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Fms-like tyrosine kinase-3 ligand alters antigen-specific responses to infections after severe burn injury.
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Burn patients are susceptible to opportunistic infections partly because of decreased immune functions, especially TH1-driven antigen-specific responses, which are regulated by dendritic cells. The dendritic cell growth factor, fms-like tyrosine kinase-3 ligand (FL), has been shown to increase
Inhibition of protein tyrosine phosphatases prevents mesenteric lymph node T-cell suppression following alcohol intoxication and burn injury.
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Previously, we have shown that acute alcohol (EtOH) intoxication before burn injury potentiates the suppression of mesenteric lymph node T-cell effector responses. Moreover, the suppression in T-cell was accompanied with a decrease in p-38 and extracellular-signal-regulated kinase (ERK) activation.
Endogenous Fms-like tyrosine kinase-3 ligand levels are not altered in mice after a severe burn and infection.
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BACKGROUND
Fms-like tyrosine kinase-3 ligand (Flt3L) is a hemopoietic cytokine and dendritic cell (DC) growth factor that promotes the proliferation and differentiation of progenitor cells into DCs. We have previously found that treatment of severely burned mice with recombinant Flt3L significantly
Enhancement of dendritic cell production by fms-like tyrosine kinase-3 ligand increases the resistance of mice to a burn wound infection.
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Fms-like tyrosine kinase-3 ligand (Flt3L) is a hemopoietic cytokine that stimulates the production of dendritic cells. This study evaluated the ability of Flt3L-enhanced dendritic cell production to increase the resistance of mice to a burn wound infection with Pseudomonas aeruginosa, a common
Fms-Like Tyrosine Kinase-3 Ligand Attenuates Local and Systemic Infection in a Model of Post-Burn Pneumonia.
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BACKGROUND
Burn injury induces immunosuppression and promotes infection with opportunistic pathogens. Pneumonia and sepsis are leading causes of post-burn morbidity and mortality. Fms-like tyrosine kinase-3 ligand (Flt3L) improves local and systemic resistance to P aeruginosa-associated burn wound
Prophylactic treatment with fms-like tyrosine kinase-3 ligand after burn injury enhances global immune responses to infection.
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Severely burned patients are susceptible to infections with opportunistic organisms due to altered immune responses and frequent wound contamination. Immunomodulation to enhance systemic and local responses to wound infections may be protective after burn injury. We previously demonstrated that
Fms-like tyrosine kinase-3 ligand increases resistance to burn wound infection through effects on plasmacytoid dendritic cells.
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Patients experiencing large thermal injuries are susceptible to opportunistic infections that can delay recovery and lead to sepsis. Dendritic cells (DC) are important for the detection of pathogens and activation of the innate and acquired immune responses. DCs are significantly decreased in burn
Tyrosine aminotransferase induction in rat liver as a response to irradiation or flash burn injuries.
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Flt3 Ligand Treatment Attenuates T Cell Dysfunction and Improves Survival in a Murine Model of Burn Wound Sepsis.
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Sepsis is a leading cause of death among severely burned patients. Burn injury disrupts the protective skin barrier and causes immunological dysfunction. In our previous studies, we found that burn injury and wound infection causes a significant decline in lymphocyte populations, implying adaptive
Plasma and urinary amino acid pattern in severe burn patients-evolution throughout the healing period.
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Plasma and urinary amino acids were measured in 12 severely burned adults (20% of body surface area or more). Measurements were made on the day of injury, and seven times thereafter until the 28th day after trauma. During the first 7 days, a decrease in plasma concentrations of some glucose
Signaling pathways targeted by curcumin in acute and chronic injury: burns and photo-damaged skin.
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Phosphorylase kinase (PhK) is a unique enzyme in which the spatial arrangements of the specificity determinants can be manipulated to allow the enzyme to recognize substrates of different specificities. In this way, PhK is capable of transferring high energy phosphate bonds from ATP to
Construction of an immunorelated protein-protein interaction network for clarifying the mechanism of burn.
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OBJECTIVE
Severe burn is known to induce a series of pathological responses resulting in increased susceptibility to systemic inflammatory response and multiple organ failure, but the underlying molecular mechanism remains unclear at present. The main aim of this study was to expand our
mTOR partly mediates insulin resistance by phosphorylation of insulin receptor substrate-1 on serine(307) residues after burn.
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Mammalian target of rapamycin (mTOR) is an important mediator for cross talk between nutritional signals and metabolic signals of insulin by downregulating insulin receptor substrate proteins. Therefore, mTOR inhibition could become a therapeutic strategy in insulin-resistant states, including
Burn injury stimulates multiple proteolytic pathways in skeletal muscle, including the ubiquitin-energy-dependent pathway.
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BACKGROUND
Burn injury is associated with increased muscle protein breakdown. However, the role of different intracellular proteolytic pathways in burn-induced muscle proteolysis is not known.
METHODS
A 30 percent total body surface area burn injury was inflicted on rats. Total and myofibrillar
Antiproteolytic action of insulin in burn-injured rats.
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BACKGROUND
Negative nitrogen balance is a typical metabolic response to burn injury resulting in decreased muscle mass and activity. Since insulin is an anabolic hormone, using insulin as a prophylactic agent in burned patients has received some attention. The present study was carried out to
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