Objective To discuss the methods and clinical effects of phased treatment of ankylosing spondylitis (AS) combined with severe hip flexion contracture.Methods The study enrolled 8 cases (12 hips) of AS combined with severe hip flexion contracture hospitalized from September 2011 to November 2012.Phased treatments included lateral hip arthrolysis,articular capsulectomy,stripping of the reflected head of rectus femoris,femoral neck osteotomy,traction and stage Ⅱ biotype total hip arthroplasty (THA).Preoperative and postoperative Harris score,hip range of motion,and complication of femoral nerve injury were detected.Results Period of follow-up was 6-12 months (mean 10 months).One case developed heterotopic ossification,which affected postoperative hip activity and received resection one year later.One case sustained fissure fracture of calcar femorale during implantation of the prosthetic femoral stem,but no special handling was provided.Of all cases,active flexion and extension of the hip were both 0° before operation,but increased to (96.25 ± 4.33) ° and (24.17 ± 4.69)° respectively after operation ; mean Harris score was improved from (26.67 ± 2.39) points preoperatively to (90.92 ± 5.66) points postoperatively (P ＜ 0.01).Besides,no femoral nerve injury was observed.Conclusion Phased treatment of AS combined with severe hip flexion contracture restores hip function and minimizes femoral nerve injury following THA.

Objective:To evaluate the role of heme oxygenase-1 (HO-1) in endotoxin-induced acute lung injury (ALI) and the relationship with the regulation of mitochondrial quality control in mice.Methods:Clean-grade healthy male adult C57BL/6 mice, aged 6-8 weeks, weighing 20-25 g, were selected.HO-1 inducible gene knockout mice (HO-1 -/-) were prepared based on CRISPER/Cas9-mediated EGE system, and HO-1 gene overexpression mice (HO-1 + /+ ) were prepared by transfection of HO-1 overexpressed adenovirus vector.The mice were divided into 2 groups ( n=6 each) using a random number table method: control group (group WT, group HO-1 -/-, group HO-1 + /+ ) and endotoxin-induced ALI group (group ALI, group HO-1 -/-+ ALI, group HO-1 + /+ + ALI). Lipopolysaccharide 15 mg/kg was injected through the tail vein to develop the model of endotoxin-induced ALI, and the equal volume of normal saline was given instead in each control group.The mice were sacrificed by bloodletting at 12 h after lipopolysaccharide or normal saline administration.The lung tissues were harvested for microscopic examination of the pathological changes which were scored, for determination of GSH and GSSG contents, for observation of the ultrastructure of mitochondria (with a transmission electron microscope) and survival within 12 h, for measurement of mitochondrial membrane potential (MMP) levels, and for determination of the expression of mitochondrial quality control-related proteins mitochondrial fusion protein 2 (Mfn2) and dynamin-related protein 1 (Drp1), peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α), nuclear respiratory factor 1 (NRF1), mitophagy marker protein PTEN-induced kinase 1 (PINK1) and E3 ubiquitin-protein ligase Parkin.The ratio of GSH/GSSG was calculated. Results:Compared with control group (group WT, group HO-1 + /+ and group HO-1 -/-), the 12-h survival rate and MMP were significantly decreased, the lung injury score was increased, GSH content and GSH/GSSG ratio were decreased, and the content of GSSG was increased in endotoxin-induced ALI groups (group ALI, group HO-1 + /+ + ALI and group HO-1 -/-+ ALI) ( P<0.05). Compared with group ALI, the 12-h survival rate and MMP were significantly decreased, the lung injury score was increased, the GSH content and GSH/GSSG ratio were decreased, the GSSG content was increased, and the expression of HO-1, Mfn2, PGC-1α, NRF1, PINK1 and Parkin was down-regulated, and Drp1 expression was up-regulated in group HO-1 -/-+ ALI, and 12-h survival rate and MMP were significantly increased, lung injury score was decreased, GSH content and GSH/GSSG ratio were increased, GSSG content was decreased, the expression of HO-1, Mfn2, PGC-1α, NRF1, PINK1 and Parkin was up-regulated, and the expression of Drp1 was down-regulated in group HO-1 + /+ + ALI ( P<0.05). Conclusions:HO-1 is involved in the process of endotoxin-induced ALI in mice, which is related to the regulation of mitochondrial quality control.

Objective:To evaluate the effect of transcutaneous electrical acupoint stimulation (TEAS) on mitochondrial quality control during endotoxin-induced acute lung injury (ALI) in mice.Methods:Twenty-four clean-grade healthy male C57BL/6J mice, aged 4-6 weeks, weighing 15-20 g, were divided into 4 groups ( n=6 each) according to the random number table method: control group (group C), endotoxin-induced ALI group (group L-ALI), endotoxin-induced ALI plus acupoint electroacupuncture group (group L-ALI+ EA), and endotoxin-induced ALI plus non-acupoint electroacupuncture group (group L-ALI+ SEA). Lipopolysaccharide (LPS) 15 mg/kg was injected via the caudal vein to develop the model of endotoxin-induced ALI in anesthetized mice.In group L-ALI+ EA, at 5 days before LPS injection, bilateral Zusanli and Feishu acupoints were stimulated with an electric stimulator for 30 min each time at a voltage of 1-2 mA and a frequency of 2/15 Hz until the end of the experiment.In group L-ALI+ SEA, stimulation was performed at the points 0.5 cm lateral to the acupoints of bilateral Zusanli and Feishu non-meridian and non-acupoint sites using the shallow puncture method, and the other treatment methods were the same as those previously described in group EA.Group C received no treatment.The mice were sacrificed by euthanasia at 12 h after LPS administration, and lung tissues were obtained for microscopic examination of the pathological changes (with a light microscope) and structure and morphology of mitochondria (with a transmission electron microscope) and for determination of the levels of reactive oxygen species (ROS) and mitochondrial DNA (mtDNA) and contents of glutathione (GSH) and glutathione oxidized (GSSG). The GSH/GSSG ratio was calculated.The expression of mitochondrial fusion proteins mitofusin 1 (Mfn1), Mfn2, optic atrophy1 (OPA1), dynamin-related protein 1 (Drp1), fission protein 1 (Fis1), peroxisome-proliferator-activated receptor γ coactivator-1α (PGC-1α), nuclear respiratory factor-1 (NRF1), NRF2, PTEN-induced putative protein kinase 1 (PINK1) and the E3 ubiquitin ligase (Parkin) was determined by Western blot. Results:Compared with group C, the level of ROS and contents of GSSG and mtDNA were significantly increased, GSH content and GSH/GSSG ratio were decreased, the expression of Mfn1, Mfn2, OPA1, NRF1, NRF2 and PGC-1α was down-regulated, and the expression of Drp1, Fis1, PINK1 and Parkin was up-regulated in L-ALI, L-ALI+ EA and L-ALI+ SEA groups ( P<0.05). Compared with group L-ALI, the level of ROS and contents of GSSG and mtDNA were significantly decreased, GSH content and GSH/GSSG ratio were increased, the expression of Mfn1, Mfn2, OPA1, NRF1, NRF2 and PGC-1α was up-regulated, and the expression of Drp1, Fis1, PINK1 and Parkin was down-regulated in group L-ALI+ EA ( P<0.05). Compared with group L-ALI+ EA, the level of ROS and contents of GSSG and mtDNA were significantly increased, GSH content and GSH/GSSG ratio were decreased, the expression of Mfn1, Mfn2, OPA1, NRF1, NRF2 and PGC-1α was down-regulated, and the expression of Drp1, Fis1, PINK1 and Parkin was up-regulated in group L-ALI+ SEA ( P<0.05). Conclusions:TEAS can reduce endotoxin-induced ALI probably through regulating mitochondrial quality control in mice.