Objective To investigate the clinical outcome of correction of unilateral delayed orbitozygomatic complex fractures with digital guide plates.Methods The study involved 14 cases of unilateral delayed orbitozygomatic complex fractures treated between September 2007 and March 2012.Craniofacial structures were measured by thin-section CT before operation,followed by data input to the image processing software.Before and after the processing of images,three dimensional skull models were produced using rapid prototyping technique and applied to have surgical simulation.Digital guild plates were produced for guiding the reduction of fractures and orbital walls were reconstructed as well.Results All cases were followed up for a period of 6-11 months,which showed basic restoration of facial structure and significant correction of diplopia and enophthalmos,with no infection or dislocation of implants buried in orbit floor.Mild ectropion of the lower eyelid occurred in one case and temporary decrease of frontal wrinkle in two cases,but all recovered in 3-6 months postoperatively.Conclusion Digital guide plate is easy in operation and reliable for treatment of unilateral delayed orbitozygomatic complex fractures.

Objective To investigate the effects of Rhizoma Alismatis extracts on oxidative stress induced by cerebral ischemia-reperfusion injury in rats,and to explore its protective mechanism in cerebral ischemia-reperfusion injury.Methods A total of 60 male SD rats were randomly divided into sham operation group,model group,Alisma orientalis group and Nimodipine positive control group (n=15,each).Cerebral ischemia-reperfusion injury model was prepared by suture method after 14 days of intragastric administration.After 24 hours,scores of neurological dysfunction,the infarct size,the water content of the brain,the malondialdehyde (MDA),superoxide dismutase (SOD),nitric oxide (NO) levels in serum and brain tissues,and the activity of inducible NO synthase (iNOS)were detected.Results As compared with the model group,Alisma orientalis group showed that the scores of neurological dysfunction,cerebral water content,cerebral infarction size,contents of MDA and NO,and the activity of iNOS were significantly reduced,and the activity of SOD was significantly increased in respectively [(2.21 ± 0.38) vs.(2.78 ± 0.43),(81.18 ± 2.09)％ vs.(88.33±4.15)％,(0.26±0.07) ％ vs.(0.35±0.04)％,(5.92±1.64) μmol/L vs.(8.21±1.47)μmol/L,(115.48±18.65) mU/L vs.(75.52±20.78) mU/L,(28.23±4.32) μmol/L vs.(41.73±3.85) μmol/L,(15.31±1.68) mU/L vs.(23.49±3.53) mU/L,(5.41±0.68) μmol/L vs.(7.58±1.49) μmol/L,(168.57±10.65) mU/L vs.(150.11±13.62) mU/L,(14.37±0.77) μmol/L vs.(22.08±1.57) μmol/L,(9.83±0.75) mU/L vs.(13.28±1.84) mU/L,respectively,all P＜0.05]Conclusions Alisma orientalis extract has the protective effect on focal cerebral ischemia reperfusion injury,and the mechanism may be related to antioxidant and scavenging free radicals.

Objective: To explore the mechanism of An-Pressing manipulation in relieving energy crisis in chronic myofascial trigger points (MTrPs) by observing the effects of An-Pressing manipulation on adenosine triphosphate (ATP), adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) pathway and mitochondrial ultrastructure of skeletal muscle cells in MTrPs rats. Methods: Forty-eight male Sprague-Dawley rats were randomly divided into a blank group, a model group, a lidocaine group, and an An-Pressing manipulation group, with 12 rats in each group. The model group, lidocaine group and An-Pressing manipulation group were used to replicate the MTrPs rat model by blunt shock and centrifugal motion method. After modeling, the An-Pressing manipulation group was subjected to 7 times An-Pressing manipulation, once every other day; the lidocaine group was treated with 3 times of injection of lidocaine at the MTrPs, once every 6 d. The blank group and the model group were fed normally without intervention. After the intervention, local muscle tissue was taken to detect the content of ATP and the expression of AMPK, phosphorylated AMPK (phospho-AMPK), PGC-1α, and glucose transporter 4 (GluT4), and the ultrastructure of mitochondria was observed under an electron microscope. Results: Compared with the blank group, the ATP content in the model group was decreased (P<0.05), the protein expression levels of phospho-AMPK, PGC-1α, and GluT4 and the ratio of phospho-AMPK to AMPK were decreased (P<0.05); under the electron microscope, the number of mitochondria decreased, and they were deformed, small in volume, and had deformed cristae. Compared with the model group, the ATP contents in the An-Pressing manipulation group and the lidocaine group were increased (P<0.05), and the protein expression levels of phospho-AMPK, PGC-1α, and GluT4 and the ratio of phospho-AMPK to AMPK were increased (P<0.05); under the electron microscope, the number of mitochondria increased, the shape and size of the mitochondria were basically normal, and the cristae could be seen. Compared with the lidocaine group, phospho-AMPK and the ratio of phospho-AMPK to AMPK in the An-Pressing manipulation group were increased (P<0.05); under the electron microscope, the numbers of mitochondria were similar, and the shape and size of the mitochondria were basically normal without swelling, and the cristae could be observed. Conclusion: An-Pressing manipulation can increase the ATP content in MTrPs tissue, improve the expression levels of PGC-1α and GluT4 proteins and the ratio of phospho-AMPK to AMPK; its mechanism may relate to the activation of AMPK/PGC-1α signaling pathway to promote the repair of mitochondrial damages.

Objective:To investigate the mechanism of trigger point deactivation induced by pressing manipulation in a rat model and to explore its potential regulation of the inflammatory response through the extracellular signal-regulated kinase(ERK)/nuclear factor-κB(NF-κB)pathway. Methods:Fifty male Sprague-Dawley rats were randomly divided into a blank group,a model group,a pressing manipulation group,an ERK agonist group,and a pressing manipulation+ERK agonist group,with 10 rats in each group.Except for the blank group,rats in other groups were used to establish the trigger point rat model using the blunt blow combined with the eccentric exercise method.The pressing manipulation group underwent pressing manipulation intervention at the trigger points.The ERK agonist group received an injection of recombinant human epidermal growth factor via the tail vein.The pressing manipulation+ERK agonist group received interventions from both the pressing manipulation and ERK agonist groups.The pressure pain threshold(PPT)was measured by a mechanical pain threshold detector before and after the intervention.The histological changes were evaluated by hematoxylin-eosin staining after the intervention;the expression levels of ERK,phosphorylated ERK(p-ERK),NF-κB p65(p65),phosphorylated NF-κB p65(p-p65),and phosphorylated NF-κB inhibitor(p-IκB)were detected by Western blotting;the levels of interleukin(IL)-1β,IL-6,and tumor necrosis factor(TNF)-α were detected by enzyme-linked immunosorbent assay. Results:The PPT increased(P<0.05);the inflammatory cells disappeared;the ratios of p-ERK/ERK,p-p65/p65,and p-IκB/β-actin,also the levels of IL-1β,IL-6,and TNF-α all decreased in the pressing manipulation group after the intervention compared with the model group(P<0.05).The PPT decreased significantly(P<0.05),the inflammatory cell presence increased,and the ratios of p-ERK/ERK and p-p65/p65 were elevated(P<0.05);additionally,the levels of IL-6 and TNF-α were significantly higher in the pressing manipulation+ERK agonist group compared with the pressing manipulation group(P<0.05).The PPT was significantly lower(P<0.05),the inflammatory cell count was higher,the ratios of p-ERK/ERK and p-IκB/β-actin and the levels of IL-1β and TNF-α were significantly higher in the ERK agonist group compared with the pressing manipulation+ERK agonist group(P<0.05). Conclusion:Pressing manipulation can effectively alleviate inflammation and pain in trigger point model rats,potentially by inhibiting the ERK/NF-κB signaling pathway.