeutic intervention with GW9508 at the peak of the disease (day 5) delayed the resolution of arthritis. In summary, the data suggest that activation of GPR40 by GW9508 enhances neutrophil activation, up regulating the pro-inflammatory properties of this cell type, and therefore, exacerbating experimental inflammatory arthritis.
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Boström, Müssener Åsa. "Cytokine regulation in rodents with experimental arthritis /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-2862-2.

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Andreń, Maria. "The role of Fc gamma receptors in experimental arthritis /." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4724.

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Dang, Thi Ngoc Dzung. "Studies of novel immunosuppressive agents in experimental arthritis /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7357-009-5/.

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Books on the topic "Experimental arthriti"

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Jean-Yves, Reginster, ed. Osteoarthritis: Clinical and experimental aspects. Berlin: Springer, 1999.

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Foong, Wai Choong. Treatment of an experimental allergic arthritis with liposome-entrapped cytotoxics. Portsmouth: Portsmouth Polytechnic, School of Pharmacy, 1985.

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Blake, Simon M. Metabolic and histological changes associated with the experimentally induced arthritis in the rabbit. Uxbridge: Brunel University, 1992.

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Lukas, Sushila Christine *. Experimental arthritis in a rabbit model. 1989.

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Glynn, L. E., and H. D. Schlumberger. Experimental Models of Chronic Inflammatory Diseases. Springer London, Limited, 2012.

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Glynn, L. E., and H. D. Schlumberger. Experimental Models of Chronic Inflammatory Diseases. Springer, 2011.

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Melnyk, Megan Cara. The role of fibrinogen-like protein 2 (FGL2)/fibroleukin in the pathogenesis of experimental autoimmune arthritis. 2005.

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Okoye, Remi. The production and contribution of tumour necrosis factor-[alpah] in the progrssion of experimental collagen-induced arthritis in mice. 1994.

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Effects of continuous passive motion and immobilization on synovitis and cartilage degradation in antigen-induced arthritis: An experimental investigation in the rabbit. Ottawa: National Library of Canada, 1996.

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Hladkykh, Fedir, Nataliia Stepaniuk, and Heorhyi Stepaniuk. Pharmacodynamics of ibuprofen in the light if pleiotropic effects of Vinboron. ТОВ «Твори», 2022. http://dx.doi.org/10.46879/2022.2.

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This monograph summarizes the experimental studies on the pleiotropic effects of vinboron on pharmacodynamics of ibuprofen which is a widely used non-steroidal anti-inflammatory drug. Data on the effect of ibuprofen and its combination with vinboron on gastric secretion, proliferation and apoptosis of gastric epitheliocytes are presented. The effectiveness of the combined use of ibuprofen and vinboron in the treatment of experimental rheumatoid arthritis was evaluated in hematological, biochemical and pathomorphological studies. The monograph will be of intersest for clinicians, pharmacologists, biochemists, pathophysiologists as well as for medical, pharmacy and biology students. Tables – 10, figures – 40, bibliography – 144 references. Монографія присвячена узагальненню експериментальних досліджень впливу лікарського засобу з політропними фармакологічними властивостями вінборону на фармакодинаміку широковживаного нестероїдного протизапального засобу – ібупрофену. Представлено дані про вплив ібупрофену та його комбінації з вінбороном на шлункову секрецію, проліферацію та апоптоз епітеліоцитів шлунку. Проведено оцінку ефективності комбінованого застосування ібупрофену та вінборону в лікуванні експериментального ревматоїдного артриту за даними гематологічних, біохімічних та патоморфологічних досліджень. Монографія буде корисною для широкого кола лікарів-клініцистів, фармакологів, біохіміків, патофізіологів та здобувачів закладів вищої освіти медичного, фармацевтичного та біологічного профілів. Таблиць – 10, рисунків – 40, бібліографія – 144 посилань.
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Book chapters on the topic "Experimental arthriti"

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Bhalla, Parinishtha, Anukriti Verma, Bhawna Rathi, Shivani Sharda, and Pallavi Somvanshi. "Exploring Molecular Signatures in Spondyloarthritis: A Step Towards Early Diagnosis." In Proceedings of the Conference BioSangam 2022: Emerging Trends in Biotechnology (BIOSANGAM 2022), 142–55. Dordrecht: Atlantis Press International BV, 2022. http://dx.doi.org/10.2991/978-94-6463-020-6_15.

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AbstractSpondyloarthritis is an acute inflammatory disorder of the musculoskeletal system often accompanied by pain, stiffness, bone and tissue damage. It majorly consists of ankylosing spondylitis, psoriatic arthritis and reactive arthritis. It follows a differential diagnosis pattern for demarcation between the spondyloarthritis subtypes and other arthritic subtypes such as rheumatoid arthritis, juvenile arthritis and osteoarthritis due to the heterogeneity causing gradual chronicity and complications. Presence of definite molecular markers can not only improve diagnosis efficiency but also aid in their prognosis and therapy. This study is an attempt to compose a refined list of such unique and common molecular signatures of the considered subtypes, by employing a reductionist approach amalgamating gene retrieval, protein-protein interaction network, functional, pathway, micro-RNA-gene and transcription factor-gene regulatory network analysis. Gene retrieval and protein-protein interaction network analysis resulted in unique and common interacting genes of arthritis subtypes. Functional annotation and pathway analysis found vital functions and pathways unique and common in arthritis subtypes. Furthermore, miRNA-gene and transcription factor-gene interaction networks retrieved unique and common miRNA’s and transcription factors in arthritis subtypes. Furthermore, the study identified important signatures of arthritis subtypes that can serve as markers assisting in prognosis, early diagnosis and personalized treatment of arthritis patients requiring validation via prospective experimental studies.
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Wilder, R. L. "Experimental animal models of chronic arthritis." In Immunopathogenetic Mechanisms of Arthritis, 157–73. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1293-9_9.

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Lubberts, Erik, and Wim B. van den Berg. "Cytokines in the Pathogenesis of Rheumatoid Arthritis and Collagen-Induced Arthritis." In Advances in Experimental Medicine and Biology, 194–202. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0171-8_11.

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Brownlie, Rebecca J., and Stephen J. Thompson. "Heat shock proteins and experimental arthritis." In Heat Shock Proteins and Inflammation, 69–82. Basel: Birkhäuser Basel, 2003. http://dx.doi.org/10.1007/978-3-0348-8028-2_6.

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Ibañez, Olga Martinez, José Ricardo Jensen, and Marcelo De Franco. "Transcriptome Profiling in Experimental Inflammatory Arthritis." In Transcriptomics in Health and Disease, 211–26. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-11985-4_12.

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Ibañez, Olga Martinez, José Ricardo Jensen, and Marcelo De Franco. "Transcriptome Profiling in Experimental Inflammatory Arthritis." In Transcriptomics in Health and Disease, 277–98. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-87821-4_12.

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Glant, Tibor T., and Vyacheslav A. Adarichev. "Immunogenetics of Experimentally Induced Arthritis." In Immunogenomics and Human Disease, 271–97. Chichester, UK: John Wiley & Sons, Ltd, 2006. http://dx.doi.org/10.1002/0470034092.ch12.

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Feldmann, Marc, Ravinder N. Maini, Jan Bondeson, Peter Taylor, Brian M. J. Foxwell, and Fionula M. Brennan. "Cytokine Blockade in Rheumatoid Arthritis." In Advances in Experimental Medicine and Biology, 119–27. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1243-1_13.

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Alavi, Azita, and John Axford. "β1,4-Galactosyltransferase Variations in Rheumatoid Arthritis." In Advances in Experimental Medicine and Biology, 185–92. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1885-3_19.

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Bellan, Mattia, Pier Paolo Sainaghi, and Mario Pirisi. "Role of Vitamin D in Rheumatoid Arthritis." In Advances in Experimental Medicine and Biology, 155–68. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56017-5_13.

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Conference papers on the topic "Experimental arthriti"

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YAMAUCHI, Morio, Kazuhisa NAKANO, Yoshiya TANAKA, and Keiichi HORIO. "Predicting Disease Activity for Biologic Selection in Rheumatoid Arthritis." In 9th International Conference on Signal, Image Processing and Pattern Recognition (SPPR 2020). AIRCC Publishing Corporation, 2020. http://dx.doi.org/10.5121/csit.2020.101913.

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In this article, we implemented a regression model and conducted experiments for predicting disease activity using data from 1929 rheumatoid arthritis patients to assist in the selection of biologics for rheumatoid arthritis. On modelling, the missing variables in the data were completed by three different methods, mean value, self-organizing map and random value. Experimental results showed that the prediction error of the regression model was large regardless of the missing completion method, making it difficult to predict the prognosis of rheumatoid arthritis patients.
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Kiapour, Ali, Vijay K. Goel, Manoj Krishna, Sarath Koruprolu, Rachit Parikh, and Devdatt Mahtre. "A Computational and Experimental Investigation Into Biomechanics of Lumbar Spine Stabilized With a Novel Posterior Dynamic Stabilization System." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-205814.

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Lumbar spinal stenosis is a progressive degenerative condition due to arthritic facet joints. Arthritic facets become inflamed and often develop osteophytes, leading to nerve compression and persistent severe back pain. When conservative treatment fails to reduce pain, surgical management may be pursued to improve the patient’s quality of life. Spinal decompression and fusion is one of the most common surgical procedures for treatment of spinal stenosis. However, fusion may result in accelerated degeneration of the adjacent motion segments and morbidity [1]. Motion preservation instrumentation is being developed to preserve motion at the involved and adjacent segments, as opposed to fusion procedure [2]. In this study, we used experimental and finite element (FE) techniques to assess and compare the biomechanics of intact spines and spines implanted with a novel posterior dynamic stabilizer device (TrueDyn™, Disc Motion Technologies, Boca Raton, FL). The effects on the adjacent segment, including motion and intra-discal pressure were analyzed.
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Chen, W., Z. Xu, H. Wee, G. S. Lewis, N. Olsen, J. Lin, and S. G. Zheng. "THU0097 Phosphodiesterases 4 (PDE4) inhibitor ameliorates experimental arthritis." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.4989.

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Andersson, Åsa, and Samra Sardar. "FRI0011 A TRANSCRIPTIONAL REGULATOR CONTROLLING SEVERITY OF EXPERIMENTAL ARTHRITIS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.7057.

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Ratkay, Leslie G., R. K. Chowdhary, Herma C. Neyndorff, Julia G. Levy, and J. D. Waterfield. "Treatment of experimental murine arthritis with transdermal photodynamic therapy." In Fifth International Photodynamic Association Biennial Meeting, edited by Denis A. Cortese. SPIE, 1994. http://dx.doi.org/10.1117/12.203424.

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Dorst, DN, M. Rijpkema, M. Buitinga, M. Brom, DL Bos, A. Freimoser, C. Klein, et al. "P107 Targeting activated synovial fibroblasts using photodynamic therapy in experimental arthritis." In 38th European Workshop for Rheumatology Research, 22–24 February 2018, Geneva, Switzerland. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2018.122.

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Fernández-Rodríguez, J. A., M. Almonte-Becerril, O. Ramil-Gómez, S. Viñas-Diz, L. Hermida-Carballo, Á. Vela-Anero, Á. Concha, M. Camacho-Encina, F. J. Blanco, and M. J. Lopez-Armada. "AB0121 Resveratrol-enhanced autophagic flux reduces severity of experimental rheumatoid arthritis." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.4468.

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Goltsev, AN, ED Lutsenko, MV Ostankov, and NA Bondarovich. "AB0078 Role of experimental research in study of rheumatoid arthritis etiopathogenesis." 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.6113.

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Xie, Changeai, Nipeng Lin, Jiaxin Zhou, Zhiqi Fan, and Wenbin Fu. "The experimental introduction of professor Fu's three-step therapy on gouty arthritis." In 2012 IEEE International Conference on Bioinformatics and Biomedicine Workshops (BIBMW). IEEE, 2012. http://dx.doi.org/10.1109/bibmw.2012.6470364.

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Wanic, K., M. Kalkgruber, B. Niederreiter, T. Shvets, J. Smolen, and S. Hayer. "P114 Tissue regeneration and bone repair upon TNF blockade in experimental arthritis." In 39th European Workshop for Rheumatology Research, 28 February–2 March 2019, Lyon, France. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2019.102.

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Reports on the topic "Experimental arthriti"

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Koleva, Kalina, Stanislav Marchev, Rumen Nikolov, Mila Vlaskovska, and Slavina Surcheva. The Role of Diabetes on Experimental Arthritis: Analgesic, Anti-inflammatory and Adverse Effects of NSAID. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, September 2020. http://dx.doi.org/10.7546/crabs.2020.09.14.

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