Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04

    • Bacterial LPS stimulates monocytes and tissue macrophages to

    2019-05-18

    Bacterial LPS stimulates monocytes and tissue macrophages to release TNF-α and IL-1, which then stimulate secondary response cytokines, including IL-6. In addition to hematopoietic cells, IL-6 is synthesized by many different types of nonhematopoietic cells, including endothelium, lasting for an extended period in response to various stimuli. Activation of the inflammatory cascade impacts the coagulation pathway, and vice versa, and affect the endothelium. Widespread involvement of endothelium and monocytes/tissue macrophages, together with the more generalized activation of inflammation and coagulation, may lead to multiple organ dysfunction. According to our results, it is speculated that LS attenuates the late response induced by LPS and further mitigated multiple organ dysfunctions at 4 h after LPS injection, while early response protein TNF-α is not suppressed by LS. According to the dosage of LS used in the previous study done by Fries et al., we applied the preliminary dosage of LS (12 μg/kg for 10 min and 0.3 μg/kg/min for 4 h), which is compatible with the dosage used in patients with nrf2 inhibitor failure. However, the study showed disappointing results in the treatment of sepsis-induced coagulopathy (data not shown). In the current study, therefore, we used a twofold dosage (24 μg/kg for 20 min and 0.6 μg/kg/min for 4 h), which did not lead to a significant decrease in blood pressure in both the control and LPS rats. However, the current study has some limitations which need to be addressed. First, we used the experimental rat model which does not imitate the clinical manifestation of sepsis. However, Patel et al. reported that polymicrobial sepsis induced by cecal ligation/perforation and endotoxemia promote microvascular thrombosis under different mechanisms. More importantly, endotoxemia, but not cecal ligation/perforation, causes significant thrombocytopenia and coagulation derangement, comparable to hemostatic features in patients with sepsis. Second, it has been shown that an initial 3-h management bundle remains very important regarding early detection of the onset of severe sepsis and septic shock. In this study, LS was given at 10 min after LPS administration, namely co-administered with LPS. Therefore, it may be a potential adjuvant of early therapy for sepsis.
    Introduction The presence of multiple heavy metal contaminants is of grave concern and has received considerable attention in Taiwan. Heavy metals such as mercury (Hg) are toxic contaminants, which can cross the placenta and affect fetal growth. Essential minerals such as iron (Fe), copper (Cu), and manganese (Mn) are both nutrients and potential toxicants, depending on the amount of exposure. These essential minerals are metabolized similarly to the heavy metals, and they are also important metallic cofactors in catalyzing redox reactions. The developing brain is highly sensitive to oxidative damage, so the concentrations of essential minerals play a crucial role in fetal brain development. Few data are available on the concentrations of both essential minerals and heavy metals in maternal/fetal medicine. Butler Walker et al reported levels of total Hg and methyl Hg were significantly higher in cord blood than in maternal blood (p<0.0001), whereas maternal Cu levels were significantly higher than those in cord blood (p<0.0001). The confounding factors were not analyzed except for ethnicity and smoking habits; furthermore, they did not evaluate the association of these metals with birth outcome. Rudge et al showed that Hg levels in cord blood were almost twice those of the mothers (n = 62), suggesting that the fetus may act as a filter for maternal Hg levels during pregnancy. Mn and Cu levels did not show statistically significant correlations between the two compartments. However, they also did not evaluate the confounding factors or association of these metals with birth outcome. A Taiwanese study (n = 308) by Lin et al demonstrated that cord blood lead was lower where the mother had a higher blood concentration of Mn (p = 0.02). Kopp et al studied the association of multiple heavy metals and trace elements between maternal and cord blood (n = 50). Hg accumulated in the fetus resulting in more than a three-fold increase in fetal exposure compared with maternal exposure. Their results also showed no association between internal exposure to any metals and maternal use of nutritional supplement during pregnancy.