1.The relationship between brain-derived neurotrophic factor and oligodendrocytes in periventricular white matter injury of premture infants
International Journal of Pediatrics 2013;40(4):378-380
It is characterized by periventricular white matter injury (PWMI) and the following failure of myelination in the brain injury of premature infants.Periventricular leukomalacia (PVL),the main form of PWMI,is mainly induced by the decrease of premyelinating oligodendrocytes.Therefore,it is critically important for the prognosis of brain injury of premature infants that oligodendrocytes are myelinated.Brain-derived neurotrophic factor (BDNF) is the richest neurotrophic factor in the brain,and widely expressed in the brain.BDNF is connected with the tyrosine receptor kinase B (Trk B).It is convinced that BDNF influences the production and myelination of oligodendrocytes.This review focuses on the advances in the relationship between BDNF and oligodendrocytes in brain injury of premature infants.
2.Effects of Smoking on Arsenic Metabolism, Methylation:a Meta-analysis
Bo ZHU ; Quanmei ZHENG ; Yuanyuan XU
Journal of Environment and Health 2007;0(12):-
Objective To investigate whether smoking affects metabolism and methylation of arsenic. Methods Six papers about the relation between smoking and arsenic metabolism, methylation were collected until December,2008, and the data were quantitatively analyzed with random and fixed effect models. Results In the group of smoking, the summary weighted mean difference of percent of inorganic in urinary was 0.59 (95% CI:-0.01-1.18). The summary weighted mean difference of percent of MMA in urinary was 2.44 (95%CI:1.95-2.94). The summary weighted mean difference of percent of DMA in urinary was -3.04 (95%CI:-4.01- -2.07). Current evidence suggested that percent of MMA was higher, percent of DMA was lower in smoking or ever smoking group compared with nonsmoking group. Conclusion Smoking may be considered a risk factor for metabolism and methylation of arsenic on human.
3.Expression changes of brain-derived neurotrophic factors in cortex and hippocampus after hypoxia-ischemia injury in immature rats
Quanmei XU ; Yong HU ; Gang QIU ; Yi YANG
Chinese Journal of Applied Clinical Pediatrics 2014;29(11):851-856
Objective To study the effect of hypoxia-ischemia (HI) on the brain-derived neurotrophic factor (BDNF) expression in the brain cortex and the hippocampus of immature rats,and to provide new therapeutic strategies for HI brain injury.Methods Three-day-old rats were divided into 2 groups.One group of rat pups were subjected to the left carotid artery ligation followed by 60 mL/L oxygen for 2.5 hours(HI-treated rats).The other group of rat pups were only subjected to the left carotid artery separation without ligation and 60 mL/L oxygen (sham-treated rats).The brain tissues were prepared at 3,7 and 14 d after treatment.Cresyl fast videt(CV) staining was used to evaluate the damage of the cortex and the hippocampus and check whether the models were successfully made.Immunostaining was used to determine the changes in BDNF positive cells in the brain cortex and the hippocampus after HI.Western blot analysis was used to evaluate the expression of BDNF protein in the brain cortex and the hippocampus after HI.Results Models were successfully made.CV staining showed that there was brain damages and area loss in the cortex and the hippocampus after HI.BDNF immunostaining showed that the number of BDNF-positive cells was significantly decreased in the cortex (t =-3.225,-2.298,all P < 0.05) and the hippocampus (t =-3.751,-2.920,all P < 0.05) in the damaged side of the brain compared to the contralateral side in the rats treated with HI and the sham-treated rats at 3 d after surgery,while increased at 7 d(t =3.924,2.838,all P < 0.05 for cortex ; t =4.136,2.256,all P <0.05 for hippocampus) and 14 d (t =3.256,2.624,all P < 0.05 for cortex ; t =3.051,2.719,all P < 0.05 for hippocampus) after surgery.Western blot analysis showed protein expressions of BDNF:(1) Hippocampus:the protein expressions of BDNF were significantly decreased in damaged side of the brain compared to the contralateral side of rats treated with HI at 3 d(t =-3.388,P < 0.05) after surgery,while increased compared to the contralateral side of rats treated with HI and the sham-treated rats at 14 d(t =4.874,4.646,all P <0.05) after surgery.(2)Cortex:the protein expression of BDNF was significantly decreased in damaged side of the brain compared to the contralateral side of rats treated with HI and the sham-treated rats at 3 d(t =-7.386,-3.256,all P < 0.05) after surgery,compared to the sham-treated rats at 7 d(t =4.439,P < 0.05) and the contralateral side of rats treated with HI and the sham-treated rats 14 d(t =24.161,3.942,all P < 0.05) after surgery.Conclusions The number of BDNF-positive cells and protein expressions are decreased in the cortex and the hippocampus at the early stage of HI injury,and increased at the late stage.BDNF may play a role in the healing stage of HI brain injury.
4.Advances in rituximab treatment of refractory myasthenia gravis
International Journal of Pediatrics 2018;45(10):772-775
Myasthenia gravis is an autoimmune disorder of the neuromuscular junction caused by circu-lating antibodies specific for the post-synaptic receptor. It results in neuromuscular transmission disorders. After optimal treatment with standard drugs,most myasthenia gravis patients can achieve a good life quality. Part of patients cannot get stable clinical remission or minimal manifestation with standard therapy. Rituximab is a chim-eric mouse/human antibody specific for the CD20 B-cell surface antigen. Studies have showed that rituximab is effective in the refractory myasthenia gravis. This review mainly discusses about the advances of rituximab in the treatment of refractory myasthenia gravis.