Objective To investigate the effectiveness of arthroscopic reduction and percutaneous fixation (ARPF) for the treatment of tibial plateau fractures. Methods Seventeen cases of tibial plateau fractures from April 1999 to June 2002 were reviewed. The fractured tibial plateau was reconstructed by “drag-and-draw” reduction and iliac crest bone graft under arthroscope. And percutaneous cancellous bone screw fixation was conducted. Results Clinical bone union was achieved in all the patients at the third postoperative month. No infection or severe osteoarthritis occurred. Conclusions ARPF for tibial plateau fractures has advantages of reduction under direct view, reliable fixation and facilitation for early activities.

BACKGROUND:A large amount of apicocoronal and buccolingual bone resorption occur in alveolar bone after tooth extraction, leading to the distinct shortage of bone mass of alveolar bone in tooth-missing area, which has a certain effect on the stability of early implantation and postoperative aesthetic outcomes and greatly affects the long-term success rate of denture implantation. Therefore, immediate-delayed implantation can shorten the time of repair. OBJECTIVE:To evaluate the effect of implant repair after immediate-delayed implantation and application of guided bone regeneration technique in anterior maxila area. METHODS:Nineteen patients (28 teeth lost) with maxilary anterior tooth loss and labial one-waled bone defects were selected. Twenty-eight OSSTEM implants were implanted at 4 weeks after tooth extraction. Guided bone regeneration technique was applied concurrently in labial bone defect area. The secondary repair was performed after 6 months. RESULTS AND CONCLUSION:The success rate of these 28 implants was 100% at 24 months after denture implantation. The peri-implant bone height loss at 6, 12 and 24 months was 0.1, 0.6 and 0.11 mm, respectively. Red aesthetic scores were satisfactory. Immediate-delayed implantation combined with application of guided bone regeneration technique for treatment of maxilary anterior tooth loss and mild bone defect can restore the height and width of peri-implant bone and acquire stable vertical bone resorption and satisfactory gingival aesthetic outcomes .

Objective To study the clinical and X-ray findings in mamma virilis devolopment.Methods Clinical and X-ray findings in 11 patients with primary mamma virilis development were presented and analysed retrospectvely.Results X-ray findings were divided into 3 groups:1)mass(n=4):round or oval mass with high density and well-defined border;2)patch(n=4):patch like uneven mass with high density and ill-defined border;3)nodule(n=3):irregular uneven nodules.Conclusion Clinical and X-ray findings of mamma virilis development have some characteristic features,it can be differentiated from mamary cancer and pseudogynecomastia.

Objective To evaluate Western blot analysis in diagnosing limb-girdle muscular dystrophy type 2A (LGMD2A). Methods The clinical records including their pathological and biochemical results of 4 patients with LGMD type 2 were reviewed. Histochemical and immunohistochemical staining were performed on muscle biopsy specimens from the four patients. The expressions of dysferlin and calpain-3 in muscles were analyzed by Western biol. Results All 4 LGMD patients shared some common clinical features, such as dorsal muscular atrophy of lower limbs and remarkably elevated CK. The immunohistochemical results showed partial or complete deficiency of dysferlin staining in all 4 LGMD patients. However, Western blot revealed that the calpain-3 protein in the muscle of patient 1 was completely absent, who was later diagnosed with LGMD2A. The other 3 patients had complete dysferlin deficiency with reduced calpain-3 expression and they were confirmed to be LGMD2B. Conclusions Western blot analysis of calpain-3 and dysfcrlin can be used to differentiate LGMD2A which shows absence of calpain-3 from other LGMD types which show dysferlin deficiency. Western blot is an invaluable method in clinical diagnosis of LGMD2A.

BACKGROUND: The deficiency of perfect animal femoral head necrosis model limited its further investigation. OBJECTIVE: To verify the feasibility of establishing rabbit femoral head necrosis models using liquid nitrogen rsfdgeration method, and to provide a foundation for subsequent research. METHODS: A total of 20 adult, New Zealand, white rabbits were selected in the study. The round ligament of femur was not cut off and femoral head was not dislocated, and the exposed femoral head were quick frozen using cotton bud carrying liquid nitrogen for successive 25 times, with 10 s per time. The specimens were examined by gross anatomy, X-ray film, MRI and histological observation at day 3, 7 and weeks 2, 4, 6, and 8 after operation. RESULTS AND CONCLUSION: The histolOgical section showed that chondrocyte, osteccyts, and myelold tissues presented necrosis in freezing and periphery at 3days after model preparation, and the repair process appeared at 2weeks after operation. The articular surface of femoral heads appeared collapse at 4 weeks after operation, and these changes became obvious at 6 weeks. The femoral head presented ostecarthdtis-like disorder, with seriously collapsed articular surface at8 weeks, and the contour of femoral head changed in 2 animals. The results demonstrated that without hip dislocation, rabbit femoral head necrosis models can be established successfully using liquid nitrogen refrigeration method. This method is simple, feesible, with high succeed rate, which can be used in subsequent research.

Objective To investigate the clinical and immune pathological features of Ullrich congenital muscular dystrophy (UCMD) with sarcolemma-specific collagen Ⅵ deficiency (SSCD). Methods The clinical aspects of 2 patients with SSCD were analyzed and the muscle specimens from them were studied by immunofluorescence. Results SSCD patients were clinically characterized by neonatal hypotonia with proximal contractures and distal hyperlaxity at birth or early infancy. Immunofluorescence staining revealed partial deficiency of collagen Ⅵ. Double immunofluorescence staining revealed sarcolemma-specific deficiency of collagen Ⅵ, while collagen Ⅳ intact in thesarcolemma. Conclusions The clinical picture and severity of UCMD with SSCD are similar to the cases with collagen Ⅵ complete deficiency. The proximal contractures and distal hyperlaxity are the clinical hallmarks of both types. Sarcolemma-specific collagen Ⅵ deficiency can be better demonstrated by double immunofluorescence staining.

Objective To investigate muscle MRI characteristics of lower limbs in Chinese patients with dysferlinopathy. Methods Detailed clinical information of 42 patients with dysferlinopathy confirmed by Western blot or DYSF genetic test were studied retrospectively, including age, course, serum creatinine kinase (CK) and modified Gardner?Medwin and Walto score, and T1WI, STIR image. Each muscle was scored according to its fatty degeneration evaluated on T1WI (fat replacement score). The patients were divided into 3 groups:Miyoshi myopathy (MM), limb girdle muscle dystrophy 2B (LGMD 2B) and preclinical stage (asymptomatic hyperCKemia or exercise intolerance). The data including the scores of each muscle between MM and LGMD 2B were compared by ANOVA analysis and Chi square test. The relationship of fatty replacement score with course and GM?W score was analyzed by Spearman rank correlation analysis. Results Thirty nine patients underwent thigh MR scanning and 36 patients underwent leg MR scanning. At the thigh level, there is no specificity that the fatty replacement was found in both the anterior and posterior parts while the rectus femoris, sartorius and gracilis were rarely involved. At the leg level, the most severely involved muscle was the soleus, followed by gastrocnemius. It formed a sandwich?like pattern that the anterior part (anterior and posterior tibial muscle and peroneus longus muscle) and the posterior part (medial and lateral gastrocnemius) were less involved than the middle part (soleus). Of 42 patients, 14 cases were MM, and 24 were LGMD 2B. The fat replacement score of each muscle between two groups showed no significant differences (F=0.066 to 3.907,P all>0.05) except for the adductor muscle (F=5.239, P=0.028), semimembranosus (F=6.703, P=0.014) and semitendinosus (F=7.689, P=0.009). Of 4 pre?symptomatic cases, 3 showed edema of posterior part of leg on STIR, especially soleus. In all patients, the fat replacement score correlated positively with course (rs=0.732, P=0.000) and GM-W score (rs=0.485, P=0.001). Conclusions The MRI of Chinese patient with dysferlinopathy was characterized by the milder involvement of rectus femoris, sartorius and gracilis muscle in the thigh and a sandwich?like pattern in the leg, which is helpful for differential diagnosis of inflammatory Myopathy versus other types of muscular dystrophy.

Objective To evaluate the relationship between extracellular signal-regulated kinase (ERK)and ketamine-induced apoptosis in rat hippocampal neurons.Methods Sprague-Dawley rats at 18 days of gestation were anesthetized.The fetal rats were obtained under the sterile condition and decapitated.The hippocampal neurons were isolated and primarily cultured for 5 days,and were seeded in 6-well plates (2 ml/well) or in 96-well plates (100μl/well) at a density of 5 × 105/ml.The cells were randomly divided into 4 groups (n =18 each):control group (group C),fibroblast growth factor (FGF-2,an ERK agonist) group (group F),ketamine group (group K) and FGF-2 + ketamine group (group FK).The cells were cultured in the plain culture medium in group C.FGF-2 50 ng/ml was added to the culture medium in group F.Ketamine was added to the culture medium in group K.FGF-2 50 ng/ml was added to the culture medium at 20 min before ketamine 100 μmol/L was added in group FK.The phosphorylation of ERK in hippocampal neurons was detected by Western blot at 10 min after treatment.At 24 h after treatment,the neuronal apoptosis was detected by Hoechst33342/PI staining,and the cell survival rate was detected by MTT assay.The apoptosis rate was calculated.Results Compared with group C,the phosphorylation of ERK in hippocampal neurons and the cell survival rate was significantly decreased and the apoptosis rate was increased in K and FK groups (P ＜ 0.05).There was no significant difference in the parameters mentioned above between F and C groups (P ＞ 0.05).The phosphorylation of ERK in hippocampal neurons and the cell survival rat was significantly higher and the apoptosis rate was lower in group FK than in group K (P ＜0.05).Conclusion Ketamine induces apoptosis in rat hippocampal neurons by inhibiting activation of ERK in hippocampal neurons.

Objective To investigate the clinical features and electron transfer flavoprotein dehydrogenase (ETFDH) gene mutations in 35 Chinese patients with lipid storage myopathy. Methods The clinical data of 35 cases with lipid storage myopathy confirmed by muscle biopsy were collected. The sequences of all 13 exons of ETFDH were analyzed. Results All 35 patients showed proximal weakness. Ten of them demonstrated masseter weakness and 28 of them showed weakness in neck flexion. Twenty-nine of 32 patients who were followed up showed improvement after treatment with VitB2 and CoQ10. Mutations of ETFDH were found in 30 of 35 patients,which included 8 homozygosises,20 compound heterozygosises and 2 single heterozygosises. Fourteen novel mutations were found, including 9 missense mutations ( c. 3G > C, c. 152G>A, c. 191G > A, c.349G>C, c.433G>C, c. 949C > A, c. 1454C > G, c. 1744A >T and c. 1763A>G), 1 nonsense mutation(c. 172G>T), 2 deletions(c. 1282_1283del and 1773_1774del) and 2 splice mutations (c. 405 + 1G > T and c. 1691 -3C > G). Nine of them showed c. 250G > A mutation and 6 of them showed c. 770A > G mutation. Conclusions Lipid storage myopathy is presented as proximal weakness. Multiple acyl-CoA dehydrogenase deficiency caused by mutations of ETFDH is the major cause of lipid storage disease in this group. ETFDH c. 250G > A and c. 770A > G mutations show a high frequency.

Objective To investigate the clinical and pathological features of Uurich congenital muscular dystrophy (UCMD). Methods The clinical aspects of 3 patients with UCMD, 2 with Duchenne muscular dystrophy (DMD) and 1 with congenital muscular dystrophy 1A (MDC1A) were analyzed. And the muscle specimens from these patients were studied using immunohistochemistry and immunofluorescence staining. Results UCMD was clinically characterized by neonatal hypotonia with proximal contracturos and distal hyperlaxity at birth or early infancy. Histochemical staining revealed muscle frber hypoplasia andinterstitium proliferation. Immunohistochemistry staining with anti-collagen Ⅵ antibody revealed complete(1/3) or partial (2/3) deficiency of collagen Ⅵ in the sarcolemma and interstitial matrix. Partial deficiency was better demonstrated by immunofluorescence staining. Conclusions The proximal contractures and distal hyperlaxity is the clinical hallmark of UCMD. Collagen Ⅵ immunolabelling can confirm the diagnosis of UCMD.