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 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.

BACKGROUNDTo determine the inhibitory effect of antisense peptide nucleic acids (PNA) of telomerase on the growth of lung cancer cell lines.

METHODSThe synthesized modified antisense PNAs of telomerase were transfected into the lung cancer cell lines A549 and NCI-H446 respectively by lipofectamine transfection. Telomerase activity was detected by RT-PCR-ELLISA, and the cell counts were determined by MTT.

RESULTSSeventy two hours after transfection with antisense PNAs of telomerase, telomerase activity (A450 value) of A549 and NCI-H446 were down regulated from 0.582 ±0.039, 0.571±0.043 to 0.294±0.048 ( P < 0.01), 0.276±0.051 ( P < 0.01) respectively, and alive cell counts (A580 value) of them from 0.485± 0.009 , 0.513±0.015 to 0.191±0.027 ( P < 0.01), 0.138±0.046 ( P < 0.01) respectively. The growth of two lung cancer cell lines were significantly inhibited.

CONCLUSIONSAntisense PNA of telomerase might inhibit not only the telomerase activity, but also the growth of lung cancer cell lines in vitro.

BACKGROUNDTo evaluate the clinical significance of telomerase activity in lung cancer and to investigate the possibility of telomerase as cancer marker for lung cancer.

METHODSThe activity of telomerase was investigated by TRAP-PCR-ELISA in lung cancer tissues and corresponding adjacent noncancerous tissues obtained from resected specimens of 48 patients with lung cancer and 42 specimens of benign pulmonary lesions were examined simultaneously.

RESULTSTelomerase activity was detected in 42 (87.5%) of the 48 tumors and only 4 (8.3%) of the 48 adjacent noncancerous lung tissue samples (Chi-Square=13.029, P < 0.01), but in none of 42 specimens of benign pulmonary lesions (Chi-Square=14.016, P < 0.01). Correlation with pathological parameters showed that the expression of telomerase activity was associated with lymph node metastasis (93.5% vs 76.4% , Chi-Square=63.511, P < 0.01), but not with histological type, location and differenciated grade of tumor.

CONCLUSIONSTelomerase activation correlates with the carcinogenesis and aggressiveness of lung cancer. Telomerase might be one of the important diagnostic and prognostic factors in patients with lung cancer.

BACKGROUNDTo investigate the expression of the SOCS3 gene and its effect on proliferation of A549 cells.

METHODSA549 cells were cotransfected with pEFSOCS3 and pSV2neo by liposome, then G418 was used to screen the positive cells. Expression of SOCS3 mRNA and protein was detected by RT-PCR and immunocytochemistry respectively before and after transfection. MTT assay was used to detect the cell growth. Flow cytometric DNA analysis was used to determine the cell cycle.

RESULTSRT-PCR and immunocytochemistry showed that no expression of SOCS3 mRNA and protein was detected in A549 cells before transfection, but a stable expression of SOCS3 gene was observed after transfection with SOCS3 gene. Compared with control group, growth of A549 cells transfected with SOCS3 gene was significantly suppressed, with a suppressive rate of 41.07%. The cells at G₀/G₁ cell phases increased, and those at S and G₂/M phases decreased significantly after transfection.

CONCLUSIONSSOCS3 protein might inhibit the proliferation of A549 cells by negatively regulating cellular signal pathways.

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.

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.