Objective:To analyze the perpendicular force on each tooth produced by the reverse-curve arch wires of various angles and depths using the method of 3-D finite element (3-D FEM) analysis. Methods:3-D FEM models of lower teeth, periodontal ligaments and alveolar bone as well as the 0.46 mm?0.64 mm inch stainless steel reverse-curve arch wires with different angles and depths were developed with the ANSYS finite element software, and the displacements of deformation of the reverse-curve arch wires were established on the models. Results:A ideal 3-D FEM was construct,including 2 709 elements and 1 969 nodes. The depth and angle of the reverse-curve arch wires produced obvious effect on the force exerted to teeth, and they could alter both the strength and the direction of the force. The force was mainly loaded on the canines, the second premolars and the molars, while less loaded on the incisors. Affected by the reverse-curve arch wires, the perpendicular force on the incisors were brought intrusively and on the molars were brought intrusively and distal upright; however, the canines and the bicuspids, in the perpendicular direction, moved along with the transformation of the angle and depth of the reverse-curve arch wires. When the angle of reverse-curve arch wires was fixed, the intrusive force on the incisors and molars was increased along with the increase of depth of the reverse-curve arch wires. Perpendicularly, the canines underwent a process from extrusion to intrusion, while the bicuspids were from intrusion to extrusion. When the depth of reverse-curve arch wires was fixed, the intrusive force on the incisors and molars was increased along with the increase of angle of the reverse-curve arch wires. The canines underwent a process from intrusion to extrusion.Conclusion:The variation of the angle and depth of the reverse-curve arch wires may produce evident effect on the force exerted to teeth.

Objective To investigate the effects of intrathecal injection of α-cyano-4-hydroxy-cinnamate (4-CIN) in rats with neuropathic pain induced by chronic constriction injury of sciatic nerve (CCI).Methods Eighteen male SD rats were divided randomly into 3 groups(n=6):sham group (group S),CCI model group (group C0) and 4-CIN group (group C1).Group C0 and C1 were operated with the model of neuropathic pain induced by chronic constriction injury of sciatic nerve ; and group S were treated as sham operated rats.Two days after operation,group C1 received intrathecal injection of 100 μmol 4-CIN dissolved in 10％ DMSO 10 μl,while group C0 received intrathecal injection of 10％ DMSO 10 μl only.The paw withdrawal thermal latency(PWTL) and paw withdrawal mechanical threshold(PWMT) were tested 1 d before operation and 1 d,3 d,7 d,10 d,14 d after operation(T0-5).Results The basic values of PWMT and PWTL before operation showed no statistically significant differences among the three groups.On T1-5,the PWMT((11.71 ±2.81) g,(9.76± 1.00) g,(8.22± 1.33) g,(6.50± 1.48) g,(4.67± 1.03) g) and PWTL((11.36±2.18) s,(11.60±2.54) s,(8.54± 1.42) s,(7.59± 1.00) s,(6.88± 0.42) s) in group C0 were significantly lower than those in group S (P＜0.05).However,there were no significant differences between group S and C1 on T2-5(P＞0.05).Conclusion Intrathecal administration of 4-CIN can attenuate neuropathic pain in rats induced by CCI.

Objective To evaluate the expression of metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1) in ovarian cancer cell lines, and to investigate the biological effects of down-regulated MALAT-1 on OVCAR3 cells.Methods qRT-PCR analysis was used to examine the expression level of MALAT-1 gene in ovarian cancer cells, including ES-2, A2780, SKOV3 and OVCAR3 cell lines.For functional research, four shRNA oligos specially targeting MALAT-1 and a empty vector were designed and constructed into pGPU6/GFP/Neo, then transfected into OVCAR3 cells.qRT-PCR was used to confirm the effective suppression of MALAT-1.Changes of proliferation and adhesion of cells were analyzed by CCK-8 and adhesion assays.Wound-healing, transwell migration and invasion assays were used to examine migration and invasion of MALAT-l-silencing cells in vitro.Results The expression of MALAT-1 gene in OVCAR3 cells was high, and qRT-PCR results confirmed successfully the knockdown of MALAT-1 after transient transfection.After successful suppression of MALAT-1, the proliferation, wound-healing and adhesion ability in vitro were inhibited to some degree.In transwell migration assay, the number of migration cells in MALAT-1-silencing group was 52.17±4.48, which is much less than that in the negative and control groups (286.50± 12.23 and 295.67±6.96, respectively).In invasion assay, the number of invasion cells passing the transwell membrane in MALAT-1-silencing group (37.33±2.40) was also decreased significantly, compared to that in the negative and control groups (239.00±15.72 and 222.67±20.85, P ＜ 0.05).Conclusions shRNA-mediated silence of MALAT-1 can effectively inhibit the proliferation, adhesion, migration and invasion abilities of ovarian cancer cell line OVCAR3 in vitro, indicating MALAT-1 is expected to be a target gene for the treatment of ovarian cancer.

OBJECTIVE:To investigate the effects of Astragalus injection combined with Salmeterol propionate powder inhala-tion on pulmonary function,cytokines and blood rheology indexes of Chronic obsrnctine pulmonary disease (COPD) patients. METHODS:104 COPD patients were divided into observation group and control group according to the randorn number table meth-od,with 52 cases in each group. Control group was given routine symptomatic treatment+Salmeterol propionate powder inhalation 1 dose,bid;observation group was additionally given Astragalus injection 30 ml added into 5% Glucose injection 250 ml,ivgtt, qd,on the basis of control group. Treatment course of 2 groups lasted for 2 weeks. Clinical efficacy,pulmonary function indexes [forced expiratory volume in one second(FEV1),forced vital capacity(FVC),FEV1/FVC],CRP,cytokine [IL-6,IL-8,TNF-α] levels,blood rheology indexes (whole blood high-shear viscosity,whole blood low-shear viscosity,fibrinogen,hematokrit and plasma viscosity),and the occurrence of ADR were observed in 2 groups. RESULTS:The total effective rate of observation group (94.23%)was significantly higher than that of control group(75.00%);compared with before treatment,FEV1,FVC and FEV1/FVC of 2 groups were significantly increased after treatment,and those of observation group were significantly higher than those of control group;CRP,IL-6,IL-8 and TNF-α of 2 groups were significantly decreased,and those of observation group were signifi-cantly lower than those of control group. The whole blood high-shear viscosity,whole blood low-shear viscosity,fibrinogen,hema-tocrit and plasma viscosity of observation group were decreased significantly after treatment,and the observation group was signifi-cantly lower than the control group,with statistical significance(P<0.05). No significant ADR was found in 2 groups. CONCLU-SIONS:Astragalus injection combined with Salmeterol propionate powder inhalation is significantly effective for COPD,improves pulmonary function of patients,improves micro inflammatory state and decreases blood rheology indexes with good safety.

Objective To evaluate the role of neuron-restrictive silencer factor (NRSF) in the spinal cord in remifentanil-induced hyperalgesia in a mouse model of incisional pain (IP) .Methods Fifty-six male Kunming mice were randomly divided into 7 groups (n=8 each):control group (group C) ,IP group (group I) ,IP +remifentanil group (group IR ) , NRSF antisense oligonucleotide group (NAS group ) , IP + NRSF antisense oligonucleotide group (I+NAS group ) ,IP + remifentanil + NRSF mismatch oligonucleotide group (IR+NMS group) , and IP + remifentanil + NRSF antisense oligonucleotide group (IR + NAS group ) . Artificial cerebrospinal fluid 5 μl was injected intrathecally once a day for 3 consecutive days in C ,I and IR groups .NRSF antisense oligonucleotide NAS 10μg was injected intrathecally once a day for 3 consecutive days in NAS ,I+NAS and IR + NAS groups . NRSF mismatch oligonucleotide 10 μg was injected intrathecally once a day for 3 consecutive days in IR+NMS group .A 1-cm longitudinal incision was made through skin ,fascia and muscle of the plantar aspect of the right hindpaw to establish the model of incisional pain in sevoflurane-anesthetized rats .At 30 min after the last injection ,normal saline 0.4 ml was infused subcutaneously in C and NAS groups ,the model was established and normal saline 0.4 ml was subcutaneously infused simultaneously in I and I+NAS groups ,and the model was established and remifentanil 0.04 mg/kg was subcutaneously infused simultaneously in IR ,IR+NMS and IR+NAS groups .At 3 days before operation (T0 ) ,4 h before operation (T1 ) and 4 ,12 ,24 and 48 h after operation (T1-5 ) ,mechanical paw withdrawal threshold to von Frey stimuli (PMWT ) and paw withdrawal latency to thermal nociceptive stimulus (PTWL ) were measured .Results Compared with C group ,the PWMT and PWTL were significantly decreased at T2-5 in I ,IR ,I+NAS ,IR+NMS and IR+NAS groups ( P<0.05) ,and no significant change was found in the PWMT and PWTL at each time point in NAS group ( P>0.05 ) .Compared with I group ,the PWMT and PWTL were significantly decreased at T2-5 in IR and IR+NMS groups ( P<0.05) , and no significant change was found in the PWMT and PWTL at each time point in I +NAS group ( P>0.05) . Compared with IR group ,no significant change was found in the PWMT and PWTL at each time point in IR+NMS group ( P>0.05) ,and the PWMT and PWTL were significantly increased at T2-5 in IR+NAS group ( P<0.05) . Conclusion NRSF in the spinal cord is involved in the development and maintenance of hyperalgesia induced by remifentanil in a mouse model of IP .

Objective To investigate the biomechanics of J-hook headgear in En mass intrusion and retraction of maxillary anterior teeth and provide guidance for clinical treatment.Methods A three-dimensional finite element model of maxillary teeth,periodontium,straight wire appliance and maxillary bone was established in ANSYS 14.0.En mass retraction of anterior teeth with force of 1.5 N through J-hook headgear was stimulated.Force was applied mesial to lateral incisor in group A and distal to lateral incisor in group B.The force direction was 30° to the sagittal plane and 20° to 60° to the occlusal plane.Force direction to the occlusal plane was changed every 5°and 18 cases were calculated.Displacement of upper anterior teeth and stress distribution in the periodontium were analyzed.Results As the degrees of force direction to the occlusal plane increased,the moving pattern of upper anterior teeth changed from clockwise rotation(lingual movement with intrusion) to bodily retraction and intrusion,and counter-clockwise rotation (intrusion with labial movement).With the force direction of 35° to occlusal plane applied mesial to lateral incisor or force direction of 45° to the occlusal plane applied distal to lateral incisor,bodily movement of upper anterior teeth without rotation was achieved.Conclusions Placement of J-hook mesial to lateral incisor enable orthodontists to maintain better en mass intrusion and retraction of upper anterior teeth.The direction of J-hook should be adjusted according to individual condition and treatment objective.

Objective To investigate the mechanism underlying the neuroprotective effect of linarin(LIN)against microglia activation-mediated inflammation and neuronal apoptosis following spinal cord injury(SCI).Methods Fifty C57BL/6J mice(8-10 weeks old)were randomized to receive sham operation,SCI and linarin treatment at 12.5,25,and 50 mg/kg following SCI(n=10).Locomotor function recovery of the SCI mice was assessed using the Basso Mouse Scale,inclined plane test,and footprint analysis,and spinal cord tissue damage and myelination were evaluated using HE and LFB staining.Nissl staining,immunofluorescence assay and Western blotting were used to observe surviving anterior horn motor neurons in injured spinal cord tissue.In cultured BV2 cells,the effects of linarin against lipopolysaccharide(LPS)-induced microglia activation,inflammatory factor release and signaling pathway changes were assessed with immunofluorescence staining,Western blotting,RT-qPCR,and ELISA.In a BV2 and HT22 cell co-culture system,Western blotting was performed to examine the effect of linarin against HT22 cell apoptosis mediated by LPS-induced microglia activation.Results Linarin treatment significantly improved locomotor function(P<0.05),reduced spinal cord damage area,increased spinal cord myelination,and increased the number of motor neurons in the anterior horn of the SCI mice(P<0.05).In both SCI mice and cultured BV2 cells,linarin effectively inhibited glial cell activation and suppressed the release of iNOS,COX-2,TNF-α,IL-6,and IL-1β,resulting also in reduced neuronal apoptosis in SCI mice(P<0.05).Western blotting suggested that linarin-induced microglial activation inhibition was mediated by inhibition of the TLR4/NF-κB signaling pathway.In the cell co-culture experiments,linarin treatment significantly decreased inflammation-mediated apoptosis of HT22 cells(P<0.05).Conclusion The neuroprotective effect of linarin is medicated by inhibition of microglia activation via suppressing the TLR4/NF-κB signaling pathway,which mitigates neural inflammation and reduce neuronal apoptosis to enhance motor function of the SCI mice.

Objective To investigate the mechanism underlying the neuroprotective effect of linarin(LIN)against microglia activation-mediated inflammation and neuronal apoptosis following spinal cord injury(SCI).Methods Fifty C57BL/6J mice(8-10 weeks old)were randomized to receive sham operation,SCI and linarin treatment at 12.5,25,and 50 mg/kg following SCI(n=10).Locomotor function recovery of the SCI mice was assessed using the Basso Mouse Scale,inclined plane test,and footprint analysis,and spinal cord tissue damage and myelination were evaluated using HE and LFB staining.Nissl staining,immunofluorescence assay and Western blotting were used to observe surviving anterior horn motor neurons in injured spinal cord tissue.In cultured BV2 cells,the effects of linarin against lipopolysaccharide(LPS)-induced microglia activation,inflammatory factor release and signaling pathway changes were assessed with immunofluorescence staining,Western blotting,RT-qPCR,and ELISA.In a BV2 and HT22 cell co-culture system,Western blotting was performed to examine the effect of linarin against HT22 cell apoptosis mediated by LPS-induced microglia activation.Results Linarin treatment significantly improved locomotor function(P<0.05),reduced spinal cord damage area,increased spinal cord myelination,and increased the number of motor neurons in the anterior horn of the SCI mice(P<0.05).In both SCI mice and cultured BV2 cells,linarin effectively inhibited glial cell activation and suppressed the release of iNOS,COX-2,TNF-α,IL-6,and IL-1β,resulting also in reduced neuronal apoptosis in SCI mice(P<0.05).Western blotting suggested that linarin-induced microglial activation inhibition was mediated by inhibition of the TLR4/NF-κB signaling pathway.In the cell co-culture experiments,linarin treatment significantly decreased inflammation-mediated apoptosis of HT22 cells(P<0.05).Conclusion The neuroprotective effect of linarin is medicated by inhibition of microglia activation via suppressing the TLR4/NF-κB signaling pathway,which mitigates neural inflammation and reduce neuronal apoptosis to enhance motor function of the SCI mice.