Values of neutrophil-lymphocyte ratio and platelet-lymphocyte ratio in predicting sensitivity to intravenous immunoglobulin in Kawasaki disease / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the values of neutrophil-lymphocyte ratio (NLR) and platelet-lymphocyte ratio (PLR) in predicting the sensitivity to intravenous immunoglobulin (IVIG) in Kawasaki disease (KD).</p><p><b>METHODS</b>A retrospective cohort study was conducted in 404 children with newly diagnosed KD. The data on routine blood tests, NLR, and PLR were collected before and after IVIG treatment. The receiver operating characteristic (ROC) curve was used to determine the cut-off values of NLR and PLR in predicting the insensitivity to IVIG. A logistic regression analysis was used to identify independent predictive factors for insensitivity to IVIG.</p><p><b>RESULTS</b>Of all patients, 31 were insensitive to IVIG. Compared with the IVIG sensitivity group, the IVIG insensitivity group had a significantly higher incidence rate of coronary artery ectasia (P<0.01), a shorter course of disease when IVIG therapy was initiated (P<0.05), and significantly higher NLR, PLR, and C-reactive protein (CRP) level before and after treatment (P<0.05). The optimal cut-off values for NLR and PLR to predict IVIG insensitivity were 4.36 and 162 before IVIG treatment and 1.45 and 196 after treatment. The multivariate regression analysis showed that the course of disease before IVIG treatment, CRP before IVIG treatment, and NLR and PLR before and after IVIG treatment were independent predictive factors for IVIG insensitivity.</p><p><b>CONCLUSIONS</b>NLR and PLR can be used to predict IVIG insensitivity in children with KD.</p>

Antitumor, analgesic, and anti-inflammatory effects of Ornithogalum caudatum extracts / 中草药

Objective: To investigate the antitumor, analgesic, and anti-inflammatory effects of Ornithogalum caudatum extract (OCE). Methods: The MFC, HepG-2, and S180 tumor-bearing mice models were established, and the tumor inhibitory rate of OCE was calculated; The analgesic effect of OCE was observed by acetic acid writhing test of mice; The anti-inflammatory effect of OCE was observed in xylene-induced ear edema model of mice. Results: OCE (5.0 and 2.5 g/kg) could effectively inhibit the growth of solid tumors in tumor-bearing mice in a dose-dependent manner (P < 0.05, 0.001); Compared with the model group, OCE (5.0 and 2.5 g/kg) could significantly inhibit the writhing response (P < 0.05, 0.001) and xylene-induced ear edama (P < 0.05, 0.01). Conclusion: OCE has certain antitumor, analgesic, and anti-inflammatory effects, suggesting they may be worth further investigation.

Mechanism of migration in CNE2 cells promoted by EBV-LMP1 / 中南大学学报(医学版)

OBJECTIVE@#To investigate the mechanism of migration phenotype change induced by EBV-LMP1 in nasopharyngeal carcinoma (NPC) cell line CNE2.@*METHODS@#Retroviruses RV-LNSX, RV-LMP1, and RV-LMP1(TRADD) prepared previously were used to infect CNE2 cells. After selection with G418, the morphology, the ability of motion and migration in extracellular matrix, expression of LMP1 and E-Cadherin in transgenic cells were observed or detected. Meanwhile, pEcad-luc was respectively co-transfected with pLNSX, pLNSX-LMP1, and pLNSX-LMP1(TRADD), to examine the effect of LMP1 on the transcriptional activity of E-Cadherin promoter in 293 cells.@*RESULTS@#Compared with CNE2 and CNE2-LNSX cells, CNE2-LMP1 cells morphologically changed from typical epithelial appearance to long-spindle fibroblastic morphology with the concomitant loss of cell-to-cell contact, and relative migration of CNE2-LMP1 cells obviously increased (n=3, P< 0.05), while the expression of E-Cadherin was negative in CNE2-LMP1 cells. The transcriptional activity of E-Cadherin promoter and the expression of E-Cadherin was suppressed by LMP1, and the level of suppression was correlated with the concentration of pLNSX-LMP1 (0.2,0.6 and 1.0 microg). LMP1(TRADD) didn't induce the changes of morphology and migration phenotype, nor suppress the transcriptional activity of E-Cadherin promoter and the expression of E-Cadherin in CNE2 cells.@*CONCLUSION@#EBV-LMP1 promotes the migration and down-regulates the expression of E-Cadherin in CNE2 cells. The mechanism is that EBV-LMP1 suppresses the transcriptional activity of E-Cadherin promoter. TRADD of carboxyl terminus of LMP1 may be the main active domain to promote the migration in NPC cells.