[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"health-studies-list:{\"conditionNormalized\":\"pathophysiology\",\"overallStatus\":[\"RECRUITING\",\"AVAILABLE\",\"NOT_YET_RECRUITING\"],\"orderBy\":\"LastUpdateSubmitDate:desc\",\"size\":25,\"offset\":0}":3,"health-study-condition:pathophysiology":25},{"pageToken":4,"total":5,"offset":6,"count":5,"results":7},null,4,0,[8,39,62,83],{"id":9,"slug":10,"hasResults":11,"nctId":12,"briefTitle":13,"officialTitle":13,"acronym":14,"eligibilityCriteria":15,"healthyVolunteers":16,"sex":17,"minAge":18,"maxAge":4,"enrollmentInfo":19,"targetDuration":4,"studyType":22,"phases":4,"briefSummary":23,"conditions":24,"keywords":4,"overallStatus":26,"whyStopped":4,"lastUpdateSubmitDate":27,"lastUpdatePostDateStruct":28,"startDateStruct":31,"completionDateStruct":33,"leadSponsor":35,"locationsCount":38},"100635818","study-of-the-hypothalamic-microglial-response-as-a-function-of-a-meals-lipid-content-in-humans-a-single-center-prospective-cohort-study-in-healthy-male-subjects-100635818",false,"NCT07557628","Study of the Hypothalamic Microglial Response as a Function of a Meal's Lipid Content in Humans. A Single-center Prospective Cohort Study in Healthy Male Subjects","GLIPID","Inclusion Criteria:\n\n* A person who has given oral consent\n* Male\n* Body Mass Index (BMI) between 18.5 and 30 kg\u002Fm²\n* Age ≥ 20 years\n\nExclusion Criteria:\n\n* A person subject to a measure of legal protection (guardianship, tutorship)\n* A person subject to a judicial protective measure\n* A person who is not enrolled in or eligible for a social security program\n* Subject does not speak French\n* Subjects with a pacemaker or any other contraindication to MRI\n* Subjects with type 1 or type 2 diabetes\n* Subjects with a chronic inflammatory condition\n* Subjects with a neuropsychiatric condition\n* Subjects taking anti-inflammatory medication or medication that affects the central nervous system\n* Known hypersensitivity to foods provided during the study",true,"MALE","20 Years",{"count":20,"type":21},20,"ESTIMATED","OBSERVATIONAL","Obesity and its complications represent a growing public health problem in our society. A better understanding of the biological mechanisms involved in regulating food intake-and, more broadly, energy metabolism-should lead to improved management of this condition.\n\nRecent studies have shown that eating a single meal can rapidly trigger the activation of the immune system. This leads to a postprandial, systemic, and transient inflammatory response (Emerson SR, Adv Nutr 2017). It is found in both healthy and obese individuals. It has also been observed in rodents, enabling preclinical studies to better understand the phenomenon. This postprandial inflammation is characterized by the activation of macrophages in the gastrointestinal tract and by elevated levels of circulating pro-inflammatory markers. At the cellular level, nutrients activate an intracellular molecular sensor called the inflammasome, which is a multiprotein complex formed by the oligomerization of proteins including NLRP3 (Nod-like receptors pyrin domain-containing 3) and ASC (Apoptosis-associated Speck-like protein containing a CARD domain). This sensor activates caspase 1, an enzyme that converts pro-interleukin 1β (pro-IL-1β) into its mature and active form, IL-1β. This molecular mechanism converts the nutritional signal into an immune response.\n\nUnder physiological conditions, this acute response appears to have beneficial effects on the body. Indeed, it plays a positive role in blood glucose control by stimulating insulin secretion and glucose utilization (Dror, Nat Immunol 2017). However, in the context of chronic overeating and excessive consumption of saturated fats and simple sugars, this systemic inflammation becomes harmful, promoting adipocyte hypertrophy, insulin resistance, hepatic steatosis, and vascular damage (Hotamisligil, Nature 2017).\n\nIn mice, our team recently demonstrated the existence of a postprandial inflammatory response in the central nervous system (Cansell, Glia 2021). This response occurs specifically in the hypothalamus, a brain structure involved in regulating food intake and controlling energy metabolism. It is characterized by microglial reactivity visible as early as 3 hours after the start of the postprandial phase. This postprandial microglial activation occurs after the ingestion of a high-fat meal, whereas it is rarely or never observed after the ingestion of a standard balanced meal. It is characterized by a morphological change in hypothalamic microglia, including an increase in the length of microglial processes and their branching. This gliosis is associated with increased expression of IL-1β in microglial cells. Thus, the postprandial gliosis observed 3 hours after a high-fat meal is inflammatory. Using a targeted genetic approach that allows for the ablation of the inflammasome in microglial cells, the team demonstrates that postprandial gliosis exerts a satiating effect, limiting subsequent food intake following a high-calorie, high-fat meal. Thus, microglial inflammation appears to be an additional component in the body's arsenal of adaptive homeostatic responses aimed at limiting energy intake.\n\nOur clinical project will involve translating our basic findings in mice to humans. This will involve investigating postprandial hypothalamic gliosis in the human brain following a standard meal or a high-fat meal. The initial studies will be conducted exclusively in healthy male subjects to avoid the influence of the hormonal cycle on the hypothalamic response. The impact of physiological aging on the hypothalamic microglial inflammatory response will also be taken into account.",[25],"Pathophysiology","NOT_YET_RECRUITING","2026-04-22",{"date":29,"type":30},"2026-04-29","ACTUAL",{"date":32,"type":21},"2026-05",{"date":34,"type":21},"2028-05",{"name":36,"class":37},"Centre Hospitalier Universitaire Dijon","OTHER",1,{"id":40,"slug":41,"hasResults":11,"nctId":42,"briefTitle":43,"officialTitle":44,"acronym":4,"eligibilityCriteria":45,"healthyVolunteers":11,"sex":46,"minAge":47,"maxAge":4,"enrollmentInfo":48,"targetDuration":4,"studyType":22,"phases":4,"briefSummary":50,"conditions":51,"keywords":4,"overallStatus":52,"whyStopped":4,"lastUpdateSubmitDate":53,"lastUpdatePostDateStruct":54,"startDateStruct":56,"completionDateStruct":58,"leadSponsor":60,"locationsCount":38},"100534125","immunological-mechanisms-underlying-mucosal-ige-responses-100534125","NCT06234761","Immunological Mechanisms Underlying Mucosal IgE Responses","On the Origin of Immunoglobulin E's: Elucidating the Immunological Mechanisms Underlying Mucosal IgE Responses in Type2 Disease","Inclusion Criteria:\n\npatients with nasal polyposis -\n\nExclusion Criteria:\n\npatients treated in the last 2 months with systemic corticosteroids\n\n\\-","ALL","18 Years",{"count":49,"type":21},50,"Background \u002F rationale: Type 2 inflammation is driving several chronic diseases in the airway. On one hand allergic rhinitis (AR) and allergic asthma (AA) are driven by allergen expose, while on the other hand eosinophilic Type 2 inflammation with late onset eosinophilic asthma (LOA) and chronic rhinosinusitis with nasal polyps (CRSwNP) are of non-allergic ethiology. For late onset type2 asthma, many risk factors have been defined, but clear insights into disease ethiology are currently lacking. Given the quintessential role of IgE in disease ethiology of both diseases, understanding the molecular immunological mechanisms underlying mucosal IgE responses is essential to understand disease ethiology.\n\nHypothesis: Distinct mechanisms drive local IgE production in AA and LOA Overall objectives: Elucidate the potential drivers of and immunological pathways leading to local IgE production in AA and LOA, and understand how dupilumab acts on these mechanisms.\n\nMethods: A unique combination of state-of-the-art methods will be applied, including single-cell RNA sequencing and receptor profiling, proteomics, determination of the microbial composition, recombinant antibody screening and disease modelling in cell cultures.\n\nExpected results: The investigators expect for the first time to discern the drivers of local IgE production in LOA and uncover the immunological pathways leading to local IgE production in AA and LOA. Moreover, the investigators will obtain insights into the role of Dupilumab in modulation mechanisms.\n\nImpact: If successful, these insights will answer a long standing, unresolved question in type 2 disease and might aid in the development of novel directed therapeutics for AA and LOA.",[25],"RECRUITING","2024-09-05",{"date":55,"type":30},"2024-09-19",{"date":57,"type":30},"2024-01-02",{"date":59,"type":21},"2028-12",{"name":61,"class":37},"University Hospital, Ghent",{"id":63,"slug":64,"hasResults":11,"nctId":65,"briefTitle":66,"officialTitle":66,"acronym":67,"eligibilityCriteria":68,"healthyVolunteers":11,"sex":46,"minAge":47,"maxAge":4,"enrollmentInfo":69,"targetDuration":4,"studyType":22,"phases":4,"briefSummary":71,"conditions":72,"keywords":4,"overallStatus":52,"whyStopped":4,"lastUpdateSubmitDate":74,"lastUpdatePostDateStruct":75,"startDateStruct":77,"completionDateStruct":79,"leadSponsor":81,"locationsCount":38},"100549558","responders-and-non-responders-in-the-management-of-heart-failure---significance-of-genetic-influence-and-identification-of-novel-informative-biomarkers-100549558","NCT06435585","Responders and Non-responders in the Management of Heart Failure - Significance of Genetic Influence and Identification of Novel Informative Biomarkers","Responders","Inclusion Criteria:\n\n1. Written informed consent\n2. Heart failure defined by symptoms and signs of heart failure as judged by the local investigator\n3. Registered in SwedeHF\n\nExclusion Criteria:\n\n1. Plasma donation within 1 month of enrolment or any blood donation\u002Fblood loss \\>500 mL during the 3 months prior to enrolment\n2. Previous allogeneic bone marrow transplant (genetics)\n3. In the opinion of the investigator, condition\u002Fs that may either put the patient at risk on participation or influence the results or the patient's ability to participate in the study.",{"count":70,"type":21},5000,"A biobank within the Swedish national heart failure quality registry SwedeHF.",[73,25],"Heart Failure","2024-05-24",{"date":76,"type":30},"2024-05-30",{"date":78,"type":30},"2021-02-17",{"date":80,"type":21},"2030-12-31",{"name":82,"class":37},"Karolinska University Hospital",{"id":84,"slug":85,"hasResults":11,"nctId":86,"briefTitle":87,"officialTitle":88,"acronym":89,"eligibilityCriteria":90,"healthyVolunteers":11,"sex":46,"minAge":47,"maxAge":4,"enrollmentInfo":91,"targetDuration":93,"studyType":22,"phases":4,"briefSummary":94,"conditions":95,"keywords":4,"overallStatus":52,"whyStopped":4,"lastUpdateSubmitDate":98,"lastUpdatePostDateStruct":99,"startDateStruct":101,"completionDateStruct":103,"leadSponsor":105,"locationsCount":38},"100422116","biobank-for-arrhythmia-and-conduction-disorders-toward-pathophysiology-based-treatment-100422116","NCT04776642","Biobank for \"Arrhythmia and Conduction Disorders: TowArd Pathophysiology Based Treatment\"","\"Arrhythmia and Conduction Disorders: TowArd Pathophysiology Based Treatment\" ADAPT Biobank","ADAPT","Inclusion criteria:\n\n* Patients visiting the AMC outpatient clinic\n* Patients included in an ongoing clinical trial linked to this biobank. Studies are listed under point \"Groups and interventions\" and include:\n\n  * MARK AF\n  * INDICO AF\n  * PREDICT AF\n  * WEIGHTLOSS AF\n  * MAD AF\n* Patients included in future clinical trial linked to this biobank. Studies may be linked to this biobank that investigates prevalent or incident cardiac arrhythmias.\n* Cardiac arrhtymias are defined as\n\n  * Supraventricular tachycardia, among which the most common are:\n\n    * Atrial Fibrillation (AF)\n    * Atrial Tachycardia (AT)\n    * Atrial Flutter (AFL)\n    * Atrioventricular Nodal Reentrant Tachycardia (AVNRT)\n    * Atrioventricular Reentrant Tachycardia (AVRT)\n  * Ventricular tachycardia, among which the most common are:\n\n    * Ventricular Tachycardia (VT)\n    * Ventricular Flutter (VFL)\n    * Ventricular Fibrillation (VF)\n  * Bradycardia:\n\n    * Sinus Node Dysfunction\n    * AV Node Dysfunction\n    * Interventricular Conduction Disorder\n  * Arrhythmogenic cardiomyopathies, among which the most common are:\n\n    * Dilated Cardiomyopathy\n    * Restrictive Cardiomyopathy\n    * Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)\n\nExclusion criteria (shared for all studies):\n\n* Age \\\u003C 18\n* Unable or unwilling to comply with study procedures\n* Pregnancy or of childbearing potential without adequate contraception\n* NYHA class IV heart failure symptoms or left ventricular ejection fraction \\\u003C35%.",{"count":92,"type":21},1000,"5 Years","The 'ADAPT' Biobank is a collection of body material and data from patients with or at risk of cardiac arrhythmias who underwent or will undergo (non-) invasive treatment for this disease. Its main objective is to obtain a comprehensive collection of patient information and material to facilitate research and gain better insight into the complex pathophysiology of the different arrhythmias, the multifactorial process, the heterogeneity in clinical presentation, and prognosis.\n\nBodily material is used for biochemical marker assessments, histological and molecular analyses for research in cardiac arrhythmias.",[96,97,25],"Arrythmia","Conduction Disorder","2024-01-24",{"date":100,"type":30},"2024-01-25",{"date":102,"type":30},"2014-12-18",{"date":104,"type":21},"2030-01",{"name":106,"class":37},"Academisch Medisch Centrum - Universiteit van Amsterdam (AMC-UvA)"]