View clinical trials related to Healthy Controls.
Filter by:Antipsychotic (AP) medications are considered to be the gold standard treatment for psychotic disorders including schizophrenia. However, APs have also been commonly associated with serious metabolic adverse effects including weight gain and Type 2 Diabetes, with younger populations disproportionately affected. In addition, young individuals treated with these agents have also been found to be at high risk for glucose dysregulation, including higher rates of prediabetes, with significant associations found between AP use and insulin resistance. Due to the concerning prevalence of these AP metabolic effects, it becomes important to further elucidate the mechanisms underlying AP effects on glucose metabolism, which are still poorly understood. One potential underlying mechanism is insulin which has been found to regulate hepatic (liver) glucose production through insulin receptors in the brain. These insulin receptors also play a role in neuronal growth and memory, or more broadly, cognition. Preliminary data in rat models has demonstrated that the AP olanzapine (OLA) inhibits the ability of a central insulin stimulus (acting at the level of the brain) to decrease endogenous glucose production (EGP), making this mechanism a prime target to translate from rodent models to human research. Furthermore, intranasal insulin (INI) administration (an analogous central insulin stimulus) has been repeatedly associated with improved cognitive performance for verbal memory and visuospatial functions in humans. Given these findings and with the goal of translational research, the present study will investigate OLA's effects in healthy human volunteers including: (a) the ability of INI to reduce EGP during a pancreatic euglycemic clamp (PEC; a glucose metabolism and insulin procedure); and (b) the ability of INI to improve cognitive performance. More specifically, the present study hypothesizes that: 1. INI will be associated with a decrease in EGP relative to intranasal placebo (INP) as measured by the PEC. This effect will be inhibited if OLA is co-administered. 2. OLA administration will be associated with decrements in cognitive measures (i.e., visuospatial, and verbal memory) as compared to placebo (PL). Additionally, OLA co-administration will block the beneficial effects of INI on cognition previously supported by other studies. 3. INI will result in adaptive changes in neurochemical and neurohemodynamic measures as studied using MRI imaging techniques.
The purpose of this study is to investigate changes in the corneal thickness of scleral contact lens wearers in a keratoconic (KC) population and compare to age-matched controls. The hypothesis is that scleral contact lens wear is associated with low levels of corneal hypoxia including measurable changes in corneal thickness. Corneal thickness will be altered post scleral lens wear compared to pre-lens wear and the amount of alteration will correlate to the fitting characteristics in the central zone of the scleral lenses. We propose to take a sample of keratoconic and control participants, fit them in scleral lenses, and to measure topographic corneal thickness after 8-10 hours of scleral lens wear after three weeks of wear, to compare two instruments in the measurement of corneal thickness, and to compare the effects of varying central corneal clearance of the scleral lens on corneal thickness.
With this study, the investigators aim to test whether acute administration of selective serotonin reuptake inhibitors (SSRI) improves motor performance in a sequential motor learning task in comparison to placebo in healthy humans.
The objective of the study is to investigate pain mechanisms, comorbidity status, biomarkers, patient reported outcome measures, ultrasonographic (US) inflammatory activity and association between these features in patients with psoriatic arthritis (PsA) intensifying anti-rheumatic treatment. Furthermore, to assess the predictive value of baseline pain profile, comorbidity status, and US joint/entheses activity on treatment outcome after 4 months. Finally, we aimed to compare baseline characteristics with I) patients with skin psoriasis without arthritis and II) healthy controls.
Aim: More insight in pathogenesis of IBS and IBD. Samples are collected in context of an European research project.
There is accumulating evidence suggesting that inflammatory processes, through microglial activation, would play a key role in the neurodegenerative process of Parkinson's disease (PD). It is considered that microglial activation would be part of self-propelling cycle of neuroinflammation that fuels the progressive dopaminergic neurodegeneration. It is however hard to evidence microglial activation in vivo, especially in the substantia nigra: first, the investigators need very high resolution imaging tools and then, the only ligand available to date, 11C-PK11195, has a low sensitivity and specificity and provided heterogeneous results. 18F-DPA-714 is a new PET ligand which labels microglial cells. The investigators aim to explore the topography and intensity of microglial activation in several different groups of PD patients: 1) de novo, drug-naïve subjects (n = 6); 2) non-fluctuating treated patients ("honeymoon") (n = 10); 3) advanced drug-responsive patients motor fluctuations (wearing-off or dyskinesia) (n = 6); 4) patients with LRRK2 gene mutation (n = 6); and 5) related to healthy patients carriers of the mutation LRRK2(n = 6). PET imaging will be performed with a new generation tomography having a very high resolution. This study might reveal significant neuroinflammatory process in the midbrain of PD patients and will determine if such process is present in both sporadic and genetic forms of PD. The results of this study might provide a new biomarker of disease pathological progression and help as identifying subjects who might most benefit from a specific anti-inflammatory drug.
This study aims to investigate whether two different measures of tactile acuity lead to comparable results in patients diagnosed with CRPS Type I of the upper extremity. Additionally patients with a neuropathy of the median nerve and healthy controls are included.
Concussed athlethes have discrete decreased abilities in motor learning. Recent research could further show, that cortical plasticity, as measured by transcranial magnetic stimulation (TMS) is reduced. This is possibly due to an increased GABAergic activity, what have been found in concussed athletes by paired pulse protocols in TMS. GABAergic acitivty can be modulated by transcranial direct current stimulation (tDCS) in a polar-specific manner: anodal tDCS was able to decrease GABA, whereas cathodal tDCS increased tDCS. Our study aimes to assess the influence of anodal tDCS on cortical plsticity in concussed athlethes. We hypothesize, that anodal tDCS is able to increase cortical plsticity in concussed athlethes.