Objective To observe the operation of Nav1.6 voltage-gated sodium channels in rats with acute cerebral injury after electroacupuncture therapy and investigate the mechanism.Methods Male Sprague-Dawley rats were randomly divided into an ischemia control group (IC,n =48),an electroacupuncture group (ET,n =48),a nimodipine therapy group (NT,n =48) and a sham operation group (SO,n =24),and were treated accordingly.A model of acute cerebral ischemia was induced by occlusion of the right middle cerebral artery using the suture method.The expression of Nav1.6,the concentration of Ca2+ and infarct volume were observed at 6 h,1 d,2 d and 3 d after ischemia with the real-time quantitative fluorescence PCR,immunofluorescence and 2,3,5-triphenyl tetrazolium chloride methods,respectively.Results The Joshua score for neural function was zero in the sham operation group,and increased gradually in the three other groups 6 h and1 and 2 d after ischemia.The average Joshua score 3 d after ischemia was significantly lower than 1 d earlier in each group.In the ET group the expression of Nav1.6 was significantly upregulated at first,followed by a significant decrease.The concentration of Ca2+ behaved similarly.However,no significant changes were observed in the infarction volume percentage.At 3 d after ischemia the expression of Nav 1.6,the Joshua grades,the Ca2+ concentrations and the infarction volume percentage were all significantly lower in the ET group compared with the IC,NT and SO groups.Conclusion Electroacupuncture therapy after acute cerebral ischemia can inhibit the expression of Navl.6,reduced Na + inflow and calcium overload,and mitigate acute cerebral ischemic injury,at least in rats.The protective effect may be attributed to inhibiting the expression of Nav 1.6.

OBJECTIVE: Treating Class II subdivision malocclusion with asymmetry has been a challenge for orthodontists because of the complicated characteristics of asymmetry. This study aimed to explore the characteristics of dental and skeletal asymmetry in Class II subdivision malocclusion, and to assess the relationship between the condyle-glenoid fossa and first molar. METHODS: Cone-beam computed tomographic images of 32 patients with Class II subdivision malocclusion were three-dimensionally reconstructed using the Mimics software. Forty-five anatomic landmarks on the reconstructed structures were selected and 27 linear and angular measurements were performed. Paired-samples t-tests were used to compare the average differences between the Class I and Class II sides; Pearson correlation coefficient (r) was used for analyzing the linear association. RESULTS: The faciolingual crown angulation of the mandibular first molar (p < 0.05), sagittal position of the maxillary and mandibular first molars (p < 0.01), condylar head height (p < 0.01), condylar process height (p < 0.05), and angle of the posterior wall of the articular tubercle and coronal position of the glenoid fossa (p < 0.01) were significantly different between the two sides. The morphology and position of the condyle-glenoid fossa significantly correlated with the three-dimensional changes in the first molar. CONCLUSIONS: Asymmetry in the sagittal position of the maxillary and mandibular first molars between the two sides and significant lingual inclination of the mandibular first molar on the Class II side were the dental characteristics of Class II subdivision malocclusion. Condylar morphology and glenoid fossa position asymmetries were the major components of skeletal asymmetry and were well correlated with the three-dimensional position of the first molar.
Anatomic Landmarks ; Cone-Beam Computed Tomography ; Crowns ; Head ; Humans ; Malocclusion* ; Molar ; Orthodontists ; Temporomandibular Joint*

Objective To investigate the effects and mechanisms of Glutamine (Gln) supplementation on neurobehavioral outcome,neuronal apoptosis,microglia polarization,and neuroinflammatory response after traumatic brain injury (TBI) in rats.Methods TBI animal models were established using Feeney's method.Sixty Wistar rats were randomly divided into three groups:control group (Con),traumatic brain injury group (TBI),and glutamine supplementation group (TBI+Gln).We measured rat behavioral outcomes by modified neurologic severity score (mNSS) tests at day 1,3,7 and 14 after TBI.Apoptotic neurons were determined by Nissl staining.The microglia polarization relatived protein (Iba-1,CD16,CD86) expressions in TBI cerebral cortices were determined by immunohistochemistry staining and western blotting,respectively.While,the serum levels of tumor necrosis factor-α (TNF-α),interleukin (IL)-1 and interferon (IFN)-γ were tested by enzyme linked immunosorbent Assay (ELISA).Results Compared with the Con group,the levels of neurobehavioral outcome,neurons apoptosis,microglia polarization and neuroinflammatory factors were significantly increased in the other two groups (P=0.00).Compared with the TBl group,glutamin supplementation improvedneurobehavioral outcome [7 d:(10.74±0.25) points vs.(8.94±0.24) points,P=0.01;14 d:(8.77± 0.16) points vs.(7.43±0.13) points,P=0.03].Meanwhile,glutamin supplementation suppressed the apoptotic rates of neurons [3d:(80.18±8.38)％ vs.(65.47±7.02)％,P=0.01;7 d:(58.90±6.12)％ vs.(42.73±4.88)％,P=0.01;14d:(39.56±2.95)％vs.(31.12±3.16)％,P=0.01],inhibited protein expressions of Iba-1 and CD16,and increased the protein expression of CD86,which promoted the phenotypic shift of microglia from M1 to M2 phenotype,inhibited microglial activation,and thus reduced TBI-induced neuroinflammatory factors [TNF-α:(125.42 ± 12.81) pg/ml vs.(74.36 ± 9.25) pg/ml,P =0.01;IL-1:(69.04±8.48) pg/ml vs.(34.73±3.92) pg/ml,P=0.01;TNF-α:(89.75±9.40) pg/ml vs.(45.62±6.64) pg/ml,P=0.02].Conclusion Glutamine supplementation can markedly reduce neuron apoptosis and improve neurological outcomes after TBI,possibly mediated by promoting the phenotypic shift of microglia from M1 to M2 phenotype and thus reducing TBI-induced neuroinflammatory factors.