Bibliographies thématiques / Masld

Sommaire

Articles de revues
Thèses
Livres
Chapitres de livres
Actes de conférences

Littérature scientifique sur le sujet « Masld »

Auteur : Grafiati

Publié le 11 janvier 2025

Mis à jour le 1 février 2025

Créez une référence correcte selon les styles APA, MLA, Chicago, Harvard et plusieurs autres

Choisissez une source :

Consultez les listes thématiques d’articles de revues, de livres, de thèses, de rapports de conférences et d’autres sources académiques sur le sujet « Masld ».

À côté de chaque source dans la liste de références il y a un bouton « Ajouter à la bibliographie ». Cliquez sur ce bouton, et nous générerons automatiquement la référence bibliographique pour la source choisie selon votre style de citation préféré : APA, MLA, Harvard, Vancouver, Chicago, etc.

Vous pouvez aussi télécharger le texte intégral de la publication scolaire au format pdf et consulter son résumé en ligne lorsque ces informations sont inclues dans les métadonnées.

Articles de revues sur le sujet "Masld"

Chen, Li. « From metabolic dysfunction-associated fatty liver disease to metabolic dysfunction-associated steatotic liver disease : Controversy and consensus ». World Journal of Hepatology 15, n^o 12 (27 décembre 2023) : 1253–57. http://dx.doi.org/10.4254/wjh.v15.i12.1253.

Texte intégral

Résumé :

The newly released nomenclature of metabolic dysfunction-associated steatotic liver disease (MASLD) in the 2023 European Association for the Study of the Liver Congress has raised great clinical concerns. This marks the second instance of significant renaming of non-alcoholic fatty liver disease since the introduction of metabolic dysfunction-associated fatty liver disease (MAFLD) in 2020. The nomenclature and definitions of MASLD and MAFLD exhibit significant disparities as well as substantial consensus. The disparities regarding the framework of nomenclature, the definitions, the clinical management, and the impact on the clinical outcomes between MASLD and MAFLD were comprehensively compared in this editorial. Additionally, the consensus reached by the MASLD and MAFLD definitions also emphasizes positive diagnosis rather than negative diagnosis within the framework of establishing a diagnostic approach. Furthermore, they acknowledged the pivotal role of metabolic dysfunction in the pathogenesis of MAFLD or MASLD and the positive role of increasing the awareness of the disease in public. Fortunately, the non-invasive tests remains effective in the MASLD and MAFLD era. Elucidating these disparities would contribute to a more comprehensive comprehension of the nature of steatotic liver disease and enhance clinical practice. Thus, more efforts are required to reach more consensus about these important topics.

Styles APA, Harvard, Vancouver, ISO, etc.

Bando, Hiroshi. « Latest Trend and Perspective of Metabolic Dysfunction Associated Steatotic Liver Disease (MASLD) as a Novel Nomenclature ». Asploro Journal of Biomedical and Clinical Case Reports 7, n^o 2 (6 avril 2024) : 84–87. http://dx.doi.org/10.36502/2024/asjbccr.6341.

Texte intégral

Résumé :

Recently, the medical term for nonalcoholic fatty liver disease (NAFLD) has been changed to a novel nomenclature: metabolic dysfunction-associated steatotic liver disease (MASLD). The latest report shows analyses of the National Health and Nutrition Examination Survey (NHANES III) using the fibrosis-4 index (FIB-4) and enhanced liver fibrosis (ELF). Among 6429 NAFLD cases, 99% met MASLD criteria. In another study with 4286 cases, 99% of steatosis cases met the MASLD definition, and 95.4% met the metabolic dysfunction-associated fatty liver disease (MAFLD) definition. Several biomarkers show a relationship with MASLD/MAFLD, such as BMI, T2D, HOMA-IR, central obesity, waist circumference, and CKD.

Styles APA, Harvard, Vancouver, ISO, etc.

Beygi, Mohammad, Salma Ahi, Samaneh Zolghadri et Agata Stanek. « Management of Metabolic-Associated Fatty Liver Disease/Metabolic Dysfunction-Associated Steatotic Liver Disease : From Medication Therapy to Nutritional Interventions ». Nutrients 16, n^o 14 (11 juillet 2024) : 2220. http://dx.doi.org/10.3390/nu16142220.

Texte intégral

Résumé :

Non-alcoholic fatty liver disease (NAFLD) is a common long-lasting liver disease that affects millions of people around the world. It is best identified with a hepatic fat build-up that ultimately leads to inflammation and damage. The classification and nomenclature of NAFLD have long been a controversial topic, until 2020 when a group of international experts recommended substituting NAFLD with MAFLD (metabolic dysfunction-associated FLD). MAFLD was then terminologically complemented in 2023 by altering it to MASLD, i.e., metabolic dysfunction-associated steatotic liver disease (MASLD). Both the MAFLD and the MASLD terminologies comprise the metabolic element of the disorder, as they offer diagnostic benchmarks that are embedded in the metabolic risk factors that underlie the disease. MASLD (as a multisystemic disease) provides a comprehensive definition that includes a larger population of patients who are at risk of liver morbidity and mortality, as well as adverse cardiovascular and diabetes outcomes. MASLD highlights metabolic risks in lean or normal weight individuals, a factor that has not been accentuated or discussed in previous guidelines. Novel antihyperglycemic agents, anti-hyperlipidemic drugs, lifestyle modifications, nutritional interventions, and exercise therapies have not been extensively studied in MAFLD and MASLD. Nutrition plays a vital role in managing both conditions, where centralizing on a diet rich in whole vegetables, fruits, foods, healthy fats, lean proteins, and specific nutrients (e.g., omega-3 fatty acids and fibers) can improve insulin resistance and reduce inflammation. Thus, it is essential to understand the role of nutrition in managing these conditions and to work with patients to develop an individualized plan for optimal health. This review discusses prevention strategies for NAFLD/MAFLD/MASLD management, with particular attention to nutrition and lifestyle correction.

Styles APA, Harvard, Vancouver, ISO, etc.

Martínez-Montoro, José Ignacio, María Antonia Martínez-Sánchez, Andrés Balaguer-Román, Virginia Esperanza Fernández-Ruiz, José Emilio Hernández-Barceló, Mercedes Ferrer-Gómez, María Dolores Frutos, María Ángeles Núñez-Sánchez, José Carlos Fernández-García et Bruno Ramos-Molina. « Triglyceride to HDL Cholesterol Ratio for the Identification of MASLD in Obesity : A Liver Biopsy-Based Case-Control Study ». Nutrients 16, n^o 9 (27 avril 2024) : 1310. http://dx.doi.org/10.3390/nu16091310.

Texte intégral

Résumé :

Associations between dyslipidemia and metabolic dysfunction-associated steatotic liver disease (MASLD) have been reported. Previous studies have shown that the triglyceride to high-density lipoprotein cholesterol (TG/HDL-C) ratio may be a surrogate marker of MASLD, assessed by liver ultrasound. However, no studies have evaluated the utility of this ratio according to biopsy-proven MASLD and its stages. Therefore, our aim was to evaluate if the TG/HDL-C ratio allows for the identification of biopsy-proven MASLD in patients with obesity. We conducted a case-control study in 153 patients with obesity who underwent metabolic surgery and had a concomitant liver biopsy. Fifty-three patients were classified as no MASLD, 45 patients as metabolic dysfunction-associated steatotic liver—MASL, and 55 patients as metabolic dysfunction-associated steatohepatitis—MASH. A receiver operating characteristic (ROC) analysis was performed to assess the accuracy of the TG/HDL-C ratio to detect MASLD. We also compared the area under the curve (AUC) of the TG/HDL-C ratio, serum TG, and HDL-C. A higher TG/HDL-C ratio was observed among patients with MASLD, compared with patients without MASLD. No differences in the TG/HDL-C ratio were found between participants with MASL and MASH. The greatest AUC was observed for the TG/HDL-C ratio (AUC 0.747, p < 0.001) with a cut-off point of 3.7 for detecting MASLD (sensitivity = 70%; specificity = 74.5%). However, no statistically significant differences between the AUC of the TG/HDL-C ratio and TG or HDL-C were observed to detect MASLD. In conclusion, although an elevated TG/HDL-C ratio can be found in patients with MASLD, this marker did not improve the detection of MASLD in our study population, compared with either serum TG or HDL-C.

Styles APA, Harvard, Vancouver, ISO, etc.

Bae, Jaehyun, Eugene Han, Hye Won Lee, Cheol-Young Park, Choon Hee Chung, Dae Ho Lee, Eun-Hee Cho et al. « Metabolic Dysfunction-Associated Steatotic Liver Disease in Type 2 Diabetes Mellitus : A Review and Position Statement of the Fatty Liver Research Group of the Korean Diabetes Association ». Diabetes & ; Metabolism Journal 48, n^o 6 (30 novembre 2024) : 1015–28. http://dx.doi.org/10.4093/dmj.2024.0541.

Texte intégral

Résumé :

Since the role of the liver in metabolic dysfunction, including type 2 diabetes mellitus, was demonstrated, studies on non-alcoholic fatty liver disease (NAFLD) and metabolic dysfunction-associated fatty liver disease (MAFLD) have shown associations between fatty liver disease and other metabolic diseases. Unlike the exclusionary diagnostic criteria of NAFLD, MAFLD diagnosis is based on the presence of metabolic dysregulation in fatty liver disease. Renaming NAFLD as MAFLD also introduced simpler diagnostic criteria. In 2023, a new nomenclature, steatotic liver disease (SLD), was proposed. Similar to MAFLD, SLD diagnosis is based on the presence of hepatic steatosis with at least one cardiometabolic dysfunction. SLD is categorized into metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction and alcohol-related/-associated liver disease, alcoholrelated liver disease, specific etiology SLD, and cryptogenic SLD. The term MASLD has been adopted by a number of leading national and international societies due to its concise diagnostic criteria, exclusion of other concomitant liver diseases, and lack of stigmatizing terms. This article reviews the diagnostic criteria, clinical relevance, and differences among NAFLD, MAFLD, and MASLD from a diabetologist’s perspective and provides a rationale for adopting SLD/MASLD in the Fatty Liver Research Group of the Korean Diabetes Association.

Styles APA, Harvard, Vancouver, ISO, etc.

Kaewdech, Apichat, et Pimsiri Sripongpun. « Navigating the Nomenclature of Liver Steatosis : Transitioning from NAFLD to MAFLD and MASLD - Understanding Affinities and Differences ». Siriraj Medical Journal 76, n^o 4 (1 avril 2024) : 234–43. http://dx.doi.org/10.33192/smj.v76i4.267556.

Texte intégral

Résumé :

The escalating prevalence of non-alcoholic fatty liver disease (NAFLD) represents a significant challenge to public health, with an increasing impact observed across various demographics. This review delivers a comprehensive evaluation of the evolving terminology in steatotic liver disease (SLD), documenting the transition from NAFLD to metabolic dysfunction-associated fatty liver disease (MAFLD), and progressing to the latest terms, metabolic dysfunction-associated fatty liver disease (MASLD) and MASLD with increased alcohol intake (MetALD). We conducted a comprehensive review of literature discussing the benefits and drawbacks of these nomenclatural changes. Clinical evidence supporting MASLD and MetALD, including the implications of alcohol consumption thresholds on disease classification and outcomes, was analyzed. The “MAFLD” and “MASLD” labels align with the pathophysiology of metabolic diseases, afford a positive disease connotation, and facilitate the identification of more severe diseases, such as significant fibrosis or advanced liver disease. However, the MAFLD criteria may underdiagnose lean, non-overweight, or non-obese individuals with MAFLD. The review underscores the understanding of liver diseases linked to metabolic dysfunction and alcohol use. The shift in terminology marks progress towards a clinical diagnosis that reflects underlying pathophysiology. However, additional studies are necessary to assess the longterm effects of these changes and their efficacy in enhancing patient care and health outcomes.

Styles APA, Harvard, Vancouver, ISO, etc.

Ahamed, Forkan, Natalie Eppler, Elizabeth Jones et Yuxia Zhang. « Understanding Macrophage Complexity in Metabolic Dysfunction-Associated Steatotic Liver Disease : Transitioning from the M1/M2 Paradigm to Spatial Dynamics ». Livers 4, n^o 3 (13 septembre 2024) : 455–78. http://dx.doi.org/10.3390/livers4030033.

Texte intégral

Résumé :

Metabolic dysfunction-associated steatotic liver disease (MASLD) encompasses metabolic dysfunction-associated fatty liver (MASL) and metabolic dysfunction-associated steatohepatitis (MASH), with MASH posing a risk of progression to cirrhosis and hepatocellular carcinoma (HCC). The global prevalence of MASLD is estimated at approximately a quarter of the population, with significant healthcare costs and implications for liver transplantation. The pathogenesis of MASLD involves intrahepatic liver cells, extrahepatic components, and immunological aspects, particularly the involvement of macrophages. Hepatic macrophages are a crucial cellular component of the liver and play important roles in liver function, contributing significantly to tissue homeostasis and swift responses during pathophysiological conditions. Recent advancements in technology have revealed the remarkable heterogeneity and plasticity of hepatic macrophage populations and their activation states in MASLD, challenging traditional classification methods like the M1/M2 paradigm and highlighting the coexistence of harmful and beneficial macrophage phenotypes that are dynamically regulated during MASLD progression. This complexity underscores the importance of considering macrophage heterogeneity in therapeutic targeting strategies, including their distinct ontogeny and functional phenotypes. This review provides an overview of macrophage involvement in MASLD progression, combining traditional paradigms with recent insights from single-cell analysis and spatial dynamics. It also addresses unresolved questions and challenges in this area.

Styles APA, Harvard, Vancouver, ISO, etc.

Guo, Wenying, Ting Weng et Yufei Song. « Association of serum selenium with MASLD and liver fibrosis : A cross-sectional study ». PLOS ONE 19, n^o 12 (31 décembre 2024) : e0314780. https://doi.org/10.1371/journal.pone.0314780.

Texte intégral

Résumé :

Background The evolution of NAFLD, MAFLD, and MASLD underscores significant advancements and nomenclatural shifts in the realm of chronic liver disorders. This study primarily aimed to investigate the possible link between serum selenium levels and the occurrence of MASLD. Methods Utilizing data from NHANES for the years 2017 through 2020, we performed an in-depth analysis. To evaluate the relationship between serum selenium concentrations and the prevalence of MASLD and liver fibrosis, we employed a comprehensive multivariable analysis. This approach accounted for a range of variables to enhance the robustness and reliability of our results by mitigating potential confounding factors. Results Through the application of linear regression models, our comprehensive data analysis revealed significant insights. Elevated serum selenium levels exhibited a distinct positive correlation with CAP, whereas an inverse relationship with LSM was observed. Multivariate logistic regression analysis indicated that higher serum selenium concentrations were significantly associated with an increased likelihood of MASLD, alongside a marked reduction in the probability of liver fibrosis. Conclusion The findings of this study highlight a significant positive association between elevated serum selenium levels, CAP, and the prevalence of MASLD, coupled with an inverse relationship with LSM and liver fibrosis.

Styles APA, Harvard, Vancouver, ISO, etc.

Martínez-Montoro, José Ignacio, Isabel Arranz-Salas, Carolina Gutiérrez-Repiso, Ana Sánchez-García, Luis Ocaña-Wilhelmi, José M. Pinazo-Bandera, Diego Fernández-García et al. « Weight Loss After Sleeve Gastrectomy According to Metabolic Dysfunction-Associated Steatotic Liver Disease Stage in Patients with Obesity : A Liver Biopsy-Based Prospective Study ». Nutrients 16, n^o 22 (12 novembre 2024) : 3857. http://dx.doi.org/10.3390/nu16223857.

Texte intégral

Résumé :

Background: The role of metabolic dysfunction-associated steatotic liver disease (MASLD) in sleeve gastrectomy (SG)-related outcomes remains uncertain. In this study, we aimed to assess the influence of preoperative biopsy-proven MASLD and its stages on weight loss after SG. Methods: One hundred sixty-three patients with obesity undergoing SG with concomitant intraoperative liver biopsy were followed up for 1 year. Fifty-eight participants were categorized as no MASLD, thirty-eight as metabolic dysfunction-associated steatotic liver (MASL), and sixty-seven as metabolic dysfunction-associated steatohepatitis (MASH). Percentage total weight loss (%TWL) and percentage excess weight loss (%EWL) 1 year after SG were calculated for the different groups. We also evaluated the association between preoperative MASLD (and its stages) and weight loss, after adjusting for potential confounders. Results: Significant differences among groups were detected in %EWL (p = 0.004, ANOVA test), but not in %TWL (p = 0.079). However, significant differences in %TWL were found when MASH and no MASH (i.e., participants with MASL and participants without MASLD) groups were compared (27.3 ± 9.9 vs. 30.7 ± 9, respectively, p = 0.025). In the linear regression model for predicting %EWL 1 year after SG, the presence of MASH was independently associated with a lower %EWL, after adjusting for age, sex, baseline body mass index (BMI), and baseline glycated hemoglobin (HbA1c) (Beta −7.1; 95% CI −13.6, −0.5; p = 0.035). The presence of MASLD, liver fibrosis, or advanced liver fibrosis (≥F2) was also associated with lower %EWL after SG in crude models, although they did not remain significant after adjusting for these confounders. The presence of MASH was inversely related to %TWL, although the association did not remain significant after adjustment (Beta −2.7; 95% CI −5.7, 0.2; p = 0.069). Conclusions: MASH may be independently associated with lower %EWL 1 year after SG in patients with obesity.

Styles APA, Harvard, Vancouver, ISO, etc.

Boccatonda, Andrea, Lorenza Del Cane, Lara Marola, Damiano D’Ardes, Gianfranco Lessiani, Nicoletta di Gregorio, Claudio Ferri et al. « Platelet, Antiplatelet Therapy and Metabolic-Associated Fatty Liver Disease : A Narrative Review ». Life 14, n^o 4 (4 avril 2024) : 473. http://dx.doi.org/10.3390/life14040473.

Texte intégral

Résumé :

Metabolic-associated fatty liver disease (MASLD) is not only related to traditional cardiovascular risk factors like T2DM and obesity, but it is also an independent risk factor for the development of cardiovascular disease. MASLD has been shown to be independently related to endothelial dysfunction and atherosclerosis. MASLD is characterized by a chronic proinflammatory response that, in turn, may induce a prothrombotic state. Several mechanisms such as endothelial and platelet dysfunction, changes in the coagulative factors, and lower fibrinolytic activity can contribute to induce the prothrombotic state. Platelets are players and aggressors of metabolic dysregulation; obesity and insulin resistance are related to platelet hyperactivation. Furthermore, platelets can exert a direct effect on liver cells, particularly through the release of mediators from granules. Growing data in the literature support the use of antiplatelet agent as a treatment for MASLD. The use of antiplatelets drugs seems to exert beneficial effects on HCC prevention in patients with MASLD, since platelets contribute to fibrosis progression and cancer development. This review aims to summarize the main data on the role of platelets in the pathogenesis of MAFLD and its main complications such as cardiovascular events and the development of liver fibrosis. Furthermore, we examine the role of antiplatelet therapy not only in the prevention and treatment of cardiovascular events but also as a possible anti-fibrotic and anti-tumor agent.

Styles APA, Harvard, Vancouver, ISO, etc.

Plus de sources

Thèses sur le sujet "Masld"

Henry, Doriane. « Etude du lien entre la MASLD et l'athérosclérose : implication du récepteur nucléaire PPARα ». Electronic Thesis or Diss., Université de Lille (2022-....), 2024. http://www.theses.fr/2024ULILS053.

Texte intégral

Résumé :

Selon l’Organisation Mondiale de la Santé (OMS), les maladies cardiovasculaires (MCV) représentent la première cause de mortalité dans le monde. La prévalence augmentée de la maladie hépatique stéatosique associée à un dysfonctionnement métabolique (MASLD) et sa relation étroite avec le syndrome métabolique laissent suggérer un rôle du foie dans le développement de ces MCV. Cependant, le lien entre MASLD et MCV reste encore peu clair. Dans ce contexte, grâce à l’utilisation d’un modèle murin adapté et de différents outils moléculaires développés au laboratoire, j’ai pu réaliser mes travaux de thèse sur l’exploration du lien entre, d’une part le foie et la MASLD et, d’autre part le développement de l’athérosclérose à l’origine de ces MCV. De plus, le récepteur nucléaire PPARα a été employé comme outil de modulation de la MASLD. Le premier objectif de ma thèse était d’évaluer l’implication du foie dans les effets athéroprotecteurs du pemafibrate, un nouvel agoniste puissant et sélectif de PPARα. Pour cela, nous avons utilisé le modèle de souris double déficient pour le récepteur aux LDL (Ldlr-/-) et pour PPARα, dans lequel l’expression du PPARα sauvage ou d’un mutant de PPARα (exerçant seulement l’activité de transrépression) a été restaurée uniquement dans les hépatocytes de souris grâce à des vecteurs adeno-associated virus (AAV) adaptés. Ces souris ont été soumises à un régime western supplémenté ou non avec le pemafibrate pendant 8 semaines. Les résultats de cette étude montrent que l’activité transrépressive du PPARα hépatocytaire associée aux effets anti-inflammatoires du PPARα dans la MASLD est essentielle et suffisante pour induire les effets athéroprotecteurs du pemafibrate. Le deuxième objectif de ma thèse était de développer un nouveau modèle de souris associant un développement progressif de MASLD et d’athérosclérose dans un contexte cardiométabolique mimant la pathologie humaine. Pour cela, des souris Ldlr-/-, à la fois mâles et femelles, et déficientes ou non en PPARα, ont été soumises à un régime chow ou à un régime enrichi en graisses et en cholestérol. Une cinétique d’évolution de la MASLD et de l’athérosclérose a été réalisée. Les résultats de cette étude montrent un développement progressif à la fois de la MASLD avec toutes les caractéristiques de la pathologie humaine (stéatose, inflammation, ballooning, fibrose) et de l’athérosclérose, dans un contexte pouvant associer obésité et insulinorésistance. De manière intéressante, des spécificités histologiques et métaboliques associées au genre et à la déficience en PPARα ont été observées. Ainsi, les résultats obtenus au cours de ma thèse ont permis de montrer l’importance du foie, et plus particulièrement de l’inflammation hépatique, dans le développement de l’athérosclérose. Le nouveau modèle murin de MASLD et d’athérosclérose permettra de mieux comprendre les mécanismes physiopathologiques mis en jeu dans la MASLD ainsi que les risques cardiovasculaires associés à cette pathologie
According to the World Health Organization (WHO), cardiovascular diseases (CVD) are the leading cause of death in the world. The increased prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) and its strong association with metabolic syndrome suggest a role of the liver in the development of CVD. However, the link between MASLD and CVD remains poorly understood. In this context, using an appropriate mouse model and various molecular tools developed in the laboratory, my thesis work explored the link between the liver and MASLD on one hand, and the development of atherosclerosis which leads to CVD, on the other. In addition, the nuclear receptor PPARα was used as a tool to modulate MASLD. The first aim of my thesis was to evaluate the involvement of liver in the atheroprotective effects of pemafibrate, a potent and selective PPARα agonist. To do this, we used a double-knockout mouse model, deficient in both LDL receptor (Ldlr-/-) and PPARα, and restored the expression of wild-type PPARα or a PPARα mutant (exerting only transrepressive activity) specifically in hepatocytes using adeno-associated virus (AAV) vectors. These mice were subjected to a western diet, with or without pemafibrate supplementation, for 8 weeks. The results of this study demonstrated that the transrepressive activity of hepatocyte PPARα, associated with its anti-inflammatory properties, is essential and sufficient to induce the atheroprotective effects of pemafibrate. The second objective of my thesis was to develop a new mouse model able of simultaneously developing progressive MASLD and atherosclerosis in a cardiometabolic context that mimics human pathology. To do this, male and female Ldlr-/- mice expressing (Pparα+/+) or lacking (Pparα-/-) PPARα were fed either a chow diet or a diet enriched in fat and cholesterol. Kinetics of MASLD and atherosclerosis progression were established. The results of this study revealed the progressive development of both MASLD, with all the human characteristics (namely steatosis, inflammation, ballooning and fibrosis), and atherosclerosis in a context that may combine obesity and insulin resistance. Interestingly, histological and metabolic features associated with sex and PPARα-deficiency were observed. In conclusion, the results obtained during my thesis demonstrate the importance of the liver, and more specifically of hepatic inflammation, in the development of atherosclerosis. The new mouse model of MASLD and atherosclerosis will help to better understand the pathophysiological mechanisms involved in MASLD and the cardiovascular risks associated with this pathology

Styles APA, Harvard, Vancouver, ISO, etc.

Nguyen, Tung Son. « Rôle de REG3A dans la maladie métabolique du foie d'origine nutritionnelle ». Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASQ044.

Texte intégral

Résumé :

REG3A est un effecteur de l'immunité innée qui joue un rôle important dans l'homéostasie du glucose et qui favorise le maintien d'une flore intestinale commensale aux propriétés anti-inflammatoires. Au cours de notre projet de recherche, nous avons étudié le rôle de REG3A dans le contexte de la maladie métabolique d'origine nutritionnelle et développé pour cela un modèle de maladie métabolique combinant un régime hyperlipidique avec des variations de poids. Les souris C57Bl/6 sauvages et REG3A-TG (exprimant REG3A dans le foie) ont été nourries pendant 1 à 3 cycles avec un régime riche en gras administré en continu ou entrecoupé de périodes d'alimentation standard. Nos résultats montrent que la succession de périodes de gain et de perte de poids favorise le développement d'une MASH chez les souris sauvages, caractérisée par une réduction de la sensibilité à l'insuline, la présence d'inflammation, de ballonnement hépatocytaire et d'une fibrose. L'analyse protéomique des foies révèle que l'alimentation riche en gras augmente le métabolisme lipidique tout en réduisant la voie de biosynthèse du cholestérol. L'expression de REG3A réduit l'hépatopathie inflammatoire et le développement de fibrose chez la souris, réduction qui est corrélée à l'activation de la voie de signalisation de l'IFN-γ/STAT1. L'alimentation hyperlipidique induit chez la souris sauvage le remodelage de la matrice extracellulaire du foie et cela, bien en amont de l'apparition de la fibrose, matrice inflammatoire remodelée qui altère la capacité d'hépatocytes en culture primaire de répondre à l'insuline. L'expression de REG3A impacte également sur la composition de cette matrice inflammatoire qui préserve alors sa capacité à sensibiliser les hépatocytes à répondre à l'insuline. En conclusion, nos travaux révèlent les effets pervers de l'alternance de périodes de gain et perte de poids chez la souris (régime yo-yo) qui favorise la sévérité de la maladie métabolique du foie d'origine nutritionnelle et le rôle protecteur que joue l'effecteur de l'immunité innée REG3A dans cette maladie
REG3A is an effector of innate immunity which plays an important role in glucose homeostasis and promotes the maintenance of a commensal gut flora with anti-inflammatory properties. In our research project, we investigated the role of REG3A in the context of nutritionally-induced metabolic disease, using a metabolic disease model combining a hyperlipidic diet with weight cycling. Wild-type C57Bl/6 and REG3A-TG mice (expressing REG3A in the liver) were fed with a high-fat diet for 1-3 cycles, either continuously or interspersed with standard feeding periods. Our results show that successive periods of weight gain and loss promote the development of MASH in wild-type mice, characterized by reduced insulin sensitivity, inflammation, hepatocyte ballooning and fibrosis. Proteomic analysis of livers reveals that high-fat diet increases lipid metabolism in mice while reducing the cholesterol biosynthesis pathway. REG3A expression reduces inflammatory hepatopathy and fibrosis development in mice, a reduction that correlates with activation of the IFN-γ/STAT1 signaling pathway. In wild-type mice, hyperlipidic feeding induces remodeling of the extracellular matrix in the liver, well before the onset of fibrosis. This remodelled inflammatory matrix impairs the ability of primary cultured hepatocytes to respond to insulin. REG3A expression also has an impact on the composition of this inflammatory matrix, which then preserves its ability to sensitize hepatocytes to respond to insulin. In conclusion, our work reveals the perverse effects of alternating periods of weight gain and loss in mice (yo-yo diet), which promotes the severity of nutritionally induced metabolic liver disease, and the protective role played by the innate immune effector REG3A in this disease

Styles APA, Harvard, Vancouver, ISO, etc.

Dubois, Michel. « MASL, langage de contrôle multi-agents robotiques ». Phd thesis, Université de Bretagne Sud, 2008. http://tel.archives-ouvertes.fr/tel-00502455.

Texte intégral

Résumé :

MASL PROPOSE UNE APPROCHE UNIFIEE ET MACROSCOPIQUE A L'EXPRESSION DE CALCULS HETEROGENES ET DISTRIBUES SUR DES AGENTS CONÇUS EN SUIVANT LE MODELE DELIBERATIF, REACTIF OU HYBRIDE. C'EST UN LANGAGE DE HAUT NIVEAU INDEPENDANT DE L'EXECUTIF OU CHAQUE AGENT, VU COMME UNE ENTITE CONCURRENTE, DETERMINE LOCALEMENT SA PARTICIPATION A DES BLOCS D'EXECUTION COLLECTIFS (E-BLOCS). CHAQUE E-BLOC EST UN PROGRAMME COLLECTIF ANONYME POUVANT S'EXECUTER SUR UN RESEAU D'AGENTS SELON DES CRITERES LOCAUX. LE MODE D'ORCHESTRATION (SCALAIRE, SYNCHRONE, ASYNCHRONE) EST DETERMINE STATIQUEMENT PAR UN ATTRIBUT DU BLOC, LES COMMUNICATIONS SUPPORTENT LE MODELE A MEMOIRE PARTAGEE, LE MODELE A ENVOI DE MESSAGES ET LE MODELE D'EVENEMENTS. L'HETEROGENEITE DES AGENTS EST ASSUREE PAR HERITAGE ET POLYMORPHISME ALORS QUE L'AUTONOMIE EST PROPOSEE PAR UN MECANISME (APPELE PERMEABILITE) DE FILTRAGE OU CHAQUE AGENT PEUT MASQUER/OUVRIR SON INTERFACE DYNAMIQUEMENT ET SELON LA POSITION DE L'EMETTEUR DANS LA HIERARCHIE D'E-BLOCS. DANS UN CONTEXTE D'ALLOCATION DYNAMIQUE DES AGENTS, DE REPRISE APRES ECHEC OU DE REMPLACEMENT D'UN AGENT ROBOTIQUE DANS UNE FLOTTE DE ROBOTS (CAS D'UNE PANNE OU PERTE DE FONCTIONNALITE COMPROMETTANT LA MISSION), LE E-BLOC PROPOSE UNE PERSPECTIVE DE POINT D'ENTREE D'UN TRAITEMENT COLLECTIF. DANS LE CAS D'E-BLOC SYNCHRONES, LE PARADIGME SOUS-JACENT EST ISSU DU MODELE DATA-PARALLELE, PERMETTANT ICI DES TRAITEMENTS ITERATIFS PAR VAGUES SUCCESSIVES D'AGENTS. AU FINAL, MASL PROPOSE DES AVANCEES DANS LE DOMAINE DES SMA (APPARTENANCE DYNAMIQUE A DES GROUPES, PRECISION DU RYTHME DES ACTIONS A ENTREPRENDRE POUR PERMETTRE UNE COOPERATION DESIREE) ET AU NIVEAU DE LA GESTION DES ERREURS.

Styles APA, Harvard, Vancouver, ISO, etc.

Dubois, Michel. « MASL, Langage de controle multi-agents robotiques ». Lorient, 2008. http://www.theses.fr/2008LORIS133.

Texte intégral

Résumé :

L'approche classique des langages pour le contrôle de Systèmes Multi-Agents (SMA), a fortiori robotiques et autonomes, consiste d'abord en un point de vue microscopique : chaque agent dispose de son propre programme de contrôle contenant des primitives de communication / synchronisation permettant la coopération / collaboration entre agents. L'émergence d'un comportement global, le point de vue macroscopique du calcul, ne peut qu'être observé a posteriori. Dans ce contexte, MASL propose une approche unifiée et macroscopique à l'expression de calculs hétérogènes et distribués sur des agents conçus en suivant le modèle délibératif, réactif ou hybride. C'est un langage de haut niveau indépendant de l'exécutif où chaque agent, vu comme une entité concurrente, détermine localement sa participation à des blocs d'exécution collectifs (e-blocs). Chaque e-bloc est un programme collectif anonyme pouvant s'exécuter sur un réseau d'agents selon des critères locaux. Le mode d'orchestration (scalaire, synchrone, asynchrone) est déterminé statiquement par un attribut du bloc, les communications supportent le modèle à mémoire partagée, le modèle à envoi de messages et le modèle d'évènements. L'hétérogénéité des agents est assurée par héritage et polymorphisme alors que l'autonomie est proposée par un mécanisme (appelé perméabilité) de filtrage où chaque agent peut masquer/ouvrir son interface dynamiquement et selon la position de l'émetteur dans la hiérarchie d'e-blocs. Dans un contexte d'allocation dynamique des agents, de reprise après échec ou de remplacement d'un agent robotique dans une flotte de robots (cas d'une panne ou perte de fonctionnalité compromettant la mission), le ebloc propose une perspective de point d'entrée d'un traitement collectif. Dans le cas d'e-bloc synchrones, le paradigme sous-jacent est issu du modèle data-parallèle, permettant ici des traitements itératifs par vagues successives d'agents. Au final, MASL propose des avancées dans le domaine des SMA (appartenance dynamique à des groupes, précision du rythme des actions à entreprendre pour permettre une coopération désirée) et au niveau de la gestion des erreurs
The classical approach for Multi-Agent System (MAS) Control, especially autonomous and robotic ones, deals first from a microscopic point of view: each agent embed a control program with communication/synchronization primitives that enable cooperation between agents. The emergence of a global behaviour from a macroscopic point of view can only be observed afterwards. In this context, MASL offers a macroscopic and unified approach with heterogeneous and distributed calculations over deliberative, reactive or hybrid agents. In this high level language, regardless of the runtime, each concurrent agent locally decides its participation in a collective execution block named an e-block. Each e-block is an anonymous collective program that runs over an agent network following local conditions. The orchestral mode (scalar, asynchronous, synchronous) is statically fixed by a shared block attribute. The communication use shared memory, events, synchronous messages passing, and asynchronous messages passing. Heterogeneous agents are managed with heritage and polymorphism. Permeability mechanism, dealing with agent autonomy, allows an agent to dynamically filter calls to its interface in respects to the sender position in the e-block hierarchy. In dynamic task allocation of agents, auto failover and recovery, agent replacement in a robot fleet (case of agent failure, loss of a mandatory functionality for the mission) an e-block is an entry point of a collaborative work. In the case of synchronous e-block, the programming paradigm is the data parallel model with iterative task for waves of agents. Finally, MASL offers advances in the field of MAS (dynamic belonging to groups, accuracy of the pace of actions to undertake to enable a desired cooperation) and for the management of errors

Styles APA, Harvard, Vancouver, ISO, etc.

Tan, Elizabeth E.-Lyn. « Immuno-metabolism in Metabolic (dysfunction) associated fatty liver disease (MAFLD) ». Thesis, The University of Sydney, 2021. https://hdl.handle.net/2123/27978.

Texte intégral

Résumé :

The findings from chronic complex diseases modelled in animals are difficult to extrapolate to humans. In metabolic (dysfunction) associated fatty liver disease (MAFLD), dietary models are commonly used to study the mechanisms for disease progression. The current dogma is that diets rich in fat, simple carbohydrates, and cholesterol can lead to systemic alterations in metabolism that leads to the accumulation of lipids in the adipose and liver tissues. This leads to lipotoxicity and a vicious cycle of inflammation and liver injury which can drive disease progression. Hence, there has been a considerable interest to model and comprehend the role of metabolism and the immune response in this disease. However, our knowledge of the underlying mechanisms in MAFLD is still limited. A major caveat is that pre-clinical models do not represent the full spectrum of human diseases. This has been a major source of failure in clinical trials. Understanding the impact of dietary challenges in animal models and where they resemble or diverge from human disease can help to resolve the current dilemmas that have hampered progress in the field. In this thesis, I used different dietary models in mice and characterised liver pathology, the liver immune profile, and the landscape of liver gene expression. Initially, we used multiple dietary models containing simple (sucrose) or complex carbohydrates, with/without cholesterol (2%), and with/without an added bile acid (cholic acid): A) normal chow (NC); B) high sucrose (HS); C) high sucrose and high cholesterol (HS_Chol2%); D) high sucrose, high cholesterol (2%) and cholic acid (HS_Chol2%_CA); E) high cholesterol (2%) and cholic acid (Chol2%_CA); F) cholic acid (CA). From a liver pathology perspective, diets containing cholesterol (Diets C to E) induced a dramatic change in liver pathology. Consistently, immune profiling of the liver of mice fed these diets induced infiltration of a broad range of immune cells including myeloid and lymphoid cells (diets C to E). Of note, the combination of cholesterol and cholate (diets D and E) had synergistic effects and dramatically enhanced liver immune cell infiltration. Subsequently, we performed RNA sequencing on the liver of mice fed these 6 diets. In agreement, we detected the highest differentially expressed genes in diets containing cholesterol and cholate (diets D and E). We conclude that this combination disturbs liver homeostatic functions the greatest. To gain a systems perspective of perturbations in liver homeostatic function, we undertook a systems approach and applied weighted gene co-expression network analysis (WGCNA) on liver transcriptomes. We noticed several gene expression modules (networks) that were associated with diets. Most of these modules were enriched for metabolic pathways and immune responses. Of interest, there was a negative correlation between immune and metabolic-related modules. This was reminiscent of immunometabolism and a co-variance in gene regulatory networks between metabolic and immune modules. The up-regulation of immune responses and down-regulation of metabolic networks within the liver were prominent in mice exposed to cholesterol and cholate. A published report and our unpublished data (not the subject of this thesis) indicated that diets containing cholesterol and cholate induce a heightened immune response with anti-tumorigenic properties. Thus, from a phenotypic perspective, this immune response and the outcomes are divergent from human fatty liver that increases the risk of liver cancer. One caveat in our dietary models was that they contained supra-physiological levels of cholesterol (2%). I detected a suppression in the expression of genes in cholesterol biosynthesis pathway in all diets that contained cholesterol (Diet C) or cholic acid (Diets D to F). This was in contrast with a study on clinical fatty liver disease (in humans) which reported up-regulation of genes in cholesterol biosynthesis pathways. I hypothesised that reduction in cholesterol biosynthesis could be related to a higher immune response. Hence, I omitted cholic acid and reduced the amount of cholesterol to 0.2% and investigated the liver pathology in mice exposed to a HS_Chol0.2% diet. This diet also induced minimal liver pathology similar to the HS diet. Despite a reduction in the cholesterol content, I detected a suppression in the expression of genes in cholesterol biosynthesis in mice exposed to the 0.2% cholesterol in the diet. This indicates a diverged response in cholesterol metabolism between mice and human liver. This diet did not induce pathological features resembling human MAFLD, however it resembled some characteristics of metabolic syndrome such as adiposity with systemic glucose intolerance. One of the models that is often used to simulate MAFLD is the MCD (methionine choline deficient) diet. This diet induced pathological features resembling human MAFLD, however, our analysis of liver transcriptome data on mice fed with MCD diet indicated down-regulation in metabolic pathways and cholesterol biosynthesis. Indeed, the behaviour of these modules in mice on the MCD diet resembles those in mice exposed to high levels of cholesterol, which are divergent from human fatty liver disease. Overall, my results have shown that mice dietary models do not fully resemble clinical fatty liver either phenotypically or at the gene expression level. A possible strategy to overcome these limitations is to use multiple models in which each model could represent a specific aspect of the disease. At the molecular level, undertaking a module-based approach to understand the link between the behaviour of preserved modules (e.g., between mice and humans) to phenotypic outcome is an alternative strategy. One unmet need in human fatty liver is dissociating liver tissue inflammation from protective immune responses (immunosurveillance), which I would like to delve into in my future endeavours.

Styles APA, Harvard, Vancouver, ISO, etc.

Hoteling, Andrew J. « MALD/I TOF PSD and CID : understanding precision, resolution, and mass accuracy and MALD/I TOFMS : investigation of discrimination issues related to solubility / ». Philadelphia, Pa. : Drexel University, 2004. http://dspace.library.drexel.edu/handle/1860/318.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Elsayed, Asmaa. « A Polymorphism in the FGF21 Gene is a Novel Risk Variant for Metabolic-Associated Steatohepatitis ». Thesis, The University of Sydney, 2020. https://hdl.handle.net/2123/22453.

Texte intégral

Résumé :

Background: Metabolic associated fatty liver disease (MAFLD) afflicts about a quarter of the global population. A proportion of these patients develop chronic inflammation which can progress to cirrhosis and cancer. Sugar consumption is a major risk factor of MAFLD progression and a human FGF21 variant (rs838133) was recently found to be a risk variant for increased sugar consumption. Whether this variant is a novel risk factor for MAFLD is unknown. Methods: We studied the association of FGF21 rs838133 with liver disease severity and the metabolic profile of patients with MAFLD. Functional investigations were undertaken using allele-specific expression of FGF21 in liver, by measurement of serum FGF21 by ELIZA, bioinformatics analysis and by complementary mouse studies. Results: FGF21 rs838133 was associated with an increased risk of metabolic associated steatohepatitis (MASH), but not simple steatosis. The variant did not affect hepatic FGF21 expression or splicing, but likely affects FGF21 mRNA structure. Compared to healthy controls, patients with MAFLD have higher serum FGF21 levels (p < 0.05). This difference was more profound in patients with MASH (162 ± 47.26, p < 0.01) compared to those with simple steatosis (155.2 ± 51.98, p < 0.01). Similarly, FGF21 levels increased with progression of the NAS score and with fibrosis (p <0.05, for both). Consistently, there was a positive correlation between FGF21 levels and blood glucose, HOMA-IR, AST, GGT, triglycerides, total bile acids and primary bile acids (p < 0.05, for all). In mouse models of liver injury, Fgf21 expression was increased by a high sucrose diet, and in two liver injury models, namely bile duct ligation (p < 0.05, for both) and a methionine and choline deficient diet (p < 0.0001). There was no correlation between serum levels of FGF21 and other FGF family proteins (FGF19, FGF23). Conclusion: FGF21 rs838133 is a novel risk variant for MASH, likely via a change in mRNA folding and subsequently, stability. FGF21 serum levels are likely increased in MASH due to hepatic resistance and correlates with markers of glycaemic profile and bile acids in these patients. Different members of the FGF family of proteins are likely regulated by different mechanisms.

Styles APA, Harvard, Vancouver, ISO, etc.

Bayoumi, Ali. « Mistranslation drives alterations in protein levels and the effects of a synonymous variant at the FGF21 locus ». Thesis, The University of Sydney, 2020. https://hdl.handle.net/2123/24549.

Texte intégral

Résumé :

Background: Fibroblast growth factor 21 (FGF21) is a liver-derived hormone with pleiotropic beneficial effects on metabolism. Paradoxically, FGF21 levels are elevated in metabolic diseases. Interventions that restore metabolic homeostasis reduce FGF21. Whether abnormalities in FGF21 secretion or resistance in peripheral tissues is the initiating factor in altering FGF21 levels and function in humans is unknown. Methods: I have studied the role of the rs838133 polymorphism in regulating FGF21 protein expression in-vivo and in-vitro. Then, I explored the mechanisms by which this single nucleotide polymorphism (SNP) modulates FGF21 production. I utilized RiboLace methodology to examine FGF21 production associated with the ribosomal translationally active fraction. Next I developed an in-vitro genetic model to help resolve the paradox of FGF21 expression in metabolic disorders. Furthermore, I studied the association between rs838133 and the expression of FGF21 receptors and activity. Finally, I related my findings back to tissue and explored the functional impact of rs838133 on hepatic inflammation. Results: I have shown that the minor (A) allele of the rs838133 polymorphism is associated with higher levels of circulating and hepatic FGF21 and it is not associated with the expression of fibroblast growth factor receptor 1 (FGFR1), Klotho-β (KLB) nor fibroblast activation protein (FAP) and hence and does not alter FGF21 signalling or activity. Then I identified an unanticipated mechanism for the FGF21 levels variation which is a genotype dependant alteration in the translational rate of FGF21. This alteration is most probably the primary event which results in FGF21 levels disturbance. Furthermore, I have demonstrated that codon bias and secondary mRNA structure are pivotal elements of the effect of rs838133 on the FGF21 translation rate. Additionally, I have proposed that ribosomal protein lateral stalk subunit P0 (RPLP0) could be the link between metabolic stress and FGF21 overexpression in metabolic disorders. Finally, I have related my results back to tissue and identified that under metabolic stress, the rs838133 has a deferential inflammatory response in-vivo and in-vitro. Conclusion: My results highlight a dominant role for translation of the FGF21 protein to explain variations in blood levels that is at least partially inherited. These results provide a framework for translational reprogramming of FGF21 to treat metabolic diseases.

Styles APA, Harvard, Vancouver, ISO, etc.

Fazal-Baqaie, Masud [Verfasser]. « Project-specific software engineering methods : composition, enactment, and quality assurance / Masud Fazal-Baqaie ». Paderborn : Universitätsbibliothek, 2016. http://d-nb.info/1115793861/34.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Maslo, Armin [Verfasser]. « Interessenwahrung und Rechtsschutz der Aktionäre beim Bezugsrechtsausschluss im Rahmen des genehmigten Kapitals. / Armin Maslo ». Berlin : Duncker & ; Humblot, 2019. http://d-nb.info/1238352022/34.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Plus de sources

Livres sur le sujet "Masld"

Ṭayyib, al-Ṭayyib Muḥammad. al- Masīd. [Khartoum : s.n.], 1991.

Trouver le texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Shabanov, Pavel. Vologodskoe maslo. Vologda : Agentstvo zhurnalistskikh rassledovaniĭ "Belorizet͡s,", 2011.

Trouver le texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Beňo, Ján. Maslo v hlave. Bratislava : Slovenský spisovatel̕, 1997.

Trouver le texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Jerovec, Leon. Žaba na maslu. Ljubljana : Mihelač, 1992.

Trouver le texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Rahi, Joginder Singh. Masle galp de. 9^e éd. Amritsar : Nanaka Singhe Pusataka Mala, 2004.

Trouver le texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

1919-1967, Masle Antun, dir. Antun Masle, 1986. Split : Logos, 1986.

Trouver le texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Federat︠s︡ii, Gosudarstvennyĭ standart Rossiĭskoĭ, dir. Nefteprodukty : Masla : metody ispytaniĭ. Moskva : IPK Izd-vo standartov, 2002.

Trouver le texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Federat︠s︡ii, Gosudarstvennyĭ standart Rossiĭskoĭ, dir. Nefteprodukty : Masla : metody ispytaniĭ. Moskva : IPK Izd-vo standartov, 2002.

Trouver le texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Rawas, Muhammed. Fiqha Abdullah bin Masud. Lahore : Idara-e-muarif-e-Islami, 1992.

Trouver le texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Huq, Mahmudul. Kafan-dafaner masla masayel. Kolkata : Mallik, 2004.

Trouver le texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Plus de sources

Chapitres de livres sur le sujet "Masld"

Sourianarayanane, Achutan. « Treatment of MASLD ». Dans Managing Complex Cases in Gastroenterology, 309–18. Cham : Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-48949-5_67.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Méndez-Sánchez, Nahum, Mariana M. Ramírez-Mejía et Mohammed Eslam. « Introduction of MASLD ». Dans Metabolic Dysfunction-Associated Steatotic Liver Disease, 1–6. Singapore : Springer Nature Singapore, 2024. https://doi.org/10.1007/978-981-97-9519-2_1.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Pan, Ziyan, et Mohammed Eslam. « MASLD : Looking Ahead ». Dans Metabolic Dysfunction-Associated Steatotic Liver Disease, 157–59. Singapore : Springer Nature Singapore, 2024. https://doi.org/10.1007/978-981-97-9519-2_13.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Vidal-Cevallos, Paulina, Norberto Chávez-Tapia et Emmanuel Tsochatzis. « Diagnostic Advances in MASLD ». Dans Metabolic Dysfunction-Associated Steatotic Liver Disease, 49–60. Singapore : Springer Nature Singapore, 2024. https://doi.org/10.1007/978-981-97-9519-2_5.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Méndez-Sánchez, Nahum, Mariana M. Ramírez-Mejía et Xingshun Qi. « Unveiling the MASLD Epidemic ». Dans Metabolic Dysfunction-Associated Steatotic Liver Disease, 7–14. Singapore : Springer Nature Singapore, 2024. https://doi.org/10.1007/978-981-97-9519-2_2.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Sood, Vikrant, Snehavardhan Pandey, Mohit Kehar, Alexandre Louvet, Mariana M. Ramírez-Mejía et Nahum Méndez-Sánchez. « MASLD in Special Populations ». Dans Metabolic Dysfunction-Associated Steatotic Liver Disease, 135–56. Singapore : Springer Nature Singapore, 2024. https://doi.org/10.1007/978-981-97-9519-2_12.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Dossaji, Zahra, Tooba Laeeq, Lubaba Haque, Magnus Chun et Robert G. Gish. « Integrative Approaches to MASLD Management ». Dans Metabolic Dysfunction-Associated Steatotic Liver Disease, 125–34. Singapore : Springer Nature Singapore, 2024. https://doi.org/10.1007/978-981-97-9519-2_11.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Córdova-Gallardo, Chantal Jacqueline, Andres Manuel Vargas-Beltran, Mariana M. Ramírez Mejía et Nahum Méndez-Sánchez. « MASLD as a Multisystemic Disease ». Dans Metabolic Dysfunction-Associated Steatotic Liver Disease, 87–94. Singapore : Springer Nature Singapore, 2024. https://doi.org/10.1007/978-981-97-9519-2_7.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Stadlbauer, Vanessa. « Mikrobiom und MASLD, Leberzirrhose und Leberkarzinom ». Dans Gastrointestinales Mikrobiom, 129–44. Berlin, Heidelberg : Springer Berlin Heidelberg, 2024. https://doi.org/10.1007/978-3-662-68455-9_11.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Francque, Sven M., et Ann Driessen. « Histopathology of MASLD : Insights into Liver Tissue Changes ». Dans Metabolic Dysfunction-Associated Steatotic Liver Disease, 61–85. Singapore : Springer Nature Singapore, 2024. https://doi.org/10.1007/978-981-97-9519-2_6.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Actes de conférences sur le sujet "Masld"

Laevens, Benjamin, Yazhou Chen, Jan Clusmann et Carolin Victoria Schneider. « Characterising MASLD using Bayesian Networks in the UK Biobank ». Dans 40. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag, 2024. http://dx.doi.org/10.1055/s-0043-1777562.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Kaya, Eda, et Yusuf Yilmaz. « Deciphering the implications of the MAFLD and MASLD definitions in the NAFLD population : Results from a single-center biopsy study ». Dans 40. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag, 2024. http://dx.doi.org/10.1055/s-0043-1777508.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Schneider, Carolin Victoria, et Kai Markus Schneider. « Discriminating between MASLD and MetALD : Insights from UK Biobank Lipidomics ». Dans 40. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag, 2024. http://dx.doi.org/10.1055/s-0043-1777563.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Yong, Helena. « P33 Sera metabolite changes in obesity-induced MASLD, assayed with metabolomic approaches ». Dans Abstracts of the British Association for the Study of the Liver Annual Meeting, 8–11 October 2024, A30. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2024. http://dx.doi.org/10.1136/gutjnl-2024-basl.42.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Rau, M., J. Kestel, S. De Monte, H. B. Leicht, F. P. Reiter, H. Hermanns et A. Geier. « Liver-related outcomes of MASLD patients in a prospective, German real-world cohort ». Dans Viszeralmedizin 2024. Georg Thieme Verlag KG, 2024. http://dx.doi.org/10.1055/s-0044-1789801.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Chen, Li, Haoyu Jia, Shanshan Li, Jing Li et Changqing Yang. « IDDF2024-ABS-0412 Intestinal NLRP3 deficiency aggravates MASLD mice via reduced butyrate production ». Dans Abstracts of the International Digestive Disease Forum (IDDF), Hong Kong, 10 – 11 August 2024, A90.1—A90. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2024. http://dx.doi.org/10.1136/gutjnl-2024-iddf.46.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Buttler, L., A. Tiede, M. Griemsmann, H. Schneider, J. B. Mauz, H. Wedemeyer, M. Cornberg, T. L. Tergast, K. L. Hupa-Breier et B. Maasoumy. « Unterschiede im klinischen Verlauf von PatientInnen mit MASLD-, MetALD- und ALD-assoziierter dekompensierter Leberzirrhose ». Dans Viszeralmedizin 2024. Georg Thieme Verlag KG, 2024. http://dx.doi.org/10.1055/s-0044-1789802.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Hussain, Nasir, Usha Gungabissoon, Linda Casillas, Sumanta Mukherjee, Andrea Ribeiro, Megan McLaughlin, Philip Newsome, Matthew Armstrong et Palak Trivedi. « O37 Pruritus and the unrecognised impact in metabolic dysfunction associated steatotic liver disease (MASLD) ». Dans 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.37.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Jegodzinski, L., D. Castven, D. Becker, J. Marques Affonso, A. Mallagaray, L. Rudolph, A. Kumar Rout et al. « Genexpressionsprofile von Leber-, subkutanem und viszeralem Fettgewebe rekapitulieren die schrittweise Progression von MASLD zu MASH ». Dans Viszeralmedizin 2024. Georg Thieme Verlag KG, 2024. http://dx.doi.org/10.1055/s-0044-1789819.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Wolf, Stephanie D., Moritz C. Malms, Sophia Müller-Dott, Tobias Lautwein, Seddik Hammad, Karl Köhrer, Julio Saez-Rodriguez, Steven Dooley, Tom Lüdde et Johannes G. Bode. « Progression of MASLD goes along with significant changes of a recruited and TGFb sensitive macrophage population ». Dans 40. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag, 2024. http://dx.doi.org/10.1055/s-0043-1777564.

Texte intégral

Styles APA, Harvard, Vancouver, ISO, etc.

Nous offrons des réductions sur tous les plans premium pour les auteurs dont les œuvres sont incluses dans des sélections littéraires thématiques. Contactez-nous pour obtenir un code promo unique!