Inflammation
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We prospectively studied (1) the relationships between angiogenic factors, their soluble receptors and organ dysfunction and (2) the effects of disseminated intravascular coagulation (DIC)-induced platelet consumption, thrombin generation, and tissue hypoxia on the expression of the factors and receptors. Fifty patients with sepsis were classified into two subgroups: 37 patients with DIC and 13 patients without DIC. DIC patients showed higher Sequential Organ Failure Assessment (SOFA) scores, the prevalence of multiple organ dysfunction syndrome (MODS) and more increased soluble fibrin and lactate levels. ⋯ The VEGF levels showed a marked correlation with the platelet counts. Soluble fibrin and lactate levels independently predicted increases in the levels of VEGF, sVEGFR1, and Ang2 in DIC patients. In conclusion, VEGF, sVEGFR1, Ang2, and Ang1/Ang2, especially Ang2, may have roles in the development of MODS in sepsis associated with DIC, and VEGF, sVEGFR1, and Ang2 serum levels correlated with the extent of DIC-induced platelet consumption, thrombin generation, and blood lactate levels.
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Patients undergoing surgical procedure develop an inflammatory response due to surgical trauma that may be modulated by anesthetics. The aim of this study was to investigate the cytokine profile in the plasma of adult patients who underwent minimally invasive surgery with balanced anesthesia with propofol, fentanyl, and sevoflurane. The study included 15 healthy patients scheduled for tympanoplasty or septoplasty under balanced anesthesia. ⋯ All other cytokines did not change either during or after balanced anesthesia (p > 0.05). In conclusion, balanced anesthesia with propofol, fentanyl, and sevoflurane anesthesia is not associated with intraoperative changes in the plasma cytokines in healthy patients undergoing minimally invasive otorhinological surgeries. Considering IL-6 results, a postoperative inflammatory response may have occurred due to surgical stress.
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This study explored the association of sepsis prognosis with dynamic changes in serum soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) and its polymorphisms. We enrolled 80 subjects with sepsis and 80 controls. Serum sTREM-1 was tested on days 1, 3, 5, 7, 10, and 14. ⋯ However, there was no relationship between TREM-1 polymorphism and dynamic concentration of sTREM-1. Logistic regression showed that sTREM-1, APACHE II, and rs2234237 polymorphism are risk factors for prognosis. Dynamic changes in serum sTREM-1 and rs2234237 polymorphism could be used in sepsis prognosis assessment.
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The present study aimed to determine whether any specific intestinal site or intestinal mucosal inflammation is highly correlated with bacterial translocation (BT). Enterostomy tubes were surgically placed in adult male Sprague-Dawley rats 5 days before induction of experimental model. After surgery, sterile water containing kanamycin (25 mg/L) was injected into each intestinal segment through the tubes for 3 days. ⋯ The endotoxemia ileum showed the highest levels of both intestinal permeability and inflammatory cytokine, while the colon showed the lowest. The present study of endotoxemia rats suggests that LPS increases gut paracellular permeability and induces BT. The ileum is the site of greatest BT risk, while the colon is the lowest, and the difference in risk between these sites is correlated with intestinal mucosal inflammation.
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Strong anti-inflammatory activity has been found in Laminaria japonica dichloromethane fraction (LDF); however, the molecular mechanisms underlying its anti-inflammatory activity are not reported. Our results indicated that LDF inhibited LPS-induced nitric oxide and prostaglandin E(2) production in a dose-dependent manner and suppressed the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) in RAW 264.7 cells. ⋯ Moreover, LDF inhibited activation of mitogen-activated protein kinases and AKT in LPS-treated RAW 264.7 cells. These results indicate that the LDF downregulates iNOS and COX-2 expressions through the suppression of NF-κB pathway associated with inhibition of multiple signaling proteins.