View clinical trials related to Burns.
Filter by:The purpose of this study is to evaluate the effect of burn injury on the human immune system with a focus on cytomegalovirus (CMV) reactivation and the immunologic correlates of latent viral reactivation. Subjects will be patients admitted to the North Carolina Jaycee Burn Center with burn injury. Blood samples will be collected over time and will be evaluated for CMV reactivation and immune cell phenotype.
The purpose of this study is to prospectively evaluate whether the addition of continuous glucose monitoring to point-of-care (POC) glucometer monitoring improves glucose control.
The purpose of this study is to evaluate the safety of a protein called BPI that is naturally made by the body's white blood cells to fight infection.
Discussion and evaluation of patients with sore and burning mouth to determine whether alpha lipoic acid is helpful in managing their symptoms.
Anorexia in children with burn injury is a common phenomenon. The study is searching for the origin of the anorexia in those children. The study correlates between the level peptides of the immune and the endocrine systems and the length of the anorexia.
The purpose of this study is to evaluate the efficacy and safety of treatment of chronic cutaneous ulcers and burn wounds with topical beta adrenergic antagonists (Timoptic®).
After severe burn injury, the full-thickness burn areas are excised (in the first week) and then temporarily covered with allograft (cryogenic preserved cadaver skin). This first covering is then replaced with thin skin meshed autograft. In this study, either the dermal substrates cellularised LG002 or uncellularised LG002 will be grafted, after excision, in symmetrical areas, in replacement of the allografts. Fourteen to twenty one days after this first covering, the dermal substrate will be covered with thin skin meshed autograft.
This study is designed to see if some tests of hand movement, strength, and function are valid for children with burns.
Skin graft fixation is essential for the success of its survival. There are several common methods for skin graft fixation including sutures, skin staples and glue. The study objective is to compare between skin graft fixation with staples and glue in burn patients. The study is retrospective. It Includes 44 patients that were hospitalized in the burn unit, Rabin Medical Center, Israel with 2nd and 3rd degree burns, total body surface area 1-50% during 1/2002-5/2003.All patients were operated for debridement and skin grafting. In 29 patients the skin graft was fixated with staples and in 15 with cyanoacrylate glue (histoacryl). The parameters that will be compared are skin graft take, hospitalization length and local infection.
Insulin resistance and hyperglycemia contribute to negative outcomes in burned patients. We will assess insulin sensitivity in traditional terms of glucose metabolism, and with regard to the responsiveness of both muscle and liver protein metabolism, in severely burned patients. Plasma free fatty acid (FFA) and tissue TG levels will be manipulated via inhibition of peripheral lipolysis with nicotinic acid or activation of plasma lipoprotein lipase activity with heparin, stimulation of tissue fatty acid oxidation and thus reduction of tissue TG with the peroxisome proliferate-activated receptor (PPAR) alpha agonist fenofibrate. Methodological approaches will include stable isotope tracer techniques to quantify kinetic responses of protein, glucose and lipid metabolism in vivo, quantification of intracellular stores of TG and glycogen by means of magnetic resonance spectroscopy (MRS), as well as quantitative analysis of tissue levels of active products of fatty acids, key intermediates of the insulin signaling pathway, glycogen, the enzyme activities of citrate synthase and glycogen synthase and the activity of the muscle mitochondria. These studies will clarify the physiological and clinical significance of the alterations of tissue lipid metabolism that occur after burn injury, thereby forming the basis for new therapeutic approaches not only in this specific clinical condition but in other clinical circumstances in which hepatic and/or muscle TG is elevated. We will investigate the general hypothesis that the accumulation of intracellular TG in liver and muscle either directly causes insulin resistance in those tissues or serves as an indictor of the intracellular accumulation of active fatty acid products, such as fatty acyl CoA and diacylglycerol, which in turn disrupt insulin action. The following specific hypotheses will be investigated: 1. Intracellular TG is elevated in both muscle and liver in severely burned patients. The reduction of the fat in the liver and the insulin resistance will improve clinical outcomes, glucose and protein metabolism. 2. The insulin signaling pathway, as reflected by phosphoinositol-3-kinase (PI3K) and PKC activity, is impaired in tissues with elevated TG. 3. Fatty acids, or their active intracellular products, are the direct inhibitors of insulin action, rather than the tissue TG itself.