AIM: To investigate the effects of fibroblast growth factor 10 ( FGF10 ) on lipopolysaccharide ( LPS)-induced microglial activation .METHODS:Mouse BV2 microglial cells were maintained in DMEM in a humidified incubator with 95%/5%( V/V) mixture of air and CO 2 at 37℃.The medium was changed every 1 or 2 d.The cells were digested and passaged every 4 or 5 d.The BV2 microglial cells were first pretreated with FGF 10 (1 mg/L) for 30 min and then stimulated with LPS (500 μg/L).The medium and the cells were collected at different time points .The morphologi-cal changes of microglia were visualized under microscope .To evaluate the microglial activation , the transcription and pro-duction of proinflammatory factor tumor necrosis factor-α( TNF-α) were examined by real-time quantitative polymerase chain reaction (RT-qPCR) and enzyme-linked immunosorbent assay (ELISA), respectively.RESULTS:The morphology of control BV2 microglia showed circular or oval shape .After exposure to LPS for 24 h, the microglia revealed spindle shaped or multipolar morphology , and the percentage of activated cells was significantly increased compared with control group.Pretreatment with FGF10 successfully inhibited the morphological change from normal to activated shape .LPS sti-mulation for 6 h significantly increased the transcription of TNF-α, while FGF10 pretreatment remarkably reversed the effect.In addition, the production of TNF-αincreased in the presence of LPS stimulation for 24 h compared with control group.Pretreatment with FGF10 suppressed LPS-induced TNF-αexpression.CONCLUSION: Pretreatment with FGF10 inhibits the morphological change from normal to activated shape , and remarkably suppressed the transcription and produc-tion of TNF-α.FGF10 successfully suppresses LPS-induced BV2 microglial activation , indicating that FGF10 is a therapeu-tic agent for the treatment of glia-mediated neuroinflammatory diseases .

Objective: To investigate the predictive factors of mortality in extremely preterm infants. Methods: The retrospective case-control study was accomplished in the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University. A total of 268 extremely preterm infants seen from January 1, 1999 to December 31, 2015 were divided into survival group (192 cases) and death group (76 cases). The potential predictive factors of mortality were identified by univariate analysis, and then analyzed by multivariate unconditional Logistic regression analysis. The mortality and predictive factors were also compared between two time periods, which were January 1, 1999 to December 31, 2007 (65 cases) and January 1, 2008 to December 31, 2015 (203 cases). Results: The median gestational age (GA) of extremely preterm infants was 27 weeks (23⁺³-27⁺⁶ weeks). The mortality was higher in infants with GA of 25-<26 weeks (OR=2.659, 95% CI: 1.211-5.840) and<25 weeks (OR=10.029, 95% CI: 3.266-30.792) compared to that in infants with GA> 26 weeks. From January 1, 2008 to December 31, 2015, the number of extremely preterm infants was increased significantly compared to the previous 9 years, while the mortality decreased significantly (OR=0.490, 95% CI: 0.272-0.884). Multivariate unconditional Logistic regression analysis showed that GA below 25 weeks (OR=6.033, 95% CI: 1.393-26.133), lower birth weight (OR=0.997, 95% CI: 0.995-1.000), stage Ⅲ necrotizing enterocolitis (NEC) (OR=15.907, 95% CI: 3.613-70.033), grade Ⅰ and Ⅱ intraventricular hemorrhage (IVH) (OR=0.260, 95% CI: 0.117-0.575) and dependence on invasive mechanical ventilation (OR=3.630, 95% CI: 1.111-11.867) were predictive factors of mortality in extremely preterm infants. Conclusions GA below 25 weeks, lower birth weight, stage Ⅲ NEC and dependence on invasive mechanical ventilation are risk factors of mortality in extremely preterm infants. But grade ⅠandⅡ IVH is protective factor.

Iron overload, as a pathological feature of many nervous system diseases, can cause oxidative stress and lead to abnormal iron metabolism and injury of nerve cells. Hypoxia inducible factor (HIF) can participate in brain iron metabolism by regulating brain iron uptake, storage, excretion and intracellular regulation. So, HIF is expected to become a therapeutic target to inhibit brain iron overload in nervous system diseases. This paper reviews the physiological/pathological mechanism of HIF in regulating brain iron metabolism, in order to provide new treatment ideas and methods for nervous system diseases characterized by brain iron overload.

Animal models play a critical role in the research on the pathogenesis and treatment of white matter injury in premature infants. Rodent modeling is often used to mimic the pathological manifestations of white matter injury in premature human infants. Currently, the most used models include the common carotid artery occlusion combined with the hypoxia model, prenatal/postpartum infection model, chronic hypoxia model, hyperoxia exposure model, neuronal excitotoxicity model, transgenic model, etc. This article reviews the modeling methods, advantages, and disadvantages of the above models.