The Journal of surgical research
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It was previously reported that both pro- and anti-inflammatory cytokines are elevated in systemic inflammatory response syndrome (SIRS). Cytokine-mediated systemic neutrophil activation is a direct consequence of SIRS, and can lead to multiple organ dysfunction syndrome (MODS). This prospective study assessed the risk of SIRS and MODS after orthognathic surgery by measuring the circulating levels of inflammatory cytokines such as IL-6 and IL-10 as well as the neutrophil functions as a marker of organ failure. ⋯ These results suggest that a few patients in whom high levels of circulating inflammatory cytokine and neutrophil-derived toxic factor continue may have a possibility of contracting severe diseases such as SIRS and MODS after orthognathic surgery. We conclude that the ratio of IL-6 to IL-10 may be a predictive factor in SIRS.
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Tumors evade T cell-mediated rejection despite the presence of tumor associated antigens (TAAs) and T cells specific for these TAAs in cancer patients. Therapeutic tumor vaccines are being developed to prevent this evasion. Previous reports revealed that anti-tumor T cell responses could be activated in mice when granulocyte macrophage-colony stimulating factor (GM-CSF) or CD40L are produced at tumor vaccine sites. We sought to test the hypothesis that production of GM-CSF and CD40L by a bystander cell line could induce an anti-tumor T cell response in an in vitro human model. ⋯ A fully autologous human model consisting of tumor cells as stimulator cells and tumor-draining lymph nodes as responder cells can be used to test immunotherapeutic strategies. T cells in these lymph nodes are unresponsive to autologous tumor cells, but this lack of responsiveness can be reversed in the presence of GM-CSF and CD40L. These data provide a rationale for testing tumor cell vaccines incorporating GM-CSF- and CD40L-expressing bystanders in clinical trials.
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Our previous work observed that vascular hyporeactivity to norepinephrine (NE) developed after hemorrhage and the response was not the same in the 4 arteries examined. To evaluate possible mechanisms involved, the present study investigated the gene expression of iNOS, eNOS, IL-1beta, IL-6, TNF-alpha, and endothelin-1 in the corresponding organs, and the roles of nitric oxide (NO) and endothelin (ET). ⋯ These findings suggest that the differential expression of NOS, cytokines, and endothelin-1 in different organs are associated with the development of vascular hyporeactivity after hemorrhagic shock and may account, at least in part, for the vascular bed diversity observed.
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Sepsis is the leading cause of morbidity and mortality in the surgical intensive care unit. We postulate that the variable clinical profile of septic patients is the product of multiple factors, including initiating insult, environment, and genetic make-up. This hypothesis was tested by changing the severity of the insult and the genetic background in an experimental murine model of sepsis. ⋯ Mortality rate and cytokine profiles after CLP vary depending on the insult severity and the genetic make-up.
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Following cardiopulmonary bypass (CPB) and cardiac global ischemia and reperfusion, pro-inflammatory cytokines are activated and cause cardiomyocytic injury. Nuclear factor (NF)-kappaB is involved in regulating inflammatory signal transduction. Curcumin inhibits NF-kappaB activation and blocks the inflammatory responses. We studied whether curcumin could decrease myocardial ischemia/reperfusion injury with cardioplegia during CPB and attenuate the appearance of apoptosis of cardiomyocytes. ⋯ Curcumin, an inhibitor of NF-kappaB, ameliorated the surge of pro-inflammatory cytokines during CPB and decreased the occurrence of cardiomyocytic apoptosis after global cardiac ischemia/reperfusion injury.