View clinical trials related to Inflammation.
Filter by:This study evaluates the relationship between alterations in the GI microbiome and GI inflammation on symptom burden in women with breast cancer receiving chemotherapy.
The commensal oral bacteria are responsible for the initiation and propagation of the disease through the process of dysbiosis, or microbial imbalance. The disease proceeds cyclically with periods of activity and quiescence until therapeutic action is taken, or the tooth and surrounding structures are destroyed by the disease process that may result in the loss of the tooth. As periodontal disease progresses from gingivitis to periodontitis, a greater number of anaerobic organisms colonize deeper periodontal pockets, such as Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis, which triggers the host inflammatory response. This response includes the production and dissemination of C-reactive protein (CRP), a biomarker of inflammation, as well as various neutrophil and macrophage compounds such as tumor necrosis factor-alpha (TNF-a), matrix metalloproteinases (MMPs), and interleukins (IL-1 and IL-8). An elevated serum CRP level suggests that the inflammation arising as a result of periodontitis may correlate with cardiovascular pathology. Additionally, smoking creates an increasingly favorable environment for the growth of periodontal pathogens, thus furthering the disease process. In recent meta-analysis, published articles on the effect of saffron supplementation on three inflammatory biomarkers (CRP, TNF-α, and IL-6) were evaluated. Combining eight eligible trials, it was demonstrated that saffron supplementation did not have a significant effect on serum levels of the three inflammatory biomarkers. However, in the subgroup analysis, saffron was found to significantly reduce CRP and TNF-α serum concentrations
Evaluating hemostasis in decompensated liver cirrhosis with novel hemostatic assays.
The study aims to evaluate or to assess: - An improvement in the peripheral inflammatory levels in depressed patients after 8 weeks of treatment with Minocycline in addition to their current antidepressant treatment; - Any improvements in depressive symptoms after 8 weeks of treatment with Minocycline given as adjuvant to the current antidepressant treatment; - Changes in the inflammatory status in the brain (in terms of microglia activation with 11C PK PET) after 8 weeks of treatment with Minocycline in addition to the current patient's treatment; - Possible structural and functional brain changes evaluated by MRI after 8 weeks of treatment with Minocycline given as adjuvant to the current patient's treatment; - Whether changes in MRI, in microglia activation, and peripheral inflammation correlate with the improvement in depressive symptoms. In order to achieve these, a total of 60 patients, male and female, aged 25-45, who have not responded to their pharmacological treatment and who have medium-high levels of inflammation (with CRP> 2 mg/L) will be included in the study. Enrolled patients will receive, in addition to their current antidepressant treatment, Minocycline (200 mg/day as total dosage) for 8 weeks. Patients will be subjected to blood collection and clinical evaluations at baseline and after 8 weeks of treatment with Minocycline. A subgroup of patients will be subjected to MRI and 11C PK PET assessment at baseline and after 8 weeks of treatment with Minocycline.
Major depressive disorder (MDD) is a chronic mental illness, with 60% lifetime risk of recurrence after the first MDD episode. Despite available treatment options for MDD, only about half to two-thirds of patients respond to first-line antidepressant treatment, and only 30% to 45% of patients achieve remission. Scholars assume that this low remission rate and high rate of treatment resistance are due to the polyetiological nature of the disease, the heterogeneity of the clinical picture of depression, and the lack of biomarkers to stratify MDD subtypes. The aetiology of MDD, although researched extensively, remains unclear. None of the known mechanisms alone explains the pathogenesis of depression, meaning that the interplay of several factors contributes to the development of MDD. Accumulated scientific evidence has supported the importance of the immune system in the etiopathogenesis of MDD. Until now, the cause of the low-grade inflammation observed in this subgroup of MDD patients has been unclear. In the proposed study, the investigators will test a new hypothesis of the immune theory of the development of MDD: the endotoxin hypothesis of neurodegeneration. This hypothesis states that endotoxin, causes or contributes to neurodegeneration. Blood plasma levels of LPS are normally low but are elevated during infections, gut inflammation, gum disease, and neurodegenerative diseases. Dysbiosis may promote increased intestinal permeability ("leaky gut"), which leads to bacterial translocation across the intestinal barrier and into the circulation, thus forming of LPS and LPS-binding protein complex, which triggers the secretion of cytokines. Data suggest that LPS-induced peripheral inflammation can activate neuroinflammation. However, it is not known whether a low-level persistent presence of LPS in the circulatory system can cause low-grade chronic neuroinflammation leading to neurodegeneration and/or symptoms of MDD. Based on existing preclinical and clinical research data, the investigators hypothesise that an increase in blood plasma endotoxin and peripheral cytokines induce BBB dysfunction, neuroinflammation and neurodegenerative processes in specific etiologically relevant structures of the brain and cause clinical manifestation of depressive symptoms and cognitive damage. In this study the investigators are also going to investigate the effects of single nucleotide polymorphisms of four genes in relation to blood plasma endotoxin and peripheral cytokines concentrations and clinical manifestation of MDD.
The study is being done to see if ziltivekimab can be used to treat participants living with heart failure and inflammation. Participants will either get ziltivekimab (active medicine) or placebo (inactive substance that looks like the study medicine but does not contain any medicine). The treatment participants get is decided by chance. Participant's chance of getting ziltivekimab or placebo is the same. Ziltivekimab is not yet approved in any country or region in the world. It is a new medicine that doctors cannot prescribe. The study is expected to last for up to 1 year and 4 months.
The goal of this clinical trial is to evaluate cardiometabolic and inflammatory parameters in kidney transplant recipients after transitioning to a plant-based diet (PBD). The main aims of the study are as follows: - To test the feasibility of transiting renal allograft recipients who are > 3 months post-transplant to a PBD - To study the effect of a PBD on cardiometabolic parameters in kidney transplant recipients - To assess the effect of a PBD on peripheral blood Th17/Treg ratio and systemic inflammation in kidney transplant recipients Participants will be asked to: - Complete a 2-week investigator-designed PBD transition program - Follow a PBD for a minimum of 16 weeks - Consent for blood draws, urine samples, and fecal samples along with physical exams - Complete intermittent food frequency questionnaires and quality of life questionnaires - Periodically meet with investigators and other study participants Researchers will compare baseline measurements with future measurements for each participant.
The present study is testing spermidine treatment in elderly patients with coronary artery disease. The study is a randomized, double-blind, placebo-controlled, two-armed, parallel-group, single centre, clinical study.
The proposed research is designed to extend previous research findings building on the knowledge of strawberries as fruits that support a healthy immune and vascular system. The proposed research leverages a recently funded proposal by the USDA to study in greater depth inflammation, glucoregulation and oxidative stress defense and their relation to improving endothelial function and insulin sensitivity. Before and after strawberry intake, blood samples will be collected for monocyte (immune cells and source of inflammatory cytokines) isolation and activation via changes in cellular NF-κB and Nrf-2 (key transcription factors of inflammation/oxidative stress defense) status along with products of their activation (ie., plasma cytokines). Because inflammation and oxidative stress impairs endothelial function and insulin sensitivity, acutely and chronically, investigators will also study changes in vascular and insulin sensitivity status, assessing changes in vascular adhesion molecules, endothelial responsiveness through flow mediated vasodilation (ie., FMD) and insulin sensitivity using the Liquid Meal Tolerance (LMTT) if intravenous glucose tolerance test (IVGTT) method cannot be used due to supply chain issues of sterile Dextrose. Glucoregulation will be assessed by placing a Continuous Glucose monitoring (CGM) machine (Dexcom-6) to participants for 10 days at the beginning and at the end of the study period of intervention. The study will be a randomized, double-blinded, 3-arm parallel, 4-week, dose-response study. Individuals with chronic low grade inflammation will be sought to test the anti-inflammation - vaso-relaxing - insulin sensitivity effects of strawberry.
Background: COVID-19 left consequences in different organs from months to years requiring different types of rehabilitation. In fact, a severe loss in the lung function, and in the respiratory and peripheral muscle strength is commonly observed in post-COVID-19 patients. Objectives: Thus, the present study investigated whether 30 days of supplementation with a nutritional blend (ImmuneRecov®; composition: whey protein concentrate, astaxanthin, creatine, selenium, vitamin C, glutamic acid, tryptophan, magnesium) would help to minimize the respiratory (lung function) and muscular (respiratory and peripheral muscles) sequelae in post-COVID-19 patients.