Bibliografie tematiche / Inflammation de bas grade

Letteratura scientifica selezionata sul tema "Inflammation de bas grade"

Autore: Grafiati

Pubblicato: 8 giugno 2024

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Articoli di riviste sul tema "Inflammation de bas grade":

Yoo, Ji Youn, Sarah Sniffen, Kyle Craig McGill Percy, Veera Bramhachari Pallaval e Bojjibabu Chidipi. "Gut Dysbiosis and Immune System in Atherosclerotic Cardiovascular Disease (ACVD)". Microorganisms 10, n. 1 (5 gennaio 2022): 108. http://dx.doi.org/10.3390/microorganisms10010108.

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Atherosclerosis is a leading cause of cardiovascular disease and mortality worldwide. Alterations in the gut microbiota composition, known as gut dysbiosis, have been shown to contribute to atherosclerotic cardiovascular disease (ACVD) development through several pathways. Disruptions in gut homeostasis are associated with activation of immune processes and systemic inflammation. The gut microbiota produces several metabolic products, such as trimethylamine (TMA), which is used to produce the proatherogenic metabolite trimethylamine-N-oxide (TMAO). Short-chain fatty acids (SCFAs), including acetate, butyrate, and propionate, and certain bile acids (BAs) produced by the gut microbiota lead to inflammation resolution and decrease atherogenesis. Chronic low-grade inflammation is associated with common risk factors for atherosclerosis, including metabolic syndrome, type 2 diabetes mellitus (T2DM), and obesity. Novel strategies for reducing ACVD include the use of nutraceuticals such as resveratrol, modification of glucagon-like peptide 1 (GLP-1) levels, supplementation with probiotics, and administration of prebiotic SCFAs and BAs. Investigation into the relationship between the gut microbiota, and its metabolites, and the host immune system could reveal promising insights into ACVD development, prognostic factors, and treatments.

Remmel, Paul, e Valérie Freiche. "Entéropathies chroniques du chat, quelles spécificités ?" Le Nouveau Praticien Vétérinaire canine & féline 19 (dicembre 2022): 60–67. http://dx.doi.org/10.1051/npvcafe/2023010.

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Les entéropathies du chat sont des affections fréquentes dont l’origine peut être infectieuse, alimentaire, dysimmunitaire ou tumorale. Leur présentation est très équivoque et dans de nombreux cas, les signes cliniques orientent vers une atteinte diffuse entérocolique. La précision des signes cliniques reste cependant déterminante dans le choix des examens complémentaires. Les chats jeunes avec des signes cliniques modérés sont le plus souvent atteints par des protozoaires ou par des troubles de la tolérance alimentaire. En présence de diarrhée, une parasitose doit être recherchée par coproscopie sur 3 prélèvements successifs et PCR tritrichomonas. La fibroplasie sclérosante éosinophilique féline est une entité récemment décrite. Elle affecte aussi les jeunes adultes et peut être suspectée lors d’éosinophilie périphérique ou de masse digestive. Chez les animaux âgés de plus de huit ans, le lymphome digestif de bas grade est une cause fréquente d’entéropathie chronique. Les principaux signes cliniques incluent un amaigrissement, une anorexie (ou une polyphagie) et des vomissements. Le diagnostic est histologique selon de nouveaux critères, récemment mieux cernés. Les entéropathies lymphoplasmocytaires, éosinophiliques et les autres néoplasies affectent des chats de tout âge et peuvent s’exprimer par des présentations cliniques variées. L’échographie abdominale couplée à l’examen cytologique en cas d’adénopathie ou de masse digestive constitue une étape préliminaire et essentielle du diagnostic. Si nécessaire, des biopsies digestives soumises à une analyse histologique et immunohistochimique sont déterminantes pour la distinction spécifique entre inflammation chronique et lymphome de bas grade.

Cooper, J., T. Dang, M. Reeson, J. Dang, L. Dieleman, K. Kroeker, D. Baumgart et al. "A113 DIAGNOSTIC ACCURACY OF COMPUTED TOMOGRAPHY ENTEROGRAPHY COMPARED TO BALLOON ASSISTED ENDOSCOPY IN CROHN’S DISEASE". Journal of the Canadian Association of Gastroenterology 6, Supplement_1 (1 marzo 2023): 61–62. http://dx.doi.org/10.1093/jcag/gwac036.113.

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Abstract Background Crohn’s disease (CD) is a chronic inflammatory condition which can affect the entire gastrointestinal tract with a wide variety of potential complications which may require endoscopic or surgical interventions. Small bowel CD beyond the reach of standard endoscopy poses a diagnostic obstacle and relies on cross sectional imaging ─ such as computed tomography enterography (CTE) ─ and balloon assisted endoscopy (BAE). BAE is the current diagnostic gold standard allowing for direct mucosal visualization as well as therapeutic capabilities; however, remains limited by access, cost, and requires specialized training. Alternatively, CTE in small bowel in CD is widely available, and less invasive than BAE. The diagnostic accuracy of CTE against the gold standard of BAE remains unclear. Purpose We aim to assess the sensitivity and specificity of CTE vs BAE in the diagnosis and evaluation of small bowel CD. Method Patients with an established diagnosis of Crohn’s disease who underwent a CTE and a BAE within 6 months between 2011 and 2018 were reviewed. Relevant findings of active inflammation (defined by mural hyperenhancement and thickening), long-segment disease (≥ 15 cm active disease), skip-segments, number of strictures, and presence of high-grade strictures (defined on BAE as inability to traverse with scope prior to dilation and on CTE as prestenotic luminal dilation ≥3cm and fecalization) were extracted from both reports and images of CTE and BAE by two independent reviewers. Sensitivity and specificity for each finding on CTE was calculated using BAE as the gold-standard diagnostic test. Result(s) A total of 42 patients with 65 corresponding CTE and BAE were identified between 2011 and 2018. CTE was found to be most sensitive for assessing presence of active inflammation and number of strictures at 75.6% [95% CI, 60.5-87.1%] and 71.4% [95% CI, 55.4-84.3], respectively. CTE was highly specific for findings of long-segment inflammation, skip lesions, number of strictures, and high-grade stricture with a specificity of 89.3% [95% CI, 78.1-96.0], 74.1% [95%, 67.2-94.7], 100% [97.5% CI, 73.5-100], and 84.4% [95% CI, 67.2-94.7] respectively. CTE showed poor specificity for active inflammation 45.0% [23.1-68.5%], and poor sensitivity for high grade strictures 54.5% [36.4-71.9] and skip lesions 54.5% [23.4-83.3] Image Conclusion(s) CTE is relatively sensitive in detecting active inflammation and number of strictures compared to BAE, but showed suboptimal sensitivity in detecting long segment inflammation, skip lesions, and high-grade strictures. CTE showed high specificity in identification of long segment inflammation, number of strictures, and high-grade strictures, but not active inflammation overall. CTE and BAE are complementary to one another and based utilized in combination to improve diagnostic accuracy. Future directions include prospective validation prospective studies to validate the results of this study looking at a broader population of Crohn’s disease patients. Please acknowledge all funding agencies by checking the applicable boxes below None Disclosure of Interest None Declared

Divella, Rosa, Graziella Marino, Stefania Infusino, Laura Lanotte, Gaia Gadaleta-Caldarola e Gennaro Gadaleta-Caldarola. "The Mediterranean Lifestyle to Contrast Low-Grade Inflammation Behavior in Cancer". Nutrients 15, n. 7 (29 marzo 2023): 1667. http://dx.doi.org/10.3390/nu15071667.

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A healthy diet and an active lifestyle are both effective ways to prevent, manage, and treat many diseases, including cancer. A healthy, well-balanced diet not only ensures that the body gets the right amount of nutrients to meet its needs, but it also lets the body get substances that protect against and/or prevent certain diseases. It is now clear that obesity is linked to long-term diseases such as heart disease, diabetes, and cancer. The main reasons for people being overweight or obese are having bad eating habits and not moving around enough. Maintaining weight in the normal range may be one of the best things to avoid cancer. It has been scientifically proven that those who perform regular physical activity are less likely to develop cancer than those who lead a sedentary lifestyle. Moving regularly not only helps to maintain a normal body weight, avoiding the effects that favor tumor growth in overweight subjects, but also makes the immune system more resistant by counteracting the growth of tumor cells. Physical activity also helps prevent cardiovascular and metabolic diseases. In this review, it is highlighted that the association between the Mediterranean diet and physical activity triggers biological mechanisms capable of counteracting the low-grade chronic inflammation found in patients with cancer. This assumes that healthy lifestyles associated with cancer therapies can improve the expectations and quality of life of cancer patients.

Rutsch, Frank, e Robert Terkeltaub. "Inflammation de bas grade et déficit en inhibiteurs physiologiques de la calcification dans les calcifications des artères: mécanismes permettant de comprendre les calcifications du cartilage". Revue du Rhumatisme 72, n. 3 (marzo 2005): 186–94. http://dx.doi.org/10.1016/j.rhum.2004.05.021.

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Hébert, Marine, Tristan Méric e Juan Hernandez. "Entéropathies inflammatoires chroniques chez le chien : actualités". Le Nouveau Praticien Vétérinaire canine & féline 19 (dicembre 2022): 50–58. http://dx.doi.org/10.1051/npvcafe/2023009.

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L’exploration et le traitement des entéropathies inflammatoires chroniques (EIC), très courantes chez le chien, reposent sur une succession de tests d’exclusion et d’essais thérapeutiques. Cette démarche, bien que codifiée, ne permet l’obtention d’un diagnostic qu’a posteriori, et peut être chronophage sans pour autant garantir une réponse clinique satisfaisante. Une meilleure compréhension des mécanismes est nécessaire pour identifier de nouveaux biomarqueurs et prédire la réponse thérapeutique. En particulier, la place du microbiote intestinal dans la pathogénie des EIC est soulignée dans les récentes études qui montrent qu’il participe à l’initiation et à l’entretien de l’inflammation digestive. Le microbiote fécal est à l’étude à la fois en tant qu’outil diagnostique et en tant que modalité thérapeutique. Par ailleurs, les dernières publications soulignent l’utilité de l’analyse immunohistochimique et de l’analyse PARR dans la distinction entre inflammation et lymphome de bas grade. L’examen par hybridation in situ en fluorescence est également de plus en plus utilisé dans l’exploration de l’implication des bactéries dans certains processus inflammatoires intestinaux. Ce document propose une synthèse de ces actualités.

Valadez-Bustos, Escamilla-Silva, García-Vázquez, Gallegos-Corona, Amaya-Llano e Ramos-Gómez. "Oral Administration of Microencapsulated B. Longum BAA-999 and Lycopene Modulates IGF-1/IGF-1R/IGFBP3 Protein Expressions in a Colorectal Murine Model". International Journal of Molecular Sciences 20, n. 17 (31 agosto 2019): 4275. http://dx.doi.org/10.3390/ijms20174275.

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The Insulin-like growth factor-I/Insulin-like growth factor-I receptor (IGF-1/IGF-1R) system is a major determinant in colorectal cancer (CRC) pathogenesis. Probiotics (Bifidobacterium longum, BF) and lycopene (LYC) have been individually researched for their beneficial effects in the prevention of CRC. However, the effect of a combined treatment of microencapsulated BF and LYC on IGF-1/IGF-1R/IGFBPs (Insulin-like growth factor-binding proteins) expression in an azoxymethane (AOM)-dextran sulfate sodium (DSS)-induced CRC model have not been demonstrated. BF was microencapsulated by the spray drying technique, with high viability, and daily gavaged with LYC for 16 weeks to CD-1 mice in an AOM-DSS model. The results indicated that BF- and BF + LYC-treated groups had significantly lower inflammation grade, tumor incidence (13–38%) and adenocarcinoma (13–14%) incidence compared to the AOM + DSS group (80%), whereas LYC treatment only protected against inflammation grade and incidence. Caecal, colonic and fecal pH and β-glucuronidase (β-GA) values were significantly normalized by BF and LYC. Similarly, BF and BF + LYC treatments significantly reduced both the positive rate and expression grade of IGF-1 and IGF-1R proteins and normalized Insulin-like growth factor-binding protein-3 (IGFBP3) expression. Based on intestinal parameters related to the specific colon carcinogenesis in an AOM-DSS-induced model, LYC and microencapsulated BF supplementation resulted in a significant chemopreventive potential through the modulation of IGF-1/IGF-1R system.

Raucci, Angela, Federica Macrì, Stefania Castiglione, Ileana Badi, Maria Cristina Vinci e Estella Zuccolo. "MicroRNA-34a: the bad guy in age-related vascular diseases". Cellular and Molecular Life Sciences 78, n. 23 (26 ottobre 2021): 7355–78. http://dx.doi.org/10.1007/s00018-021-03979-4.

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AbstractThe age-related vasculature alteration is the prominent risk factor for vascular diseases (VD), namely, atherosclerosis, abdominal aortic aneurysm, vascular calcification (VC) and pulmonary arterial hypertension (PAH). The chronic sterile low-grade inflammation state, alias inflammaging, characterizes elderly people and participates in VD development. MicroRNA34-a (miR-34a) is emerging as an important mediator of inflammaging and VD. miR-34a increases with aging in vessels and induces senescence and the acquisition of the senescence-associated secretory phenotype (SASP) in vascular smooth muscle (VSMCs) and endothelial (ECs) cells. Similarly, other VD risk factors, including dyslipidemia, hyperglycemia and hypertension, modify miR-34a expression to promote vascular senescence and inflammation. miR-34a upregulation causes endothelial dysfunction by affecting ECs nitric oxide bioavailability, adhesion molecules expression and inflammatory cells recruitment. miR-34a-induced senescence facilitates VSMCs osteoblastic switch and VC development in hyperphosphatemia conditions. Conversely, atherogenic and hypoxic stimuli downregulate miR-34a levels and promote VSMCs proliferation and migration during atherosclerosis and PAH. MiR34a genetic ablation or miR-34a inhibition by anti-miR-34a molecules in different experimental models of VD reduce vascular inflammation, senescence and apoptosis through sirtuin 1 Notch1, and B-cell lymphoma 2 modulation. Notably, pleiotropic drugs, like statins, liraglutide and metformin, affect miR-34a expression. Finally, human studies report that miR-34a levels associate to atherosclerosis and diabetes and correlate with inflammatory factors during aging. Herein, we comprehensively review the current knowledge about miR-34a-dependent molecular and cellular mechanisms activated by VD risk factors and highlight the diagnostic and therapeutic potential of modulating its expression in order to reduce inflammaging and VD burn and extend healthy lifespan.

Hirano, F., D. Van der Heijde, F. A. Van Gaalen, R. B. M. Landewé, C. Gaujoux-Viala e S. Ramiro. "SAT0375 DETERMINANTS OF PATIENT’S GLOBAL ASSESSMENT OF WELL-BEING IN EARLY AXIAL SPONDYLOARTHRITIS; 5-YEAR LONGITUDINAL DATA FROM THE DESIR COHORT." Annals of the Rheumatic Diseases 79, Suppl 1 (giugno 2020): 1135–36. http://dx.doi.org/10.1136/annrheumdis-2020-eular.816.

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Background:A framework has been proposed to explain which disease outcomes impact quality of life or well-being in patients with axSpA; this was based on cross-sectional data and patients with radiographic axSpA.1Objectives:To investigate the determinants of patient’s well-being over time, and the influence of contextual factors on these relationships in patients with early axSpA.Methods:Five-year data from DESIR, a cohort of early axSpA, were analysed. Clinical data were collected every 6 months up to 2 years and annually thereafter. X-rays and MRI of the spine and SIJ were performed at baseline, 2, and 5 years. The outcome was BAS-G, the patient’s global assessment of the disease impact on well-being. Generalized estimating equations (GEE) were used to test the relationship between potential explanatory variables from 5 domains (disease activity, physical function, spinal mobility, structural damage, spinal and SIJ inflammation) and BAS-G over 5 years. Longitudinal relationships were analysed using an autoregressive GEE model. Contextual factors (patient’s educational level, gender and age) were tested as potential effect modifiers or confounders.Results:A total of 708 patients were included, mean age 33.7 (SD 8.6) years, 46% male, 41% lower educated. Higher scores of the individual questions of BASDAI on fatigue (Q1) (β [95% CI]: 0.17 [0.13-0.22]), back pain (Q2) (0.51 [0.46-0.56]), peripheral joint pain (Q3) (0.08 [0.04-0.12]) and severity of morning stiffness (Q5) (0.08 [0.03-0.13]), and BASFI (0.14 [0.08-0.19]) were independently associated with a higher BAS-G over time (Table 1). In the autoregressive GEE model, all variables except for the BASDAI Q5 showed true longitudinal associations with BAS-G. Age, gender and educational level were neither effect modifiers nor confounders.Table 1.Factors associated with BAS-G over time.Multivariable GEE modelMultivariable autoregressive GEE model §Coefficient (95% CI)Coefficient (95% CI)BASDAI Q1 (fatigue, 0-10)0.17 (0.13 to 0.22)*0.15 (0.10 to 0.20)*BASDAI Q2 (back pain, 0-10)0.51 (0.46 to 0.56)*0.54 (0.47 to 0.60)*BASDAI Q3 (peripheral joint pain, 0-10)0.08 (0.04 to 0.12)*0.13 (0.08 to 0.19)*BASDAI Q4 (enthesitis, 0-10)0.03 (-0.01 to 0.07)0.02 (-0.04 to 0.08)BASDAI Q5 (severity of morning stiffness, 0-10)0.08 (0.03 to 0.13)*0.06 (-0.01 to 0.13)BASDAI Q6 (duration of morning stiffness, 0-10)0.03 (-0.01 to 0.07)0.05 (-0.01 to 0.11)SJC28 (0-28)0.01 (-0.11 to 0.13)0.10 (-0.11 to 0.31)TJC53 (0-159) ¶-0.01 (-0.02 to 0.01)-0.01 (-0.03 to 0.01)MASES (0-39)0.00 (-0.02 to 0.02)-0.00 (-0.03 to 0.02)CRP (mg/L)0.01 (-0.00 to 0.01)0.00 (-0.01 to 0.01)Any EAM (presence vs absence)-0.05 (-0.21 to 0.11)-0.09 (-0.28 to 0.10)BASFI (0-10)0.14 (0.08 to 0.19)*0.08 (0.00 to 0.16)*BASMI linear (0-10)-0.07 (-0.16 to 0.02)-0.10 (-0.22 to 0.02)mNY grading (0-8)0.01 (-0.03 to 0.06)0.06 (0.01 to 0.12)*mSASSS (0-72)-0.01 (-0.04 to 0.02)0.00 (-0.03 to 0.04)* p-value < 0.05¶ Each joint graded 0-3§Adjusted for the outcome (i.e. BAS-G) one year before, in order to disentangle the cross-sectional and longitudinal relationships between outcomes and allow the interpretation of a longitudinal relationshipConclusion:A higher level of back pain was associated with a worsening of the patient’s well-being in early axSpA, as were, though to a lesser extent, higher levels of fatigue, morning stiffness, peripheral joint pain and physical disability. Contextual factors like age, gender and educational level did not have an impact on these relationships. Thus, the previously proposed framework of disease outcomes also applies to patients with early axSpA and to outcomes over time.References:[1]Machado, P. ARD 2011.Disclosure of Interests:Fumio Hirano Paid instructor for: Ono pharmaceuticals, Astellas Pharma Inc, Sumitomo Dainippon Pharma, Chugai Pharmaceutical Co., Ltd., Désirée van der Heijde Consultant of: AbbVie, Amgen, Astellas, AstraZeneca, BMS, Boehringer Ingelheim, Celgene, Cyxone, Daiichi, Eisai, Eli-Lilly, Galapagos, Gilead Sciences, Inc., Glaxo-Smith-Kline, Janssen, Merck, Novartis, Pfizer, Regeneron, Roche, Sanofi, Takeda, UCB Pharma; Director of Imaging Rheumatology BV, Floris A. van Gaalen: None declared, Robert B.M. Landewé Consultant of: AbbVie; AstraZeneca; Bristol-Myers Squibb; Eli Lilly & Co.; Galapagos NV; Novartis; Pfizer; UCB Pharma, Cecile Gaujoux-Viala: None declared, Sofia Ramiro Grant/research support from: MSD, Consultant of: Abbvie, Lilly, Novartis, Sanofi Genzyme, Speakers bureau: Lilly, MSD, Novartis

Desjardins, Clément, Khê Hoang-Xuan e Caroline Houillier. "Lymphome de bas grade". Revue Neurologique 178 (aprile 2022): S143. http://dx.doi.org/10.1016/j.neurol.2022.02.009.

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Tesi sul tema "Inflammation de bas grade":

Alentorn, Agusti. "Caractérisation génomique et génétique des gliomes diffus de bas grade de l’adulte". Thesis, Paris 11, 2014. http://www.theses.fr/2014PA11T011.

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La caractérisation moléculaire multidimensionnelle des tumeurs et des tumeurs gliales en particulier est une étape importante pour l’identification de biomarqueurs (diagnostique, pronostique, théranostique et/ou de prédisposition), pour l’identification de cibles thérapeutiques et pour une meilleure compréhension de l’oncogénèse moléculaire.Nos travaux ont permis de confirmer et de consolider certaines données de la littérature comme par exemple : (i) la valeur pronostique favorable de la codélétion 1p/19q, (ii) la valeur pronostique favorable de la mutation IDH, (iii) le caractère mutuellement exclusive des mutations TP53 et de la codélétion 1p/19q et (iv) la rareté des altérations génétiques du PDGFRA dans les gliomes de bas grade (GDBG). De manière plus originale, nous avons identifié plusieurs sous-groupes génomiques de GDBG pertinents sur le plan clinico-biologique, notamment au sein des GDBG non 1p/19q codélétés : (i) 19q-délété ; (ii) 11p-délété, (iii) 7-gagné, (iv) 19-gagné et (v) inclassés. La perte du bras chromosomique 19q annule la valeur pronostique favorable de la mutation IDH dans les GDBG non 1p/19q codélétés. Nous avons également identifié des mutations géniques originales dans les GDBG (i.e. mutation TEP1 et RNF40) qui renforcent le rôle des télomères et du remodelage de la chromatine au sein des GDBG.Enfin, nous nous sommes concentrés sur la caractérisation des GDBG 11p-délétés qui sont de phénotype majoritairement astrocytaire et de moins bon pronostic. Ces GDBG surexpriment des gènes des cellules immunitaires (les GIM -Glioma infiltrating microglia-, les macrophages de type 1, les macrophages de type 2) et sont infiltrés par des cellules macrophagiques et microgliales. Ce microenvironnement dérégulé peut constituer une cible thérapeutique au sein des GDBG 11p-délétés. En conclusion, nos travaux participent à la dissection clinico-moléculaire des GDBG et à préciser la biologie d’un sous-type de GDBG caractérisé la perte du bras chromosomique 11p
Multildimensional molecular characterization of tumors and more specifically of gliomas is of pivotal importance to identify: (i) new biomarkers (i.e. diagnostic, prognostic, theranostic or predisposing), (ii) new therapeutic targets and (iii) to improve our understanding of molecular oncogenesis.Our work has confirmed and consolidated previous data published in the literature, for example that: (i) 1p/19q co-deletion is associated with better prognosis, (ii) IDH mutation is associated with better prognosis, (iii) TP53 mutations and 1p/19q codeletion are mutually exclusive and (iv) PDGFRA is rarely altered, at genomic level, in low-grade gliomas (LGG).More originally, we have identified several genomic groups, with clinical and biological relevances, in LGG and more specifically in LGG without 1p/19q co-deletion: (i) 19q-deleted, (ii) 11p-deleted, (iii) 7-gained, (iv) 19-gained and (v) unclassified. Interestingly, 19q deletion abrogates the positive prognostic value of IDH mutation in LGG without 1p/19q codeletion.We have also identified new recurrent somatic gene mutations in LGG (i.e. TEP1 and RNF40 mutations), supporting the critical role of telomeres and chromatin remodelling in LGG.Finally, we have characterized further 11p-deleted LGG that exhibit mostly astrocytic phenotype and poor prognosis. This subgroup includes LGG overexpressing genes of inflammatory/immune cells (GIM -Glioma infiltrating microglia-, M1 macrophages and M2 macrophages) and infiltrated by macrophagic/microglial cells. This peculiar microenvironment detected in 11p-deleted LGG might be used as a therapeutic target. In conclusion, our work participates to characterize clinico-biological portrait of LGG and to describe a singular genomic subgroup of LGG characterized by 11p loss

Allouche, Rania. "Effet anti-inflammatoire d’hydrolysats de protéines de surface ou intracellulaires de Streptococcus thermophilus obtenus après action de protéases digestives". Electronic Thesis or Diss., Université de Lorraine, 2022. http://www.theses.fr/2022LORR0344.

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L'inflammation offre une protection contre les blessures, traumatismes ou infections causées par des cellules endommagées, des irritants ou des agents pathogènes. Ce processus élimine les agents nuisibles et les composants des tissus endommagés. Néanmoins, une inflammation chronique de bas grade est associée à diverses pathologies. L'alimentation pourrait être un levier d'action. En effet, des peptides bioactifs issus de protéines alimentaires pourraient moduler des facteurs clés de l'inflammation et retarder l'apparition de ces maladies chroniques. En outre, les bactéries lactiques, composantes des produits laitiers fermentés, présentent des propriétés anti inflammatoires in vitro et in vivo. Parmi elles, Streptococcus thermophilus (ST) est régulièrement consommée par une part importante de la population. Certaines souches de ST présentent une activité anti inflammatoire in vitro dont le mécanisme est inconnu. Dans ce travail, l'hypothèse a été émise que des peptides libérés après hydrolyse par des protéases digestives des protéines de surface ou intracellulaires de ST pourraient être impliqués dans cette activité. Des hydrolysats ont été obtenus après rasage des protéines de surface par la trypsine ou la pepsine suivi ou non d'une trypsinolyse. La caractérisation des peptides par spectrométrie de masse en tandem a montré que la majorité appartenait aux protéines de surface. L'activité anti-inflammatoire des hydrolysats a été évaluée dans deux modèles cellulaires enflammés. L'hydrolysat obtenu après rasage trypsique et trypsinolyse des protéines de surface de ST LMD 9 a significativement diminué la sécrétion de la cytokine pro inflammatoire IL 8 dans les cellules HT 29 stimulées par le lipopolysaccharide (LPS) et réduit la production d'IL 8 et de la cytokine pro-inflammatoire IL 1β ainsi que les niveaux d'expression protéique de Pro IL 1β et COX 2 dans les macrophages THP 1 stimulés par le LPS. Les peptides actifs pourraient être issus de la digestion de la protéase de surface PrtS. Pour vérifier cette hypothèse, des hydrolysats ont été préparés par rasage par la pepsine suivi ou non d'une trypsinolyse des protéines de surface de deux souches phénotypiquement distinctes de ST : LMD 9 (PrtS+) et CNRZ 21N (PrtS-). La modulation de IL 8, IL 1β, Pro IL 1β et COX 2 a été évaluée dans les macrophages THP 1 et celle de IL 8 dans les cellules HT 29, stimulés par le LPS. Les hydrolysats issus des deux souches ont montré une action anti inflammatoire mais avec des différences selon la souche, l'hydrolysat et la concentration. Néanmoins, même la souche dépourvue de la protéase PrtS montre une activité anti inflammatoire. Les peptides libérés à partir des protéines de surface de ST par des protéases du tractus gastro intestinal lors de la digestion d'un produit contenant cette bactérie pourraient exercer des effets anti-inflammatoires et réduire le risque de maladies chroniques liées à l'inflammation. Enfin, les protéines intracellulaires des souches LMD 9 et CNRZ 21N ont été récupérées par sonication et hydrolysées par la Corolase PP, un mélange de protéases pancréatiques. Les hydrolysats générés à partir d'une fraction de ces protéines issues des deux souches ont démontré une action anti-inflammatoire par modulation des médiateurs pro inflammatoires dans les macrophages THP 1 stimulés par le LPS. A notre connaissance, il s'agit de la première étude mettant en évidence l'activité anti-inflammatoire de peptides issus de protéines de surface et d'une fraction des protéines intracellulaires de ST. Ces paraprobiotiques ou postbiotiques, pouvant être libérés dans le tractus digestif du consommateur, pourraient participer à l'effet anti-inflammatoire global mis en évidence avec certaines souches et avoir des effets bénéfiques sur la santé humaine et ainsi constituer un ingrédient bioactif prometteur pour le développement d'aliments fonctionnels pour la prévention de l'inflammation de bas grade
Inflammation is a mechanism that provides protection against injury, trauma, or infection caused by damaged cells, irritants, or pathogens. This process removes harmful agents and damaged tissue components. Nevertheless, chronic low-grade inflammation is often associated with various pathologies. Diet could be a promising way of action. Indeed, bioactive peptides derived from the hydrolysis of dietary proteins could modulate key inflammatory factors and consequently delay the onset of these chronic diseases. Furthermore, lactic acid bacteria, components of fermented milk products, exhibit anti-inflammatory properties both in vitro and in vivo studies. Among them, Streptococcus thermophilus (ST) is regularly consumed by a significant part of the population. Studies have shown that some strains of ST display anti inflammatory activity in vitro with an unknown mechanism of action. In this work, it was hypothesized that peptides released after hydrolysis by digestive proteases of the surface or intracellular proteins of this bacterium could be involved at least partially in this activity. Firstly, hydrolysates were obtained by shaving surface proteins with trypsin or pepsin followed or not by trypsinolysis. The tandem mass spectrometry analysis indicated that the majority of the identified peptides belonged to the surface proteins of this bacterium. Secondly, the anti inflammatory activity of the hydrolysates was evaluated in two inflamed cell models. The hydrolysate obtained after tryptic shaving and trypsinolysis of surface proteins of ST LMD 9 significantly decreased the secretion of the pro-inflammatory cytokine IL 8 in lipopolysaccharide (LPS) stimulated HT 29 cells. The same hydrolysate also reduced production of IL 8 and of the pro-inflammatory cytokine IL 1β as well as protein expression levels of Pro IL 1β and COX 2 in LPS-stimulated THP 1 macrophages. It was proposed that the surface protease PrtS could be a source of active peptides during gastrointestinal digestion. To verify this hypothesis, hydrolysates were prepared by shaving with pepsin followed or not by trypsinolysis of the surface proteins of two phenotypically distinct strains of ST: LMD 9 (PrtS+) and CNRZ 21N (PrtS-). Modulation of pro-inflammatory mediators IL 8, IL 1β, Pro IL 1β and COX 2 was assessed in LPS-stimulated THP 1 macrophages and IL 8 in LPS stimulated HT 29 cells. The hydrolysates from the two strains showed an anti inflammatory action but modulation of all these inflammatory mediators was strain, hydrolysate, and concentration dependent. Interestingly, the strain lacking PrtS also showed anti-inflammatory activity. Therefore, peptides released from surface proteins of ST strains by proteases of the gastrointestinal tract during digestion of a product containing this bacterium could exert anti-inflammatory effects and thus could reduce the risk of inflammation related chronic diseases. Finally, the intracellular proteins of the LMD 9 and CNRZ 21N strains were recovered by sonication and hydrolysed with Corolase PP, a mixture of pancreatic proteases. Hydrolysates generated from a fraction of these proteins of both strains demonstrated anti inflammatory action by modulating some of the pro-inflammatory mediators in LPS stimulated THP 1 macrophages. To our knowledge, this is the first study demonstrating the anti inflammatory activity of peptides derived from surface proteins and a fraction of the intracellular proteins of ST strains. These paraprobiotics or postbiotics, likely to be released in the digestive tract of the consumer, could participate in the overall anti inflammatory effect of S. thermophilus which had been demonstrated with certain strains. They could display beneficial effects on human health and therefore could be a promising bioactive ingredient for the development of novel functional foods for the prevention of low grade inflammation

Lasselin, Julie. "L’inflammation chronique à bas bruit et ses relations avec la fatigue et les altérations cognitives chez les patients souffrant de troubles métaboliques". Thesis, Bordeaux 2, 2012. http://www.theses.fr/2012BOR22001/document.

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Les cytokines, produites lors de l’activation du système immunitaire, ont la capacité d’agir au niveau du système nerveux central et d’induire diverses altérations comportementales. Lorsque l’activation du système de l’immunité innée devient chronique, ces altérations comportementales peuvent évoluer en véritables symptômes neuropsychiatriques. La physiopathologie des symptômes neuropsychiatriques qui se développent dans un contexte d’inflammation chronique à bas bruit, c’est-à-dire caractérisé par une activation chronique des processus immunitaires mais à un niveau relativement faible, est peu connue et reste à déterminer. L’implication de l’inflammation chronique à bas bruit dans les symptômes de fatigue et les altérations cognitives constitue l’élément d’étude principal de ce travail de thèse. Les troubles métaboliques, tels que l’obésité et le diabète de type 2, sont de bons modèles pour une telle étude. Ces deux pathologies sont en effet caractérisées par une inflammation chronique à bas bruit qui proviendrait, au moins en partie, du tissu adipeux. De plus, la fatigue et les altérations cognitives sont fréquentes chez les patients souffrant de troubles métaboliques. Compte tenu du rôle connu de l’inflammation dans la physiopathologie de ces altérations comportementales, leur développement dans des contextes de troubles métaboliques pourrait également être lié à l’activation chronique à bas bruit de processus inflammatoires. Différents objectifs ont été définis pour tester cette hypothèse : 1) caractériser et spécifier les symptômes de fatigue et les altérations cognitives chez des patients diabétiques ou obèses ; 2) évaluer la relation entre inflammation systémique et état inflammatoire du tissu adipeux ; 3) étudier l’association de l’inflammation chronique à bas bruit avec les symptômes de fatigue et les altérations cognitives des patients souffrant de troubles métaboliques. Nos résultats indiquent que la fatigue, en particulier la fatigue générale et physique, représente une caractéristique fondamentale des troubles métaboliques. Des perturbations cognitives, se traduisant par un ralentissement psychomoteur dans un test de temps de réaction ainsi qu’une altération de performance dans une tâche de planification spatiale, ont également été décelées chez les patients diabétiques de type 2, particulièrement ceux sous insulinothérapie, et chez les patients obèses. Des altérations mineures étaient également mesurées dans une tâche d’empan spatial rétrograde chez les patients obèses. En ce qui concerne les données biologiques, nos résultats indiquent diverses associations entre l’inflammation systémique et l’expression des marqueurs inflammatoires (cytokines inflammatoires, dont le MCP1, et marqueurs des cellules T) dans le tissu adipeux viscéral des patients obèses. De façon intéressante, l’inflammation systémique à bas bruit était associée aux dimensions de fatigue (générale, mentale, réduction des activités et de la motivation) et aux altérations de performance dans les tests ciblant les fonctions exécutives. Dans l’ensemble, ces résultats supportent l’hypothèse de l’implication des macrophages et des lymphocytes T du tissu adipeux dans l’état inflammatoire systémique associé à l’obésité. Il suggère en outre que l’inflammation systémique à bas bruit pourrait participer au développement de la fatigue et des altérations cognitives chez les patients souffrant de troubles métaboliques. Ce travail de thèse offre une caractérisation précise des symptômes de fatigue et des altérations cognitives associées aux troubles métaboliques. En outre, ce travail apporte d’importantes informations sur les relations de l’inflammation chronique à bas bruit avec ces symptômes, et permet d’affiner les hypothèses relatives à l’implication de processus inflammatoires dans la physiopathologie de ces altérations
Cytokines produced during the activation of the immune system have the ability to act within the central nervous system and to induce a large number of behavioral alterations. When the activation of immune system becomes chronic and unregulated, these behavioral alterations may lead to the development of neuropsychiatric symptoms. The pathophysiology of neuropsychiatric symptoms that develop in conditions of chronic low-grade inflammation context (i.e., characterized by a chronic but low activation of inflammatory processes), remains unknown. The main aim of this thesis was to investigate the involvement of low-grade inflammation in the development of fatigue symptoms and cognitive alterations in patients with metabolic disorders including obesity and type 2 diabetes. These conditions are characterized by a chronic low-grade inflammatory state, manifesting by higher blood concentrations of inflammatory factors. This inflammatory state would originate, at least partially, from the adipose tissue. Moreover, fatigue symptoms and cognitive alterations are common in metabolic disorders. Given the role of inflammation in the physiopathology of these symptoms, their development could also rely on chronic low-grade inflammatory processes. Several objectives were defined to test this hypothesis: 1) to characterize fatigue symptoms and cognitive alterations in obese and diabetic patients; 2) to assess the relationship of systemic inflammation with the inflammatory state of the adipose tissue; and 3) to investigate the association of low-grade inflammation with fatigue symptoms and cognitive alterations in patients with metabolic disorders. Fatigue symptoms and cognitive function were respectively assessed using the multidimensional fatigue inventory (MFI) and the neuropsychological tests automated battery CANTAB in diabetic patients (type 1 and type 2) and in obese patients before and after bariatric surgery. A control group was included for each model (obesity and type 2 diabetes). Circulating concentrations of inflammatory markers, as well as expression of inflammatory markers in the visceral adipose tissue of obese patients, were measured. Our results indicate that fatigue symptoms, especially in the dimensions of general and physical fatigue, represent fundamental characteristics of patients suffering from metabolic disorders. In addition, cognitive alterations (psychomotor slowing and alterations in spatial planning performance) were measured in type 2 diabetic patients, more particularly those under insulin treatment, and in obese patients. Slight alterations in the test of backward spatial span were measured in obese patients. With respect to biological data, our results indicate significant relationships between systemic inflammation and inflammatory markers (inflammatory cytokines, including MCP1, and T-cell markers) in the visceral adipose tissue of obese patients. Interestingly, chronic low-grade inflammation was associated with fatigue symptoms (general fatigue, mental fatigue, reduced activity and motivation) and performance alterations in tests assessing executive functions. Altogether, these data support the hypothesis of the involvement of the adipose macrophages and T lymphocytes in the systemic inflammatory state associated with obesity. Moreover, these results suggest that systemic low-grade inflammation associated with metabolic disorders may contribute to the physiopathology of fatigue and cognitive alterations in these conditions. In conclusion, these studies provide a precise characterization of fatigue symptoms and cognitive alterations associated with metabolic disorders, such as obesity or type 2 diabetes. In addition, this thesis work gives interesting information about the relationships of chronic low-grade inflammation and fatigue and cognitive symptoms, and refines hypotheses regarding the involvement of inflammatory processes in the physiopathology of these symptoms in patients with diabetes or obesity

Pépin, Léopold. "Astrocytomes de bas-grade : apport de l'imageri moderne". Montpellier 1, 1992. http://www.theses.fr/1992MON11055.

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Rorive, Sandrine. "Les astrocytomes de bas-grade: caractérisation moléculaire et implications cliniques". Doctoral thesis, Universite Libre de Bruxelles, 2010. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210181.

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La malignité des astrocytomes est établie sur base de critères morphologiques définis au sein de la classification de l’Organisation Mondiale de la Santé (OMS). Ce système de gradation, qui s’échelonne de I à IV, constitue actuellement l’outil pronostique le plus fiable. Par facilité, les cliniciens regroupent les astrocytomes de grade I (astrocytomes pilocytiques) et les astrocytomes diffus de grade II sous le terme d’« Astrocytomes de bas-grade » par opposition aux astrocytomes de haut-grade, constitués des astrocytomes anaplasiques (grade III) et des glioblastomes (GBM ;grade IV). Cette terminologie conduit à des prises en charge cliniques inadéquates car elle englobe des tumeurs très différentes en terme d’agressivité :les astrocytomes de grade I, majoritairement non infiltrants, non évolutifs et indolents et les astrocytomes diffus de grade II, toujours infiltrants et évolutifs, progressant systématiquement en astrocytomes de haut-grade et entraînant le plus souvent le décès prématuré du patient. Bien que ces tumeurs soient définies par la classification de l’OMS comme des entités clinicopathologiques distinctes, peu de données sont disponibles dans la littérature pour expliquer leurs particularités biologiques et la pratique quotidienne montre que les différencier peut être difficile.

Le but des études entreprises au cours de ce travail de thèse est d’apporter une contribution à la compréhension des mécanismes de tumorigenèse qui différencient l’astrocytome de grade I des astrocytomes diffus (grade II-IV), de manière à identifier des voies biologiques qui permettraient, au moins en partie, d’expliquer ces différences de comportement.

Au cours de la première partie de ce travail, nous avons caractérisé les profils d’expression génomique des astrocytomes de grade I et de grade II, en comparant les données d’expression de gènes (évaluées par des technologies de micropuces d’ADN) de travaux publiés entre 2000 et 2005. L’expression des gènes identifiés a été validée par des analyses de RT-PCR quantitative sur une série indépendante d’astrocytomes de grade I, II et IV. Les fonctions biologiques des protéines codées par chacun de ces gènes ont fait l’objet de recherches bibliographiques détaillées afin de proposer un modèle permettant d’approcher les différences de comportement de ces tumeurs. Cette analyse nous a permis d’identifier TIMP4 (tissue inhibitor of metalloproteinases 4) et IGFBP2 (insulin-like growth factor binding protein 2) comme gènes candidats pour améliorer la caractérisation biologique et clinique des astrocytomes de grade I par rapport aux astrocytomes diffus. TIMP4 et IGFBP2 codent respectivement pour un inhibiteur endogène des métalloprotéinases matricielles (MMPs) et une protéine de liaison capable d’inhiber l’action des « insulin-like growth factors » (IGFs, dont IGFI et IGFII), des facteurs impliqués dans la croissance et la migration des astrocytes normaux et tumoraux.

Sur base de la surexpression de TIMP4 et d’IGFBP2 dans les astrocytomes de grade I, en comparaison aux astrocytomes diffus de grade II, nous avons posé l’hypothèse suivante :« L’absence d’agressivité des astrocytomes de grade I, en comparaison aux astrocytomes diffus (grade II-IV) pourrait en partie être liée à l’inhibition par TIMP-4 de la protéolyse des complexes IGFBP2-IGFII au sein de ces tumeurs ». Cette protéolyse, qui diminue l’affinité d’IGFBP2 pour IGFII, pourrait contribuer à libérer IGFII dans la matrice extracellulaire (MEC), favoriser la liaison d’IGFII à son récepteur IGF-IR et stimuler la croissance et la migration des cellules astrocytaires tumorales. Pour tester cette hypothèse, nous avons réalisé différentes analyses biochimiques afin i) de caractériser les actions protéolytiques de MMP-2, MMP-9 et MT1-MMP sur le complexe IGFBP2-IGFII, ii) d’identifier la libération d’IGFII lors du clivage de ce complexe, et iii) d’étudier l’action inhibitrice de TIMP-4. A l’aide d’un modèle cellulaire in vitro (lignée astrocytaire tumorale LN229), nous avons ensuite observé l’influence de la protéolyse du complexe IGFBP2-IGFII sur la croissance et la motilité cellulaire. Cette étude a montré :(1) la protéolyse du complexe IGFBP2-IGFII par MMP-9, (2) l’inhibition partielle de cette protéolyse par TIMP-4, (3) la libération d’IGFII résultant de cette protéolyse et (4) les effets stimulants de la libération d’IGFII sur la croissance et la motilité des cellules LN229. Cette étude souligne le rôle important de la protéolyse des complexes IGFBP2-IGFII dans l’agressivité des astrocytomes diffus. Elle confirme les effets stimulants propres d’IGFII, d’IGFBP2 et de MMP-9 sur la motilité et/ou la croissance des cellules astrocytaires tumorales. Enfin, elle identifie un rôle inhibiteur potentiel de TIMP-4 sur la protéolyse du complexe IGFBP2-IGFII, qui pourrait contribuer à expliquer le caractère plus indolent des astrocytomes de grade I en comparaison aux astrocytomes diffus.

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Doctorat en Sciences médicales
info:eu-repo/semantics/nonPublished

Gerin, Chloé. "Modélisation et étude histologique de gliomes diffus de bas grade". Phd thesis, Université Paris-Diderot - Paris VII, 2012. http://tel.archives-ouvertes.fr/tel-00820353.

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Les gliomes diffus de bas grade (GBG) sont des tumeurs cérébrales primaires. Après une phase de croissance lente, ils évoluent en gliomes de haut grade, entrainant une issue fatale. Ce sont des tumeurs très diffuses donc difficiles à traiter. Une meilleure connaissance de ces tumeurs pourrait permettre de les guérir ou, à défaut, d'optimiser les traitements. Nous avons étudié la croissance des GBG grâce à un modèle mathématique simple, ce qui nous a amené à spéculer (i) qu'ils surviennent à l'adolescence, (ii) que l'âge de la tumeur au moment du diagnostic peut être calculé facilement et (iii) que la vitesse de croissance est un fac- teur pronostique important. Cette dernière prédiction concorde avec les observations cliniques. Pour vérifier ce modèle spatial, nous avons caractérisé quantitativement des tissus de biopsies étagées de GBG humains, en particulier la présence d'œdème. L'analyse de ces données micro- scopiques étaie l'idée que l'œdème est à l'origine de l'anomalie de signal IRM en séquence T2. Pour prendre en compte ce résultat nouveau, nous avons incorporé l'œdème au modèle initial comme conséquence de la présence de cellules tumorales. Ce modèle permet d'expliquer la longue décroissance du rayon tumoral pendant des dizaines de mois après la radiothérapie : les cellules tumorales désormais moins nombreuses, le drainage de l'œdème devient prédominant. Ce mo- dèle, qui ne comprend que trois paramètres libres, a été validé grâce à des données cliniques sur une vingtaine de patients.

Gerin, Chloé. "Modélisation et études histologiques de gliomes diffus de bas grade". Paris 7, 2012. http://www.theses.fr/2012PA077066.

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Les gliomes diffus de bas grade (GBG) sont des tumeurs cérébrales primaires. Après une phase de croissance lente, ils évoluent en gliomes de haut grade, entrainant une issue fatale. Ce sont des tumeurs très diffuses donc difficiles à traiter. Une meilleure connaissance de ces tumeurs pourrait permettre de les guérir ou, à défaut, d'optimiser les traitements. Nous avons étudié la croissance des GBG grâce à un modèle mathématique simple, ce qui nous a amené à spéculer (i) qu'ils surviennent à l'adolescence, (ii) que l'âge de la tumeur au moment du diagnostic peut être calculé facilement et (iii) que la vitesse de croissance est un facteur pronostique important. Cette dernière prédiction concorde avec les observations cliniques. Pour vérifier ce modèle spatial, nous avons caractérisé quantitativement des tissus de biopsies étagées de GBG humains, en particulier la présence d'œdème. L'analyse de ces données microscopiques étaie l'idée que l'œdème est à l'origine de l'anomalie de signal IRM en séquence T2. Pour prendre en compte ce résultat nouveau, nous avons incorporé l'œdème au modèle initial comme conséquence de la présence de cellules tumorales. Ce modèle permet d'expliquer la longue décroissance du rayon tumoral pendant des dizaines de mois après la radiothérapie : les cellules tumorales désormais moins nombreuses, le drainage de l'œdème devient prédominant. Ce modèle, qui ne comprend que trois paramètres libres, a été validé grâce à des données cliniques sur une vingtaine de patients
Diffuse low-grade gliomas (LGG) are primary brain tumors. After a slow growth, they evolve to high-grade gliomas, resulting into death. These tumors are very diffuse, thus diffîcult to treat. A better knownledge of them could allow to cure them or, failing that, to optimize treatments. We studied the growth of LGG with a simple mathematical model, which led us to speculate (i) that they arise in adolescence, (ii) that the age of the tumor at diagnosis can be calculated easily, and (iii) that the growth rate is an important prognostic factor. This last prediction is consistent with clinical observations. To test this spatial model, we have quantitatively characterized biopsy tissues of human LGG, particularly the presence of edema. The microscopic analysis of these data underpins the idea that edema is the cause of the abnormality seen on T2-weighted MR imaging. To take this new result into account, we have incorporated edema into the initial model as a consequence of the presence of tumor cells. This model helps explain the long decay of the tumor radius for tens of months after radiation therapy: as tumor cells become less numerous, drainage of the edema becomes predominant. This model, which has only three free parameters, has been validated thanks to clinical data from twenty patients

Darlix, Amélie. "Gliomes diffus de bas grade : données épidémiologiques et hypothèses étiologiques". Thesis, Montpellier, 2016. http://www.theses.fr/2016MONTT011/document.

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L’épidémiologie et les facteurs de risque des gliomes diffus de bas grade (GDBG, ou gliomes diffus de grade II OMS) sont à ce jour mal connus. Ce travail de thèse s’est intéressé à décrire les caractéristiques épidémiologiques (taux d’incidence, données démographiques) et à rechercher, dans la littérature et par nos travaux, des arguments en faveur de facteurs de risque environnementaux, fonctionnels et moléculaires. Epidémiologie descriptive : l’analyse d’une série exhaustive de cas incidents de GDBG diagnostiqués entre 2006 et 2011, à l’échelle nationale, a permis de déterminer l’incidence des GDBG dans leur ensemble (incidence standardisée sur la population française : 0,775/105 personnes-années) et pour chacun de leurs sous-types histologiques définis par la classification 2007 de l’OMS. Facteurs de risque environnementaux : nous avons pu mettre en évidence des différences significatives dans la distribution géographique des gliomes diffus de grade II et III OMS en France métropolitaine, avec une incidence plus élevée dans le Nord-Est et le centre de la France. Cette hétérogénéité semble en faveur de facteurs de risque environnementaux, même s’il n’existe à ce jour aucun facteur de risque environnemental démontré dans les GDBG. Facteurs de risque biologiques : notre travail a permis de démontrer l’existence d’une dichotomie sur le plan moléculaire entre les GDBG de topographie frontale, plus fréquemment mutés IDH et codélétés 1p19q, et les GDBG temporo-insulaires, moins fréquemment mutés IDH et codélétés 1p19q, suggérant des voies de gliomagénèse différentes pour ces deux patterns tumoraux. Facteurs de risque fonctionnels : enfin, comme le montrent les données de la littérature, il existe deux arguments principaux en faveur de facteurs de risque fonctionnels dans les GDBG. D’une part, ces tumeurs présentent des localisations intracérébrales spécifiques et distinctes des autres gliomes, et impliquent préférentiellement les zones dites « fonctionnelles ». D’autre part, des modifications macroscopiques cérébrales ont été rapportées en lien avec l’apprentissage d’une tâche ou une expertise particulière. Les mécanismes microscopiques qui sous-tendent ces modifications sont encore incertains mais une implication (directe ou indirecte) des cellules gliales, semble probable, ce qui pourrait faire le lit de la gliomagénèse. Peu d’études se sont intéressées jusqu’à présent aux corrélations entre les activités du sujet et le risque de GDBG, et nous proposons donc, dans les suites de ce travail de thèse, une étude cas-témoins en ce sens. En conclusion, même s’il n’existe à ce jour aucun facteur de risque démontré de GDBG, certains éléments bibliographiques, et les travaux de cette thèse, suggèrent l’implication de facteurs environnementaux, fonctionnels et biologiques dans la genèse des GDBG
The epidemiology and risks factors of diffuse low-grade gliomas (DLGG, or WHO grade II diffuse gliomas) are yet poorly known. This thesis aimed at describing the epidemiology (incidence rates, demographic data) and at looking for arguments in favor of environmental, functional and molecular risk factors, in the literature and by our works. Descriptive epidemiology: The analysis of an exhaustive series of incident cases of DLGG diagnosed between 2006 and 2011 allowed the determination of DLGG incidence (incidence rate standardized on the French population: 0,775/105 person-years) as well as that of each histological subtype described by the 2007 WHO classification. Environmental risk factors: We were able to demonstrate significant differences in the geographical distribution of WHO grade II and III diffuse gliomas in metropolitan France, with higher incidence rates in the North-East and Center regions. This heterogeneity stands in favor of environmental risk factors, even though there is to date no proven environmental risk factor for DLGG. Biological risk factors: Our work demonstrated the existence of a clear dichotomy, regarding molecular biology, between frontal DLGG, more frequently IDH-mutated and 1p19q codeleted, and temporo-insular tumors, less frequently IDH-mutated and 1p19q codeleted, suggesting different gliomagenesis pathways for these two patterns of tumors. Functional risk factors: Finally, data from the literature provide two main arguments in favor of the existence of functional risk factors in DLGG. First, the intra-cerebral location of these tumors is specific and distinct from that of other gliomas, with a preferential implication of “functional” areas. Second, macroscopic intra-cerebral changes have been reported following training on specific tasks, or in relation with a specific expertise. The microscopic mechanisms that underlie these modifications are uncertain but an implication (direct or indirect) of glial cells seems probable, and could favor gliomagenesis. To date, only few studies have investigated the correlation between the subject’s activity and the risk of DLGG. We thus propose, following this thesis, a case-control study to further investigate this issue. In conclusion, even though there is no demonstrated risk factor for DLGG, data from the literature, and conclusions from the present work, suggest the implication of environmental, functional and biological factors in DLGG genesis

Lopes, Manuel. "Chirurgie des gliomes de bas grade en zone fonctionnelle : réflexions éthiques". Paris 5, 2002. http://www.theses.fr/2002PA05N116.

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Les controverses thérapeutiques du Gliome de Bas grade succèdent à la difficulté de leur définition histologique, et donc, à la mauvaise connaissance de l'histoire naturelle de cette maladie. Il en découle des indications chirurgicales hétérogènes ( depuis l'abstention jusqu'à l'exérèse chirurgicale la plus complète possible, y compris en zone fonctionnelle) dues à la difficulté de déterminer la meilleure attitude pour chaque patient, posant alors des questions d'ordre éthique, engendrées par le manque de consensus. Cette réalité est objectivée tant sur le plan pratique en France 'résultats d'une enquête menée dans le cadre de ce travail
Therapeutic controversies abouy low-grade gliomas arise both from the difficulties in clearly defining them from a histological point of view and from the subséquent imperfect knowledge of the natural history of the disease. The surgical attitude is thus heterogeneous ( from abstention to maximal possible resection involving in some cases functional areas), resulting from the difficulty in determining the best indication for each individual patient ; this lack of consensus generates several ethical issues. This fact has been assessed both practically

Claessens, Yann-Erick. "Etude de la dysérythropoièse au cours des syndromes myélodysplasiques de bas grade". Paris 5, 2004. http://www.theses.fr/2004PA05P632.

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L'anémie est une anomalie communément rencontrée dans les syndromes myélodysplasiques (SMD) de bas grade. Les mécanismes qui en sont responsables restent à ce jour non résolus. Nous décrivons un modèle en culture liquide permettant le développement in vitro de la lignée érythroi͏̈de à partir de cellules CD34+ issues de patients porteurs de SMD de bas grade. Nous retrouvons une augmentation de l'apoptose et une diminution des capacités d'expansion dans les cultures de SMD. Le couple Fas-Fas ligand est responsable du défaut de développement de la lignée érythroi͏̈de dans notre modèle. Nous modulons ce système par l'utilisation d'un dominant négatif de l'adaptateur FADD permettant l'inhibition de la caspase-8, permettant d'envisager une nouvelle cible thérapeutique. La signification de la surexpression du système Fas reste néanmoins inconnue à ce jour
Anemia is a common feature in low grade myelodysplastic syndromes (MDS). However mechanisms responsible for this are unresolved. We describe a model of liquid cultures allowing the in vitro development of the erythroid lineage from CD34+ cells from MDS and control patients. We found an increased apoptosis and a decrease in expansion properties in MDS cultures. The Fas-Fas ligand system was responsible for the impairment of the erythroid development. We modulate this apoptotic signalling via inhibition of caspase-8 using a dominant negative of the adapter FADD, thus openening new therapeutic pathways. Significance of the enhanced apoptotic pathway mediated by Fas remains unresolved so far

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Libri sul tema "Inflammation de bas grade":

Capacchione, Vito. Infiammazione Silente (low-Grade Inflammation). Independently Published, 2018.

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Tunjic, Luka. Mechanical Stimulation Low-Grade Inflammation Weight Gain: Muscles Upward Lifting Activity Weight Loss. Independently Published, 2021.

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music theory in practice grade 1. abrms, 1991.

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Taylor, Eric. Music Theory In Practice Grade 1. Associated Board of the Royal School of Music, 1990.

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Carrero, Juan Jesús, e Peter Stenvinkel. The role of inflammation in chronic kidney disease. A cura di David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0110.

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Low-grade persistent inflammation is a common feature of chronic kidney disease. This chapter provides an overview of the pathogenesis and clinical consequences of elevated pro-inflammatory cytokines in the uraemic milieu with an emphasis on dialysis stages. It reviews the multifactorial dialysis- and non-dialysis-related causes of inflammation and its purported role in the development of protein energy wasting, vascular calcification, endocrine disorders, and depression. The chapter also discusses the use and the need of monitoring C-reactive protein levels regularly in the clinical setting and comments on possible therapeutic approaches to reduce inflammation in these patients.

Lafeber, Floris P. J. G., Nick J. Besselink e Simon C. Mastbergen. Synovium and capsule. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0006.

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Synovium is an integrated tissue of the diarthrodial joints that interacts with all the other joint tissues and specifically is important in nourishment and lubrication of the articular cartilage, removal of waste products, and immunological surveillance. Chronic as well as recurrent low-grade synovial inflammation definitely contributes to progression and symptoms of certain patients with osteoarthritis. Low-grade inflammation may even be causative in the disease. The challenge is that osteoarthritis is a heterogeneous disorder with inflammation not only of the synovial tissue but with its mediators also present in cartilage and bone. Therefore, despite the presence of inflammatory mediators, in some cases synovitis may be seen as a bystander and not as a driving force in pathogenesis. Future research must be directed toward defining the risk-to-benefit ratio for (systemic) anti-inflammatory therapy, especially when targeting mediators of low-grade inflammation.

Schiller, Adalbert, Adrian Covic e Liviu Segall. Chronic tubulointerstitial nephritis. A cura di Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0086_update_001.

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Chronic tubulointerstitial nephropathies (CTINs) are a group of renal diseases, characterized by variable interstitial inflammation and fibrosis and tubular atrophy, and a slow course towards end-stage renal disease (ESRD). The causes of CTIN are numerous, including nephrotoxic drugs and chemicals, infections, autoimmune diseases, obstructive uropathies, and metabolic disorders. Taken together, CTIN are responsible for less than 10% of all ESRD cases requiring renal replacement therapy. The clinical manifestations of CTIN typically comprise low-grade proteinuria, leucocyturia, and variably reduced glomerular filtration rate (GFR), whereas the blood pressure is usually normal or moderately increased. Tubular abnormalities are common, including type 2 (proximal) renal tubular acidosis, Fanconi syndrome, nephrogenic diabetes insipidus, and type 1 (distal) renal tubular acidosis, with hypokalaemia and nephrolithiasis. Radiology exams reveal shrunken kidneys, sometimes with irregular outlines. A renal biopsy is often required for the diagnosis of CTIN and its aetiology. The treatment of CTIN mainly involves discontinuation of exposure to nephrotoxins and specific therapy of renal infections, urinary tract obstruction, or underlying systemic diseases. Agents like ACE inhibitors and pirfenidone, which might reduce interstitial inflammation and fibrosis, are still under clinical evaluation.

Sahetya, Sarina. Acute Uncomplicated Bronchitis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0029.

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Acute bronchitis is a respiratory illness characterized predominantly by cough with or without sputum production that lasts for up to 3 weeks in the presence of normal chest radiography. Additional presenting symptoms include rhinorrhea, congestion, sneeze, sore throat, wheezing, low-grade fever, myalgia, and fatigue. Causative organisms include viral and bacterial pathogens. The disease course is characterized by self-limited inflammation of the airways. Chest radiographs should be utilized to distinguish acute bronchitis from pneumonia or interstitial disease. Therapeutic recommendations are typically supportive; however, studies reveal that between 60% and 80% of patients receive unwarranted antibiotic therapy. Only those patients at high risk for serious complications (including patients over 65 with a history of hospitalization, diabetes mellitus, congestive heart failure, or current use of oral glucocorticoids) usually require routine antibiotic therapy directed toward both typical and atypical bacterial pathogens.

Tobar, Ximena, e Shannon B. Putman. Viral Gastroenteritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0030.

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Viral gastroenteritis is a diarrheal disease associated with nausea, vomiting, headache, abdominal cramping, myalgias, and low-grade fever. Stools are often described as watery, with bouts of diarrhea and emesis that can occur on an hourly basis. Blood or mucus in the stool is suggestive of a bacterial or parasitic process. Additionally, the presence of fecal leukocytes excludes viral infection, as it is suggestive of colonic inflammation. Treatment is mainly supportive with appropriate hydration, including oral rehydration and/or intravenous fluids, being the key intervention. Specific antiviral agents are not available. Prevention and control of spread are important issues for viral gastroenteritis. Hand washing alone may reduce the spread of infection. The use of alcohol-based hand sanitizers and daily disinfection of surfaces with quaternary ammonium wipes has reduced the spread of Norovirus and was found superior to handwashing alone.

Capitoli di libri sul tema "Inflammation de bas grade":

Wang, Lihui, Xianhua Yu e Jun-Ping Liu. "Telomere Damage Response and Low-Grade Inflammation". In Regulation of Inflammatory Signaling in Health and Disease, 213–24. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-5987-2_10.

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Das, Undurti N. "Metabolic Syndrome X and low-grade systemic inflammation". In A Perinatal Strategy For Preventing Adult Disease: The Role Of Long-Chain Polyunsaturated Fatty Acids, 61–93. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4419-8564-4_6.

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Das, Undurti N. "Low-grade Systemic Inflammation is Present in Common Diseases/Disorders". In Molecular Basis of Health and Disease, 175–79. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-0495-4_6.

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Piuri, Gabriele. "Individual Food Clusters Excess and Low-Grade Inflammation in Pregnancy". In Metabolic Syndrome and Complications of Pregnancy, 23–33. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-16853-1_2.

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Ortega, Eduardo, Isabel Gálvez e Leticia Martín-Cordero. "Extracellular Hsp70 and Low-Grade Inflammation- and Stress-Related Pathologies". In Heat Shock Proteins and Stress, 13–38. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-90725-3_2.

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Fioranelli, Massimo, Marco Del Prete, Jahaira Carolina Aracena, Maria Grazia Roccia, Carlo Dal Lin e Claudio Tomella. "Low-Dose Therapy for the Treatment of Low-Grade Chronic Inflammation". In Integrative Cardiology, 27–38. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-40010-5_3.

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Guarner, Verónica, e Maria Esther Rubio-Ruiz. "Low-Grade Systemic Inflammation Connects Aging, Metabolic Syndrome and Cardiovascular Disease". In Interdisciplinary Topics in Gerontology, 99–106. Basel: S. KARGER AG, 2014. http://dx.doi.org/10.1159/000364934.

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Daly, Robin M. "Dietary Factors and Chronic Low-Grade Systemic Inflammation in Relation to Bone Health". In Nutrition and Bone Health, 659–80. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2001-3_39.

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Daly, Robin M. "Nutrition, Aging, and Chronic Low-Grade Systemic Inflammation in Relation to Osteoporosis and Sarcopenia". In Nutritional Influences on Bone Health, 1–18. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-2769-7_1.

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Das, Undurti N. "Adult Diseases and Low-Grade Systemic Inflammation Have Their Origins in the Perinatal Period". In Molecular Basis of Health and Disease, 513–49. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-0495-4_16.

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Atti di convegni sul tema "Inflammation de bas grade":

Campana, F., U. Ugo Ordioni, J. Del Grande e N. Fakhry. "Adénocarcinome polymorphe de bas grade : A propos d’une localisation labiale". In 62ème Congrès de la SFCO. Les Ulis, France: EDP Sciences, 2014. http://dx.doi.org/10.1051/sfco/20146203008.

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Lautenbach, Anne, Fabian Stoll, Oliver Mann, Philipp Busch, Tobias B. Huber, Heike Kielstein, Ina Bähr e Jens Aberle. "65 Langfristige Verbesserung der chronischen Low-Grade-Inflammation nach bariatrischer Chirurgie". In Adipositas-Kongress 2021 – 37. Jahrestagung der Deutschen Adipositas-Gesellschaft e.V. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1735687.

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van den Borst, Bram, Harry R. Gosker, Geertjan Wesseling, Wilco de Jager, Valery A. C. V. Hellwig, Frank J. Snepvangers e Annemie M. W. J. Schols. "Low-Grade Adipose Tissue Inflammation In Patients With Mild-To-Moderate COPD". In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4124.

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Wopereis, Suzan, Willem J. van den Brink, Tim J. van den Broek, Wilrike J. Pasman e Femke P. M. Hoevenaars. "Postprandial Composite Biomarkers of Low-Grade Inflammation to Evaluate Nutritional Intervention Effects". In European Nutrition Conference. Basel Switzerland: MDPI, 2024. http://dx.doi.org/10.3390/proceedings2023091141.

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Tabei, S., L. Scheffler, R. Chakaroun, S. Ziesche, A. Crane, M. Stumvoll, A. Dietrich, M. Blüher, M. Gericke e P. Kovacs. "Low-grade inflammation in insulin resistance associates with bacterial load in adipose tissue". In Diabetes Kongress 2019 – 54. Jahrestagung der DDG. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1688193.

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Leipe, Jan, Anna-Isabelle Kaelsch, Marcus Kleber, Hubert Scharnagl, Wolfgang Sattler, Winfried März, Ernst Malle e Bernhard Kraemer. "FRI0660 LONG- AND SHORT-TERM ASSOCIATION OF LOW-GRADE SYSTEMIC INFLAMMATION WITH CARDIOVASCULAR MORTALITY". 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.7919.

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Horishnyi, I. M., e O. V. Chernyshov. "Low-grade inflammation in patients with asthma and risks of SARS-CoV-2 infection". In MODERN MEDICINE: THE USE OF CREATIVE INDUSTRIES IN THE HEALTHCARE SYSTEM. Baltija Publishing, 2021. http://dx.doi.org/10.30525/978-9934-26-182-4-7.

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Lo Tam Loi, Adèle T., Susan Hoonhorst, nick hacken ten, J. W. J. Lammers e Leo Koenderman. "Low Body Mass Index Is Associated With Low Grade Systemic Inflammation In Stable COPD Patients". In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2553.

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Fornasiero, Massimiliano, Iain Pierce, Matthew Webber, Kathryn E. Keenan, Karl F. Stupic, Rüdiger Bruehl, Bernd Ittermann et al. "11 A medical device-grade T2 phantom for quality assurance of inflammation imaging by CMR". In British Society of Cardiovascular Magnetic Resonance 2021 Annual Meeting. BMJ Publishing Group Ltd and British Cardiovascular Society, 2021. http://dx.doi.org/10.1136/heartjnl-2021-bscmr.11.

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Rapporti di organizzazioni sul tema "Inflammation de bas grade":

Akkus, Ozan. Regeneration of Musculoskeletal Tissues by Prolonged Low-Grade Inflammation. Fort Belvoir, VA: Defense Technical Information Center, ottobre 2011. http://dx.doi.org/10.21236/ada562974.

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Yang, Chao, Tao-junjin Lu, Jie Wang, Qing Zhang, Ze-Fen Wang e Zhi-Qiang Li. Association of systemic immune-inflammation index with grade and prognosis in glioma patients: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, aprile 2022. http://dx.doi.org/10.37766/inplasy2022.4.0072.

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Mateș, Letiția, Marius Emil Rusu, Ionel Fizeșan, Daniela-Saveta Popa e Daniel Leucuța. Walnut intake interventions targeting biomarkers of metabolic syndrome and inflammation in middle-aged and older adults: a systematic review and meta-analysis of randomized controlled trials research protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, giugno 2022. http://dx.doi.org/10.37766/inplasy2022.6.0058.

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Review question / Objective: The aim of this study was to conduct a systematic review and meta-analysis of randomized controlled trials (RCTs) in order to properly examine the evidence on the effects of walnut consumption on chosen indicators of inflammation and metabolic syndrome in mature adults. Condition being studied: Metabolic syndrome (MetS), chronic, low-grade inflammation, and oxidative stress are all important risk factors for morbidity and death, with a higher frequency in the elderly population. Information sources: We conducted a comprehensive search in five databases: Pubmed, EMBASE, Scopus, Cochrane, ClinicalTrials, from inception.

Platz, Elizabeth A. Prospective Evaluation of Intraprostatic Inflammation and Focal Atrophy as a Predictor of Risk of High-Grade Prostate Cancer and Recurrence after Prostatectomy. Fort Belvoir, VA: Defense Technical Information Center, luglio 2014. http://dx.doi.org/10.21236/ada610016.

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Schreiber, Martin A. The Effect of Hypotensive Resuscitation and Fluid Type on Mortality, Bleeding, Coagulation and Dysfunctional Inflammation in a Swine Grade V Liver Injury Model. Fort Belvoir, VA: Defense Technical Information Center, gennaio 2008. http://dx.doi.org/10.21236/ada490734.

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Schreiber, Martin. The Effect of Hypotensive Resuscitation and Fluid Type on Mortality, Bleeding, Coagulation, & Dysfunctional Inflammation in a Swine Grade V Liver Injury Model. Fort Belvoir, VA: Defense Technical Information Center, gennaio 2006. http://dx.doi.org/10.21236/ada446801.

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Schreiber, Martin A. The Effect Of Hypotensive Resuscitation And Fluid Type On Mortality, Bleeding,Coagulation And Dysfunctional Inflammation In A Swine Grade V Liver Injury Model. Fort Belvoir, VA: Defense Technical Information Center, gennaio 2012. http://dx.doi.org/10.21236/ada559947.

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Liu, Yangjun, Wei Xie, Zbigniew Ossowski, Juan Li, Juan Yang, Yiming Luo, Xia Wu e 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, marzo 2023. http://dx.doi.org/10.37766/inplasy2023.3.0051.

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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.

Czerwaty, Katarzyna, Karolina Dżaman, Krystyna Maria Sobczyk e Katarzyna Irmina Sikrorska. The Overlap Syndrome of Obstructive Sleep Apnea and Chronic Obstructive Pulmonary Disease: A Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, novembre 2022. http://dx.doi.org/10.37766/inplasy2022.11.0077.

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Review question / Objective: To provide the essential findings in the field of overlap syndrome of chronic obstructive pulmonary disease and obstructive sleep apnea, including prevalence, possible predictors, association with clinical outcomes, and severity compared to both chronic obstructive pulmonary disease and obstructive sleep apnea patients. Condition being studied: OSA is characterized by complete cessation (apnea) or significant decrease (hy-popnea) in airflow during sleep and recurrent episodes of upper airway collapse cause it during sleep leading to nocturnal oxyhemoglobin desaturations and arousals from rest. The recurrent arousals which occur in OSA lead to neurocognitive consequences, daytime sleepiness, and reduced quality of life. Because of apneas and hypopneas, patients are experiencing hypoxemia and hypercapnia, which result in increasing levels of catecholamine, oxidative stress, and low-grade inflammation that lead to the appearance of cardio-metabolic consequences of OSA. COPD is a chronic inflammatory lung disease defined by persistent, usually pro-gressive AFL (airflow limitation). Changes in lung mechanics lead to the main clini-cal manifestations of dyspnea, cough, and chronic expectoration. Furthermore, patients with COPD often suffer from anxiety and depression also, the risk of OSA and insomnia is higher than those hospitalized for other reasons. Although COPD is twice as rare as asthma but is the cause of death eight times more often.