1.Bipolar radial head replacement for treatment of comminuted radial head fractures:a preliminary report
Xiaoen WEI ; Haiping HONG ; Weiguo SHEN
Orthopedic Journal of China 2006;0(06):-
[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.
2.Research progress on mechanism of antibody-dependent enhancement
Weizhuang YUAN ; Yicheng YANG ; Xuling LIU ; Xiaoen HE ; Yuan HUI ; Yujing LIU ; Ying LI ; Wei ZHAO
Chinese Journal of Zoonoses 2017;33(7):650-657
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.
3.MAPK-ERK1/2 signaling pathway regulates osteogenic gene expression in rat osteoblasts in vitro.
Daofang DING ; Linghui LI ; Yi SONG ; Guoqing DU ; Xiaoen WEI ; Yuelong CAO
Journal of Southern Medical University 2013;33(10):1432-1436
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