Objective To investigate the mechanical stability and clinical outcome of minimally invasive plate osteosynthesis of pubic ramus fractures.Methods Stability of minimally invasive plate osteosynthesis and traditional open fixation of pubic ramus fractures was compared in finite element analysis.A retrospective analysis was performed on fractures of pubic rami (126 sides) in 101 consecutive patients treated with minimally invasive plate osteosynthesis from 2005 to 2012.Operation time,intraoperative blood loss and follow-up of fracture healing were evaluated.Results In finite element analysis,traditional open fixation and minimally invasive plate osteosynthesis resulted in the maximum pelvic force of 7.35 MPa and 5.59 MPa,maximum fracture displacement of 4.31 mm and 4.38 mm and relative fracture gap displacement of 0.029 mm and 0.012 mm.Displacement of fracture gap after minimally invasive plate osteosynthesis and traditional open fixation was reduced 26％ and 59％ respectively.In the clinical study,the surgery acquired for pubic ramus fractures averaged 65 minutes with mean blood loss of 94 ml.Follow-up duration was 5-50 months (mean,24.3 months).Reduction of the fracture as assessed using Matta' s criteria was excellent in 118 sides (93.7％),good in eight sides (6.3％).Totally,the fracture was healed within postoperative 12 weeks in 117 sides and within postoperative 6 months in 9 sides.No iatrogenic nerve or vascular injury occurred.Conclusions Minimally invasive plate osteosynthesis is a safe and effective technique for fixation of pubic ramus fractures.Moreover,satisfactory results can be achieved together with less trauma and better cosmetic effect.

Objective To discuss the surgical technique of delayed acetabular fractures and its possible prognosis factors.Methods From April 2001 to November 2008,61 patients with delayed acetabular fractures were surgically treated.There were 47 males and 14 males,with an average age of 38 years.According to Letourael classification,16 simple fractures included 7 cases of posterior wall fractures,2 of posterior column fractures,1 of anterior column fractures and 6 of transverse fractures.Forty-five patients with mixed fractures included 3 cases with both fractures posterior column and wall,7 of transverse and posterior wall fractures,4 of T-shape fractures,6 of posteriorly semi-transverse fractures and 25 of both-columns fractures.Fifty-two patients suffered from traffic accident;6 patients were caused by falling from height and 3 suffered from crush injuries.Brain injuries occurred in 11 cases,thorax-abdominal injuries in 15,urinary tract injuries in 7,multiple fractures in 25.The injury of sciatic nerve was found in 3 patients preoperatively.The average interval form injury to surgery was 39 days.A single approach was employed in 13 cases,and combined antero-posterior approaches were employed in 48.The operation time was (248±45) min with a blood loss of (2160±100) ml averagely.Results The average follow-up was (61±8) months.The clinical result was evaluated by Matta reduction criteria,modified Merle d'Aubingne and Postel scoring system.Anatomical reduction was achieved in 45 cases;however,13 were unsatisfactory and 3 were poor.For clinical results,38 were graded as excellent,13 as good,6 as fair and 4 as poor.Osteonecrosis of the femoral head occurred in 3 cases (4.9%),and heterotopic ossification developed in 28 cases (45.9%).Additionally,4patients (6.6%) had a transient sciatic nerve paralysis.Conclusion Open reduction and internal fixation is a liable method for delayed acetabular fractures.Single approach is suitable for simple fractures;in principle and combined approaches are for compound delayed acetabular fractures.The reduction quality is closely related to surgeon's experience.

Objective To investigate the variations of mtDNA from high and low metastatic mouse hepatocarcinoma cell sublines Hca-F and Hca-P, and the relationship between mutations of mtDNA and carcinogenesis. Methods The variations of D-loop, ND3 and tRNA Met+Glu+Ile gene fragments of mtDNA from Hca-F and Hca-P cells were analyzed by PCR-RFLP and sequencing techniques. Results No amplification fragment length polymorphism and restriction fragment length polymorphism were observed in tRNA Met+Glu+Ile , ND3 and D-loop of mtDNA from the 2 cell sublines. Sequence difference between these 2 cell sublines were found in mtDNA D-loop region by sequencing. Conclusions Genetic alteration of mtDNA non-coding region in tumors, which may reflect the environmental and genetic influences operative during tumor progression, can be linked to their tumorigenic phenotype.

Objective To study the 4 977 bp deletion of mitochondrial DNA in lung cancer, paraneoplastic tissue and normal lung tissue from non-lung cancer subjects and its significance in the development of cancer. Methods Lung cancer tissues and paraneoplastic tissues from 37 non-small lung cancer patients, and normal lung tissues from 20 patients without lung cancer were analyzed by long PCR technique. Results Mitochondrial DNA 4 977 bp deletion was detected in 54.1%(20/37) of lung cancer tissues, 59.5%(22/37) of paraneoplastic tissues and 30.0%(6/30) of normal lung tissues. The correlation between 4 977 bp deletion and age, smoking was present in our data. Conclusion Mitochondrial DNA 4 977 bp deletion, which may reflect the environmental and genetic influences during tumor progression, is not specific to lung cancer and unlikely to play an important role in carcinogenesis.

Objective To investigate the effects of sodium butyrate on the activity of RAW264.7 cells and the osteoclast differentiation.Methods The RAW264.7 cells were treated by sodium butyrate at concentrations of 0,0.25,0.50,1.00,2.00,3.00,4.00 and 5.00 mmol/L,with 3 double pores for each concentration.The cytotoxicity of sodium butyrate on RAW264.7 cells was detected by a CCK-8 kit.The effects of sodium butyrate (0,0.25,0.50 and 1.00 mmol/L) on apoptosis of RAW264.7 cells were detected by Hoechst33342 staining.RAW264.7 cells were induced into osteoclasts by osteoclast differentiation factors.The experiment was carried out in 2 groups (n =3).After induced maturation,the experimental group was treated with 1.00 mmol/L sodium butyrate and the control medium was added only with the same volume of solvent.The number of osteoclasts and the area of bone resorption were observed and compared.The differentiation of RAW264.7 cells was detected by tartrate-resistant acid phosphatase (TRAP) staining.Western blotting was used to detect the effects of sodium butyrate (0,0.25,0.50 and 1.00 mmol/L) on NF-κB-related signaling pathway in RAW264.7 cells.Results Compared with the group of 0 mmol/L sodium butyrate,the activity of cells treated with 1.00,2.00,3.00,4.00 and 5.00 mmol/L sodium butyrate for 24 h was significantly decreased (P ＜ 0.05).Treatment with 1.00 mmol/L sodium butyrate for 24 h induced apoptosis.The number of osteoclasts in the control group and the experimental group were 9.33 ± 2.08 and 4.67 ± 1.16,respectively,showing a significant difference between the 2 groups (t =3.395,P =0.027).The percentages of bone resorption area in the control group and the experimental group were 52.43％ ± 5.38％ and 14.28％ ± 2.72％,respectively,also showing a significant difference between the 2 groups (t =10.970,P ＜ 0.001).Western blot results showed that,compared with other concentrations of sodium butyrate,treatment with 1 mmol/L sodium butyrate on RAW264.7 cells for 24 h led to an increase in the expression levels of cytoplasmic p65,B lymphoma-2 associated X protein and cleaved-caspase 3 and the acetylation of Histone H3 but a decrease in the phosphorylation level of α/β subunit of NF-κB kinase.Conclusions With the increased concentration of sodium butyratecan,the activity of NF-κB may be suppressed and the number of apoptotic cells may increase.1.00 mmol/L sodium butyrate can reduce osteoclast formation and bone resorption area.

Due to increasing incidence of open fracture and increasing application of orthopedic implants, chronic osteomyelitis prevails in recent years, leading to failure of internal fixation, sinus tract formation, long-term abscess discharge and delayed recovery, etc., affecting prognosis and quality of life of the patients, and causing a huge medical and economic burden.The treatment of osteomyelitis has recently progressed from mere debridement to debridement + Masquelet bone reconstruction or osteotomy + llizarov bone transfer which has significantly improved the therapeutic efficacy. However, multiple surgeries, long healing time and massive surgical trauma of the current treatment cause poor compliance in the patients. Therefore, new therapeutic strategies are imperative. Various causes of chronic osteomyelitis involve autoimmunity, inflammatory factors, oxidative stress, local blood supply in osteomyelitis region, drug-resistant bacteria, bacterial virulence and bacterial biofilm which, as an important form of bacteria in the body, has a particularly significant impact on chronic osteomyelitis. Resistance to a variety of eliminating effects by bacteria is achieved mainly by biofilm, including reducing antibiotics concentration, barrier against immune clearance, improving bacterial resistance, spreading bacteria and promoting signal communication between bacteria. Aiming at the key factors and pathways for target research and intervention is the hotspot and trend in the research and treatment of osteomyelitis. Here we review the literature about the role of biofilm in chronic osteomyelitis, which is conducive for further understanding of the biofilm influence on chronic osteomyelitis and related targets, and for prevention and treatment of chronic osteomyelitis as well.

IL-34 can promote osteoclast differentiation and activation, which may contribute to steroidinduced osteonecrosis of the femoral head (ONFH). Animal model was constructed in both BALB/c and IL-34 deficient mice to detect the relative expression of inflammation cytokines. Micro-CT was utilized to reveal the internal structure. In vitro differentiated osteoclast was induced by culturing bone marrow-derived macrophages with IL-34 conditioned medium or M-CSF. The relative expression of pro-inflammation cytokines, osteoclast marker genes, and relevant pathways molecules was detected with quantitative real-time RT-PCR, ELISA, and Western blot. Up-regulated IL-34 expression could be detected in the serum of ONFH patients and femoral heads of ONFH mice. IL-34 deficient mice showed the resistance to ONFH induction with the up-regulated trabecular number, trabecular thickness, bone value fraction, and down-regulated trabecular separation. On the other hand, inflammatory cytokines, such as TNF-α, IFN-γ, IL-6, IL-12, IL-2, and IL-17A, showed diminished expression in IL-34 deficient ONFH induced mice. IL-34 alone or works in coordination with M-CSF to promote osteoclastogenesis and activate ERK, STAT3, and non-canonical NF-κB pathways. These data demonstrate that IL-34 can promote the differentiation of osteoclast through ERK, STAT3, and non-canonical NF-κB pathways to aggravate steroid-induced ONFH, and IL-34 can be considered as a treatment target.