Objective To explore the alterations of resting-state neural networks in females with migraine at attack stage in low-and high-frequency ranges compared to healthy controls. Methods Resting-state magnetoencephalography data from 20 females with migraine ( migraine group ) and 20 age-and gender-matched healthy controls ( control group ) were collected to compute the neural network parameters through graph theory analysis.Independent samples t test was used to compare the difference of the network parameters between the two groups.The Pearson coefficient was used to assess the relationship between the abnormal network parameters and clinical manifestations of migraine.Results Compared with control group, females in migraine group at attack stage showed increased functional connectivity in the 0.1 -1 Hz, 4 -8 Hz, 12 -30 Hz, 30 -80 Hz band; increased shortest path length in the 80-250 Hz band; increased clustering coefficient and degree in the 0.1 -1 Hz band;decreased clustering coefficient and degree in the 4 -8 Hz, 12 -30 Hz band ( P<0.05 -0.01 ) .The functional connectivity of females with migraine at attack stage was positively correlated with number of years with migraine in the 12-30 Hz ( r=0.56, P=0.01 ) .Conclusion These results indicate that inherent neural networks are significantly impaired in low-and high-frequency ranges in females with migraine at attack stage and may contribute to the clinical manifestations of this disorder.

OBJECTIVE:To establish an HPLC method for the determination of the contents of Decussatin,Bellidifodin,Methylswertianin and Swerchirin in Swertia macrosperma C.B.Clark.METHODS:The determination was performed on VP-ODS C18(150 mm? 4.60 mm,5 ? m),with the mobile phase consisting of methanol-water-phosphoric acid(70∶ 30∶ 0.4),the detection wavelength set at 254 nm,the flow rate at 1.0 mL? min-1 and the column temperature at 20℃.RESULTS:The calibration curves of Decussating,Bellidifodin,Methylswertianin and Swerchirin were in good linearity in the range of 0.172～ 0.86 ? g,0.224～ 1.344 ? g,0.144～ 0.72 ? g and 0.154～ 0.77? g,respectively.The average recoveries were 98.18%(RSD=1.19%),99.32%(1.52%),98.44%(1.23%)and 97.68%(1.57%),respectively.CONCLUSION:The method is rapid and precise,with accurate and reliable results.

AIM: To study the antioxidative effect of three kinds of xanthone:methylswertianin(MET), bellidifodin(BEL) and decussatin (DEC) extracted from Swertia macrosperma C.B. clark. METHODS: Hydroxy radical was generated from H_2O_2 and VC-Fe~ 2+ system; MDA contents in liver homogenate and mitochondria were measured by thiobabituric acid assay; the hemolysis of RBC and the swelling extent of mitochondria were detected by spectrophotometric methods. RESULTS: Xanthones could inhibit the generation of MDA, the hemolysis of RBC, and the swelling of mitochondria. The inhibitory effect of BEL was stronger than that of MET and DEC. CONCLUSION: Xanthones possess a good antioxidant activity.

Objective: To seek the optimum technology of drying and to solve the problem of powder sticking clump. Methods : On the basis of major drying condition, such as duration of drying, temperature of drying, evaluating different drying technology; On the basis of the quantity of the powder sticking on the wall and the hygroscopicity of one, investigating different excipients how to affect the spray drying. Seeking the optimum kinds and quantity of excipients. Results : The best properties of the granules are from the spray drying process. ?-cyclodextrin and lactose have the effects on solving the powder sticking on the wall. Conclusion : The spray drying process is the optimum one. Adding 3～5 percent of ?-cyclodextrin has an effect on improving the phenomenon of powder sticking on the wall in process of the spray drying.

Animals ; Brain ; drug effects ; metabolism ; Calmodulin ; metabolism ; Female ; Lead ; toxicity ; Male ; Maternal Exposure ; Pregnancy ; Protein Kinase C ; metabolism ; Rats ; Rats, Wistar

Objective To investigate the expressions of receptor for advanced glycation endproducts (RAGE) and nuclear factor κB(NF-κB) in brain hippocampus of rat with chronic fluorosis,and to reveal the mechanism of brain damage resulted from chronic fluorosis.Methods Sixty clean grade SD rats were randomly divided to three groups(20 rats in each group,10 female and 10 male) fed with different contents of fluoride,control group with normal tap-water(＜ 0.5 mg/L fluoride),small dosage of fluoride exposure group(10 mg/L fluoride in tap-water) and large dosage of fluoride exposure group(50 mg/L fluoride) for six months.Then the rats were killed by femoral artery bleeding and hippocampus was removed.Protein and mRNA levels of RAGE and NF-κB in the hippocampus were determined by Western blotting and quantitative real time PCR,respectively.Results As compared to the control groups[(100.00 ± 2.60)％,(100.00 ± 7.80)％],the expressions of RAGE and NF-κB at protein level in the hippocampus were significantly increased in the small dosage of fluoride exposure groups [(205.00 ± 15.30)％,(156.00 ± 12.20)％] and the large dosage of fluoride exposure groups[(232.00 ± 10.90)％,(162.00 ± 9.80)％,all P ＜ 0.05]; for the mRNA level of RAGE and NF-κB,the expressions were higher in the small dosage of fluoride exposure groups(1.27 ± 0.09,0.83 ± 0.15) and the large dosage of fluoride exposure groups (2.60 ± 0.19,1.27 ± 0.19) than those of the control groups(0.66 ± 0.18,0.32 ± 0.08,all P＜ 0.05).Conclusions The increased expressions of RAGE and NF-κB in the hippocampus of rat brain are caused by chronic fluorosis,and these changes may be associated with the mechanism of nerve injury.

Objective Aim of the study is to investigate the expression of syndecan-4 and nuclear factor κB(NF-κB) in the kidney of rat with chronic fluorosis,and to reveal the mechanism of kidney damage resulted from the toxicity of excessive amount of fluoride.Methods According to body mass and sex,sixty SD rats were randomly divided to three groups according to body mass and fed with different contents of fluoride:control group with normal tap-water(＜ 0.5 mg/L fluoride),small dosage of fluoride exposure group (adding 10 mg/L fluoride in tap-water) and large dosage of fluoride exposure group (50 mg/L fluoride) for six months.The protein level of syndecan-4 and NF-κB in the kidney was detected by Western blotting and syndecan-4 mRNA level by quantitative real time PCR.Results As compared to the control group[(100.0 + 8.1)％],the expression of syndecan-4 at protein level in the kidney of rat was significantly increased in the small dosage of fluoride exposure group [(198.5 + 5.6)％,P ＜ 0.05] and large dosage of fluoride exposure group [(209.2 + 13.0)％,P ＜ 0.05]; the protein levels of NF-κB in the small dosage of fluoride exposure group[(284.4 + 11.1)％,P ＜ 0.05] and in the large dosage of fluoride exposure group[(343.2 + 2.9)％,P ＜ 0.05] were significantly increased than that of the control group[(100.0 ± 10.7)％].The mRNA levels of syndecan-4 in the kidney in the small dosage of fluoride exposure group and large dosage of fluoride exposure group(0.431 + 0.058 and 0.453 ± 0.065,both P ＜ 0.05,respectively) were significantly increased than that of the control(0.128 + 0.026).Conclusions The increased expression of NF-κB in the kidney is induced by increased expression of syndecan-4,which may be involved in kidney damage of chronic fluorosis.

Ischemic heart disease (IHD), which has been considered to be exclusively caused by stenosis or occlusion of coronary artery, is a significant cause of morbidity and mortality worldwide. Mitochondrial dysfunction is the main pathological basis of ischemic heart disease and reperfusion injury, and moderate mitochondrial autophagy can selectively remove damage proteins and organelles to maintain intracellular homeostasis, so mitochondrial autophagy is important for maintaining the homeostasis of cardiomyocytes. Natural drugs from plants are widely used in ischemic heart disease. In recent years, more and more natural drugs have been proven to alleviate myocardial cell damage after ischemia/reperfusion through mitochondrial autophagy. This paper reviews the research progress of natural drugs from plants medicines regulating mitochondrial autophagy in the treatment of ischemia heart disease.

Objective To explore the localization and expression of dopaminergic neurons in olfactory bulb of cynomolgus monkeys damaged by 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).Methods Three adult cynomolgus monkeys were injected with MPTP to induce the damage of dopamine neurons ( MPTP group ) and three adult cynomolgus monkeys were as a control group .Immunohistochemical staining was performed to examine the localization and expression of dopaminergic neurons in the olfactory bulb in normal and MPTP group monkeys .The numbers of DA-positive and DARPP32-positive cells were counted and the average absorbance was measured in normal and MPTP group .Results DA and DARPP32 positive neurons were concentrated in the glomerular layer ( GL) of olfactory bulb.DA positive nerve fibers were distributed in the GL while DARPP 32 positive nerve fibers appeared in all layers , and most nerve fibers were in GL and external plexiform layers (EPL).After MPTP injury, compared with the normal control group , DA and DARPP32 positive neurons and nerve fibers decreased in MPTP group and DA neurons and nerve fibers decreased significantly . Conclusions DA neurons and nerve fibers are in the GL of cynomolgus monkey olfactory bulb .DA neurons and fibers are significantly reduced in the olfactory bulb of cynomolgus monkeys damaged by MPTP , which may be associated with the dysosmia in Parkinson ’ s disease .

Objective:To survey the expression of MMP-1,MMP-2 of human periodontal ligament cells(HPDLCs)treated by tea polyphenols(TP)and lipopolysaccharide(LPS).Methods:HPDLCs were in vitro cultured in vitro and treated by TP(200 μg/ml) and /or LPS(100 μg/ml)for 24,48 and 72 h respectively,the secretion of MMP-1 and MMP-2 were examined by ELISA,MMP-1 and MMP-2 mRNA expression was examined by real-time PCR.Results:The secression and mRNA expression of MMP-1 and MMP-2 of HPDLCs increased by LPS treatment and significantly inhibited by TP at the different times.Conclusion:TP can inhibit the col-lagen degradation of HPDLCs mediated by LPS.