Mediators of inflammation
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Mediators of inflammation · Jan 2013
Impact of the body mass on complications and outcome in multiple trauma patients: what does the weight weigh?
Obesity is known as an independent risk factor for various morbidities. The influence of an increased body mass index (BMI) on morbidity and mortality in critically injured patients has been investigated with conflicting results. To verify the impact of weight disorders in multiple traumatized patients, 586 patients with an injury severity score >16 points treated at a level I trauma center between 2005 and 2011 were differentiated according to the BMI and analyzed regarding morbidity and outcome. ⋯ In brief, obesity was the highest risk factor for development of a multiple organ dysfunction syndrome (MODS) (OR 4.209, 95%-CI 1.515-11.692) besides injury severity (OR 1.054, 95%-CI 1.020-1.089) and APACHE II score (OR 1.059, 95%-CI 1.001-1.121). In obese patients as compared to those with overweight, normal weight, and underweight, the highest levels of CRP were continuously present while increased systemic IL-6 levels were found until day 4. In conclusion, an altered posttraumatic inflammatory response in obese patients seems to determine the risk for multiple organ failure after severe trauma.
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Mediators of inflammation · Jan 2013
NF-κB inhibition after cecal ligation and puncture reduces sepsis-associated lung injury without altering bacterial host defense.
Since the NF-κB pathway regulates both inflammation and host defense, it is uncertain whether interventions targeting NF-κB would be beneficial in sepsis. Based on the kinetics of the innate immune response, we postulated that selective NF-κB inhibition during a defined time period after the onset of sepsis would reduce acute lung injury without compromising bacterial host defense. ⋯ Transiently blocking NF-κB activity after the onset of CLP-induced sepsis can effectively reduce acute lung injury in mice without compromising bacterial host defense or survival after CLP.
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Mediators of inflammation · Jan 2013
Early serum procalcitonin level after primary total hip replacement.
Procalcitonin (PCT) is a useful surrogate marker for the differentiation of postoperative infection and unspecific inflammatory reaction after surgery. It is known that postoperative course of the PCT serum level varies with type of surgery. No data exists about the postoperative course of serum PCT levels after primary total hip replacement (THR). ⋯ Similar to observations in cardiothoracic, intestinal, and neural surgeries, postoperative course of PCT after primary THR showed a uniform low-level course with a peak at the second postoperative day but below expected levels in systemic infections.
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Mediators of inflammation · Jan 2013
Dexmedetomidine inhibits inflammatory reaction in lung tissues of septic rats by suppressing TLR4/NF-κB pathway.
Dexmedetomidine has been reported to reduce mortality in septic rats. This study was designed to investigate the effects of dexmedetomidine on inflammatory reaction in lung tissues of septic rats induced by CLP. After induction of sepsis, the rats were treated with normal saline or dexmedetomidine (5, 10, or 20 μg/kg). ⋯ IL-6 and TNF-α levels in BALF and plasma, NF-κB activity, and TLR4/MyD88 expression in rat lung tissues were markedly enhanced after CLP. Dexmedetomidine (10 and 20 μg/kg) significantly decreased mortality and pulmonary inflammation of septic rats, as well as suppressed CLP-induced elevation of TNF- α and IL-6 and inhibited TLR4/MyD88 expression and NF-κB activation. These results suggest that dexmedetomidine may decrease mortality and inhibit inflammatory reaction in lung tissues of septic rats by suppressing TLR4/MyD88/NF-κB pathway.
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Mediators of inflammation · Jan 2013
Protective effects of necrostatin-1 against concanavalin A-induced acute hepatic injury in mice.
Necrostatin-1 (Nec-1) inhibits receptor-interacting protein 1 (RIP1) kinase and programmed necrosis. This study was designed to examine the protective effects and mechanisms of Nec-1 in concanavalin A- (ConA-) induced hepatitis in mice. ⋯ These results demonstrate that Nec-1 prevents ConA-induced liver injury via RIP1-related and autophagy-related pathways.