View clinical trials related to Mitochondrial Dysfunction.
Filter by:The goal of this observational study is to evaluate the presence of mitochondrial dysfunction related to oxidative stress and its possible role in frailty, with and without multimorbidity, and to identify possible frailty biomarkers correlated with mitochondrial dysfunction. The main questions it aims to answer are: - What is the role of oxidative stress-related mitochondrial dysfunction in frailty, taking into account the interaction with multimorbidity. - What could be the specific biomarkers associated with mitochondrial dysfunction in the assessment of frailty. In order to reach the study goals, we will enroll three categories of older adults: - Non-Frail without Multimorbidity (NFWoM); - Frail with Multimorbidity (FWM); - Frail without Multimorbidity (FWoM). Each individual will undergo an assessment of frailty phenotype and multimorbidity, and the collection of blood samples to isolate Peripheral Blood Mononuclear Cells (PBMCs). The identification of frailty biomarkers in each group of participants will be performed by combining untargeted metabolomics-based approaches and functional studies on specific mitochondrial dysfunctions performed on PBMCs and their subpopulations. Multivariate statistical and machine learning techniques will characterize the three clinical phenotype groups based on molecular data.
To date, little is understood regarding post-COVID fatigue or cancer fatigue though it is known to affect a large proportion of patients (10-70% depending on the population). This study aims to investigate potential mitochondrial function and metabolic changes in brain to provide further information regarding the etiology of these changes leading to fatigue. This study hypothesized that Post-COVID fatigue is ensued by perturbations in metabolism and mitochondrial function in the brain. This is a case-control study. In this study, 30 patients (experimental group) complaining of persistent fatigue lasting longer than 4 weeks after recovering from SARS-CoV-2 infection and the age/gender-matched control of 30 healthy subjects (control group 1) and 30 patients suffering from cancer-related fatigue patients longer than 4 weeks after remission (control group 2). Both the experimental group (post-COVID fatigue) and control group 2 (cancer fatigue) will be recruited from NUH outpatient clinic will undergo a session of MRI, 3D Arterial Spin Labelling (ASL) and 1H magnetic resonance spectroscopy (MRS) and the Chalder Fatigue Scale, Health Questionnaire (EQ-5D-5L) and Hamilton Depression Rating Scale at baseline and follow-up visit.
In surgical patients early risk prediction of postoperative complications and organ dysfunctions is still an important clinical challenge whereas appropriate risk predictors are still missing. In this regard, fatigue is a complex phenomenon, is affected by many factors and has been shown to be associated with delayed return to normal activity after surgery. The investigators hypothesize that early tiredness (acute fatigue) assessed shortly after surgery is associated to postoperative complications and organ dysfunctions and might be used for risk stratification. Therefore, in this prospective, observational study the investigators introduce and evaluate a newly developed score to assess early fatigue during the perioperative period ("Acute Fatigue Score", AFS). The AFS and the Identity-Consequence Fatigue Scala will be used to assess early fatigue and perioperative time courses and inter-rater-variability will be evaluated. The rating of these two fatigue scores will be evaluated regarding the association with hemodynamic, immunologic, endothelial, metabolic, gastrointestinal measures as well as organ dysfunction and complications after surgery. Furthermore, hemodynamic, immunologic, endothelial, metabolic and gastrointestinal measures are investigated with respect to the intraoperative course and postoperative organ dysfunction and complications. In a subgroup of patients, patients will undergo specialized metabolic measures to investigate mitochondrial dysfunction during the perioperative period.
Part A: The study is a double-blind, randomized, single ascending doses, study in 24 healthy elderly male and female volunteers. Each subject will be randomized for two subsequent doses in three cohorts. Part B: The study is a double-blind, randomized, multiple ascending doses study in 36 healthy elderly male and female volunteers. Subjects will be randomized to receive study product or placebo for 28 days.
The symptoms and severity of arterial disease is secondary to perfusion deficit. The specific alteration of the mitochondrial function of ischemic skeletal muscle plays an important role, and therapeutic enhancing mitochondrial function are associated with a clinical improvement with increase in the walking distance of the patient. In severe ischemia, reperfusion required is accompanied by a deleterious episode through a worsening of endothelial dysfunction (impaired pathway of nitric oxide (NO)), majorant alteration of cellular energy and the hormonal and inflammatory responses. This is reperfusion syndrome, which can lead to grave consequences. Our goal is to limit mitochondrial and endothelial dysfunction (increased by the reperfusion) by stimulating the NO pathway by in situ addition of its precursor, L-arginine. Our working hypothesis is that this cellular improvement will be accompanied by an increase in systolic pressure index and an improvement in the walking distance. Method: This is a trial with direct individual benefit, comparative, randomized, prospective, single-center, double-blind, versus placebo.
The purposes of this study are to evaluate if switching an antiretroviral medication from efavirenz (EFV) to atazanavir/ ritonavir (ARV/r) will, in a 96-week period, change: 1. the amount of fat in HIV patients with lipoatrophy, 2. metabolic lab values such as your lipid (fat) profile, glucose (blood sugar), and insulin (a hormone that regulates glucose) in HIV patients with lipoatrophy.
Obesity and type 2 diabetes are occurring at epidemic rates in the United States and worldwide. The global burden of diabetes is estimated to double over the next 25 years. Obese children are at risk for the development of insulin resistance, relative insulin deficiency and type 2 diabetes mellitus (DM). The prevention of type 2 DM is hindered by the lack of a non-invasive predictive test, knowledge as to individual risk and effective preventative measures. There is increasing evidence that alterations in mitochondria contribute to the development of diabetes in humans. Therefore, it is important to explore mitochondrial dysfunction as a potential predictor of diabetes in children and a potential target for prevention. The aims of the proposed protocol are to determine whether an intensive exercise intervention can improve mitochondrial function in children identified as having mitochondrial dysfunction and insulin resistance. The use of a non-invasive imaging technique will allow for a functional in vivo assessment of mitochondrial activity. The investigators propose the investigation of an intensive exercise protocol designed to improve mitochondrial function in children who are insulin resistant and have documented mitochondrial dysfunction by magnetic resonance spectroscopy. The study is designed to investigate the plasticity of abnormal mitochondrial function in high risk children. In summary, the proposed projects will investigate mitochondrial function as a non-invasive predictive marker for the development of insulin resistance and type 2 diabetes mellitus in children and attempt to modify mitochondrial function with an intensive exercise intervention. The study of mitochondrial dysfunction in children may both identify those at risk for disease and provide a molecular therapeutic target for prevention and treatment. The investigators hypothesize that children with insulin resistance and mitochondrial dysfunction who are randomized to intensive exercise versus standard lifestyle advice will show improvement in mitochondrial function and insulin sensitivity.