AIM: To establish a model of staphylococcal enterotoxin B (SEB)-induced steroid resistance in human peripheral blood mononuclear cells (PBMCs), and to investigate the potential mechanism of SEB superantigen-induced steroid resistance in vitro. METHODS: PBMCs were isolated from normal children blood by Ficoll-Hypaque gradient centrifugation and stimulated with SEB at different concentrations. The proliferation rate of cells was measured by MTT assay. The subcellular localization of glucocorticoid receptor α (GRα) was examined by confocal microscopy. Protein phosphorylation was measured by means of Western blotting. RESULTS: SEB induced steroid resistance in a range of 10-500 μg/L and no significant difference among concentrations was observed. In SEB-stimulated PBMCs, the GRα did not translocate to the nuclear after dexamethasone treatment. ERK inhibitor U0126 significantly attenuated the inhibition of GRα nuclear translocation in SEB-stimulated PBMCs. SEB also induced more rapid and sustained phosphorylation of ERK1/2 in PBMCs. CONCLUSION: This study demonstrates that SEB may contribute to steroid resistance through ERK pathway and is associated with abrogation of GRα nuclear translocation.

Objective:To explore the effects of health education on the knowledge and awareness of hypertension in primary and secondary school students.Methods:Twenty seven primary and secondary schools in Emin County of Xinjiang Uygur Autonomous Region were selected in 2014 as study sites; among which 24 schools were randomly assigned as the intervention group and 3 schools were assigned as control group. According to the education methods (classroom teaching, publicity manual, hypertension class reports and the combination of the three) and the frequency of education (1, 2, 3 times per semester), the intervention group were further randomly divided into 12 subgroups with 2 schools in each group. The intervention study was carried out for 3 years.Results:A total 13 402 students were involved in the study, and there were 11 333 students in the intervention group and 2 069 students in the control group. The awareness rates of hypertension concept [41.8% (4 738/11 333) vs. 24.6% (511/2 069), χ 2=154.86, P<0.01], the adverse consequences of hypertension [85.8% (9 735/11 333) vs. 75.4% (1 561/2 069),χ 2=25.80, P<0.01], the hypertension risk factors [84.3% (9 564/11 333) vs. 72.5%(1 501/2 069), χ 2=12.83, P<0.01), and the health behaviors after hypertension [84.9% (9 629/11 333) vs. 67.7%(1 402/2 069), χ 2=187.24, P<0.01] in intervention group were all significantly higher than those in control group. The stratified analysis showed that among students in elementary school, junior high school and high school, there were significant differences in the awareness rate of adverse consequences [94.4% (2 019/2 138) vs. 81.6% (3 829/4 690), 86.2% (3 887/4 505), χ 2=199.31, P<0.01], awareness rate of risk factor [86.8% (1 857/2 138) vs.86.1% (4 038/4 690), 81.4% (3 669/4 505) , χ 2=49.96, P<0.01); and awareness rate of correct behavior [89.9% (1 923/2 138) vs. 86.1% (4 037/4 690), 81.4% (3 669/4 505) χ 2=89.77, P<0.01]. Up to 95.9% (10 868/11 333) students in the intervention group liked the hypertension health education. Conclusion:Based on the school health education curriculum, the intervention measures of hypertension health education are effective, and the awareness rate of hypertension related knowledge among senior high school students is significantly improved.

BACKGROUND:The mechanism underlying Wal erian degeneration fol owing peripheral nerve injury is complex. Immune regulation on Wal erian degeneration is beneficial for early repair of perpheral nerve injury.
OBJECTIVE:To investigate the effects of Tol-like receptor 4 (TLR4) antagonist on Wal erian degeneration and axonal regeneration after early peripheral nerve injury in rats.
METHODS:Fifty male Wistar rats were recruited and randomly divided into treatment group (n=20), model group (n=20) and sham group (n=10). The right sciatic nerves of rats in treatment and model groups were cut and sutured end-to-end, while the sciatic nerves of rats in sham group were only exposed. In the treatment group rats were intravenously injected with 0.15 mg/kg TAK-242 via tail vein 1 hour preoperatively and 7 days postoperatively, and the rats in the other two groups were given intravenous injection of the same volume of normal saline. The sciatic nerves were removed at 24 hours, 3, 4 and 7 days after surgery.
RESULTS AND CONCLUSION:Real-time PCR indicated that the mRNA expressions of interleukin-1βand monocyte chemoattractant-1 were significantly increased in the model group compared with the sham group at 24 hours after surgery (both P<0.001), while the expressions were significantly decreased after TAK-242 injection (both P<0.001). Immunofluorescence showed that compared with the model group, down-regulated expression of CD68+and iba1+cel s appeared in the treatment group at 3 days after surgery (P<0.01, P<0.05). Luxol fast blue staining revealed that demyelination at the sciatic nerve stump appeared in both model and treatment groups at postoperative 7 days, but myelin debris clearance in the treatment group was significantly reduced compared with the model group (P<0.05). Hematoxylin-eosin staining showed that a lot of inflammatory cel s, Schwann cells and regenerated nerve fibers at the sciatic nerve stump were found in the model group, while there were few inflammatory cells, Schwann cel s and regenerated nerve fibers in the treatment group at 7 days after surgery. Immunohistochemistry found that the expression of growth-associated protein-43 in the treatment group was significantly lower than that in the model group at 4 days postoperatively (P<0.05). Besides, compared with the model group, a significantly decreased sciatic functional index was found in the treatment group at 20, 30 and 40 days after surgery (P<0.05). These results show that TLR4 antagonists delay early nerve regeneration in rats after sciatic nerve injury probably by inhibiting the TLR4 signaling pathway.

Inflammation plays an important role in the pathophysiological process of ischemic stroke. Experimental results have shown that the lipocalin-2 (LCN2) produced by astrocytes is involved in the inflammatory mechanism of ischemic stroke and aggravates the ischemic brain damage. Clinical studies have shown that the increased LCN2 in peripheral blood of patients with ischemic stroke is associated with the poor outcomes and risk of death. Further research is needed to reveal the specific mechanism of LCN2 in cerebral ischemia-reperfusion injury, especially the signaling pathway mediated by LCN2, and look for possible treatments targeting LCN2.

Objective To evaluate the safety and perinatal outcomes of thoracoamniotic shunting in the treatment of fetuses with severe primary hydrothorax. Methods 22 cases of suspected severe primary fetal hydrothorax which underwent thoraco-amniotic shunting in Shanghai First Maternity and Infant Hospital,Fetal Medicine Unit and Prenatal Diagnosis Center from January 2012 to December 2017 were analyzed retrospectively. Hydrothorax associated with structural or chromosomal abnormalities, infections and immune fetal hydrops were excluded. Results Totally ,28 shunts were placed in 22 fetuses. The median gestational age at TAS was 31.3 weeks. Preterm membrane rupture within 7 days after the procedure occurred in 9.1％(2/22) cases. Catheter displacement occurred in 18％(4/22) cases. The interval from shunting to delivery was 26.0 days. One fetus ended in induced abortion; 21(95％,21/22) babies were born alive, and their median gestational age at delivery was 34.4 weeks. 62％(13/21)newborns required ventilator supports; 4 neonatal deaths were attributed to pulmonary hypoplasia. The overall perinatal survival rate was 81％(17/21). The perinatal survival rate with hydrops and without hydrops were 10/13 and 7/8 respectively. Conclusion Thoraco-amniotic shunting is a safe procedure for intrauterine therapy and could improve the perinatal outcomes of severe primary fetal hydrothorax.

Inhibition of human epidermal growth factor receptor 2 mediated cell signaling pathway is an important therapeutic strategy for HER2-positive cancers. Although monoclonal antibodies are currently used as marketed drugs, their large molecular weight, high cost of production and susceptibility to proteolysis could be a hurdle for long-term application. In this study, we reported a strategy for the development of artificial antibody based on