Academic literature on the topic 'Fibrotic and inflammatory conditions'

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Journal articles on the topic "Fibrotic and inflammatory conditions"

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Binatti, Eleonora, Alessio Gerussi, Donatella Barisani, and Pietro Invernizzi. "The Role of Macrophages in Liver Fibrosis: New Therapeutic Opportunities." International Journal of Molecular Sciences 23, no. 12 (June 14, 2022): 6649. http://dx.doi.org/10.3390/ijms23126649.

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Chronic inflammation is the hallmark of fibrotic disorders and is characterized by the activation of immune cells in the damaged tissues. Macrophages have emerged as central players in the fibrotic process since they initiate, sustain and amplify the inflammatory reaction. As regards the liver, distinct populations of phagocytic cells, like Kupffer cells and monocyte-derived macrophages, are indisputably key cells implicated in the pathogenesis of several chronic liver diseases. In this review, we summarize the current knowledge on the origin, role and functions of macrophages in fibrotic conditions, with a specific focus on liver fibrosis; then, we discuss some innovative therapeutic strategies targeting macrophages in fibrotic liver diseases.
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Sgambellone, Silvia, Silvia Marri, Stefano Catarinicchia, Alessandro Pini, Dilip K. Tosh, Kenneth A. Jacobson, Emanuela Masini, Daniela Salvemini, and Laura Lucarini. "Adenosine A3 Receptor (A3AR) Agonist for the Treatment of Bleomycin-Induced Lung Fibrosis in Mice." International Journal of Molecular Sciences 23, no. 21 (November 1, 2022): 13300. http://dx.doi.org/10.3390/ijms232113300.

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Adenosine receptors (ARs) are involved in the suppression and development of inflammatory and fibrotic conditions. Specifically, AR activation promotes differentiation of lung fibroblasts into myofibroblasts, typical of a fibrotic event. Pulmonary fibrosis is a severe disease characterized by inflammation and fibrosis of unknown etiology and lacking an effective treatment. The present investigation explored the action of MRS5980, a new, highly potent and selective A3AR agonist, in an established murine model of lung fibrosis. The effects of either vehicle or MRS5980 were studied in mice following intratracheal bleomycin administration. We evaluated the role of the A3AR agonist on lung stiffness, studying the airway resistance to inflation, oxidative stress (8-OHdG and MDA), inflammation, pro- and anti-inflammatory marker levels (IL-1β, IL-6, TNF-α, IL-10 and IL-17A) and fibrosis establishment, evaluating transforming growth factor (TGF)-β expression and α-smooth muscle actin (α-SMA) deposition in lungs. Bleomycin administration increased lung stiffness, TGF-β levels, α-SMA deposition, and inflammatory and oxidative stress markers. The treatment with MRS5980 attenuated all the analyzed functional, biochemical and histopathological markers in a dose-dependent manner. Our findings support the therapeutic potential of A3AR agonists in lung fibrosis by demonstrating reduced disease progression, as indicated by decreased inflammation, TGF-β expression and fibrotic remodeling.
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Filidou, Eirini, Leonidas Kandilogiannakis, Gesthimani Tarapatzi, Michail Spathakis, Paschalis Steiropoulos, Dimitrios Mikroulis, Konstantinos Arvanitidis, Vasilis Paspaliaris, and George Kolios. "Anti-Inflammatory and Anti-Fibrotic Effect of Immortalized Mesenchymal-Stem-Cell-Derived Conditioned Medium on Human Lung Myofibroblasts and Epithelial Cells." International Journal of Molecular Sciences 23, no. 9 (April 20, 2022): 4570. http://dx.doi.org/10.3390/ijms23094570.

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Idiopathic pulmonary fibrosis (IPF) is caused by progressive lung tissue impairment due to extended chronic fibrosis, and it has no known effective treatment. The use of conditioned media (CM) from an immortalized human adipose mesenchymal stem cell line could be a promising therapeutic strategy, as it can reduce both fibrotic and inflammatory responses. We aimed to investigate the anti-inflammatory and anti-fibrotic effect of CM on human pulmonary subepithelial myofibroblasts (hPSM) and on A549 pulmonary epithelial cells, treated with pro-inflammatory or pro-fibrotic mediators. CM inhibited the proinflammatory cytokine-induced mRNA and protein production of various chemokines in both hPSMs and A549 cells. It also downregulated the mRNA expression of IL-1α, but upregulated IL-1β and IL-6 mRNA production in both cell types. CM downregulated the pro-fibrotic-induced mRNA expression of collagen Type III and the migration rate of hPSMs, but upregulated fibronectin mRNA production and the total protein collagen secretion. CM’s direct effect on the chemotaxis and cell recruitment of immune-associated cells, and its indirect effect on fibrosis through the significant decrease in the migration capacity of hPSMs, makes it a plausible candidate for further development towards a therapeutic treatment for IPF.
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Zhang, Xiwen, Joseph K. Ritter, and Ningjun Li. "Sphingosine-1-phosphate pathway in renal fibrosis." American Journal of Physiology-Renal Physiology 315, no. 4 (October 1, 2018): F752—F756. http://dx.doi.org/10.1152/ajprenal.00596.2017.

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Renal fibrosis is defined as the excessive deposition and modification of extracellular matrix (ECM) in the renal parenchyma in response to injury and inflammation, resulting in renal function loss. This condition is common to many chronic kidney diseases occurring under diverse pathological conditions, such as diabetic and hypertensive nephropathy. Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid metabolite involved in the regulation of cardiovascular functions and the pathogenesis of various cardiovascular diseases. S1P has also been considered an important regulator of fibrotic diseases, playing significant roles in the differentiation of fibroblasts to myofibroblasts and in the induction of inflammatory responses during the early stages of fibrotic diseases. This minireview summarizes recent research findings regarding the importance of the sphingosine kinase-1-S1P-S1P receptor axis and its interactions with other classic fibrotic signaling pathways and the immune inflammatory response to reveal novel therapeutic targets for the treatment or prevention of renal fibrosis.
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Herbelet, Sandrine, Boel De Paepe, and Jan L. De Bleecker. "Abnormal NFAT5 Physiology in Duchenne Muscular Dystrophy Fibroblasts as a Putative Explanation for the Permanent Fibrosis Formation in Duchenne Muscular Dystrophy." International Journal of Molecular Sciences 21, no. 21 (October 24, 2020): 7888. http://dx.doi.org/10.3390/ijms21217888.

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Duchenne muscular dystrophy (DMD) is characterized by chronic inflammation and fibrotic tissue production by fibroblasts. The promyogenic factor nuclear factor of activated T-cells 5 (NFAT5) is virtually present in all cells, responding to hyperosmolar or pro-inflammatory stress. In embryogenic fibroblasts, absence of NFAT5 results in cell cycle arrest. Here, unaffected skeletal muscle fibroblasts from one healthy donor showed NFAT5 nuclear translocation upon hyperosmolar stress and normal cell viability. Absence of NFAT5 translocation under pro-inflammatory conditions resulted in decreased cell growth (Incucyte ZOOM). In DMD skeletal muscle fibroblasts from one DMD patient, NFAT5 was merely located in the nucleus. Exposure to hyperosmolar conditions or pro-inflammatory cytokines IFN-γ, IL-1β and TNF-α had no influence on NFAT5 physiology (immunofluorescence, western blotting, RT-qPCR). Hyperosmolarity resulted in decreased cell viability and pro-inflammatory stress in unaltered cell growth. These findings suggest that NFAT5 is vital to DMD fibroblast survival. Exposure to pro-inflammatory or hyperosmolar stress in DMD fibroblasts results in an unexpected NFAT5 response, where fibroblasts are not triggered by inflammatory cytokines and do not withstand hyperosmolarity. Chronic inflammation could be viewed as a non-restrictive factor in the formation of fibrosis in DMD. Abnormal NFAT5 physiology could provide a molecular explanation for permanent fibrotic matrix production by DMD fibroblasts.
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Pham, Tho X., Yoojin Lee, Minkyung Bae, Siqi Hu, Hyunju Kang, Mi-Bo Kim, Young-Ki Park, and Ji-Young Lee. "Spirulina supplementation in a mouse model of diet-induced liver fibrosis reduced the pro-inflammatory response of splenocytes." British Journal of Nutrition 121, no. 7 (February 26, 2019): 748–55. http://dx.doi.org/10.1017/s0007114519000126.

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AbstractTreatment of liver fibrosis is very limited as there is currently no effective anti-fibrotic therapy. Spirulina platensis (SP) is a blue-green alga that is widely supplemented in healthy foods. The objective of this study was to determine whether SP supplementation can prevent obesity-induced liver fibrosis in vivo. Male C57BL/6J mice were randomly assigned to a low-fat or a high-fat (HF)/high-sucrose/high-cholesterol diet or an HF diet supplemented with 2·5 % SP (w/w) (HF/SP) for 16 or 20 weeks. There were no significant differences in body weight, activity, energy expenditure, serum lipids or glucose tolerance between mice on HF and HF/SP diets. However, plasma alanine aminotransferase level was significantly reduced by SP at 16 weeks. Expression of fibrotic markers and trichrome stains showed no differences between HF and HF/SP. Splenocytes isolated from HF/SP fed mice had lower inflammatory gene expression and cytokine secretion compared with splenocytes from HF-fed mice. SP supplementation did not attenuate HF-induced liver fibrosis. However, the expression and secretion of inflammatory genes in splenocytes were significantly reduced by SP supplementation, demonstrating the anti-inflammatory effects of SP in vivo. Although SP did not show appreciable effect on the prevention of liver fibrosis in this mouse model, it may be beneficial for other inflammatory conditions.
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Rizzi, Manuela, Stelvio Tonello, Davide D’Onghia, and Pier Paolo Sainaghi. "Gas6/TAM Axis Involvement in Modulating Inflammation and Fibrosis in COVID-19 Patients." International Journal of Molecular Sciences 24, no. 2 (January 4, 2023): 951. http://dx.doi.org/10.3390/ijms24020951.

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Gas6 (growth arrest-specific gene 6) is a widely expressed vitamin K-dependent protein that is involved in many biological processes such as homeostatic regulation, inflammation and repair/fibrotic processes. It is known that it is the main ligand of TAMs, a tyrosine kinase receptor family of three members, namely MerTK, Tyro-3 and Axl, for which it displays the highest affinity. Gas6/TAM axis activation is known to be involved in modulating inflammatory responses as well as fibrotic evolution in many different pathological conditions. Due to the rapidly evolving COVID-19 pandemic, this review will focus on Gas6/TAM axis activation in SARS-CoV-2 infection, where de-regulated inflammatory responses and fibrosis represent a relevant feature of severe disease manifestation. Furthermore, this review will highlight the most recent scientific evidence supporting an unsuspected role of Axl as a SARS-CoV-2 infection driver, and the potential therapeutic advantages of the use of existing Axl inhibitors in COVID-19 management. From a physiological point of view, the Gas6/TAM axis plays a dual role, fostering the tissue repair processes or leading to organ damage and loss of function, depending on the prevalence of its anti-inflammatory or profibrotic properties. This review makes a strong case for further research focusing on the Gas6/TAM axis as a pharmacological target to manage different disease conditions, such as chronic fibrosis or COVID-19.
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Hortobagyi, David, Tanja Grossmann, Magdalena Tschernitz, Magdalena Grill, Andrijana Kirsch, Claus Gerstenberger, and Markus Gugatschka. "In vitro mechanical vibration down-regulates pro-inflammatory and pro-fibrotic signaling in human vocal fold fibroblasts." PLOS ONE 15, no. 11 (November 19, 2020): e0241901. http://dx.doi.org/10.1371/journal.pone.0241901.

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Introduction Voice rest following phonotrauma or phonosurgery has a considerable clinical impact, but clinical recommendations are inconsistent due to inconclusive data. As biopsies of the vocal folds (VF) for molecular biology studies in humans are unethical, we established a new in vitro model to explore the effects of vibration on human vocal fold fibroblasts (hVFF) in an inflammatory and normal state, which is based on previously published models. Methods By using a phonomimetic bioreactor we were able to apply predefined vibrational stress patterns on hVFF cultured under inflammatory or normal conditions. Inflammatory and pro-fibrotic stimuli were induced by interleukin (IL)1β and transforming growth factor (TGF)β1, respectively. Mechanical stimulation was applied four hours daily, over a period of 72 hours. Outcome measurements comprised assessment of extracellular matrix (ECM)-related components, angiogenic factors, and inflammatory and fibrogenic markers on gene expression and protein levels. Results Under inflammatory conditions, the inflammatory cytokine IL11, as well as the myofibroblast marker alpha smooth muscle actin (α-SMA) were significantly reduced when additional vibration was applied. The desirable anti-fibrotic ECM component hyaluronic acid was increased following cytokine treatment, but was not diminished following vibration. Conclusion Our experiments revealed the effect of vibrational stress on hVFF in an inflammatory state. Elevated levels of certain pro-inflammatory/pro-fibrotic factors could be mitigated by additional vibrational excitation in an in vitro setting. These findings corroborate clinical studies which recommend early voice activation following an acute event.
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Hazel, K., N. McGinley, A. O’Toole, and S. Keely. "P087 The role of bile acids in mediating fibrosis in inflammatory bowel disease." Journal of Crohn's and Colitis 15, Supplement_1 (May 1, 2021): S187. http://dx.doi.org/10.1093/ecco-jcc/jjab076.216.

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Abstract Background Crohn’s disease is a chronic inflammatory disorder of the gastrointestinal tract that affects approximately 15,000 people in Ireland. 10% of these patients will develop fibrostenosing disease, usually requiring surgery. There are currently no antifibrotic medications in use for the treatment of fibrostenosing CD. Bile acids (BAs), produced in the liver and classically known for their roles in facilitating fat absorption from the diet, have previously been shown to have the capacity to regulate fibroblast activation and to exert protective effects against both hepatic fibrosis and intestinal inflammation. Therefore, altered mucosal fibroblast function in response to luminal BAs may be an important factor in the pathogenesis of fibrostenosing Crohn’s disease. Our aim is to determine if treatment of fibroblasts under pro-fibrotic conditions with naturally occurring BAs decreases markers associated with fibrosis. Methods NIH/3T3, a murine fibroblast cell line, were treated with TGF-ß (5 ng/ml) to induce their activation and transition to myofibroblasts in the absence or presence of varying concentrations of the naturally-occurring BAs, deoxycholic acid (DCA) and ursodeoxycholic acid (UDCA) over 24 hours. qPCR was employed to determine expression of alpha-smooth muscle actin (aSMA), an important marker for ECM deposition and fibrosis. Results Treatment of fibroblasts with DCA within the range of normal physiological concentrations (50 to 200 µM) induced a significant inhibition of TGF-ß-induced aSMA expression. At a concentration of 100 µM, DCA reduced TGF-ß-induced responses by 50%, compared to cells treated with TGF-ß-alone (RQ=2.17; RQ=4.58, respectively) (n=6) (p=0.0031) (Figure 1). Similarly, treatment with UDCA at supraphysiological concentrations (500 µM) decreased aSMA expression following TGF-ß stimulation (RQ=1.75; RQ=3.69, respectively) (n=5) (Figure 2). Treatment with conjugated BAs TDCA and TUDCA suggest an intracellular mechanism of action by DCA and UDCA. INT-777, the specific agonist of the TGR5 bile acid receptor, also reduced TGF-ß-induced aSMA expression, suggesting this receptor may be involved in mediating the effects of naturally-occurring BAs. Figure 1: Figure 2: Conclusion We have shown that treatment of fibroblasts under pro-fibrotic conditions with the BAs, DCA and UDCA, results in a significant decrease in aSMA expression. These data suggest that BAs represent a promising target for the development of new anti-fibrotic agents to treat/prevent fibrostenosing CD.
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Laaninen, Matias, Merja Bläuer, Juhani Sand, Isto Nordback, and Johanna Laukkarinen. "Difference in Early Activation of NF-κB and MCP-1 in Acinar-Cell-Rich versus Fibrotic Human Pancreas Exposed to Surgical Trauma and Hypoxia." Gastroenterology Research and Practice 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/460363.

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Objectives.Previously we have shown that a pancreas with over 40% acinar cells is exposed to postoperative pancreatitis and other complications after pancreaticoduodenectomy (PD). Our aim was to analyze the expression of NF-κB and MCP-1 in the cut edge of human pancreas after PD in both acinar-cell-rich and fibrotic pancreata.Methods.Several pancreatic samples from six patients, three with acinar-cell-rich and three with fibrotic pancreata, were exposed to surgical trauma in PD, and thereafter to hypoxemia for 15 minutes, 2–2.5 hours, 4 hours, or 6 hours, to mimic postoperative conditions of the pancreatic remnant in a patient. Immunohistochemical analysis of inflammation markers (NF-κB, MCP-1) was performed.Results.In the acinar-cell-rich pancreata, intra-acinar NF-κB and MCP-1 expression increased from mild at 15 minutes to high during the first 4 hours, whereas in ductal cells MCP-1 staining was highly intense at both time points. Acinar cell NF-κB and MCP-1 expression and ductal cell MCP-1 expression were also observed in the fibrotic pancreata, but the activation remained low throughout the 6 hours.Conclusions.In acinar-cell-rich pancreas, an extensive inflammatory cascade begins almost immediately after surgical trauma. Fibrosis may limit the progression of inflammatory process in pancreas.
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Dissertations / Theses on the topic "Fibrotic and inflammatory conditions"

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Pustilnik, Leslie Royce 1964. "The pulmonary inflammatory and fibrotic response induced by glass fibers." Thesis, The University of Arizona, 1987. http://hdl.handle.net/10150/276624.

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The present study was initiated to evaluate the pulmonary inflammatory and fibrotic responses induced by single and repeated exposures to glass fibers. Single and repeated intratracheal injections of glass fibers induced an acute inflammatory response which progressed to a chronic inflammatory and fibrotic response. Mice exposed to glass fibers in single or repeated doses demonstrated elevated numbers of eosinophils, neutrophils and macrophages and increases in cell-free protein in lung lavage fluid at five days post-exposure. These parameters, in addition to relative lung/body weight ratios and lung tissue hydroxyproline levels, were elevated in comparison to saline control animals at five weeks post-exposure. Although repeated exposures to glass fibers did not potentiate the cellular inflammatory response, they did induce a marked infiltration of eosinophils, a response not observed with either asbestos or silica exposures. These observations suggest that glass fibers may be more toxic to the lungs than previously thought.
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Montague, Samantha J. "Platelet activation in trauma and other inflammatory conditions." Thesis, University of Birmingham, 2017. http://etheses.bham.ac.uk//id/eprint/7147/.

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Platelets play critical roles in thrombosis, inflammation, and wound healing, which are essential in response to trauma. These processes are primarily driven through the immunoreceptor tyrosine-based activation motif (ITAM)-containing receptors, glycoprotein VI (GPVI) and C-type lectin-like receptor 2 (CLEC-2). This study aimed to investigate; (i) the effects of Alarmins released following trauma on platelet reactivity and the mechanisms involved; (ii) establish whether soluble GPVI (sGPVI), a platelet activation marker is elevated in trauma and other inflammatory conditions; (iii) determine whether the CLEC-2 ligand, podoplanin, is elevated in inflammatory conditions and (iv) establishing the role of GPVI and platelets in cutaneous wound healing. The nuclear-related Alarmin, histones, induced robust platelet activation both in vitro and in vivo. Histone-induced platelet activation was mediated through GPVI in vitro However, this pathway was found not to underlie histone-induced lowering of platelet count in vivo and is most likely to result from mediators released following vascular damage. GPVI shedding was shown to be induced following activation by thrombin, through a pathway dependent on fibrin generation. sGPVI was found to be a marker for platelet activation during a variety of inflammatory disorders, notably in association with sepsis. Furthermore, GPVI shedding reflects platelet activation by collagen and potentially thrombin-induced fibrin generation.
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Zhang, Qing, and 張清. "Comparison of mycophenolate mofetil and cyclophosphamide on inflammatory and fibrotic processes in the pathogenesis of lupusnephritis: animal and in vitro studies." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43085222.

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Htwe, Su Su. "Studying the role of spatial cell distribution and substrate stiffness in inflammatory and fibrotic responses in human lung using bioengineered platforms." Thesis, University of Nottingham, 2017. http://eprints.nottingham.ac.uk/48045/.

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The extracellular matrix (ECM) has emerged as a major regulator of cell behaviours. Changes in extracellular matrix, especially its composition, organization/ dimensionality, and rigidity have been implicated in various aspects of cellular functions including cell growth, migration, and differentiation. In my thesis, I have focused on the effect of two biophysical properties of the extracellular matrix namely dimensionality and rigidity in the inflammatory and fibrotic pathologies of human lung. To study the role of matrix dimensionality, firstly electrospun scaffold based three-dimensional (3D) culture with similar architecture of human lung was developed. By applying this 3D model, inflammatory response was studied in an in vivo like environment by using NF-κB transcription factor activation as a tool for probing inflammatory response in human lung fibroblasts. According to my observations, it was confirmed that the matrix dimensionality together with spatial organisation of cells is crucial in lung inflammatory response, evidenced by the observation of the differences in the level and pattern of inflammatory response between 2D and 3D culture systems. To study the role of matrix rigidity in progression of lung fibrosis, we developed the ECM-based hydrogel platform with tuneable stiffness level relevant to normal and fibrotic lung. By using this disease relevant platform, I have shown that stiff matrix but not soft matrix can induce the myofibroblast differentiation and fibroblast proliferation, the two major features of lung fibrosis. To date, the molecular mechanisms underpinning this cellular mechanosensing process in response to matrix stiffening remains unknown. To achieve this, I further investigated the involvement of two potential mechanosensitive signalling pathways namely, Rho associated coiled coil forming kinase (ROCK) signalling and talin- (focal adhesion adaptor) signalling in this process. Interestingly, my data show that ROCK signalling differentially regulated stiffness induced myofibroblast differentiation between soft normal and stiff fibrotic matrix. Moreover, both ROCK isoforms 1 and 2 are synergistically important in myofibroblast differentiation driven by rigid matrix and the absence of one ROCK isoform can exaggerate myofibroblast differentiation on stiff fibrotic matrix. Regarding talin signalling, my preliminary data confirms that talin1 can control both stiffness induced fibroblast proliferation and myofibroblasts differentiation on stiff matrix. In contrast to talin1, talin2 showed a protective role in controlling myofibroblast differentiation. In conclusion, we have successfully developed two in vitro lung models for studying the effect of matrix dimensionality and rigidity in lung inflammation and fibrosis. Overall my PhD work has elucidated the significant contribution of biophysical cues of external cellular environment in lung inflammation and fibrosis.
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Lee, Chung Bomy. "Theranostic nanoparticles for the management of inflammatory diseases and conditions." Thesis, Massachusetts Institute of Technology, 2017. http://hdl.handle.net/1721.1/112504.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Chemical Engineering, 2017.
Cataloged from PDF version of thesis.
Includes bibliographical references.
Atherosclerosis, the gradual buildup of plaques within arteries, is the main cause of cardiovascular diseases (CVDs). The World Health Organization reports that CVDs are the number one cause of death in the world. In the United States alone, around 85 million people suffer from CVDs; this is associated with a cost of over $316 billion per year and responsible for about a third of all deaths in the US. Recent findings have shown that inflammation plays a pivotal role in atherosclerosis. Although statins have traditionally been prescribed for their lipid-lowering benefits, studies have indicated that they can have other effects as well (so-called "pleiotropic effects"), including anti-inflammatory, anti-oxidant, and anti-thrombotic benefits. This thesis presents a novel theranostic (therapeutic + diagnostic) nanoparticle platform for the treatment and diagnosis of atherosclerosis. Given the anti-inflammatory effects of statins when cells are directly treated, the aim of this nanoparticle platform was to target macrophages within plaques given their central role in plaque development and progression. First, simvastatin-loaded nanoparticles were designed and optimized. The particles consisted of a biodegradable polymer core and a lipid shell. Using bulk nanoprecipitation methods, as well as microfluidic devices, the physical characteristics of the particles could be controlled and fine-tuned to meet the desired specifications: 100 to 200 nm in size, -15 to -20 mV in zeta potential, and 70%+ simvastatin loading efficiency. Imaging agents, such as iron oxide nanocrystals used for magnetic resonance imaging (MRI), were successfully incorporated into the nanoparticles and can offer diagnostic capabilities to the nanoparticles. Next, various nanoparticle formulations were shown to be therapeutically effective in cell and mice models of atherosclerosis. For instance, in vitro treatment of macrophages led to decreases in the expression of TNF-a and MCP-1 by roughly 20% and 50%, respectively. This pattern has also been observed in murine models, with researchers showing that simvastatin-loaded particles can halt plaque development (and even decrease plaque area) while reducing the expression of pro-inflammatory genes (e.g., of TNF-a, IL- IP) by an order of magnitude. Overall, this thesis presents a new and innovative nanoparticle platform that has the potential for the simultaneous treatment and diagnosis of atherosclerosis. Given their anti-inflammatory benefits, these nanoparticles have the potential to impact the treatment of not only atherosclerosis but also various other inflammatory conditions and diseases as well.
by Bomy Lee Chung.
Ph. D.
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Zhang, Qing. "Comparison of mycophenolate mofetil and cyclophosphamide on inflammatory and fibrotic processes in the pathogenesis of lupus nephritis : animal and in vitro studies /." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43085222.

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Zhang, Chenzhu, and 张辰珠. "The effects of rapamycin and mycophenolic acid on inflammatory and fibrotic processes in the pathogenesis of lupus nephritis: animal and in vitro studies." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B45898935.

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Collins, John Samuel Andrew. "A morphometric study of inflammatory conditions of the upper gastrointestinal tract." Thesis, Queen's University Belfast, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336208.

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Isebor, Peter. "Positive psychological interventions in chronic conditions : gratitude and inflammatory bowel disease." Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/21308/.

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Petit, Maxime. "Residency and trafficking of ILC2 in steady steate and th2 induced inflammatory conditions." Thesis, Université de Paris (2019-....), 2019. http://www.theses.fr/2019UNIP7095.

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Les ILC2s sont retrouvées au niveau des muqueuses comme les poumons et l’intestin, ainsi que dans divers ganglions et organes liés au métabolisme comme les tissus adipeux (ATs). Elles jouent un rôle important dans l’induction des réponses immunitaires de type Th2 comme équivalents innées dans lymphocytes Th2. Elles sont activées par des alarmines (IL-25 et IL-33) et des activateurs environnementaux (allergènes, métabolites et neuromédiateurs). Les ILC2s sécrètent des cytokines de type Th2 permettant de recruter et d’activer des cellules myéloïdes, d’augmenter la production de mucus et la contraction musculaire, ainsi que d’initier la réparation et le renouvellement des tissus. Cependant, une activation non contrôlée des ILC2s participe au développement de maladies chroniques. Les ILCs sont généralement considérées comme des cellules résidentes. Cependant, plusieurs études ont suggéré que la migration pourrait être un processus important pour la maturation des capacités effectrices. La circulation des ILCs reste peu documentée, et aucun mécanisme n’est pour l’instant capable d’expliquer le renouvellement des ILC2s pour agir dans de nombreux tissus suite à une stimulation. Nous avons montré que des quantités significatives d’ILC2s matures et immatures peuvent être collectées dans la lymphe du canal thoracique de souris canulées durant plusieurs heures. Les ILC2s circulantes forment 3 groupes distincts avec des expressions de molécules d’adhésion et récepteurs de migration spécifiques. Nos expériences de transferts cellulaires montrent que ces groupes spécifiques de molécules exprimées sont liés à des tropismes particuliers pour l’intestin, les poumons ou les ATs. Pour analyser le comportement des ILC2s dans un contexte de réponse de type Th2, nous avons injecter les cytokines IL-25 et IL-33 et étudié la lymphe de ces souris. La stimulation à l’IL-33 augmente le nombre de cellules ILC2s circulants dans la lymphe. Les différents groupes d’ILC2s montrent des réponses différentes à l’IL-33. Ainsi, les ILC2s migrants vers l’intestin sont majoritairement prolifératives tandis que le groupe migrant vers les poumons et les ATs secrètent de l’IL-5, de l’IL-13 et de l’Areg. Cela suggère que les ILC2s migrants de façon spécifique possèdent une empreinte fonctionnelle. Nous confirmons les fonctions des groupes d’ILC2s circulants en utilisant des modèles plus physiologiques mimant des réactions allergiques et des infections parasitaires (stimulation par la papaïne et le succinate). Les migrations vers l’intestin et les poumons jouent un rôle primordial dans l’induction de réponse de type Th2 par sécrétion d’IL-5 et d’IL-13, et à l’initiation de la réparation tissulaire par production d’Areg. De façon intéressante, les ILC2s migrants vers les poumons participent au renouvellement des populations résidentes participant principalement à la production d’Areg. Finalement, nous caractérisons un rôle important du trafic des ILC2s à différents temps suivant l’infection par Nippostrongulus brasiliensis, confirmant la fonction des ILC2s migrantes
ILC2s are found in mucosal tissues as lung and intestine, in lymph nodes, and in metabolic tissues such as the adipose tissues. They play important role in maintaining or inducing type-2 immune responses as innate equivalent of Th2 lymphocytes. They are activated by alarmins (IL-25 and IL-33) and by external activators (allergens, metabolites and neuromediators). ILC2s are secreting type-2 cytokines to facilitate the activation of other cells and to induce an important repair program. Their activation allows large type of events as diverse as myeloid cells recruitment and activation, mucus production, muscle contractility and tissue repair. They have key role in lung and adipose tissue development and maintain their homeostasis by early responding against parasitic pathogens. Abnormal activation of ILC2s is also participating to chronic diseases.ILCs are mostly considered as resident cells. However, different studies suggested that migration could be important for the maturation of their effector capacities and to correctly target the injured tissue. Circulation and trafficking of ILC subsets is still unclear. No mechanism is yet available to explain the turnover of ILC2s and how they can act in many tissues following stimuli.We found that large numbers of mature and immature ILC2s could be collected in the thoracic duct lymph of mice perfused over several hours, showing that ILC2s are in fact actively circulating through the hemo-lymphatic circuit. Furthermore, circulating mature ILC2s could be separated into three distinct subsets depending on their pattern of receptor and adhesion molecule expression. Cell transfer experiments proved that specific patterns are representative of specific tropism for gut, lung and adipose tissues.To analyse ILC2 behaviour in the context of a type-2 response, we injected IL-25 and IL-33 before lymph collection. IL-33 stimulation largely enhanced the number of circulating ILC2s in the lymph. These different ILC2 tissue targeted subsets responded differently to IL-33. Specifically, gut-trafficking ILC2s were mainly stimulated to proliferate whereas lung and adipose tissue subsets were stimulated to produce IL-13, IL-5 and Areg. This suggests that, in ILC2s, specific tissue targeting is associated with already imprinted functions while transiting through the hemo-lymphatic system. We confirmed these functions of circulating ILC2 subsets in more physiological context by mimicking allergy and helminth infection (stimulation by papain and succinate) where specific migration to lungs and intestine play important roles in mounting the type-2 response by IL-5/IL-13 secretion, and also initiating tissue repair by Areg production. Interestingly, we showed that lung migrating ILC2s participated to resident pool renewal that main function is Areg production. Finally, we characterized important trafficking of ILC2 at different stages of Nippostrongulus brasiliensis infection, confirming the functional relevance of ILC2 trafficking
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Books on the topic "Fibrotic and inflammatory conditions"

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Inflammatory conditions of the colon. New York: Nova Science Publishers, 2009.

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Church, Martin, and Clive Robinson, eds. Eicosanoids in Inflammatory Conditions of the Lung, Skin and Joints. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1283-0.

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1942-, Bonney R. J., ed. Inflammatory disease therapy: Preclinical and clinical developments. Basel: Birkhäuser Verlag, 1993.

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Hashefi, Mandana. PET/CT applications in non-neoplastic conditions. Edited by New York Academy of Sciences. Boston, Mass: Published by Blackwell Pub. on behalf of the New York Academy of Sciences, 2011.

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Black, Jessica K. Eating your way back to health: A guide to inflammatory cooking - reduce inflammation to help heal cardiovascular disease, arthritis, fibromyalgia, diabetes, allergies, and many more conditions. McMinnville, Ore: A Family Healing Center, 2004.

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Yaqoob, Muhammad M., Katherine Bennett-Richards, and Islam Junaid. Retroperitoneal fibrosis. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0357.

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Retroperitoneal fibrosis (RPF) is a rare but multifaceted disease which encompasses a range of conditions characterized by the presence of a fibro-inflammatory tissue, which usually surrounds the abdominal aorta, iliac arteries, and extends into the retroperitoneum to entrap ureters with resultant unilateral or bilateral obstruction, usually at the junction between the middle and lower thirds of the ureter. The condition is progressive: initially, the fibrous tissue is fairly cellular, later becoming relatively acellular. The mechanism by which obstruction occurs is probably due to loss of peristalsis. A histological diagnosis should be obtained if at all possible, and laparotomy is required in order to obtain a sufficiently large sample to differentiate between idiopathic and secondary causes of RPF. Treatment of idiopathic RPF is by corticosteroids in the first instance with ureteric stents or ureterolysis initially and requires regular monitoring.
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Recipes for the Specific Carbohydrate Diet: The Grain-Free, Dairy-Free, Sugar-Free Solution to IBD, Celiac Disease, Autism, Cystic Fibrosis, and other ... Conditions (Healthy Living Cookbooks). Fair Winds, 2008.

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G, Poór, and Gergely P, eds. Miscellaneous inflammatory musculoskeletal conditions. [Netherland]: Elsevier, 2004.

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Gyula, Poór, and Gergely Peter, eds. Miscellaneous inflammatory musculoskeletal conditions. London: Baillière Tindall, 2004.

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F, Lioté, and Pascual E, eds. Miscellaneous non-inflammatory musculoskeletal conditions. London: Bailliè Tindall, 2003.

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Book chapters on the topic "Fibrotic and inflammatory conditions"

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Wright, Fred W. "Tracheal and Bronchial Developmental Abnormalities, and Inflammatory Diseases including Bronchiectasis, Cystic Fibrosis and Bronchiolitis." In Radiology of the Chest and Related Conditions, 103–36. London: CRC Press, 2022. http://dx.doi.org/10.4324/9780429272967-3.

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Order, Stanley E., and Sarah S. Donaldson. "Inflammatory Conditions." In Radiation Therapy of Benign Diseases, 176–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-58719-1_61.

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Caldarelli, Massimo. "Inflammatory Conditions." In Principles of Pediatric Neurosurgery, 216–26. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2800-4_16.

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Daróczy, Judit. "Inflammatory Conditions." In The Dermal Lymphatic Capillaries, 87–99. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73480-9_12.

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Ibba-Manneschi, Lidia, Irene Rosa, and Mirko Manetti. "Telocytes in Chronic Inflammatory and Fibrotic Diseases." In Advances in Experimental Medicine and Biology, 51–76. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-10-1061-3_4.

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Owens, Scott R., and Henry D. Appelman. "Noninfectious Inflammatory Conditions." In Atlas of Esophagus and Stomach Pathology, 17–25. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8084-6_3.

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Oliveira, Margarida Alexandre, and Anna Ciechomska. "Inflammatory Allied Conditions." In Musculoskeletal Ultrasonography in Rheumatic Diseases, 271–313. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15723-8_12.

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Ansell, I. D. "Prostate — Inflammatory Conditions." In Atlas of Male Reproductive Pathology, 69–72. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-4868-6_15.

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Ansell, I. D. "Testis — Inflammatory Conditions." In Atlas of Male Reproductive Pathology, 45–48. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-4868-6_9.

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Rogler, Gerhard. "Challenges of Translation of Anti-Fibrotic Therapies into Clinical Practice in IBD." In Fibrostenotic Inflammatory Bowel Disease, 295–305. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-90578-5_20.

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Conference papers on the topic "Fibrotic and inflammatory conditions"

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Kapnisis, Konstantinos, Dina Halwani, Brigitta Brott, Jack Lemons, Peter Anderson, and Andreas Anayiotos. "Stent Overlapping and Geometric Curvature Influence the Structural Integrity and Surface Characteristics of Coronary Stents." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80231.

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A common clinical practice in interventional procedures, is the deployment of two or more overlapping stents, especially in areas of branches and bifurcations where the stenotic area is diffuse and cannot be covered by a single stent or in the cases of treating long or recurrent lesions. However, complex in vivo conditions such as vessel tortuousity, high curvature, vascular wall stresses as well as blood flow wall shear stresses and diffuse calcification, may cause additional interactions within overlapping stents resulting in enhanced surface damage and fracture of stents. Preliminary studies have revealed that some stents undergo corrosion and fatigue-induced fracture in vivo, with significant release of metallic ions into surrounding tissues. A direct link between corrosion and in-stent restenosis has not been clearly established; nonetheless in vitro studies have shown that relatively high concentrations of heavy metal ions can stimulate both inflammatory and fibrotic reactions, which are the main steps in the process of restenosis. This study presents the outcome of in vitro accelerated biomechanical testing of Nitinol stents placed in mock arteries in single and overlapping configurations with various degrees of curvature. The effect of overlapping dissimilar materials was also investigated by testing multiple alloy stent combinations combining NiTi with CoCr or SS stents.
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Dudas, Paul L., Fang Teng, Karen I. Becker, Patrick F. Wilkinson, Jennifer L. Luongo, Anuk M. Das, and Francis X. Farrell. "Interleukin-1± Pulmonary Pro-Inflammatory / Pro-Fibrotic Activity." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3530.

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Kamoun, S., N. Khalil, K. A. Johannson, V. Marcoux, M. R. J. Kolb, J. H. Fisher, H. Manganas, C. J. Ryerson, and D. Assayag. "Progressive Fibrotic Interstitial Lung Disease in Autoimmune Inflammatory Myopathy." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a2742.

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Schmidkonz, C., S. Rauber, A. Atzinger, TI Götz, A. Soare, M. Cordes, O. Prante, et al. "Disentangling inflammatory from fibrotic disease activity by fibroblast activation protein imaging." In NuklearMedizin 2021 – digital. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1726701.

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Moraes Ferreira, Renilson, Maysa A R Brandao-Rangel, Anamei Silva-Reis, Thiago G Gibson-Alves, Helida C Aquino-Santos, Victor H Souza-Palmeira, Claudio R Frison, and Rodolfo P Vieira. "Aerobic Training Improves Pulmonary and Systemic Inflammatory and Fibrotic Response in Asthmatics." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.oa2935.

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Carbajal, M. P., Z. Mark, A. Kumar, N. Daphtary, M. Aliyeva, A. Jegga, J. H. T. Bates, and V. Anathy. "The Anti-Inflammatory, Pro-Fibrotic Role of Osteopontin in Influenza A Infection." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a2619.

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Kamata, Hirofumi, Sasatomo Tasaka, Ken-ichiro Inoue, Naoki Hasegawa, Rina Takamiya, Hirohisa Takano, and Akitoshi Ishizaka. "Carbon Black Nanoparticle Enhances Bleomycin-induced Inflammatory And Fibrotic Changes In The Lung." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1960.

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Humphries, B., M. Saunders, S. Cruwys, and B. Humphries. "Inhaled NXP002 attenuates LPS-induced inflammatory and fibrotic mediator production in the rat lung." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.2955.

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Gagnon, L., M. Leduc, M. Tremblay, C. Shimbori, F. Sarra-Bournet, A. Felton, T. Yanagihara, et al. "Anti-Inflammatory/Anti-Fibrotic Compound PBI-4425 Alleviates Bleomycin- and TGF-ß1-Induced Pulmonary Fibrosis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2389.

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Dufour, A. M., M. Alvarez, S. Lemeille, M. E. Truchetet, N. C. Brembilla, and C. Chizzolini. "FRI0411 Dual pro-inflammatory and anti-fibrotic role of il-17a in systemic sclerosis skin." 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.6784.

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Reports on the topic "Fibrotic and inflammatory conditions"

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Schwartz, Bertha, Vaclav Vetvicka, Ofer Danai, and Yitzhak Hadar. Increasing the value of mushrooms as functional foods: induction of alpha and beta glucan content via novel cultivation methods. United States Department of Agriculture, January 2015. http://dx.doi.org/10.32747/2015.7600033.bard.

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During the granting period, we performed the following projects: Firstly, we differentially measured glucan content in several pleurotus mushroom strains. Mushroom polysaccharides are edible polymers that have numerous reported biological functions; the most common effects are attributed to β-glucans. In recent years, it became apparent that the less abundant α-glucans also possess potent effects in various health conditions. In our first study, we explored several Pleurotus species for their total, β and α-glucan content. Pleurotuseryngii was found to have the highest total glucan concentrations and the highest α-glucans proportion. We also found that the stalks (stipe) of the fruit body contained higher glucan content then the caps (pileus). Since mushrooms respond markedly to changes in environmental and growth conditions, we developed cultivation methods aiming to increase the levels of α and β-glucans. Using olive mill solid waste (OMSW) from three-phase olive mills in the cultivation substrate. We were able to enrich the levels mainly of α-glucans. Maximal total glucan concentrations were enhanced up to twice when the growth substrate contained 80% of OMSW compared to no OMSW. Taking together this study demonstrate that Pleurotuseryngii can serve as a potential rich source of glucans for nutritional and medicinal applications and that glucan content in mushroom fruiting bodies can be further enriched by applying OMSW into the cultivation substrate. We then compared the immune-modulating activity of glucans extracted from P. ostreatus and P. eryngii on phagocytosis of peripheral blood neutrophils, and superoxide release from HL-60 cells. The results suggest that the anti-inflammatory properties of these glucans are partially mediated through modulation of neutrophileffector functions (P. eryngiiwas more effective). Additionally, both glucans dose-dependently competed for the anti-Dectin-1 and anti-CR3 antibody binding. We then tested the putative anti-inflammatory effects of the extracted glucans in inflammatory bowel disease (IBD) using the dextran sulfate sodium (DSS)–induced model in mice. The clinical symptoms of IBD were efficiently relieved by the treatment with two different doses of the glucan from both fungi. Glucan fractions, from either P. ostreatus or P. eryngii, markedly prevented TNF-α mediated inflammation in the DSS–induced inflamed intestine. These results suggest that there are variations in glucan preparations from different fungi in their anti-inflammatory ability. In our next study, we tested the effect of glucans on lipopolysaccharide (LPS)-induced production of TNF-α. We demonstrated that glucan extracts are more effective than mill mushroom preparations. Additionally, the effectiveness of stalk-derived glucans were slightly more pronounced than of caps. Cap and stalk glucans from mill or isolated glucan competed dose-dependently with anti-Dectin-and anti-CR-3 antibodies, indicating that they contain β-glucans recognized by these receptors. Using the dextran sulfate sodium (DSS)-inflammatory bowel disease mice model, intestinal inflammatory response to the mill preparations was measured and compared to extracted glucan fractions from caps and stalks. We found that mill and glucan extracts were very effective in downregulatingIFN-γ and MIP-2 levels and that stalk-derived preparations were more effective than from caps. The tested glucans were equally effective in regulating the number of CD14/CD16 monocytes and upregulating the levels of fecal-released IgA to almost normal levels. In conclusion, the most effective glucans in ameliorating some IBD-inflammatory associated symptoms induced by DSS treatment in mice were glucan extracts prepared from the stalk of P. eryngii. These spatial distinctions may be helpful in selecting more effective specific anti-inflammatory mushrooms-derived glucans. We additionally tested the effect of glucans on lipopolysaccharide-induced production of TNF-α, which demonstrated stalk-derived glucans were more effective than of caps-derived glucans. Isolated glucans competed with anti-Dectin-1 and anti-CR3 antibodies, indicating that they contain β-glucans recognized by these receptors. In conclusion, the most effective glucans in ameliorating IBD-associated symptoms induced by DSS treatment in mice were glucan extracts prepared from the stalk of P. eryngii grown at higher concentrations of OMSW. We conclude that these stress-induced growing conditions may be helpful in selecting more effective glucans derived from edible mushrooms. Based on the findings that we could enhance glucan content in Pleurotuseryngii following cultivation of the mushrooms on a substrate containing different concentrations of olive mill solid waste (OMSW) and that these changes are directly related to the content of OMSW in the growing substrate we tested the extracted glucans in several models. Using dextran sulfate sodium (DSS)–inflammatory bowel disease (IBD) mice model, we measured the colonic inflammatory response to the different glucan preparations. We found that the histology damaging score (HDS) resulting from DSS treatment reach a value of 11.8 ± 2.3 were efficiently downregulated by treatment with the fungal extracted glucans, glucans extracted from stalks cultivated at 20% OMSWdownregulated to a HDS value of 6.4 ± 0.5 and at 80% OMSW showed the strongest effects (5.5 ± 0.6). Similar downregulatory effects were obtained for expression of various intestinal cytokines. All tested glucans were equally effective in regulating the number of CD14/CD16 monocytes from 18.2 ± 2.7 % for DSS to 6.4 ± 2.0 for DSS +glucans extracted from stalks cultivated at 50% OMSW. We finally tested glucans extracted from Pleurotuseryngii grown on a substrate containing increasing concentrations of olive mill solid waste (OMSW) contain greater glucan concentrations as a function of OMSW content. Treatment of rat Intestinal epithelial cells (IEC-6) transiently transfected with Nf-κB fused to luciferase demonstrated that glucans extracted from P. eryngii stalks grown on 80% OMSWdownregulatedTNF-α activation. Glucans from mushrooms grown on 80% OMSW exerted the most significant reducing activity of nitric oxide production in lipopolysaccharide (LPS) treated J774A.1 murine macrophages. The isolated glucans were tested in vivo using the Dextran Sodium Sulfate (DSS) induced colitis in C57Bl/6 mice and found to reduce the histology damaging score resulting from DSS treatment. Expression of various intestinal cytokines were efficiently downregulated by treatment with the fungal extracted glucans. We conclude that the stress-induced growing conditions exerted by OMSW induces production of more effective anti-inflammatory glucans in P. eryngii stalks.
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Chou, Roger, Jesse Wagner, Azrah Y. Ahmed, Ian Blazina, Erika Brodt, David I. Buckley, Tamara P. Cheney, et al. Treatments for Acute Pain: A Systematic Review. Agency for Healthcare Research and Quality (AHRQ), December 2020. http://dx.doi.org/10.23970/ahrqepccer240.

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Objectives. To evaluate the effectiveness and comparative effectiveness of opioid, nonopioid pharmacologic, and nonpharmacologic therapy in patients with specific types of acute pain, including effects on pain, function, quality of life, adverse events, and long-term use of opioids. Data sources. Electronic databases (Ovid® MEDLINE®, PsycINFO®, Embase®, the Cochrane Central Register of Controlled Trials, and the Cochrane Database of Systematic Reviews) to August 2020, reference lists, and a Federal Register notice. Review methods. Using predefined criteria and dual review, we selected randomized controlled trials (RCTs) of outpatient therapies for eight acute pain conditions: low back pain, neck pain, other musculoskeletal pain, neuropathic pain, postoperative pain following discharge, dental pain (surgical or nonsurgical), pain due to kidney stones, and pain due to sickle cell disease. Meta-analyses were conducted on pharmacologic therapy for dental pain and kidney stone pain, and likelihood of repeat or rescue medication use and adverse events. The magnitude of effects was classified as small, moderate, or large using previously defined criteria, and strength of evidence was assessed. Results. One hundred eighty-three RCTs on the comparative effectiveness of therapies for acute pain were included. Opioid therapy was probably less effective than nonsteroidal anti-inflammatory drugs (NSAIDs) for surgical dental pain and kidney stones, and might be similarly effective as NSAIDs for low back pain. Opioids and NSAIDs were more effective than acetaminophen for surgical dental pain, but opioids were less effective than acetaminophen for kidney stone pain. For postoperative pain, opioids were associated with increased likelihood of repeat or rescue analgesic use, but effects on pain intensity were inconsistent. Being prescribed an opioid for acute low back pain or postoperative pain was associated with increased likelihood of use of opioids at long-term followup versus not being prescribed, based on observational studies. Heat therapy was probably effective for acute low back pain, spinal manipulation might be effective for acute back pain with radiculopathy, acupressure might be effective for acute musculoskeletal pain, an opioid might be effective for acute neuropathic pain, massage might be effective for some types of postoperative pain, and a cervical collar or exercise might be effective for acute neck pain with radiculopathy. Most studies had methodological limitations. Effect sizes were primarily small to moderate for pain, the most commonly evaluated outcome. Opioids were associated with increased risk of short-term adverse events versus NSAIDs or acetaminophen, including any adverse event, nausea, dizziness, and somnolence. Serious adverse events were uncommon for all interventions, but studies were not designed to assess risk of overdose, opioid use disorder, or long-term harms. Evidence on how benefits or harms varied in subgroups was lacking. Conclusions. Opioid therapy was associated with decreased or similar effectiveness as an NSAID for some acute pain conditions, but with increased risk of short-term adverse events. Evidence on nonpharmacological therapies was limited, but heat therapy, spinal manipulation, massage, acupuncture, acupressure, a cervical collar, and exercise were effective for specific acute pain conditions. Research is needed to determine the comparative effectiveness of therapies for sickle cell pain, acute neuropathic pain, neck pain, and management of postoperative pain following discharge; effects of therapies for acute pain on non-pain outcomes; effects of therapies on long-term outcomes, including long-term opioid use; and how benefits and harms of therapies vary in subgroups.
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The Copper T 380 Intrauterine Device: A Summary of Scientific Data. Population Council, 1992. http://dx.doi.org/10.31899/cbr1992.1000.

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Intrauterine devices are the most widely used of all reversible contraceptive methods worldwide. Modern IUDs are among the most effective and long-acting methods of family planning and are acceptable options for many women. This monograph presents highlights of the clinical performance of the Copper T 380 over eight years, including the latest data on effectiveness, expulsions, and continuation rates. It incorporates data from Population Council and World Health Organization studies, and work by scientists at Family Health International and in several countries. Clinical studies of the three models of the Copper T 380 have provided substantial evidence of the safety, effectiveness, convenience, acceptability, and long-acting quality of this IUD. The bulk of the material in this document presents preclinical and clinical performance, including mechanisms of action, effectiveness, outcome of accidental pregnancy, rates of expulsion and ectopic pregnancy, side effects, continuation rates, return to fertility, and lactation and IUD use. There is also discussion of the data on IUD use and pelvic inflammatory disease, and the importance of performing skilled insertions under aseptic conditions.
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