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Статті в журналах з теми "Balance inflammatoire"
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Buron, F., P. Malvezzi, E. Villar, C. Chauvet, B. Janbon, L. Denis, R. Cahen, et al. "Effet du sirolimus sur la balance inflammatoire en transplantation rénale : étude sirilygre." Néphrologie & Thérapeutique 8, no. 5 (September 2012): 268. http://dx.doi.org/10.1016/j.nephro.2012.07.305.
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SAUVET, F., M. CHENNAOUI, S. BANZET, C. BOURRILHON, F. CANINI, L. BOURDON, and N. KOULMANN. "Coup de chaleur d’exercice, système cardiovasculaire et vulnérabilité systémique." Médecine et Armées Vol. 40 No. 3, Volume 40, Numéro 3 (June 1, 2012): 231–40. http://dx.doi.org/10.17184/eac.6611.
Повний текст джерелаАнотація:
L’un des problèmes posés par le coup de chaleur d’exercice réside dans la précocité des troubles neurologiques qui sont la conséquence de mécanismes pernicieux généraux et cérébraux aboutissant à un déficit de perfusion tissulaire et à une ischémie cérébrale. Au niveau général, la redistribution vasculaire et les modifications de la vasomotricité d’origine inflammatoire, favorisent l’apparition d’un collapsus vasculaire. L'ischémie cérébrale, liée à l’oedème cérébral et à l’hypoperfusion, favorise un état de déséquilibre énergétique qui s'accompagne d'une cytotoxicité, d’une inflammation locale et d'une augmentation de la production de radicaux libres qui majorent la diminution des débits sanguins. Ainsi, les modifications vasculaires observées sont liées à des réponses physiopathologies locales et générales, parfois contradictoires et complexes, qui entrent en compétition et déséquilibrent dans un sens ou dans l’autre la balance vasoconstriction/vasodilatation. Ces déséquilibres modifient les résistances vasculaires, créant des mécanismes vicieux qui favorisent la diminution de la tolérance à la chaleur. Dans ce travail, nous décrierons l’implication du système cardiovasculaire dans la diminution de la tolérance à la chaleur et la survenue d’un coup de chaleur d’exercice. Nous aborderons également les mécanismes qui augmentent la vulnérabilité individuelle et les effets des contremesures protectrices.
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Horiuchi, I., Y. Kawano, M. Minohara, and J. Kira. "Th1Th2 balance in inflammatory neurologic diseases." Journal of Neuroimmunology 90, no. 1 (September 1998): 81. http://dx.doi.org/10.1016/s0165-5728(98)91665-4.
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Adrie, Ch, and M. R. Pinsky. "The inflammatory balance in human sepsis." Intensivmedizin und Notfallmedizin 36, no. 5 (June 25, 1999): 419–28. http://dx.doi.org/10.1007/s003900050260.
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Adrie, C., and M. R. Pinsky. "The inflammatory balance in human sepsis." Intensive Care Medicine 26, no. 4 (April 26, 2000): 364–75. http://dx.doi.org/10.1007/s001340051169.
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Tedgui, A., and Z. Mallat. "Pro- and anti-inflammatory balance and atherosclerosis." Atherosclerosis 151, no. 1 (July 2000): 165. http://dx.doi.org/10.1016/s0021-9150(00)80751-0.
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Hutcheson, Jack. "Adipokines influence the inflammatory balance in autoimmunity." Cytokine 75, no. 2 (October 2015): 272–79. http://dx.doi.org/10.1016/j.cyto.2015.04.004.
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Ferrarelli, Leslie K. "New connections: Restoring immune balance." Science Signaling 13, no. 661 (December 8, 2020): eabf9854. http://dx.doi.org/10.1126/scisignal.abf9854.
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Wagener, Frank, Carine Carels, and Ditte Lundvig. "Targeting the Redox Balance in Inflammatory Skin Conditions." International Journal of Molecular Sciences 14, no. 5 (April 26, 2013): 9126–67. http://dx.doi.org/10.3390/ijms14059126.
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Esmaelzadeh, Abbas, Hassan Vosooghinia, Mohammad Reza Sheikhian, Hadi Bagheri Hosseini, Daryoush Hamidi Alamdari, Fatemeh Ahmadi, Maryam Emadzadeh, and Seyed Mahdi Pakdaman Shahri. "Pro-Oxidant Antioxidant Balance in Inflammatory Bowel Disease." International Journal of Clinical Medicine 07, no. 05 (2016): 334–41. http://dx.doi.org/10.4236/ijcm.2016.75035.
Повний текст джерелаДисертації з теми "Balance inflammatoire"
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Motta, Jean-Paul. "Rôle de la balance protéolytique dans l'immunité de la muqueuse intestinale." Toulouse 3, 2012. http://thesesups.ups-tlse.fr/1883/.
Повний текст джерелаАнотація:
Le traitement des patients atteints de Maladies Inflammatoires Chroniques de l'Intestin (MICI) représente un enjeu d'avenir. La réponse inflammatoire dans l'intestin impliquent la libération de plusieurs médiateurs, comme les protéases. Dans cette thèse, nous avons montré qu'il y avait un déséquilibre entre ces protéases et leurs inhibiteurs au cours des MICI. D'une part, les tissus coliques de ces patients libéraient davantage d'activité protéolytique en comparaison aux tissus sains. D'autre part, les patients atteints de MICI exprimaient dans la muqueuse intestinale une quantité réduite d'ARN messager de l'élafine, un inhibiteur de protéase. Nous avons donc émis l'hypothèse que l'inflammation peut être réduite en rééquilibrant cette balance grâce à l'administration d'élafine. Nous avons utilisé des souris transgéniques pour l'expression de l'élafine de façon constitutive. Puis, nous avons utilisé un virus et des bactéries lactiques pour exprimer de façon transitoire cette molécule dans le côlon. En parallèle, nous avons développé des approches in vitro pour connaître le rôle de l'élafine dans la physiologie des cellules épithéliales de l'intestin. Grâce à ces différentes approches, nous avons montré que l'élafine réduisait : les symptômes de la maladie dans différents modèles, la libération de cytokines pro-inflammatoire, l'infiltration des cellules immunitaire et restaurait l'homéostasie de l'épithélium intestinal au cours de l'inflammation. Ces résultats nous ont permis de proposer que l'utilisation d'inhibiteurs de protéases dans l'intestin au cours de l'inflammation constitue une nouvelle piste thérapeutique contre les MICITreatment of Inflammatory Bowel Disease (IBD) represents a major medical challenge. Inflammatory processes in the gut are induced by several cells and mediators. Among them, serine proteases are mediators involved in many pathways leading to inflammation in the gut. During this thesis, we have shown that serine proteases and their inhibitors were dysregulated during IBD. On one hand, colonic biopsies from IBD patients released higher amount of proteolytic activity than healthy controls did. On the other hand, the expression of elafin mRNA (i. E. A protease inhibitor) was downregulated in the mucosa of patients suffering from IBD. We have hypothesized that gut inflammation could be reduced by re-equilibrating that balance in the gut, using elafin inhibitor. We have developed several in vivo approaches to evaluate the therapeutic properties of elafin. We used transgenic mice expressing elafin constitutively, we have used recombinant viral vectors and recombinant lactic acid bacteria to express transiently elafin in the gut during colitis. We have also evaluated in vitro the role of elafin in the physiology of human intestinal epithelial cells. Using those different approaches, we have demonstrated that elafin reduced the clinical score of colitis in different models in mice, reduced the release of pro-inflammatory cytokines, reduced immune cell infiltration and also restored epithelium homeostasis during inflammation. Those results led us to think that protease inhibitors have a promising therapeutic potential for the treatment of IBD
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Tournadre, Anne. "Immunité innée, balance th1/th17 et précurseurs musculaires dans les myopathies inflammatoires." Phd thesis, Université Claude Bernard - Lyon I, 2010. http://tel.archives-ouvertes.fr/tel-00715926.
Повний текст джерелаАнотація:
Cette thèse, consacrée aux myopathies inflammatoires, démontre le rôle dans les maladies auto-immunes des Toll-like récepteurs (TLRs), véritable passerelle entre immunité innée et adaptative, et plus spécifiquement dans le muscle, le rôle fondamental de la cellule musculaire elle-même. Après une présentation globale des myopathies inflammatoires et des différents aspects immunopathologiques, la réponse immunitaire adaptative est abordée en rapportant notamment dans le muscle des myopathies inflammatoires une accumulation de cellules dendritiques matures, et la présence des lymphocytes Th1 et Th17, avec un profil prépondérant Th1. L'implication de l'immunité innée est démontrée in vivo par l'expression musculaire des TLR3 et 7, et des C-type lectin récepteurs, spécifique des myopathies inflammatoires. In vitro, l'activation de la voie TLR3 induit la production par les cellules musculaires d'IL6, de la βchémokine CCL20, contribuant au recrutement et à la différentiation des cellules dendritiques et lymphocytes T, et de l'IFNβ qui participe à la surexpression des antigènes HLA de classe I. Les mécanismes de régulation impliquent une balance cytokinique Th1 et Th17. Finalement, l'importance des précurseurs musculaires immatures est soulignée. Contrairement au tissu musculaire normal, une surexpression des antigènes HLA de classe I, des TLRs, des auto-antigènes et de l'IFNβ, par les précurseurs musculaires immatures, est caractéristique des myopathies inflammatoires. Le rôle central de ces cellules musculaires immatures à potentiel de régénération pourrait expliquer un défaut de réparation associé au processus auto-immun de destruction musculaire.
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Lorvellec, Marie. "Dialogue entre le complément C1 et l'alarmine HMGB1 dans l'inflammation." Electronic Thesis or Diss., Université Grenoble Alpes, 2024. http://www.theses.fr/2024GRALV033.
Повний текст джерелаАнотація:
La protéase C1s est un élément central dans l’initiation de la voie classique du système du complément. Elle était auparavant considérée comme ciblant exclusivement les protéines C2 et C4 dans cette cascade protéolytique. Des découvertes récentes ont cependant mis en lumière la présence de C1s libre constitutivement active dans certaines pathologies, suggérant un rôle plus large de cette protéase au-delà de l'activation du complément. Parmi les cibles non-canoniques identifiées de C1s figure la protéine HMGB1, initialement décrite comme une protéine nucléaire impliquéedans la condensation de la chromatine et l'expression des gènes. Des études récentes ont démontré que HMGB1 peut également être localisée dans différents compartiments cellulaires et qu'elle joue un rôle crucial dans l'inflammation lorsqu'elle est libérée dans le milieu extracellulaire. Ce projet de thèse avait pour objectif principal d'élucider le rôle du clivage de HMGB1 par C1s dans la modulation de la réponse inflammatoire. Nos travaux ont démontré que les fragments de digestion de HMGB1 possèdent des effets distincts de la protéine entière sur l'activation du complément et laréponse cytokinique des macrophages. Nous avons notamment confirmé que la protéine entière active la voie classique du complément lorsqu’elle est fixée à une surface et qu’elle favorise la polarisation M1 des macrophages en réponse aux LPS. En revanche, le fragment f2 est capable d'activer la voie classique du complément même lorsqu’il est en solution, tandis que le fragment f3 inhibe la sécrétion de cytokines pro-inflammatoires dans les études cellulaires. De plus, nous avons exploré l'impact de l'état d'oxydo-réduction des cystéines sur les effets de HMGB1 et de ses fragmentsen utilisant des mutants mimétiques. La digestion de HMGB1 est restreinte lorsque la protéine est sous forme disulfure, suggérant un rôle important du pont disulfure dans l’accès aux sites de digestion par C1s. Les formes redox de la protéine entière ne semblent pas affecter sa capacité à activer le complément, tandis que le fragment f2 oxydé pourrait perdre sa capacité d'activation en solution. Ces résultats révèlent que le clivage de HMGB1 par C1s agit comme un chronomètre de l’inflammation, orchestrant la réponse inflammatoire via la transition d’une phase d’amplification pro-inflammatoireà une phase de résolution. Ces découvertes ouvrent de nouvelles perspectives pour la compréhension des mécanismes complexes de l'inflammation et le développement de thérapies pour le traitement de pathologies inflammatoiresC1s protease is a central component in the initiation of the classical pathway of the complement system. It was originally believed to exclusively target proteins C2 and C4 in this proteolytic cascade. However, recent discoveries have highlighted the presence of constitutively active free C1s in certain pathologies, suggesting a broader role for this protease beyond complement activation. Among the non-canonical targets identified for C1s is the HMGB1 protein, initially described as a nuclear protein involved in chromatin condensation and gene expression.Recent studies have shown that HMGB1 can also be localized in different cellular compartments and plays a crucial role in inflammation when released into the extracellular environment. The main objective of this thesis project was to elucidate the role of C1s cleavage of HMGB1 in modulating the inflammatory response. Our work has shown that HMGB1 digestion fragments have distinct effects from the whole protein on complement activation and macrophage cytokine responses.In particular, we confirmed that the whole protein activates the classical complement pathway when bound to a surface and promotes M1 macrophage polarization in response to LPS. In contrast, fragment f2 is capable of activating the classical complement pathway, even when in solution, while fragment f3 inhibits the secretion of pro-inflammatory cytokines in cell studies. In addition, we explored the impact of cysteine redox state on the effects of HMGB1 and its fragments using mimetic mutants. HMGB1 digestion is restricted when the protein is in disulfide form, suggesting an important role of the disulfide bridge in access to the C1s digestion site. The redox forms of the whole protein do notappear to affect its ability to activate complement, while oxidized fragment f2 may lose its ability to activate it in solution. These results reveal that C1s cleavage of HMGB1 acts as an inflammation timer, orchestrating the inflammatory response through the transition from a pro-inflammatory amplification phase to a resolution phase. These findings open new perspectives for understanding the complex mechanisms of inflammation and the development of therapies for the treatment of inflammatory diseases
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Gormley, Sheena Mary Catherine. "Plasma and urinary cytokine balance and renal function during cardiac surgery." Thesis, Queen's University Belfast, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326410.
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McLean, Gavin W. "An investigation into the balance of pro- and anti-inflammatory cytokines in cardiac surgery and hip fracture surgery." Thesis, Queen's University Belfast, 2017. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.727756.
Повний текст джерелаАнотація:
The aim of this study was to investigate the balance of pro- and anti-inflammatory cytokines in patients undergoing cardiac and hip fracture surgery in relation to the development of postoperative acute kidney injury (AKI). 400 patients undergoing elective cardiac surgery and 237 patients undergoing emergency hip fracture surgery were recruited. For each patient blood and urine samples were analysed preoperatively and postoperatively to determine how cytokine balance alters in those patients who develop postoperative AKI. In both patients groups, the balance of pro- and anti-inflammatory cytokines in the blood was maintained, regardless of whether or not the patient developed postoperative AKI. This demonstrates that the underlying process responsible for AKI in these patients was not located within the systemic circulation. In the cardiac surgery patients who developed postoperative AKI, it was found that there was a local imbalance of pro- and anti-inflammatory cytokines in the urine, indicating that the pathological cause of AKI is located within the kidney. What was observed was an inadequate anti-inflammatory response to the pro-inflammatory insult of surgery, thus, leaving the kidney vulnerable to the pro- inflammatory onslaught and, subsequently renal injury. A different picture was seen in the hip fracture patients, where elevated pro- and anti-inflammatory mediators were observed preoperatively due to the trauma that occurred in sustaining the hip fracture. This showed an important finding that the hip fracture patients had been undergone cytokine preconditioning as a result of trauma, prior to surgery. In this group the cytokines behaved quite differently to the cardiac surgery group. In the absence of preconditioning, postoperative AKI is associated with an inadequate anti- inflammatory cytokine response to the pro-inflammatory rise associated with surgery. However, when preconditioning is present, the cytokine levels must be analysed more carefully with the clinical context in mind.
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Cabrera, Rojas Natalia. "Efficacité et tolérance des agents biologiques dans les rhumatismes inflammatoires à début juvénile dans les essais cliniques randomisés et les études observationnelles." Thesis, Lyon, 2019. http://www.theses.fr/2019LYSE1191/document.
Повний текст джерелаАнотація:
Les rhumatismes inflammatoires juvéniles sont des maladies chroniques débutant avant l’âge de 16 ans. Comprennent des pathologies classées dans un continuum, allant de la dérégulation de l’immunité innée à la dérégulation de l‘immunité adaptative. L’arthrite juvénile idiopathique (AJI) reste la plus fréquemment diagnostiqué. Les options thérapeutiques se sont élargies à partir des années 2000 avec le développement des thérapies ciblées, les biothérapies, associés aux traitements standard utilisés en rhumatologie pédiatrique (ex : anti-inflammatoires non stéroïdiens, corticostéroïdes, méthotrexate, et autres immunosuppresseurs). L’objectif de ce travail de thèse était d’estimer la relation bénéfice-risque des biothérapies utilisés dans les rhumatismes inflammatoires juvéniles à partir des essais cliniques randomisés (ECR) et d’explorer la tolérance à long cours à partir des essais observationnels. Premièrement, en utilisant une approche méta-analitique, les données des ECR en double aveugle contre placebo ou en ouvert dans l’AJI ont été analysées pour modéliser la relation bénéfice-risque des biothérapies avec le bénéfice net. Pour cela, l’efficacité clinique, mesuré par un score composite clinique et biologique (ACRped30), a été confronté à la tolérance clinique pendant la phase randomisée des ECR. Le critère de tolérance était la survenue d’un évènement indésirable (EI) grave (EIG). La balance bénéfice-risque reste favorable pour les biothérapies. Cependant, ces résultats sont limités par le suivi de faible durée, qui peut sous-estimer l’incidence des EI. Deuxièmement, nous avons conduit une étude observationnelle pour étudier la tolérance à moyen et long-terme des biothérapies utilisant les EI et les EIG décrits dans une base de données multicentrique rétrospective. La sécurité globale des biothérapies a été acceptable chez les enfants atteints de rhumatismes inflammatoires. Nous avons observé une variation des EIG au cours du temps et que la prescription concomitante des immunosuppresseurs a représenté un risque indépendant pour la survenue des EI. Afin d’explorer ces éléments et connaître la tolérance au long-terme, une méta-analyse des études observationnelles a été fait. Nous avons utilisé les EIG pour étudier précisément la tolérance à court et à long termeJuvenile inflammatory rheumatism is a chronic disease that begins before the age of 16. Includes conditions classified along a continuum, ranging from the deregulation of innate immunity to the deregulation of adaptive immunity. Juvenile idiopathic arthritis (JIA) remains the most frequently diagnosed disease. Therapeutic options have expanded since the 2000s with the development of targeted therapies: biological agents (BAs). They can be combined with standard treatments used in paediatric rheumatology (e.g. non-steroidal anti-inflammatory drugs, corticosteroids, methotrexate, and other immunosuppressive drugs). The objective of the work of this thesis was to model the benefit-risk balance of BAs used in JIA from randomized clinical trials (RCTs) and to explore long-term tolerance from observational trials. First, using a meta-analytical approach, the data from double-blind, placebo-controlled or open RCTs in JIA were analysed for modelling the benefit-risk balance of BAs. For this purpose, the efficacy measured by a composite clinical and biological score (ACRped30), was compared with clinical safety during the randomized phase of RCTs. Safety criterion was the occurrence of adverse events (AEs). The risk-benefit balance remains favourable for biotherapies. However, these results are limited by the short follow-up period, which may underestimate the incidence of AEs. Second, we conducted an observational study to investigate the medium- and long-term safety of biotherapies using AEs and serious AEs described in a retrospective multicentre database. The overall safety of biotherapies has been acceptable in children with inflammatory rheumatic diseases. We observed a variation in the SAEs over time and that the concomitant prescription of immunosuppressants represented an independent risk for the occurrence of AEs. In order to explore these elements and long-term safety, a meta-analysis of observational studies was conducted. We used the SAEs to study precisely the short and long-term tolerance
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Henno, Priscilla. "Dysfonctions vasculaire et bronchique dans deux modèles de bronchopathies chroniques inflammatoires chez l’homme : tabagisme et mucoviscidose. Voies de l’endothéline-1 et de la balance NOS/arginases." Thesis, Paris Est, 2010. http://www.theses.fr/2010PEST0043.
Повний текст джерелаАнотація:
L'endothélium artériel pulmonaire joue un rôle déterminant dans la régulation du tonus vasomoteur en libérant des substances vasodilatatrices et vasoconstrictrices. Toute perturbation des fonctions endothéliales entraîne une perte de l'équilibre physiologique très finement régulé entre réponse vasoconstrictrice et vasodilatatrice, avec perte conjointe du contrôle de la prolifération des cellules musculaires lisses vasculaires et de l'effet antiagrégant plaquettaire. Ces modifications conduisent à un remodelage du lit vasculaire pulmonaire avec une augmentation des résistances vasculaires parfois à l'origine d'une hypertension pulmonaire (HTP) irréversible. Le rôle de l'hypoxémie n'y est pas exclusif. Le réseau bronchique est soumis quant à lui à des agressions physiques par les particules inhalées. Celles-ci peuvent entraîner un remodelage bronchique et une perturbation du tonus bronchique et de la broncho-réactivité, dont les médiateurs peuvent être en partie partagés par la dysfonction vasculaire.Le but de ce travail était d'évaluer dans un premier temps l'existence d'une dysfonction endothéliale, en tant que précurseur potentiel d'une HTP, dans deux modèles de bronchopathies chroniques à des stades opposés de la sévérité de l'atteinte respiratoire : la mucoviscidose terminale et le tabagisme avec peu ou pas d'impact sur la fonction respiratoire.Nous avons ainsi montré à partir d'explants pulmonaires qu'une dysfonction endothéliale était fréquente au cours de la mucoviscidose au stade pré-greffe et qu'elle était au-moins en partie liée à une surexpression vasculaire pulmonaire de l'ET-1 et de ses récepteurs ET-A.Nous avons montré par ailleurs que 25% environ des sujets fumeurs à fonction respiratoire normale ou peu altérée présentaient également une telle dysfonction. Nous en avons étudié ici deux voies physiopathologiques potentielles, celle de l'ET-1 et celle qui gouverne la synthèse du NO : la balance NO Synthases (NOS)/arginases. Nous avons mis en évidence une surexpression des récepteurs ET-A de l'ET-1 chez les sujets avec dysfonction ainsi qu'une corrélation inverse entre cette expression et la réponse vasoactive à l'Acétylcholine (Ach). Par ailleurs, si le NO a entre autres un effet anti-prolifératif sur les cellules musculaires lisses, la voie des arginases - système enzymatique compétitif avec les NOS - mène quant à elle à la réparation et au remodelage. Nous avons étudié l'expression vasculaire de ces différentes enzymes ainsi que l'effet pharmacologique d'inhibiteurs des NOS ou des arginases sur la réponse vasoactive à l'Ach. Nous avons montré qu'il n'existait pas de déficit d'expression des NOS et qu'il ne semblait pas y avoir d'effet délétère des arginases dans la dysfonction endothéliale dans ce modèle.Parallèlement aux mécanismes sous-tendant le remodelage vasculaire au cours du tabagisme nous avons recherché l'existence d'une « dysfonction » bronchique chez ces fumeurs, qui pourrait précéder le remodelage bronchique qui les caractérise. La présence d'une hyperréactivité bronchique est un marqueur prédictif de remodelage des voies aériennes et de l'obstruction bronchique qui en découle. Le rôle de la balance NOS/arginases dans le contrôle du tonus bronchique est encore méconnu. Notre premier objectif était d'évaluer l'expression de cette balance enzymatique dans le tissu bronchique de ces patients et le second d'étudier les effets de l'inhibition des NOS et des arginases sur la réponse bronchoconstrictrice à l'Ach. Nous avons montré qu'une augmentation d'expression bronchique de la NOS 2 chez les fumeurs était impliquée dans la régulation du tonus bronchique et dans l'obstruction bronchique, tandis qu'une augmentation de l'activité des arginases était impliquée dans la sensibilité bronchiquePulmonary arteriel endothelium has a key role in the regulation of vascular tone by the release of dilating and constrictive mediators. Impairment of endothlium functions leads to a loss of the physiological equilibrium between vasoconstriction and vasodilation, together with the loss of vascular smooth muscle cells (SMC) proliferation. These alterations induce pulmonary vascular remodeling and elevation of vascular resistance which can lead to an irreversible pulmonary hypertension (PH). The role of hypoxemia is not exclusive. Airways are exposed to physical aggressions by inhaled particles, which can lead to bronchial remodeling and impaired bronchial tone and reactivity, the mediators of which can be partly shared by endothelial dysfunction.Our goal was to evaluate the existence of endothelial dysfunction as a precursor of PH in 2 models of chronic bronchopathy of opposite stages of disease severity: end-stage cystic fibrosis (CF) and tobacco smoking with or without impaired lung function. We showed that in end-stage CF pulmonary explants, endothelial dysfunction is frequent and that it was at least partly due to a vascular upregulation of the endothelin (ET)-1 pathway.Furthermore, approximately ¼ of smokers with normal or poorly impaired lung function also displayed a similar endothelial dysfunction. We studied therein 2 potential physiopathological pathways, that of ET-1 and that which governs nitric oxide (NO) synthesis: the NO synthases (NOS)/arginases balance. We showed an upregulation of ET-A receptor expression and an inverse correlation between this expression and the vasoactive response to acetylcholine (Ach). If NO has an anti mitogenic effect on SMC, the arginases pathway-competitive with the NOS- leads to tissue repair and remodeling.We studied the vascular expression of these enzymes and the pharmacological effect of NOS and arginases inhibitors on response to Ach. We showed that the expression of NOS was not deficient and that arginases did not seem to have a deleterious effect on endothelial function in this model.Concomitantly to these mechanisms leading to vascular remodeling, wr searched for a bronchial dysfunction in smokers which could antecede bronchial remodeling, a well known feature of tobacco smoking. Bronchial hyperresponsiveness is a predictive marker of airway remodeling and subsequent bronchial obstruction. The role of the NOS/arginases pathway in the control of bronchial tone is still unknown. We evaluated the bronchial expression of the NOS/arginases balance in smokers and the effects of NOS and arginases inhibitors on bronchoconstrictive response to Ach. We found that an upregulation of NOS2 expression in COPD patients is involved in airway tone regulation and functional airflow limitation, whereas increased arginase activity is involved in airway sensitivity
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Costa, Fernando Oliveira. "Efeito agudo da galantamina em parâmetros hemodinâmicos e autonômicos em portadores da síndrome metabólica: estudo clínico prospectivo randomizado." Universidade Nove de Julho, 2014. http://bibliotecadigital.uninove.br/handle/tede/1152.
Повний текст джерелаАнотація:
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The metabolic syndrome (MetS) consists of a combination of conditions that tend to cluster together, and increase the risk of type 2 diabetes and cardiovascular disease. The components of the metabolic syndrome include central (abdominal) obesity, elevated fasting glucose, dyslipidemia (abnormally high triglycerides and low high-density lipoprotein cholesterol), and elevated blood pressure. MetS is also associated with proinflammatory and prothrombotic states, non-alcoholic liver steatosis, obstructive sleep apnea and reproduction disorders. Although a common unifying physiopathological mechanism is not known, central obesity and inflammation play a major role in MetS and upon each of its components. The MetS has reached epidemic proportions and to date there are no proven pharmacological interventions that simultaneously target all of the components of this syndrome. Inflammation plays an important role in the pathogenesis of the MetS. Recently, it was discovered that inflammation can be regulated by neural, cholinergic mechanisms and a cholinergic drug, the acetylcholinesterase inhibitor galantamine suppresses abnormal inflammation and alleviates MetS pathologies in rodents. The fact that galantamine is an approved drug, used to treat patients with Alzheimer´s disease with a known safety profile, will facilitate its clinical application in another situations. We hypothesize that treatment of subjects with the MetS with galantamine will result in alleviation in the MetS clinical conditions and inflammation. The objective of our study was to initiate an investigation on the safety profile of galantamine in MetS patients, with special attention on autonomic, hemodynamic and cognitive parameters. A randomized, double-blind, prospective study evaluated clinical, autonomic, hemodynamic and cognitive variables of patients with MetS in two moments: before treatment (basal state) and after 28 days of treatment with galantamine 8 mg daily. There was a statistical tendency in reducing systolic blood pressure in the HRV with Finometer® in patients under galantamine (124.4 ± 4 vs 119.7 ± 3.7 mmHg, basal and 28 days values, respectively) and also a reduction in diastolic blood pressure (72.5 ± 1.3 vs 67.2 ± 1.7 mmHg, basal and 28 days values, respectively). Paradoxically, an increase in the sympathetic modulation of the heart was observed with the HRV study measuring the LF (nu) value (46.2 ± 3.8 vs 57.1 ± 3.4 basal and 28 days, respectively) and a decrease in the parasympathetic modulation HF (nu) value (53.8 ± 3.8 vs 43.0 ± 3.4, basal and 28 days, respectively). We did not observe any significant change in cognitive domains. Our conclusion is that treatment with galantamine 8 mg exhibits a safe clinical profile and can be used in MetS patients.
A síndrome metabólica consiste na combinação de condições agrupadas e aumentam o risco para diabetes tipo 2 e doença cardiovascular. Seus componentes incluem obesidade central, níveis aumentados de glicose, dislipidemia caracterizada por aumento de triglicérides e baixos níveis de HDL e aumento da pressão arterial. Também está associada a um estado proinflamatório, a um estado protrombótico, a esteatose hepática não-alcoólica, apnéia obstrutiva do sono e a desordens reprodutivas. Apesar da não determinação de um mecanismo fisiopatológico unificador, obesidade central e inflamação parecem ser centrais na síndrome metabólica e nos seus componentes individuais. A síndrome metabólica tem alcançado proporções epidêmicas universais e até o presente não há intervenção farmacológica comprovada que atue simultaneamente em todos os seus componentes. Sabe-se hoje que o processo inflamatório tem um papel importante na patogenia da síndrome. Recentemente foi evidenciado que a inflamação pode ser regulada por mecanismos neurais colinérgicos, e que a galantamina, um inibidor da acetilcolinesterase, suprime a inflamação e atua nos componentes da síndrome diminuindo a patogenia em roedores. O fato de a galantamina ser uma droga já aprovada e de perfil seguro em portadores de demência facilita seu uso em outras situações clínicas. Considerando a hipótese de que a galantamina causará melhora da inflamação e dos outros distúrbios relacionados, o objetivo deste estudo foi iniciar a investigação sobre o perfil de segurança da galantamina em pacientes com síndrome metabólica, em especial, em parâmetros hemodinâmicos, autonômicos e de cognição. Realizamos um estudo prospectivo, duplo-cego e randomizado, que avaliou os dados clínicos e os parâmetros descritos, no momento basal e após 28 dias de uso de galantanima (8mg por dia), em portadores de síndrome metabólica. Houve uma tendência à redução da PAS, avaliada batimento-a-batimento com o Finometer no grupo que usou galantamina (124,4 ± 4 vs 119,7 ± 3,7 mmHg, respectivamente basal e após 28 dias de uso, p=0,04), o mesmo ocorrendo com a PAD (72,5 ± 1,3 vs 67,2 ± 1,7, p=0,005), respectivamente basal e após 28 dias de uso). De forma paradoxal, ocorreu um aumento da atividade simpática na modulação autonômica para o coração, avaliada por meio do estudo da variabilidade da freqüência cardíaca como atestado por um valor LF (nu) (46,2 ± 3,8 vs 57,1 ± 3,4 , p=0,0005)), e redução da modulação parassimpática, representada pelo valor do HF (nu) (53,8 ± 3,8 vs 43,0 ± 3,4, p=0,0005) respectivamente basal e após 28 dias de uso. Não observamos alterações significativas nos testes que avaliam o domínio cognitivo dos indivíduos. Concluímos que a dose utilizada de galantamina tem um perfil de segurança clínica que permite expandir seu uso em pacientes portadores de síndrome metabólica.
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Werncke, Daíse. "Relação entre restrição nutricional e acidose ruminal com as alterações na produção e composição do leite." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2017. http://hdl.handle.net/10183/163326.
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O estudo consistiu de dois experimentos com o objetivo de avaliar os efeitos da acidose ruminal e restrição nutricional na ocorrência de processos inflamatórios nos animais e relacionar com as alterações na produção e composição do leite. Foram utilizadas doze vacas Holandês e Mestiças Holandês Jersey. Experimento 1: Na fase de adaptação, os animais receberam uma dieta formulada para atender 100% das necessidades nutricionais de energia e proteína. Na indução foi administrada uma dieta com restrição de 50% das necessidades em energia e proteína. Na recuperação os animais receberam uma das três dietas experimentais, para recuperar a estabilidade do leite: (1) suprimento somente de energia; (2) suprimento somente de proteína; (3) suprimento de energia e proteína. A restrição nutricional em energia e/ou proteína afeta negativamente a produção de leite, o peso vivo e o escore de condição corporal. Além de reduzir a eficiência de utilização de proteína da dieta e provocar uma maior instabilidade do leite ao teste do álcool. Entretanto, não altera o perfil sanguíneo e metabólico. Experimento 2: Os animais foram divididos em dois grupos (1) controle e (2) acidose. O delineamento experimental foi reversível simples com dois tratamentos e dois períodos experimentais. Foram analisados parâmetros referente às características físico-quimica, saúde da glândula mamária, medidas fisiológica, perfil metabólico e parâmetros sanguíneos. A indução da acidose ruminal subaguda (SARA) causou redução da produção e estabilidade do leite ao teste do álcool, pH urinário, pH fecal, pH ruminal. Entretanto, a indução a SARA não alterou os parâmetros sanguíneos avaliados. A SARA altera as características físico-químicas do leite, sem influenciar nas concentrações proteínas de fase aguda, caracterizando uma resposta inflamatória. A SARA pode acometer os animais sem apresentar mudanças no perfil sanguíneo dos mesmos.The study consisted of two experiments with the aim of evaluating the effects of ruminal acidosis and nutritional restriction on the occurrence of inflammatory processes in animals and correlate with changes in milk production and composition. Twelve Holstein and cross bred Holstein and Jersey cows were used. In the first study, in the adaptation phase, the animals received a diet formulated to supply 100% of the nutritional needs of energy and protein. In the induction, a diet composed by 50% restriction of energy and protein requirements was administered. In the recuperation, the animals received one of the three experimental diets to recover milk stability: (1) only energy supply; (2) supply only of protein; (3) supply of energy and protein. The nutritional restriction in energy and / or protein can affects negatively milk production, weight and condition score body. In addition to reduce the efficiency of protein utilization of the diet and cause greater instability of the milk to the alcohol test. However, it does not changed the blood and metabolic profile. In second study, the animals were divided into two groups (1) control and (2) acidosis. The experimental design was simple reversible with two treatments and two experimental periods. Physiochemical characteristics, health of the mammary gland, physiological measures, metabolic profile and blood parameters were analyzed. Losses in milk production, reduction of alcohol stability test, urinary pH, fecal pH, ruminal pH were caused by Subacute ruminal acidosis (SARA) induction. However, induction of SARA did not changed the blood parameters evaluated. SARA changes the physical-chemical characteristics of the milk, without influencing the acute phase proteins concentrations, characterizing an inflammatory response. SARA can affect the animals without demostrate changes in the blood profile of the animals.
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Bäck, Christer Matthias [Verfasser], Uwe [Akademischer Betreuer] Conrath, and Frank [Akademischer Betreuer] Tacke. "MCP-1 dependent balance of inflammatory pathways and interplay of immune cells in the liver during injury, fibrosis and injury regression : unterschiedliche MCP-1-abhängige Entzündungsmechanismen und Interaktionen von Immunzellen in der Leber / Christer Matthias Bäck ; Uwe Conrath, Frank Tacke." Aachen : Universitätsbibliothek der RWTH Aachen, 2015. http://d-nb.info/1129787419/34.
Повний текст джерелаКниги з теми "Balance inflammatoire"
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Farmer, Jenna. Managing IBD: A Balanced Guide to Inflammatory Bowel Disease. Hammersmith Health Books, 2017.
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Lundin, Mia, and Ulrika Davidsson. Hormone Balance Cookbook: 60 Anti-Inflammatory Recipes to Regulate Hormonal Balance, Lose Weight, and Improve Brain Function. Skyhorse Publishing Company, Incorporated, 2018.
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The hormone balance cookbook: 60 anti-inflammatory recipes to regulate hormonal balance, lose weight, and improve brain function. 2018.
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Holmes, Aubree, Carla Choy, and Alyssa Yuhas. Way We Eat: Finding Balance and Nourishment Through Delicious Anti-Inflammatory Cooking. Aubree Holmes, LLC, 2024.
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Günşen, Uğur, and Ramazan Mert Atan. Role of Nutrition in Providing Pro-/Anti-Inflammatory Balance: Emerging Research and Opportunities. IGI Global, 2020.
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Atan, Ramazan Mert, and Uğur Günşen. Role of Nutrition in Providing Pro-/Anti-Inflammatory Balance: Emerging Research and Opportunities. IGI Global, 2020.
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Günşen, Uğur, and Ramazan Mert Atan. Role of Nutrition in Providing Pro-/Anti-Inflammatory Balance: Emerging Research and Opportunities. IGI Global, 2020.
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Atan, Ramazan Mert, and Uğur Günşen. Role of Nutrition in Providing Pro-/Anti-Inflammatory Balance: Emerging Research and Opportunities. IGI Global, 2020.
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Senger, Lillian. New Anti-Inflammatory Cookbook 2022: Recipes to Lose Weight, Balance Hormones and Reverse Disease. Independently Published, 2022.
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Maclachlan, Rosie. Complete Anti-Inflammatory Cookbook: 498 Quick and Simple Anti-Inflammatory Recipes, Reduce Inflammation, Balance Hormones and Lose Weight. Including 28-Days Meal Plan. Independently Published, 2022.
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Kang, Melissa, and Temitope O. Keku. "Single Nucleotide Polymorphisms in Obesity and Inflammatory Genes in African Americans with Colorectal Cancer." In Impact of Energy Balance on Cancer Disparities, 131–63. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-06103-0_7.
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Vetter, Douglas E., and Kathleen T. Yee. "Corticotropin Releasing Factor Signaling in the Mammalian Cochlea: An Integrative Niche for Cochlear Homeostatic Balance Against Noise." In Inflammatory Mechanisms in Mediating Hearing Loss, 31–60. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-92507-3_3.
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Al Marmour, Doha. "The Medicinal Importance of the Indian Spice Plant, Curry Leaves Murraya Koenigii." In Medicinal Spices, 143–52. Istanbul: Nobel Tip Kitabevleri, 2024. http://dx.doi.org/10.69860/nobel.9786053359340.9.
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The medicinal significance of curry leaf, an Indian spice plant, is often studied in traditional Indian medicine and modern scientific research. Also known as Curry leaf, Murraya koenigii, the leaves of this plant contain antioxidants, anti-inflammatory compounds and a number of vitamins and minerals. These leaves contain active compounds that may improve the digestive system, balance blood sugar levels, lower cholesterol, and even have anti-cancer properties. Additionally, curry leaves are known to be beneficial for hair health.
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Gunes Kocinkag, Vezire, and Muhammed Kocinkag. "Medical Use of Cardamom (Elettaria Cardamomum L.)." In Medicinal Spices, 239–46. Istanbul: Nobel Tip Kitabevleri, 2024. http://dx.doi.org/10.69860/nobel.9786053359340.15.
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Cardamom (Elettaria cardamomum L.) is a spice that is widely used especially in Asian cuisine and is also valuable for medicinal purposes. Thanks to the active ingredients it contains, Cardamom supports digestive health and can relieve stomach discomfort. Additionally, it has antioxidant properties and can reduce inflammation, thus having anti-inflammatory effects. Some research shows that cardamom has the ability to balance blood sugar levels, suggesting it may play a potential role in diabetes management. Additionally, cardamom has antimicrobial properties and can therefore be used to support oral health.
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Konsman, Jan Pieter, and Rainer H. Straub. "Energy Balance and Neuroendocrine-Immune Regulation in Chronic Inflammatory and Neoplastic Diseases: An Evolutionary Perspective." In Masterclass in Neuroendocrinology, 323–42. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-21358-8_13.
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Tahseen, Rabia, Mohammad Parvez, G. Sravan Kumar, and Parveen Jahan. "Prognostic Importance of Th1:Th2 (IL-1β/IL-10) Cytokine Ratio in Adult Onset-Bronchial Asthma." In Proceedings of the Conference BioSangam 2022: Emerging Trends in Biotechnology (BIOSANGAM 2022), 176–87. Dordrecht: Atlantis Press International BV, 2022. http://dx.doi.org/10.2991/978-94-6463-020-6_18.
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AbstractBronchial asthma is a complex respiratory disorder, exhibits several endotypes and phenotypes due to different underlying cellular and molecular mechanisms. Globally it affects 300 million individuals, with the prevalence of 2–3% in India, contributing to morbidity and mortality. Over 50 cytokines have been identified in asthma. The dysregulation in Th1 and Th2 cytokines is implicated in the patho-mechanism of pulmonary inflammation and airway remodeling. The aim of the current study was to access the circulating levels of IL-1β (pro-inflammatory) and IL-10 (anti-inflammatory) cytokines using sandwich enzyme-linked immunosorbent assay (ELISA). In this case-control study we recruited a total of 164 subjects (104 adult onset asthma patients and 60 non-asthmatic healthy controls) from south India. Data exhibited increased levels of IL-1β and decreased levels of IL-10 in asthma patients compared to the healthy controls. Subgroup analysis revealed significant elevation in the circulating levels of IL-1β and Th1:Th2 (IL-1β/IL-10) ratio in patients with uncontrolled and long-standing disease (>10 years). Receiver operating curve analysis of individual cytokines and ratios showed good and excellent discriminating capacity respectively for health vs disease and controlled vs uncontrolled. However, IL-1β showed better incisive capacity for disease duration. Based on our observation it appears that rather than individual cytokine(s), the balance between pro and anti-inflammatory cytokines are crucial in the patho-mechanism of asthma. However, developing a signature profile of multiple cytokines using cut-off values may prove to be more promising for diagnostic, prognostic and therapeutic purposes of bronchial asthma.
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Batu, Ozlem. "Oxytocin." In Brain Biochemistry and Its Disease, 23–38. Istanbul: Nobel Tip Kitabevleri, 2024. http://dx.doi.org/10.69860/nobel.9786053359371.2.
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Oxytocin is a peptide hormone secreted from the posterior pituitary. Its best-known function is to increase milk secretion in breastfeeding women. It can be used pharmacologically to induce uterine contractions and sustain labour. However, it is thought that its contribution to birth is minimal at physiologically normal blood levels. This hormone, which acts as a neurotransmitter in the central nervous system, is also effective in regulating blood circulation. It balances the mood and is important in regulating behaviour in different emotional states. It helps to experience positive emotions. It has anti-inflammatory properties and this feature also increases the healing speed of wounds on the body. It reduces stress by lowering cortisol levels. It increases the pain threshold. It enables socialisation and prevents falling into an introverted mood. It increases sexual arousal and it makes it easier to empathize. Oxytocin is no longer the simple "love hormone" and, like many other hormones, has complex interactions with human health and behaviour. Although good progress has been made, much more research is needed to understand the effects of oxytocin fully.
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Cetik Yildiz, Songul. "Brain and Oxidative Stress." In Brain Biochemistry and Its Disease, 149–65. Istanbul: Nobel Tip Kitabevleri, 2024. http://dx.doi.org/10.69860/nobel.9786053359371.9.
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Brain tissue is more sensitive to oxidative damage due to many different properties than other tissues. So, the need for protection of brain tissue, which is more prone to oxidative damage than other tissues and organs, is greater than other tissues. Oxidative stress is brought on by a disturbance in the balance between antioxidants and free radicals, which have a scavenging effect on them in biological systems. Increased ROS causes cell damage by causing damage to cell membranes, deterioration in the structure and functions of intracellular proteins, and structural damage to DNA. Oxidative stress is responsible for the pathogenesis of many diseases, especially cancer, diabetes, neurological and cardiovascular diseases, atherosclerosis and inflammatory disorders. Brain tissue is prone to free radical damage because it produces more toxic radicals than other organs. Because the brain has a poorer antioxidant defense system and a higher oxidative metabolism than other organs, it is more vulnerable to ROS-induced damage that can lead to neuronal death. Regional differences in antioxidant system activities and variable metabolic rates in brain tissue may also cause regional accumulation of oxidative damage. In the light of this information, it is aimed to evaluate oxidative stress, the mechanism of oxidative stress formation and the mechanisms of action of oxidative stress on the brain, its effects on intracellular structures and the destruction products formed in oxidative stress with the results of biochemical studies.
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Nasa, Prashant, Rajesh Kumar, Deven Juneja, and Supradip Gosh. "The Case for Albumin as Volume Expander and beyond." In Rational Use of Intravenous Fluids in Critically Ill Patients, 227–42. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-42205-8_10.
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AbstractThis chapter discusses the importance of endogenous albumin, the most abundant plasma protein in the body. Albumin has diverse functions such as antioxidant, anti-inflammatory activities, intravascular buffering, drug metabolism, transport, distribution, and restoration of vascular endothelial integrity. It is also crucial for maintaining the endothelial glycocalyx layer in blood vessels. Critically ill patients may experience hypoalbuminemia, defined as serum albumin <35 g/L, due to reduced synthesis, malnutrition, increased loss, or increased catabolism. Observational studies show hypoalbuminemia as an independent predictor of worse outcomes, with a 10 g/L decrease in serum albumin linked to a higher risk of mortality, morbidity, longer ICU/hospital stays, and increased resource utilisation. Administering exogenous albumin targeting serum albumin >30 g/L may reduce complications, but further trials are needed. Exogenous albumin is used in the ICU for various indications, including resuscitation and deresuscitation. Evidence on its use as a plasma expander is inconclusive. Both high- (20%) and low-concentration (4 and 5%) albumin can be used for resuscitation if patients require additional fluid, despite receiving crystalloids. Albumin is safe and effective for plasma expansion in patients with sepsis and septic shock but should be avoided in traumatic brain injury. Judicious and vigilant use of albumin is recommended due to its cost and potential risks. Albumin administration should be based on clinical indications, and monitoring fluid balance and clinical parameters is critical to prevent fluid accumulation and oedema formation.
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Hatipoglu, Abdulkerim. "Brain and Nutrition." In Brain Biochemistry and Its Disease, 109–30. Istanbul: Nobel Tip Kitabevleri, 2024. http://dx.doi.org/10.69860/nobel.9786053359371.7.
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In the current section, the functions of nutrients such as polyunsaturated fatty acids (PUFAs), B group vitamins, calcium, zinc, iron, magnesium in the brain and the effect of diet on neurodegenerative diseases such as Alzheimer’s, Parkinson’s, Amyotrophic Lateral Sclerosis and Multiple Sclerosis are discussed. PUFAs (Linoleic acid, α-Linoleic acid, eicosapentaenoic acid and docosahexaenoic acid), which maintain membrane fluidity necessary for synaptic vesicle fusion and neurotransmitter transmission within neural networks, are essential components of neuronal cell membranes. In older brains, there is a deficiency in PUFA levels in the cortex, hippocampus and cerebellum, which are associated with cognitive and motor functions. The brain has four times the amount of circulating methyltetrahydrofolate (folate) than plasma. The production of cholesterol, phospholipids, amino acids, fatty acids, steroid hormones and neurotransmitters is facilitated by pantothenic acid, which is a substrate for the synthesis of coenzyme A (CoA), which contributes to the structure and function of brain cells. Pyridoxine (vitamin B6) is a rate-limiting cofactor in the production of neurotransmitters such as dopamine, noradrenaline, serotonin, γ-aminobutyric acid (GABA) and melatonin hormone. Calcium is a very important factor in the normal functioning of neurons and the neuromuscular junction, as it transmits depolarizing impulses and contributes to synaptic activity. Since zinc is mostly stored in the hippocampus, amygdala, cortical regions and telencephalon, it has important effects on memory, cognition and emotional balance. Iron is essential due to its role in cellular metabolism, myelin production, and neurotransmitter synthesis. Magnesium is essential for controlling the activity of neurotransmitter receptors. It is known that there are significant amounts of microglial cells and activated pro-inflammatory cytokines in the postmortem brain tissue of Alzheimer’s patients, meaning that there is an important relationship between inflammation and the pathophysiology and cognitive failures of Alzheimer’s patients. Parkinson’s disease risk may be affected by dietary consumption of PUFAs and MUFAs (monounsaturated fatty acids). On the other hand, high consumption of PUFAs and vitamin E supplementation may protect against Amyotrophic Lateral Sclerosis (ALS). In Multiple Sclerosis (MS) patients with dysphagia, brain signaling defects affect respiratory muscle strength, making normal food intake difficult.
Тези доповідей конференцій з теми "Balance inflammatoire"
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Dinatt, Roberto Fontella, Bruna Zorzo Marques, Paloma Trevisan Vogel, and Lucas Cardeal de Oliveira. "Analysis of the importance of a balanced diet to prevent diseases associated with aging." In III Seven International Medical and Nursing Congress. Seven Congress, 2024. http://dx.doi.org/10.56238/iiicongressmedicalnursing-051.
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A balanced diet plays an essential role in promoting healthy aging and preventing chronic diseases associated with advancing age, such as cardiovascular disease, type 2 diabetes, osteoporosis, and neurodegenerative disorders. Adequate intake of nutrients, including vitamins, minerals, fiber, and antioxidants, contributes to maintaining health and reducing inflammatory processes and oxidative stress, key factors in the development of several pathologies. This paper reviews the scientific evidence on the importance of a balanced diet in preventing diseases related to aging and highlights the main nutritional recommendations for this population, aiming to improve the quality of life and increase the longevity of elderly individuals.
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Saber Hmimass, M., Driss Azzouzi, Mohamed Borahma, Maryeme Kadiri, Fatima Zahra Chabib, Camelia Berhili, Nawal Lagdali, and Fatima Zahra Ajana. "P319 The etiological profile of chronic disturbances of the liver balance during chronic inflammatory bowel diseases." In BSG LIVE’24, 17-20 June 2024, ICC Birmingham. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2024. http://dx.doi.org/10.1136/gutjnl-2024-bsg.401.
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Liu, Xiaoqing, Nalin Lai, Ting Cheng, Xiaojuan Mao, and LI Xiaofeng. "AB0470 IMMUNOREGULATORY THERAPY EFFECTIVELY PROMOTES THE BALANCE BETWEEN TREG CELLS AND PRO-INFLAMMATORY LYMPHOCYTES IN SYSTEMIC LUPUS ERYTHEMATOSUS." 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.2151.
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Petrović, Miloš, Radojica Đoković, Vladimir Kurćubić, Snežana Bogosavljević-Bošković, Simeon Rakonjac, and Milun Petrović. "Intracellular and extracellular Hsp70 in cows: Similarities and differences in physiological and pathophysiology conditions." In Zbornik radova 26. medunarodni kongres Mediteranske federacije za zdravlje i produkciju preživara - FeMeSPRum. Poljoprivredni fakultet Novi Sad, 2024. http://dx.doi.org/10.5937/femesprumns24025p.
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Heat shock proteins (Hsp), also called chaperones, are proteins that are indispensable for the proper formation of the polypeptide chain; and have a role in its translocation within the cell. Hsp70 in cells helps to re-establish the native conformation of proteins that have denatured under the influence of various stressogens, by preventing their aggregation, which results in protecting the cell from apoptosis and having an anti-inflammatory effect. These proteins are classified on the basis of molecular mass, and the most significant is heat shock protein 70 (Hsp70) with a molecular mass of about 70 kDa, which is designated as "a master player in protein homeostasis". The concentration of Hsp increases significantly when exposed to a stressor originating from the cell itself or from the external environment. Many chaperones are induced under the influence of high ambient temperatures, when the universal heat shock response (HSR) develops, which is why the name heat shock proteins was defined. Intracellular Hsp70 (iHsp70) shows its protective and anti-inflammatory effects. Induced iHsp70 protects the cell from apoptosis by reducing or blocking the activation of caspases, binding to apoptosis-inducing factor (AIF) and inhibiting AIF-induced chromatin condensation or preventing mitochondrial damage and nuclear fragmentation. It blocks cell morphological changes caused by tumor necrosis factor-induced apoptosis, and has been found to aid in cell repair of damage caused by inflammation. The anti-inflammatory effect of iHsp70 is reflected in the fact that it inhibits the response to lipopolysaccharides and blocks the production of inflammatory mediators such as tumor necrosis factor Alpha (TNF-a), and other mechanisms have been described. he expression of the gene for the production of Hsp70 has been well studied in ruminants or their cell cultures exposed to high ambient temperatures, and the multiple increase of iHsp70 in the cells results in a better adaptation to heat stress. The study of eHsp70 has become relevant due to the availability of diagnostic kits for determining its concentration, and the latest results show that it is a very useful predictor of mortality in patients with septic shock. Hsp70 moves to the extracellular space in several ways: after leaving necrotic cells, under the action of various stress factors and inflammation in undamaged cells, it can be produced in the liver as an acute phase protein, and transport by exosomes and direct contact with the lipid membrane of cells have also been described. The pro-inflammatory effect of eHsp70 is realized by inducing immune cells, which further induces the secretion of inflammatory cytokines (TNF-a, IL-1b, IL-6), inducible nitric oxide synthase (iNOS) expression and nuclear translocation of nuclear factor-cB (NF-cB). According to the chaperone balance theory, the higher the value of eHsp70 compared to iHsp70, the more pronounced its proinflammatory effects. This hypothesis was also confirmed in dairy cows in the periparturient period.
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Balajadia, Januaria M., Lori Shimoda, William Greineisen, and Helen Turner. "Abstract 2884: ER stress and autophagy induced in pro-inflammatory mast cells exposed to stimuli associated with a positive energy balance." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-2884.
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Nakstad, Britt, and Torstein Lyberg. "LOCAL ACTIVATION OF COAGULATION AND FIBRINOLYSIS IN LUNG DISEASE IS REFLECTED IN BR0NCH0ALVE0LAR LAVAGE FLUID." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643054.
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Fibrin deposition in the alveolar space and the lung interstitium is a prominent feature of many types of pulmonary inflammatory diseases.Ce11s of the monocyte/ macrophage lineage have a dualistic role in the balance between coagulation and fibrinolysis having the ability to synthesize both procoagulant factors and plasminogen activators. In the present studies bronchoa1veo1 ar lavage were performed on 128 patients with various lung diseases and 29 healthy controls.Both lung alveolar macrophages (LAM) and the supernatant bronchoalveolar lavage fluid (BALF) expressed two types of procoagulant activities a)thromboplastin and b) a direct factor X activator.The procoagulant in BALF was associated with membrane vesicles which sedimented at 100000g,lh.By electron microscopy the BALF ultrasediment was seen to consist for a large part of membrane material and this was confirmed by monitoring the content of different marker enzymes for specific subcellular structures. LAM from patients had significantly higher specific thromboplastin activity than LAM from controls (4,36 -0.98(SEM)vs.0.81± 0.14 U/mg cell protein).BALF collected from patients had significantly higher levels than BALF from controls of a ) thrombop1 astin(0.66-0.18vs.0.07 ±0.01 U/ml) b ) factor VII activity(1.33±0.31vs.0.48±0.06 U/ml) c)fibrin degradation products(presentin 28,7vs.0% of the cases) and d) fibronectin(491±103 vs.35±5 ng/ml ) In addition,the level of plasminogen activator was higher in controls than in patients(294±68 vs.!02±14 m U/m1).These studies show that activation products of the coagulation and fibrinolytic systems can be detected in BALF and that lung disease often is associated with abberations in the balance between these systems.Fibrin serves as a substrate for fibronectin and the increases in lavage fibronectin may reflect the development of lung fibrosis.
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Muhammad, Shayma, Suhaila Darogha, and Ahmed A Al-Naqsbbandi. "Association of IL-18 Promoter -607 C/A Polymorphism with Severity of Covid-19 in Kurdish Patients." In 5th International Conference on Biomedical and Health Sciences. Cihan University-Erbil, 2024. http://dx.doi.org/10.24086/biohs2024/paper.1448.
Повний текст джерелаАнотація:
Coronavirus disease 2019 is a viral infection that throws the immune system out of balance, sets off an inflammatory cytokine storm, and has the potential to drastically alter the makeup of immune cells in circulation. Methods: In order to estimate serum IL-18 levels and genotyped SNPs in IL-18 using the ARMS-PCR technique, a case-control research including 210 Kurdish Covid-19 patients visiting three hospitals in Erbil-city and 70 healthy controls was carried out from July to December 2021. Based on their symptoms, the patients who were recruited in this research were classified into three groups: mild, moderate, and severe. Results: The study results indicated that most Covid-19 patients were 51 years and older (60%). With respect to gender, women were more affected than male (53% vs. 47%). When compared to healthy controls, the median level of IL-18 in the blood of patients in the Covid-19 group was considerably higher. The group with severe symptoms exhibited the greatest level. The primary findings also showed that homozygous for strongly displayed CC was protected against Covid-19 severity, but heterozygous CA showed an elevated risk for Covid-19 severity. Conclusion: there is a substantial correlation between the severity of Covid-19 and elevated blood levels of IL-18. Additionally, heterozygous CA genotype at the IL-18 -607 position was positively correlated with Covid-19 patients.
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Sazdova, Lyubomira. "ASPECTS OF PHYSIOTHERAPY AFTER NONOPERATIVE TREATMENT OF LATERAL ANKLE SPRAIN." In INTERNATIONAL SCIENTIFIC CONGRESS “APPLIED SPORTS SCIENCES”. Scientific Publishing House NSA Press, 2022. http://dx.doi.org/10.37393/icass2022/148.
Повний текст джерелаАнотація:
ABSTRACT Introduction: Lateral ankle sprain is a common injury and, if not treated properly, could result in chronic ankle pain and instability. Well-structured and timely applied appropriate physiotherapy program is of great importance for the purpose of good functional recovery. The study aims to outline the main aspects of physiotherapy after nonoperative treatment of lateral ankle sprain and to assess its effectiveness on the functional outcome in patients with this kind of injury. Material and methods: The study was conducted on seven patients undergoing nonoperative treatment with an acute lateral ankle sprain. Depending on the phases of the soft tissue regeneration, the physiotherapeutic program included specialized manual techniques and exercises for controlling inflammatory process, stress to collagen fibers for proper orientation along the stress lines, restoring ROM, reactivation of the fibular muscles, training of the dynamic stabilization and improvement of the muscle strength, progressive neuromuscular, proprioceptive and postural control training, as well as return to recreational and sport-specific training. The functional outcome was assessed by Foot and Ankle Disability Index, Y balance test, and One-leg stance test. Results: The results of the conducted functional tests at the latest follow-up showed statistically significant improvement in all of the studied indicators, but some deficit in proprioception and the dynamic stabilization still persists. To achieve optimal functional results, the implementation of the supervised physiotherapeutic program should continue. Conclusion: Early mobilization after lateral ankle sprain and an individualized physiotherapeutic program could reduce the deficit in proprioception, muscular imbalance and impaired neuromuscular control, and the risk of recurrent sprain.
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Ueno, Augusto Yoshiro, Ivo Emilio da Cruz Jung, Ivana Beatrice Mânica da Cruz, and Fernanda Barbisan. "Depression and psychological distress in elders are influenced by the antioxidant enzyme SOD2." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.003.
Повний текст джерелаАнотація:
Introduction: Depression and psychological stress have high prevalence and incidence rates, affecting the individual welfare and increasing the risks for non-infectious chronic diseases. Studies have shown relations between inflammation and oxidative stress. In genetics, the single nucleotide polymorphism (SNP), inside the superoxide dismutase gene (Val16Ala-SOD2), is an important study subject to comprehend the risks of developing depression because its different genotypes can impact the balance between superoxide and hydrogen peroxide. The genotype VV favors the superoxide, the AA favors the peroxide and the AV generates similar amounts. Objectives: Evaluate the relation between oxidative unbalance, generated by Val16Ala-SOD2 SNP, and the rates of depression in elders. Methods: The study, approved by the ethics committee of UFSM, was a case-control analysis to examine the association between Val16Ala-SOD2 SNP, depression and stress in elders. Genetical analysis was made by polymerase chain reactions. The sample had 612 elders from Gravataí (RS). Depression was diagnosed using the geriatric depression scale- 15 and the stress by self perception. Statistical analysis was made by SSPS. Results: From the 612 elders (with similar ages and lifestyles), 115 were diagnosed with depression; the other 497 composed the control group. The analyses showed significantly higher frequency of the genotype VV in those who had depression, compared with the allele A. Conclusion: The results indicate strong association of the Val16Ala-SOD2 SNP, the risks of depression and psychological stress, probably due to the increasing oxidative stress and inflammatory state associated with the recessive genotype, VV.
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Ahmed, Saad, Zackary Harris, and Russell David Levi. "Relationship Between Gut Microbiota and Dementia." In 28th Annual Rowan-Virtua Research Day. Rowan University Libraries, 2024. http://dx.doi.org/10.31986/issn.2689-0690_rdw.stratford_research_day.90_2024.
Повний текст джерелаАнотація:
This paper explores the complex relationship between gut microbiota, dietary habits, and dementia, focusing particularly on Alzheimer's disease (AD). Growing evidence suggests a significant link between the composition of gut bacteria, dietary choices, and susceptibility to dementia. Notably, individuals with dementia demonstrate a noticeable reduction in gut bacteria diversity, highlighting the crucial role of a balanced microbiome in maintaining cognitive health. Conversely, dietary preferences characterized by excessive consumption of processed foods and sugars are associated with an increased risk of dementia, emphasizing the critical influence of diet on shaping gut microbiota and subsequent neurocognitive outcomes. Importantly, dietary interventions featuring a diverse range of fiber and fermented foods emerge as promising strategies for reducing dementia risk, creating an optimal gut environment conducive to the production of anti-inflammatory agents and short-chain fatty acids. While ongoing research continues to elucidate the intricate mechanisms governing the gut-brain axis, current evidence underscores the importance of dietary modifications as a fundamental approach in dementia prevention and management. Specifically, adherence to dietary patterns resembling the Mediterranean diet or emphasizing high-fiber intake holds significant potential in alleviating the burden of dementia. Through a comprehensive examination of existing literature, this study provides valuable insights into the complex interplay between gut microbiota, dietary influences, and dementia risk, laying the groundwork for future medical interventions aimed at preserving cognitive function and mitigating the impact of dementia.
Звіти організацій з теми "Balance inflammatoire"
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Liu, Yangjun, Wei Xie, Zbigniew Ossowski, Juan Li, Juan Yang, Yiming Luo, Xia Wu, and Liying Liu. Physical activity, abdominal obesity and inflammatory response in the elderly: a systematic review and meta-analysis of randomized-controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2023. http://dx.doi.org/10.37766/inplasy2023.3.0051.
Повний текст джерелаАнотація:
Review question / Objective: The purpose of this study was to explore the effects of physical activity (i.e., type of exercise, FITT criteria, control group, other interventions) on abdominal obesity and inflammatory response in elderly? The study method was a randomized controlled trial. Condition being studied: An increasing number of studies have demonstrated that chronic inflammation is closely associated with the initiation and progression of a broad range of age-related diseases, such as cardiovascular disease, cancer, diabetes, Alzheimer’s disease, and other neurodegenerative diseases and is an independent risk factor for mortality in healthy adults. Moreover, there is strong evidence that the development of age-related diseases is linked to low-grade elevation of circulating inflammatory mediators. Therefore, future interventional researches should focus on preserving overall homeostatic balance and controlling inflammatory status in the aging patient.