Systemic lupus erythematosus(SLE) is an autoimmune disease with diverse clinical manifestations, and the mechanism of its immune disorder has not been fully defined.Previous studies have shown that type I interferon plays an important role in SLE.Type I interferon is mainly produced by macrophages and dendritic cells, and the interferon-stimulated genes in various immune cells of SLE children were significantly increased.Researchers have found that in addition to interacting with neutrophil extracellular traps, IFN-α can regulate the function of B cells, maintain and amplify autoantibodies, affect the balance of T cell subsets, ultimately aggravate autoimmune abnormalities in SLE patients.Here we review the immunological effects of type I interferon in SLE patients.

Objective:To determine the potency of epidural ropivacaine in inhibiting breakthrough pain in primiparae undergoing labor analgesia with programmed intermittent epidural bolus (PIEB).Methods:American Society of Anesthesiologists Physical Status classification Ⅰ or Ⅱ primiparae of full-termpregnancy, with a singleton fetus in vertex presentation, aged ≥18 yr, with body mass index < 30 kg/m 2, presenting with breakthrough pain during labor analgesia with PIEB, were enrolled in this study. Ropivacaine 10 ml was epidurally administered, and the concentration was determined by up-and-down sequential allocation. The initial concentration was set at 0.15% in the first patient in each group. Each time the concentration increased/decreased in the next patient depending on whether the patients showed breakthrough pain relief, and the ratio between the two successive doses was 0.9. The criterion of breakthrough pain relief was defined as numerical rating scale score < 4 points within 30 min after epidural injection of ropivacaine. The median effective concentration (EC 50) and 95% confidence interval of ropivacaine in inhibiting breakthrough pain were calculated by Dixon-Massey′s method. Results:Twenty-six patients were finally included in this study.The EC 50 (95% confidence interval)of ropivacaine in inhibiting breakthrough pain was 0.102% (0.088%-0.117%). Conclusions:The EC 50(95% confidence interval) of epidurally administered ropivacaine 10 ml is 0.102%(0.088%-0.117%) when used for inhibiting breakthrough pain during labor analgesia with PIEB in primiparae.

Background Arsenic can enter the hypothalamus to induce estrogen effect and interfere with the function of the neuroendocrine system. The thyroid endocrine system (hypothalamic-pituitary-thyroid axis) is one of the main endocrine systems, and the mechanism of arsenic-induced thyroid endocrine toxicity is still unclear. Objective To investigate the effects of different arsenic exposure levels on estradiol (E2), hypothalamic thyrotropin-releasing hormone (TRH), and their receptor (ERα, ERβ, and TRHR) mRNAs in rats and the possible hypothalamic toxic pathway and mechanism. Methods Seventy Wister rats were randomly divided a control group (sterile water); low-, medium-, and high-dose arsenic exposure groups [0.8, 4.0, and 20.0 mg·kg⁻¹ sodium arsenite (NaAsO₂)]; estrogen receptor inhibitor (ICI182780) intervention + low-, medium-, and high-dose arsenic exposure groups; with 10 animals in each group, half male and half female. Rats in the arsenic exposure groups were exposed to NaAsO₂ by drinking water for 19 weeks, and rats in the intervention groups were injected with 0.5 mg·kg⁻¹ ICI182780 via tail vein at week 9, 3 times a week. The levels of E2 and TRH in serum of rats were detected by ELISA. The expression levels of estrogen receptor α (ERα), estrogen receptor β (ERβ), and TRH receptor (TRHR) mRNAs in hypothalamus of rats were detected by real-time PCR (RT-PCR). Results (1) E2 and its receptor mRNA: Compared with the control group, the serum E2 level of female rats was increased in the low-dose and the medium-dose arsenic exposure groups (P<0.05), and the serum E2 level of male rats was increased in the low-dose, the medium-dose, and the high-dose arsenic exposure groups (P<0.05), and the change of female E2 was greater than that of male rats. Compared with the control group, the relative expression levels of ERα mRNA and ERβ mRNA in female rats were increased in the low-dose, the medium-dose, and the high-dose arsenic exposure groups (P<0.05), so were the relative expression levels of ERα mRNA in male rats (P<0.05). (2) TRH and its receptor mRNA: Compared with the control group, the serum TRH level of female rats was increased in the high-dose arsenic group (P<0.05), the relative expression level of TRHR mRNA was increased in the low-dose, the medium-dose, and the high-dose arsenic exposure groups (P<0.05). Results (1) and results (2) suggested that females were more likely than males to have abnormal changes in E2, TRH, and related receptor genes after arsenic exposure. (3) Compared with female rats in the medium-high dose arsenic exposure group, the expressions of TRH and TRHR induced by arsenic exposure were inhibited after the intervention of ICI182780 (P<0.05), suggesting that arsenic in the hypothalamus may have toxic effects on TRH and TRHR by inducing estrogen-like effects. Conclusion Arsenic exposure can induce estrogen-like effects in the hypothalamus, interfere with thyroid function, and show dose-dependent and sex differences. E2 and TRH and their receptors may be the toxic pathway of arsenic-related estrogen-like effect.