[Objective]To seek for a method to rebuild radial head for comminuted radial head fractures,and recommend a new technique of bipolar radial head replacement.[Method]Five patients with fresh comminuted radial head fractures were treated by Tornier cement stem and bipolar radial prothesis.Among them,three were females and two were males,with the average age of 37.4Y(29-48Y).Four cases were to Mason type Ⅲ and one Mason type Ⅳ.All the patients underwent operation within 3-11 days with an average of 6 days after injury.Rehabilitation began in Mason type Ⅲ radial head fracture patients 48 h postoperatively.Both medial and lateral ligaments were repaired in one case of Mason type Ⅳ fracture.Plastic brace were used for 3 weeks during functional rehabilitation.The postoperative elbow joint was evaluated clinically by Broberg and Morrey score.[Result]All the patients healed by first intention were followed up for 7 to 50 months,with an average of 30 months.According to elbow functional evaluation criteria by Broberg and Morrey scores,there were excellent results in three and good in two respectively with an average of 92.2 points.[Conclusion]Cement stem and bipolar radial head prothesis replacement is a good technique for treating comminuted radial head fractures because it meets the designing principle of modern orthopaedics.

In many pathogens infection,especially virus,antibody-dependent enhancement(ADE) can aggravate the infection and lead to severe diseases.In this immunopathological phenomenon,virus-specific antibodies enhance the entry of virus into monocytes,macrophages and granulocytic cells and even the replication of virus through different mechanism.This phenomenon has been reported in numerous pathogens including virus,bacteria and parasite and the mechanisms of ADE vary from different species.Further study of ADE can promote the vaccine research and development to make the most use of vaccine and prevent human body from pathogens,which will be helpful to control the spread of pathogens including Zika virus.In the present review,we review the research progress of ADE mechanism in recent years,including antibodies mediating,receptors mediating,complement mediating,viral proteins mediating and cellular mediating ADE.In addition,dengue virus,human immunodeficiency virus,Coxsackie virus,Ebola virus,Zika virus and other pathogens will be illustrated respectively.This review provides insights on the different mechanism of ADE in different pathogens.

OBJECTIVETo investigate the effect of inhibition and activation of MAPK-ERK1/2 pathway on the expression of osteogenic genes and proliferation of rat osteoblasts in vitro.

METHODSPrimarily cultured rat osteoblasts, identified by cell morphology studies and ALP staining, were exposed to 1% or 5% rat serum for 24 h or to the specific MAPK-ERK1/2 inhibitor PD0325901. The downstream molecules of MAPK-ERK1/2 pathway including p-ERK1/2 and ERK1/2, osteogenic genes such as Runx2 and Type I collagen, and proliferating cell nuclear antigen (PCNA) were detected by Western Blotting, and alkaline phosphatase activities were analyzed quantitatively.

RESULTSCompared with 1% rat serum-treated cells, exposure of the cells to a higher concentration (5%) of rat serum caused a significantly increased phosphorylation level of p-ERK1/2 (P<0.05) and obviously enhanced expressions of the osteogenic genes (Runx2, type I collagen and ALP) and PCNA (P<0.05). Inhibition of the MAPK-ERK1/2 pathway with PD0325901 resulted in suppressed expressions of the osteogenic genes and PCNA.

CONCLUSIONThe activation of MAPK-ERK1/2 pathway promotes the expression of osteogenic genes such as Runx2, type I collagen and ALP and enhances the proliferative activity of the osteoblasts, while inhibition of this pathway suppresses the expressions of these genes and the cell proliferation, suggesting that this pathway may potentially serve as a therapeutic target for osteoporosis.

Alkaline Phosphatase ; metabolism ; Animals ; Antineoplastic Agents ; pharmacology ; Benzamides ; pharmacology ; Cell Proliferation ; drug effects ; Cells, Cultured ; Collagen Type I ; metabolism ; Core Binding Factor Alpha 1 Subunit ; metabolism ; Diphenylamine ; analogs & derivatives ; pharmacology ; Female ; Gene Expression Regulation ; drug effects ; MAP Kinase Signaling System ; drug effects ; Male ; Mitogen-Activated Protein Kinase 1 ; metabolism ; Mitogen-Activated Protein Kinase 3 ; metabolism ; Osteoblasts ; cytology ; metabolism ; Phosphorylation ; drug effects ; Proliferating Cell Nuclear Antigen ; metabolism ; Rats ; Rats, Sprague-Dawley

Objective To investigate the effect of inhibition and activation of MAPK-ERK1/2 pathway on the expression of osteogenic genes and proliferation of rat osteoblasts in vitro. Methods Primarily cultured rat osteoblasts, identified by cell morphology studies and ALP staining, were exposed to 1%or 5%rat serum for 24 h or to the specific MAPK-ERK1/2 inhibitor PD0325901. The downstream molecules of MAPK-ERK1/2 pathway including p-ERK1/2 and ERK1/2, osteogenic genes such as Runx2 and Type I collagen, and proliferating cell nuclear antigen (PCNA) were detected by Western Blotting, and alkaline phosphatase activities were analyzed quantitatively. Results Compared with 1%rat serum-treated cells, exposure of the cells to a higher concentration (5%) of rat serum caused a significantly increased phosphorylation level of p-ERK1/2 (P<0.05) and obviously enhanced expressions of the osteogenic genes (Runx2, type I collagen and ALP) and PCNA (P<0.05). Inhibition of the MAPK-ERK1/2 pathway with PD0325901 resulted in suppressed expressions of the osteogenic genes and PCNA. Conclusion The activation of MAPK-ERK1/2 pathway promotes the expression of osteogenic genes such as Runx2, type I collagen and ALP and enhances the proliferative activity of the osteoblasts, while inhibition of this pathway suppresses the expressions of these genes and the cell proliferation, suggesting that this pathway may potentially serve as a therapeutic target for osteoporosis.

Objective To investigate the effect of inhibition and activation of MAPK-ERK1/2 pathway on the expression of osteogenic genes and proliferation of rat osteoblasts in vitro. Methods Primarily cultured rat osteoblasts, identified by cell morphology studies and ALP staining, were exposed to 1%or 5%rat serum for 24 h or to the specific MAPK-ERK1/2 inhibitor PD0325901. The downstream molecules of MAPK-ERK1/2 pathway including p-ERK1/2 and ERK1/2, osteogenic genes such as Runx2 and Type I collagen, and proliferating cell nuclear antigen (PCNA) were detected by Western Blotting, and alkaline phosphatase activities were analyzed quantitatively. Results Compared with 1%rat serum-treated cells, exposure of the cells to a higher concentration (5%) of rat serum caused a significantly increased phosphorylation level of p-ERK1/2 (P<0.05) and obviously enhanced expressions of the osteogenic genes (Runx2, type I collagen and ALP) and PCNA (P<0.05). Inhibition of the MAPK-ERK1/2 pathway with PD0325901 resulted in suppressed expressions of the osteogenic genes and PCNA. Conclusion The activation of MAPK-ERK1/2 pathway promotes the expression of osteogenic genes such as Runx2, type I collagen and ALP and enhances the proliferative activity of the osteoblasts, while inhibition of this pathway suppresses the expressions of these genes and the cell proliferation, suggesting that this pathway may potentially serve as a therapeutic target for osteoporosis.

Objective:To investigate the clinical effect of bridging fixation with locking plate for the Seinsheimer type V subtrochanteric femoral fracture. Methods:From March 2009 to September 2014,18 cases of Seinsheimer type V sub-trochanteric femoral fracture were treated by open reduction and bridging fixation with locking plate through proximal and distal approach including 16 males and 2 females with an average age of 41 years old ranging from 22 to 67 years old. Among them , 12 cases caused by traffic accident,5 cases by falling,1 case by heavy aboving. All cases were fresh and closed fractures. Time between injury and operation was from 4 to 9 days with an average of 6.2 days. Of them ,11 cases were fixed with reverse LISS and the other 7 cases were fixed with anatomical locking plates of proximal femur. Results:The mean time of operation was 110 min (ranged from 90 to 155 min). The mean blood loss during operation was 425 ml (ranged from 350 to 650 ml) and 16 cases got blood transfusion which was meanly 300 ml. The mean hospital time was 14 days (ranged from 12 to 18 days). The mean duration of followed up was 11.8 months (ranged from 8 to 22 months). The mean time of bone union was 6.6 months (ranged from 5 to 8 months). There was not any complication such as infection,implant failure,hip varus,external rotation deformity of low limb or fat embolism. The Sanders hip scores were 53.22±6.48,the result was excellent in 12 cases and good in 6 cases at the last follow up. Conclusion:Under the principle of biological osteosynthesis ,treatment of Seinsheimer type V sub-trochanteric femoral fracture with bridging locking plate fixation has such advantages as high mechanism ,less interference of blood supply,stable fixation and little complication. It is a safe and idea way for the treatment of the Seinsheimer type V sub-trochanteric femoral fracture.