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.

Acidolysis kinetics on the process of the hydrolysis acidification by using glucose as the only energy sources was researched.It was concluded that the acidolysis kinetics constants are V_(max)=8.45d~(-1) and K_s=1089mg/L,under the circumstances of a temperature 37℃?0.5℃and the influent pH value 6.5.The results show that the rate of anaerobic acidification process is greater than that of completed an- aerobic or anoxic process.

AIM: To investigate whether Janus kinase/signal transducer and activator of transcription ( JAK/STAT) signaling pathway mediates high glucose-induced damage in human umbilical vein endothelial cells ( HUVECs ) . METHODS:The cell viability was examined by CCK-8 assay.The expression levels of JAK2, STAT3, caspase-9 and en-dothelial nitric oxide synthase ( eNOS) were detected by Western blot .The intracellular levels of reactive oxygen species ( ROS) were tested by DCFH-DA staining followed by photofluorography .Mitochondrial membrane potential ( MMP) was measured by rhodamine 123 staining followed by photofluorography .RESULTS:Treatment of HUVECs with high glucose (40 mmol/L glucose) for 6~12 h enhanced the protein level of phosphorylated JAK 2, peaking at 9 h.Treatment of the cells with high glucose for 6~12 h also increased the protein level of p-STAT3 with the peak value at 12 h.Pretreatment with the inhibitor of JAK/STAT pathway AG490 for 1 h before exposure of the HUVECs to high glucose significantly inhibi-ted the high glucose -induced injury , as evidenced by an increase in the cell viability , decreases in the expression of caspase-9 and the intracellular ROS production , and increases in MMP and the expression of eNOS .CONCLUSION:JAK/STAT signaling pathway is involved in the high glucose-induced damage in HUVECs .

OBJECTIVETo determine Ligustilide in volatile oil from Ligustrcum chuanxiong with RP-HPLC.

METHODODS2 column (4.6 mm x 200 mm, 5 microm) was used and nitrendipine was used as internal standard. The mobil phase consisted methanol, acetontrile and water (33:21:46). The ligustilide was at 275 nm.

RESULTThe linear range was 2.92-29.2 mg x L(-1) for ligustilide. The average recovery of ligustilide was 95.1% and RSD was 2.3%.

CONCLUSIONThis method is simple and can be used to determine ligustilide with satisfactory accuracy and reproducibility.

4-Butyrolactone ; analogs & derivatives ; analysis ; Chromatography, High Pressure Liquid ; methods ; Ligusticum ; chemistry ; Oils, Volatile ; chemistry ; isolation & purification ; Plants, Medicinal ; chemistry ; Rhizome ; chemistry

0.05). CONCLUSION: Genotype of VDR is related to BMD, but there is no enough evidence to support genotype of VDR as a genetic marker in predicting the risk of developing osteoporosis in Guangzhou postmenopausal women.

Objective The aim of the study was to investigate the expression of P-glycoprotein (P-gp)and nuclear factor κB (NF-κB) in the cerebral cortex of rat with chronic fluorosis,and to reveal the mechanisms of damaged nervous system resulted from the toxicity of fluoride.Methods Sixty SD rats were randomly divided into three groups.The rats in each group were given drinking water containing different levels of fluoride:control group less than 0.5 mg/L,small amount of fluoride exposure group 10.0 mg/L and large amount of fluoride exposure group 50.0 mg/L.The animals were examined at the sixth month after initiating the experiment.Protein levels of P-gp and NF-κB in brain tissues were detected by immunocytochemistry and Western blotting,and the P-gp protein and mRNA level by quantitative real time PCR method.Results As compared to the control group(28.21 ±6.13),the numbers of positive staining cells by P-gp antibody in the cortex of rat brains were significantly increased in both the small and the large amount of fluoride exposure groups[(48.46 ± 8.00),(53.72 ± 9.15),respectively,all P ＜ 0.05] ; the protein levels in the control group(100.00 ± 3.86)％ detected by Western blotting were significantly increased in the cortex of rat brains treated with fluoride in both the small and the large amount of fluoride exposure groups[(189.47 ± 3.14)％,(191.36 ± 11.09)％,respectively,all P ＜ 0.05].The significantly increased expression of NF-κB at the protein level was observed in the cortex of rat brains of the small and the large amount of fluoride exposure groups[(365.97 ± 6.04)％ and (417.15 ± 10.89)％,respectively] as compared with the control group[(100.00 ± 10.07)％,all P ＜ 0.05].The mRMA level of P-gp in the cortex of rat brains of the small and the large amount of fluoride exposure groups(2396 ± 427,3479 ± 371,respectively) were higher than that of the control group(260 ± 106,all P ＜ 0.05).Conclusion The increased expressions of P-gp and NF-κB in the cortex of rat brains are induced by chronic fluorosis,which might be connected with the mechanism of brain damages.

Objective To investigate the changes of reactive oxygen species(ROS) level and mitochondria fission-fusion-balance in cortical neurons of rats with chronic fluorosis and reveal the correlation between these two factors. Methods One hundred and twenty rats were randomly divided into 3 groups(control group, low-dose fluorosis group, high-dose fluorosis group) and 40 rats were in each group according to body weight and the experiments were carried out for 3 months or 6 months. The rats were fed with different concentrations of fluoride (NaF) to establish fluorosis models. Controls were fed with tap water( < 0.5 mg/L), experimental animals in low- or high-dose group were fed with water containing NaF 10.0,50.0 mg/L, respectively. The level of ROS and the morphology in mitochondria fission-fusion balance in neurons of the cortex of rat brains prepared with cortical frozen sections were detected with ROS fluorescent probe and MitoTracker RED probe, respectively. Results Significant differences of the level of ROS and the numbers of abnormal mitochondria in morphology in the cortical neurons were found between 3 groups at the experiment period of 3 month and 6 month(F= 3.07,3.06,3.05,3.07, all P < 0.05). As compared with control group(10.43 ± 5.98,4.12 ± 3.86) at the experiment period of 3 month, the level of ROS and the numbers of abnormal mitochondria in morphology in the cortical neurons were obviously increased in high-dose fluorosis group(25.48 ± 6.09,20.47 ± 6.09, all P < 0.05), whereas no significant changes were found in low-dose fluorosis group(11.67 ± 3.49,6.68 ± 3.48, all P> 0.05). Furthermore, the increases in both ROS level and abnormal numbers of mitochondria were significant observed in the cortical neurons of low-dose fluorosis group (63.02 ± 8.15, 49.33 ± 8.61) and high-dose fluorosis group(65.60 ± 7.40,53.10 ± 6.95) as compared with the control group (25.26 ± 6.41,20.26 ± 6.41) at the experimental period of 6 month (all P < 0.05). The abnormal numbers of mitochondria correlated with ROS level(r = 0.93,0.81, all P < 0.05). Conclusions Taking excessive amount of fluoride results in high level of oxidative stress and impaired the balance of mitochondrial fission-fusion,which is dependent on the feeding times and doses of fluoride. The mechanism of the mitochondrial abnormalities might be associated with the high level of oxidative stress induced by chronic fluorosis.

AIM: To explore whether strontium ranelate ( Sr ) promotes osteogenic differentiation of rat bone mesenchymal stem cells (BMSCs) through the Hedgehog/Gli1 signaling pathway.METHODS:BMSCs were isolated from 4-week-old rats by adherent culture and induced to differentiate into osteoblasts .According to the experimental purposes , the cells were exposed to different concentrations of Sr , cyclopamine ( Cy, an inhibitor of Hedgehog receptor ) or Gli1-siR-NA.The expression of Gli1 and Runx2 in the cells was detected by Western blotting .The activity of alkaline phosphatase ( ALP) was measured by the method of colorimetry , and the mineralized nodules were observed under microscope with aliz-arin red staining .RESULTS:Exposure to Sr at concentrations of 0.1 to 5 mmol/L for 7 d markedly increased the expres-sion of Gli1 in the BMSCs , and the increase in Gli1 expression was the most obvious following Sr exposure at concentration of 3 mmol/L.Cy at concentration of 10 μmol/L inhibited Sr-induced up-regulation of Gli1 expression.Transfection of the BMSCs with Gli1-siRNA not only obviously inhibited Sr-induced up-regulation of Gli1 and Runx2 ( a downstream protein of Gli1) expression, but also antagonized Sr-induced enhancement of ALP activity and the formation of mineralized nodules . CONCLUSION:The Hedgehog/Gli1 pathway is involved in Sr-induced osteogenic differentiation of rat BMSCs .

OBJECTIVETo study the combination of Mandibular distraction and orthognathic techniques for the reconstruction of adult hemifacial microsomia.

METHODSThe three-dimensional CT reconstruction data was used with Mimics for preoperation design. The osteotomy location, distraction vector, distraction distance were decided before operation with a surgical guider. At the first stage, internal distractor was implanted after ostetomy through an extra-oral approach. The distraction begun 5-7 days after operation with a frequency of 1 mm/day. After distraction, the distractor was maintained for 3-6 months. At the second stage, the distractor was removed. Le Fort I osteotomy was performed in order to correct the cross-bite and improve the facial contour. Usually, bone graft was inserted into the gap after Le Fort I osteotomy. The genioplasty was also performed if necessary.

RESULTS9 cases of adult hemifacial microsomia with severe mandibular deviation were treated. The facial asymmetry were improved greatly. 1 patient suffered an wound infection in the maxillary region after Le Fort I osteotomy and healed uneventfully with wound irrigation.

CONCLUSIONSMandibular distraction combined with orthognathic surgery is an effective procedure for adult hemifacial microsomia with complicated mandibular hypoplasia.

Adult ; Aged ; Bone Transplantation ; Facial Asymmetry ; surgery ; Goldenhar Syndrome ; surgery ; Humans ; Mandible ; surgery ; Osteogenesis, Distraction ; methods ; Osteotomy, Le Fort ; methods