Active clinical trials for "Inflammation"

Hypothesis: The investigators propose that obese parturients will have an increased inflammatory response and a decreased anti-inflammatory response to the surgical and anesthetic insult of caesarean section and that this will be associated with a higher rate of perioperative complications, as compared to non-obese parturients.2 Background: Obese patients exhibit higher levels of inflammatory markers than non-obese patients. Furthermore, obese patients have a higher incidence of perioperative complications, especially wound infections, and this is well documented in the caesarean section population. The pregnant population is unique as a result of the immunologic changes that occur at baseline, and an increase in pro-inflammatory markers is seen in serum and in placental tissue of obese subjects, and has been demonstrated to correlate with adverse fetal outcomes. Specific Objectives: To determine the baseline levels of three established markers of inflammation in term pregnant obese and non-obese patients (defined by a BMI > and < 35 kg/M2 respectively), and examine how they change in response to the stress of surgery/anesthesia. The investigators will correlate the inflammatory response with the incidence of postoperative wound infections. Methods: Patients will be recruited to the study prior to the planned caesarean section. Blood samples for inflammatory marker levels will be performed preoperatively, immediately postoperatively, and at 24 hours postoperatively. Samples will be analyzed for pentraxin-3 (a relatively novel inflammatory marker), C reactive protein (CRP) (a well-known and clinically relevant inflammatory marker), and interleukin-10 (IL-10) (an established anti-inflammatory marker). Plasma will be analyzed by ELISA to determine levels of each biomarker. Patient charts will be reviewed to determine which patients have experienced surgical complications in the 30 days postoperatively. Surgical complications will then be correlated with the measured levels of inflammatory markers. Assuming that the levels of inflammatory cytokines in obese patients will be 15% higher in obese parturients and assuming an alpha error level of 5% and a beta error level of 20%, the investigators would need to study 18 patients per group to prove our hypothesis that inflammatory cytokine levels are correlated with postoperative infections. The investigators plan to study 20 patients per group to account for a potential patient attrition rate of 10% during the study. Significance/Importance: The connection between obesity and dysregulation of the perioperative inflammatory response has not been well established nor has perioperative inflammation in the obese population been linked to the observed increased in perioperative morbidity. The investigators hope to demonstrate these connections and hopefully will be able to identify at risk patients earlier, and in a subsequent study intervene to reduce the risk of postoperative wound infections with pharmacokinetically targeted antimicrobial prophylaxis.

Background: - Studies have shown that inflammation plays an important role in depression. Brain inflammation may contribute to depression, and may make it more difficult to treat some kinds of depression with current therapies. Researchers want to use magnetic resonance imaging (MRI) and positron emission tomography (PET) scanning to study inflammation in the brain. To do so, they will use a contrast agent, which is a chemical that can show inflammation during an imaging study. Objectives: - To see if people with major depressive disorder have increased inflammation in the brain. Eligibility: - Individuals at least 18 years of age who have major depressive disorder. Design: Participants will be screened with a physical exam and medical history. They will provide blood samples before the scanning sessions. Participants will have a PET scan after the screening visit. They will have a dose of the contrast agent before the study. This scan will look for possible brain inflammation. Participants will also have an MRI scan. This scan will take pictures of the brain for comparison studies. Treatment will not be provided as part of this study.

After an allergen challenge, the allergic inflammatory response disappears spontaneously. The initiation of the resolution of the inflammatory response is now recognized as a dynamic process, involving active biochemical programs that enable inflamed tissues to return to homeostasis. Recent data established key roles of different specific lipid mediators in the endogenous counter-regulation of inflammation and activation of resolution. Only little is known about kinetics of these specialized pro-resolving lipid mediators during acute allergic inflammation. Therefore, the primary propose of our study is to characterize the temporal evolution of cellular inflammation and specific lipid mediators after allergen challenge.

hypothesis: sleep restriction in healthy subject trigger alteration of decision making associated with immuno-inflammatory changes inclusion criterias: healthy subjects, men, under 35 years, BMI<26, no sleep troubles, intermediate chronotype design: 12 subjects, longitudinal study 2 days of baseline, 7 night of sleep restriction (4h sleep/night), recovery (1, 2, 3 and 9 normal sleep nights). parameters: decision making tests, reaction time, wakefulness test, biological parameters (cathecholamines, pro-inflammatory cytokines...), heart rate, blood pressure control of sleep restriction: continuous polysomnographic survey

A. BACKGROUND Accumulation of fat in the liver due to non-alcoholic causes (NAFLD) is associated with hepatic insulin resistance, which impairs the ability of insulin to inhibit the production of glucose and VLDL . This leads to increases in serum glucose, insulin and triglyceride concentrations as well as hyperinsulinemia. Recent epidemiologic studies have shown that a major reason for the metabolic syndrome as well as the accompanying increased risk of cardiovascular disease and type 2 diabetes is overconsumption of simple sugars. The investigators have recently shown that overeating simple sugars (1000 extra calories/day, "CANDY" diet) increases liver fat content by 30% within 3 weeks (4), and recapitulates features of the metabolic syndrome such as hypertriglyceridemia and a low HDL cholesterol concentration. The fatty acids in intrahepatocellular triglycerides may originate from peripheral lipolysis, de novo lipogenesis, uptake of chylomicron remnants by the liver and from hepatic uptake of fatty acids released during intravascular hydrolysis of triglyceride-rich lipoproteins (the spillover pathway). A classic study using stable isotope methodology by the group of Elisabeth Parks showed that in subjects with NAFLD, the excess intrahepatocellular triglycerides originate from peripheral lipolysis and de novo lipogenesis. It is well-established that ingestion of a high carbohydrate as compared to high fat diet stimulates de novo lipogenesis in humans. Meta-analyses comparing isocaloric high fat and high carbohydrate diets have shown that high carbohydrate but not high fat diets increase increase serum triglycerides and lower HDL cholesterol. Since hypertriglyceridemia results from overproduction of VLDL from the liver, these data suggest the composition of the diet influences hepatic lipid metabolism. Whether this is because overfeeding fat leads to preferential deposition of fat in adipose tissue while high carbohydrate diets induce a relative greater increase in liver fat is unknown. There are no previous studies comparing effects of chronic overfeeding of fat as compared to carbohydrate on liver fat or and the sources of intrahepatic fatty acids. A common polymorphism in PNPLA3 at rs738409 (adiponutrin) gene is associated with a markedly increase liver fat content. This finding has been replicated in at least 20 studies across the world. The investigators have shown that PNPLA3 is regulated by the carbohydrate response element binding protein 1. Mice overexpressing the human I148M PNPLA3 variant in the liver exhibit an increase in liver triglycerides and cholesteryl esters on a high sucrose but not high fat diet. These data suggest that overfeeding a high carbohydrate as compared to a high fat diet may increase liver fat more in subjects carrying the I148M allele than in non-carriers. B. HYPOTHESIS The investigators hypothesize that overfeeding a high fat as compared to an isocaloric high carbohydrate diet influences the source of intrahepatocellular triglycerides. During a high fat diet, relatively more of intrahepatocellular triglycerides originate from peripheral lipolysis and less from DNL than during a high carbohydrate diet in the face of a similar increase in liver fat. It is also possible given the lack of previous overfeeding data comparing 2 different overfeeding diets that the high fat diet induces a smaller increase in liver fat than a high carbohydrate diet even in the face of an identical increase in caloric intake because a greater fraction of ingested fat is channeled to adipose tissue than the liver. The investigators also hypothesize that liver fat may increase more in carriers than non-carriers of the I148M variant in PNPLA3 during a high carbohydrate than a high fat diet. C. SPECIFIC AIMS The investigators wish to randomize, using the method of minimization (considers baseline age, BMI, gender, liver fat, PNPLA3 genotype) 40 non-diabetic subjects with NAFLD as determined by the non-invasive score developed in our laboratory or previous knowledge of liver fat content based on MRS to overeat either a high carbohydrate or high fat diet (1000 extra calories per day) for 3 weeks. Before and after the overfeeding diets, will measure liver fat content by 1H-MRS and the rate of adipose tissue lipolysis using doubly labeled water (DDW) and [1,1,2,3,3-2H5] glycerol as described in detail below. The investigators also wish to characterize glucose, insulin, fatty acid and triacylglyceride profiles before and while on the experimental diet. An adipose tissue biopsy is taken to determine whether expression of genes involved in lipogenesis or lipolysis, or those involved in adipose tissue inflammation change in response to overfeeding, and for measurement of LPL activity. After overfeeding, both groups will undergo weight loss to restore normal weight as described in our recent study. The metabolic study is repeated after weight loss.

The purpose of this research study is to investigate how and why the loss of muscle mass occurs with aging. Tissue collected from young subjects will be compared to previously collected tissue from elderly subjects, as well as previously collected data on muscle function/mass to further investigate cellular and molecular pathways that have recently been shown to be important for the aging process in muscle. The Principal Investigator (PI) and the study team will look for specific proteins (called biomarkers) that can be present in the muscle tissue in various amounts in different individuals. This study will increase the investigators understanding of the processes of muscle atrophy (loss of mass) and functional loss at older age and will help to find new treatments and interventions aimed at improving the quality of life and independence of America's rapidly expanding elderly population.

Polar lipids have a specific chemical structure: they are an essential component of human cell membranes, play a major role in the nervous system and also influence the metabolic pathways including the cholesterol metabolism. Polar lipids are used in food-processing industry for their emulsification properties. The most famous emulsifier is soya lecithin but milk also naturally contains natural emulsifiers such as polar lipids. The purpose of this research is to study plasma cholesterol variation after daily intake of milk polar lipids-fortified cheese products. The volunteers will have to consume 100 g of cheese product during four weeks instead of their usual cheese products. It is a bi-centric study with a centre in LYON (Centre de Recherche en Nutrition Humaine Rhône-Alpes) and CLERMONT-FERRAND (Centre de Recherche en Nutrition Humaine Auvergne).

This study aims to determine if different diabetes treatments have different effects on inflammation; in particular, kidney inflammation. This type of inflammation is common in people with diabetes, and can lead to kidney failure. This study will investigate the effect of different types of diabetes treatment on kidney inflammation. This will help us to decide if certain types of medicine should be preferred in people with evidence of inflammation in their kidneys, as this may help prevent major complications including kidney failure.

The objective of this randomized, double-blinded, placebo-controlled, parallel trial is to determine whether consuming avenanthramide-enriched oats daily for 8 weeks on can improve biomarkers of inflammation in older, obese adults.

The objective of this randomized, double-blind, placebo-controlled, parallel-design clinical trial is to investigate the potential antioxidant benefits of a cranberry beverage. The investigators hypothesize the chronic consumption of this beverage will improve indices of oxidative stress, inflammation, endothelial function, and glucoregulation. The investigators also hypothesize that these benefits will be particularly evident following an oral glucose tolerance test.