Objective To investigate the role of PAG in migraine Methods A transformed superior sinus stimulation migraine model was applied to observe Fos expression and co localization of 5 HT with Fos in PAG following the stimulation of dual matter adjacent to the superior sagittal sinus in rats Results 5 HT immunoreactive neurons, densely located in ventrolateral and ventromedial sectors, were found throughout the PAG Fos like immunoreactivity neurons were obviously increased in stimulated group than in unstimulated and control groups The double labelled neurons accounted for 15 0%?2 8% of 5 HT immunoreactive neurons and 24 0%?4 3% of Fos like immunoreactivity The double labelled population mainly distributed in ventrolateral sector Conclusions It suggests that neurons in PAG, especially in ventrolateral sector in caudal segment, might be excited in migraine model of rat The excited cells and 5 HTnic neurons might have a similar distribution pattern in PAG, with part of excited cells being 5 HTnic neurons Other types of excited neurons and the subtype of 5 HT receptor were not included in the experiment, and would be studied further as to getting a better understanding of the pathophysiology of migraine

A themostable intracellular β-galactosidase from a thermophilic Bacillus stearothermophilus was purified by a combination of (NH4)2SO4 fractionation, ion-exchange (DEAE-22)and gel filtration (Sephades G-75). The optimum temperature and pH of the enzyme acivity were 60Cand pH6.4 respectively. The β-galatosidase activity exhibited thermosttability at 50 C. The enzyme was significaantly activated by alkali and alkali-earth metal ions. The activity was inhibited by Zn2+ 、 Fe3+ 、 Cu2+Reducing agents enhanced β- galactosidase activity. Thiol-binding agents drastically decreased the enzyme activity. The enzyme was specific for β-D glycosidic linkages,and the identity of the aglycone moiety also influenced enzyme activity. At 55Cthe Km for O-nitrophenyl-β-D-galactosidase (ONPG)and lactose were 2. 63mmol/L and 4.39mmol/L, respectively,and Vmax for both substrates were 1.93 × 10-5mmol. min-1 mg-1protein6.54 ×105 mmol. min-1. mg-1protein,respectively. The enzyme was inhibited by glucose (the products of lactose hydrolysis,ki 2.47mmol/L),but not by galactose. In addition,the enzyme possessed transgalactosylation activity. Galacto-oligosaccharides,both tri- and tetrasaccharide,were involved in the products during lactose hydrolysi

Brain-computerinterface(BCI) is a kind of direct channel for information communication and control established between the human brain and computer or other electronic equipment.BCI is a novel information communication system which does not depend on the conventional brain information pathways.The asynchronous brain-computer interface technology is based on alpha wave control,and can automatically switch system mode between working and idle and select the larger EEG signal associated with motion imagination.In this paper,the basic knowledge of BCI and alpha wave-based asynchronous BCI technology were introduced.The key technology and application prospect of the novel alpha wave-based asynchronous BCI technology were summarized,and the status and existing problems were analyzed.

MAGED4B belongs to the melanoma-associated antigen family; originally found in melanoma, it is expressed in various types of cancer, and is especially enriched in glioblastoma. However, the functional role and molecular mechanisms of MAGED4B in glioma are still unclear. In this study, we found that the MAGED4B level was higher in glioma tissue than that in non-cancer tissue, and the level was positively correlated with glioma grade, tumor diameter, Ki-67 level, and patient age. The patients with higher levels had a worse prognosis than those with lower MAGED4B levels. In glioma cells, MAGED4B overexpression promoted proliferation, invasion, and migration, as well as decreasing apoptosis and the chemosensitivity to cisplatin and temozolomide. On the contrary, MAGED4B knockdown in glioma cells inhibited proliferation, invasion, and migration, as well as increasing apoptosis and the chemosensitivity to cisplatin and temozolomide. MAGED4B knockdown also inhibited the growth of gliomas implanted into the rat brain. The interaction between MAGED4B and tripartite motif-containing 27 (TRIM27) in glioma cells was detected by co-immunoprecipitation assay, which showed that MAGED4B was co-localized with TRIM27. In addition, MAGED4B overexpression down-regulated the TRIM27 protein level, and this was blocked by carbobenzoxyl-L-leucyl-L-leucyl-L-leucine (MG132), an inhibitor of the proteasome. On the contrary, MAGED4B knockdown up-regulated the TRIM27 level. Furthermore, MAGED4B overexpression increased TRIM27 ubiquitination in the presence of MG132. Accordingly, MAGED4B down-regulated the protein levels of genes downstream of ubiquitin-specific protease 7 (USP7) involved in the tumor necrosis factor-alpha (TNF-α)-induced apoptotic pathway. These findings indicate that MAGED4B promotes glioma growth via a TRIM27/USP7/receptor-interacting serine/threonine-protein kinase 1 (RIP1)-dependent TNF-α-induced apoptotic pathway, which suggests that MAGED4B is a potential target for glioma diagnosis and treatment.
Humans ; Tumor Necrosis Factor-alpha ; DNA-Binding Proteins/metabolism* ; Ubiquitin-Specific Peptidase 7 ; Cisplatin ; Temozolomide ; Transcription Factors ; Glioma ; Cell Proliferation ; Melanoma ; Cell Line, Tumor ; Apoptosis ; Nuclear Proteins/genetics*