Active clinical trials for "Inflammation"

The purpose of this study is to help improve our understanding of the biology involved in the body's response to serious trauma or burn injury. The host response to trauma and burns is a collection of physiological and pathophysiological processes that depend critically upon the regulation of the human innate immune system, with particular emphasis on the inflammatory component of that system. No single research center or small group of centers has the capacity to delineate the integrated response of this complex biological system, which involves multiple molecular and genetic interactions that vary in time. Our proposal promotes the identification of important dynamic relationships that regulate the integration of this complex biological system, with the expectation that this understanding will ultimately impact the diagnosis, prognosis, and treatment of the hospitalized, severely injured patient.

The investigators prospectively document infectious, neurological, and other complications or adverse events occurring during peripheral regional anesthesia via a catheter using computer-based data recording.

The histological characteristics of alcoholic liver disease (ALD) and non-alcoholic steatohepatitis (NASH) related to overweight and obesity suggest the presence of partly common physiopathological mechanisms. We reported that the ponderal overload was an independent risk factor of alcoholic cirrhosis. The adipose tissue was considered for a long time as a simple place of storage of fat. However, it is now recognized that the adipose tissue can secrete cytokines called ADIPOKINES. The adipose tissue can secrete others cytokines such as TNF-alpha, IL6, IL10 and IL1-Ra. Increase in the production of the leptin and TNF-alpha by the adipose tissue after alcohol administration in the rat, as well as the role of leptin in inflammation and liver fibrogenesis in the murine model of chemical hepatotoxicity strongly suggest that activation of adipocytes by alcohol can explain the strong correlation observed between the body mass index (BMI) and the severity of ethanol-induced liver injury. Conversely, it was suggested in a murine model that the reduction in adiponectin production would sensitize the liver with the toxicity of alcohol. The PPAR alpha and gamma are the receptors which play a role both in inflammation and glucide and lipid metabolism. Taking into account the inhibiting role of PPAR alpha on the proliferation of the hepatic stellate cells, responsible for the fibrosis, the PPAR could also be implied in the relation between the overweight and the hepatic fibrosis in the alcoholic.

To investigate the association of selected genetic markers of inflammation and endothelial activation with the occurrence of non-fatal acute myocardial infarction (MI).

To investigate biochemical and genetic markers of inflammation and endothelial dysfunction as determinants of hypertension.

To investigate the relationship between genetic variation in genes for inflammation and carotid artery atherosclerosis.

To test the theory that accelerated inflammation-promoted atherosclerosis occurs in patients with rheumatoid arthritis (RA).

To determine the relation between cardiovascular disease risk factors and systemic markers of vascular inflammation in the Framingham Study cohort.

This study evaluates the local inflammatory and resolution response of patients undergoing peripheral vascular intervention like an angioplasty of the superficial femoral artery (SFA) or popliteal artery, or stenting of the iliac artery or SFA, through the use of Positron emission tomography-magnetic resonance imaging (PET/MRI). PET/MRI will be performed prior to intervention, one day and one week after intervention.

According to the World Health Organization, cardiovascular diseases (CVDs) are the number 1 cause of death globally. Systemic and local tissue inflammation is now recognized as a key etiological process leading to CVD. Hence, elevated blood levels of inflammation markers are classified among the well-established risk factors for the development of CVD. Among nutritional strategies to prevent and/or reduce chronic inflammation, long-chain omega 3 PUFA (LCn-3PUFA), notably eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have raised tremendous interest for their purported anti-inflammatory effects. Previous meta-analysis of randomized controlled trials (RCTs) substantiated the anti-inflammatory effect of LCn-3PUFA supplementation as evidenced by significant reductions in plasma concentrations of specific inflammation markers such as C-reactive protein (CRP) and tumor necrosis factor alpha (TNF-alpha). However, it is stressed that almost all of the reported RCTs have used a mix of EPA and DHA in various ratios, as EPA and DHA occur concomitantly and naturally in food (fish oils) and in most dietary supplements. Yet, several recent RCTs have recently been undertaken to test the hypothesis that not all LCn-3PUFAs are equal, at least when it comes to their anti-inflammatory effects. Accordingly, there is increasing interest and evidence for potential distinctive effects of DHA compared to EPA on systemic inflammation, raising the question: Is DHA a more potent anti-inflammatory nutrient than EPA? To formally answer this question, we will conduct a systematic review and meta-analysis of RCTs to assess and compare the individual anti-inflammatory effects of DHA and of EPA. The present work will be a pairwise and network meta-analysis focusing on RCTs comparing the effects of EPA and DHA on surrogate markers of systemic inflammation. The findings generated by these analyses will provide invaluable and timely comparative information on the specific efficacy of DHA and EPA as one of the key nutritional modalities for the treatment of chronic inflammation in high-risk men and women. This is important considering that LCn-3PUFA supplements are increasingly being used by the population and an ever growing market in the dietary supplements' industry.