La核糖核蛋白6对人血管内皮细胞增殖与凋亡的作用

Objective To investigate regulatory effect of Acheron (Achn) on proliferation and apoptosis of human vascular endothelial cell. Methods ( 1 ) Eahy926 cells were cultured in serum-free DMEM medium (96-well plates) and were divided into Achn inhibition group (transfected with plasmid psi-Achn), psi4.1 group (transfected with psi4. 1 empty vector), Achn induction group (transfected with pcDNA-Achn), pcDNA3.1 group (transfected with pcDNA3.1 empty vector), cotransfection group [cotransfected with pcDNA-Achn + psi-calcium/calmodulin-dependent serine protein kinase (CASK)] , blank control group (treated with PBS) according to the random number table (the same method below). The cell proliferation was determined by MTT assay at post transfection hour (PTH) 1, 24, 48, 72, with expression of absorbance value. (2) Total protein of Eahy926 cells were extracted and quantitated by BCA assay, and then they were divided into Achn antibody precipitation group (100 μg protein) , CASK antibody precipitation group ( 100 μg protein), IgG antibody group ( 100 μg protein), Western blot group (20 μg protein).Achn and CASK protein levels were determined by immunoprecipitation and Western blot. (3) Synchronously cultured Eahy926 cells were divided into LPS induction group (treated with 5 mol/L LPS), Achn transfection group (transfected with pcDNA-Achn), cotransfection group (cotransfected with psi-CASK and pcDNA-Achn) , KCl group (treated with 5 mol/L KCl), and blank control group (treated with 5 mol/LPBS). Cells in transfection groups were stimulated by LPS for 12 hours after PTH 24. Caspase-3 protein level was detected by immunohistochemistry. (4) Synchronously cultured Eahy926 cells were divided into Achn inhibition group (transfected with psi-Achn vector), Achn induction group ( transfected with pcDNA-Achn vector), and blank control group ( treated with PBS). Apoptosis rate was determined by FITC/PI with flow cytometry. Data were processed with one-way analysis of variance and t test. Results ( 1 ) The cell proliferation in Achn inhibition group was lower than that in psi4.1 group from PTH 24, and the differences were statistically significant at PTH 48, 72 (with t value respectively 10. 777, 6.112, P values all below 0. 05 ).The cell proliferation in Achn induction group during PTH 24-72 were higher that in pcDNA3. 1 group (with t value respectively 5. 367, 6. 053, 9. 831, P values all below 0.05 ). The cell proliferation in cotransfection group at PTH 48, 72 were significantly lower than that in Achn induction group ( with t value respectively 5.481, 9. 517, P values all below 0. 05). (2) Achn protein was detected in CASK antibody precipitation group while CASK protein was also detected in Achn antibody precipitation group. (3) Caspase-3 level in Achn transfection group was lower [( 15.6 ± 0. 5 ) %] as compared with that in LPS induction group [(32. 8 ±2.6)%, t = 10. 083, P ＜ 0. 05], and that in cotransfection group showed further inhibition [(7.0 ±2.0)%,t =9.827, P ＜0.01]. (4) Apoptosis rate in Achn inhibition group[(45.6 ± 10.9)%] was higher than that in blank control group [(13.2±4.3) %, t =7.043, P ＜0.05]; while that in Achn inductiongroup [(5.3 ±2.9)%] was lower than that in blank control group ( t =6.499, P ＜0.05).Conclusions Achn can promote human vascular endothelial cell proliferation, and inhibit its apoptosis induced by LPS or burn serum, and the effect is related to CASK.     

La核糖核蛋白6对人血管内皮细胞增殖与凋亡的作用

目的 研究La核糖核蛋白6(Achn)在人血管内皮细胞增殖和凋亡中的调节作用.方法 (1)DMEM无血清培养基培养人血管内皮细胞株Eahy926细胞,按随机数字表法(下同)分为Achn抑制组(转染Achn抑制表达载体psi-Achn)、psi4.1空载体组(转染psi4.1)、Achn诱导组(转染Achn诱导表达载体pcDNA-Achn)、pcDNA3.1空载体组(转染pcDNA3.1)、Achn与钙/钙调蛋白依赖性丝氨酸蛋白激酶(CASK)共转染组(转染pcDNA-Achn与CASK抑制表达载体psi-CASK)、空白对照组(PBS处理),分别于转染后1、24、48、72 h用噻唑蓝法测定各组细胞570 nm波长下的吸光度值.(2)取Eahy926细胞,裂解细胞总蛋白,二辛丁酸法定量后分为蛋白质印迹组(总蛋白量为20μg)、Achn蛋白沉淀组、CASK蛋白沉淀组、IgG对照组,后3组细胞蛋白总量各为100μg,免疫共沉淀法检测各组Achn、CASK蛋白水平.(3)取Eahy926细胞分为LPS组(5 mol/L LPS处理)、氯化钾组(5 mol/L氯化钾处理)、空白对照组(5 mol/L PBS处理)、Achn诱导转染组(转染pcDNA-Achn)、Achn与CASK共转染组(转染pcDNA-Achn与psi-CASK),转染组转染24 h后加入LPS刺激12 h,免疫组织化学法检测各组半胱氨酸天冬氨酸蛋白酶3(caspase-3)蛋白表达.(4)取Eahy926细胞分为Achn诱导组(转染pcDNA-Achn)、Achn抑制组(转染psi-Achn)、对照组(PBS处理),24 h后加入烧伤患者血清处理12 h,流式细胞仪检测各组细胞凋亡率.对实验数据行t检验和单因素方差分析.结果 (1)Achn抑制组细胞增殖水平从24 h开始低于psi4.1空载体组,48、72 h时差异均有统计学意义(t值分别为10.777、6.112,P值均小于0.05);转染后24、48、72 h Achn诱导组细胞增殖水平均显著高于pcDNA3.1空载体组(t值分别为5.367、6.053、9.831,P值均小于0.05);Achn与CASK共转染组细胞增殖水平48、72 h均显著低于Achn诱导组(t值分别为5.481、9.517,P值均小于0.05).(2)CASK蛋白沉淀组CASK抗体沉淀物中可同时检测到CASK蛋白和Achn蛋白,而Achn蛋白沉淀组Achn抗体沉淀物中可同时检测到Achn蛋白和CASK蛋白.(3)Achn诱导转染组血管内皮细胞caspase-3阳性表达率为(15.6±0.5)%,低于LPS组[(32.8±2.6)%,t=10.083,P＜0.05];Achn与CASK共转染组caspase-3阳性细胞表达率[(7.0±2.0)%]进一步降低,显著低于LPS组(t=9.827,P＜0.01).(4)Achn抑制组细胞凋亡率为(45.6±10.9)%,显著高于对照组的(13.2±4.3)%,t=7.043,P＜0.05;Achn诱导组的细胞凋亡率为(5.3±2.9)%,显著低于对照组(t=6.499,P＜0.05).结论Achn能促进入血管内皮细胞增殖,抑制LPS或烧伤血清诱导细胞凋亡并与CASK的作用相关联.

Abstract：

Objective To investigate regulatory effect of Acheron (Achn) on proliferation and apoptosis of human vascular endothelial cell. Methods ( 1 ) Eahy926 cells were cultured in serum-free DMEM medium (96-well plates) and were divided into Achn inhibition group (transfected with plasmid psi-Achn), psi4.1 group (transfected with psi4. 1 empty vector), Achn induction group (transfected with pcDNA-Achn), pcDNA3.1 group (transfected with pcDNA3.1 empty vector), cotransfection group [cotransfected with pcDNA-Achn + psi-calcium/calmodulin-dependent serine protein kinase (CASK)] , blank control group (treated with PBS) according to the random number table (the same method below). The cell proliferation was determined by MTT assay at post transfection hour (PTH) 1, 24, 48, 72, with expression of absorbance value. (2) Total protein of Eahy926 cells were extracted and quantitated by BCA assay, and then they were divided into Achn antibody precipitation group (100 μg protein) , CASK antibody precipitation group ( 100 μg protein), IgG antibody group ( 100 μg protein), Western blot group (20 μg protein).Achn and CASK protein levels were determined by immunoprecipitation and Western blot. (3) Synchronously cultured Eahy926 cells were divided into LPS induction group (treated with 5 mol/L LPS), Achn transfection group (transfected with pcDNA-Achn), cotransfection group (cotransfected with psi-CASK and pcDNA-Achn) , KCl group (treated with 5 mol/L KCl), and blank control group (treated with 5 mol/LPBS). Cells in transfection groups were stimulated by LPS for 12 hours after PTH 24. Caspase-3 protein level was detected by immunohistochemistry. (4) Synchronously cultured Eahy926 cells were divided into Achn inhibition group (transfected with psi-Achn vector), Achn induction group ( transfected with pcDNA-Achn vector), and blank control group ( treated with PBS). Apoptosis rate was determined by FITC/PI with flow cytometry. Data were processed with one-way analysis of variance and t test. Results ( 1 ) The cell proliferation in Achn inhibition group was lower than that in psi4.1 group from PTH 24, and the differences were statistically significant at PTH 48, 72 (with t value respectively 10. 777, 6.112, P values all below 0. 05 ).The cell proliferation in Achn induction group during PTH 24-72 were higher that in pcDNA3. 1 group (with t value respectively 5. 367, 6. 053, 9. 831, P values all below 0.05 ). The cell proliferation in cotransfection group at PTH 48, 72 were significantly lower than that in Achn induction group ( with t value respectively 5.481, 9. 517, P values all below 0. 05). (2) Achn protein was detected in CASK antibody precipitation group while CASK protein was also detected in Achn antibody precipitation group. (3) Caspase-3 level in Achn transfection group was lower [( 15.6 ± 0. 5 ) %] as compared with that in LPS induction group [(32. 8 ±2.6)%, t = 10. 083, P ＜ 0. 05], and that in cotransfection group showed further inhibition [(7.0 ±2.0)%,t =9.827, P ＜0.01]. (4) Apoptosis rate in Achn inhibition group[(45.6 ± 10.9)%] was higher than that in blank control group [(13.2±4.3) %, t =7.043, P ＜0.05]; while that in Achn inductiongroup [(5.3 ±2.9)%] was lower than that in blank control group ( t =6.499, P ＜0.05).Conclusions Achn can promote human vascular endothelial cell proliferation, and inhibit its apoptosis induced by LPS or burn serum, and the effect is related to CASK.     

高表达蛋白hSav1对人胚肾HEK293增殖能力的影响

Objective To elucidate the effects of human Salvador 1 (hSav1 ) on cell proliferation of human embryonic kidney cell line HEK293. Methods The plasmid CFP-N1-hSav1 was constructed and transfected into HEK293 cells with lipofectamine 2000. The transfection efficiency was detected by fluorescent microscopy. The effects of hSav1 on cell proliferation were measured by MTT and BrdU incorporation. Results The transfection efficiency was about 70% -80%. The MTT results showed that the inhibition rate of cell proliferation in transfected group at the 12th, 24th, 36th, and 48th h was 2% , 5% , 15% , and 23% , respectively;while that in the control group was 2% , 3% , 2% , and 2% respectively. The BrdU incorporation revealed that the BrdU incorporation rate in transfected group (12. 9 ±5. 3)% was significantly lower than in control group (27.3±3.8)% (P<0.05). Conclusion hSav1 is a newly identified protein that can cause cell proliferation inhibition in HEK293 cells.     

高表达蛋白hSav1对人胚肾HEK293增殖能力的影响

Objective To elucidate the effects of human Salvador 1 (hSav1 ) on cell proliferation of human embryonic kidney cell line HEK293. Methods The plasmid CFP-N1-hSav1 was constructed and transfected into HEK293 cells with lipofectamine 2000. The transfection efficiency was detected by fluorescent microscopy. The effects of hSav1 on cell proliferation were measured by MTT and BrdU incorporation. Results The transfection efficiency was about 70% -80%. The MTT results showed that the inhibition rate of cell proliferation in transfected group at the 12th, 24th, 36th, and 48th h was 2% , 5% , 15% , and 23% , respectively;while that in the control group was 2% , 3% , 2% , and 2% respectively. The BrdU incorporation revealed that the BrdU incorporation rate in transfected group (12. 9 ±5. 3)% was significantly lower than in control group (27.3±3.8)% (P<0.05). Conclusion hSav1 is a newly identified protein that can cause cell proliferation inhibition in HEK293 cells.     

人血管内皮生长因子165基因转染人骨髓间充质干细胞的实验研究

Objective To establish an effective method of transfecting human marrow mesenchymal stem cells (MSC) with human vascular endothelial growth factor 165 ( VEGF 165) gene. Methods MSCs isolated and cultured in vitro were divided into transfection group (pShuttle-CMV/VEGF 165 plasmid was transfected into MSCs through liposome-mediating method), empty plasmid group (pShuttle-CMV vehi-cle was transfected into MSCs as control), liposome group (liposome was transfected into MSCs as control) and control group(normal culture). Expressions of Mrna and protein of MSCs were determined by RT-PCR, enzyme-linked immunosorbent assay and Western Blot. Sensitivity to MSCs on VEGF plasmid transfec-tion was detected by MTT test. Results Expression level of VEGF 165 gene Mrna in transfection group, empty plasmid group, liposome group, and control group was respectively 0.89 ± 0.03, 0. 34 ± 0.04, 0.40 ± 0.03, and 0.30 ± 0.03, and the difference between transfection group and the other three groups was statistically significant ( P <0. 01 ). Content of VEGF protein in transfection group, empty plasmid group, liposome group, and control group was respectively (778 ± 35 ), (543 ± 24), (561 ± 28), (571 ± 23) pg/Ml, and the difference between transfection group and the other three groups was statistically significant ( P <0.01 ). In the transfection group, expression level of VEGF protein peaked on 7th day after transfec-tion, which was decreased gradually later. In transfection group, expression level of V EGF 165 protein was obviously higher than that of the other three groups ( P <0. 01 ), and no inhibitory effect of VEGF plasmid transfection on MSCs proliferation was found. Conclusions The method for transfecting human VEGF 165 gene into MSCs is established in this research, through which target gene and protein can express effectively.     

RhoA基因沉默对肝癌HepG2细胞增殖和迁移能力的影响

Objective To construct a RhoA-siRNA expression vector and determine its role on the malig-nant behavior of HepG2 cells.Methods A RhoA-siRNA DNA fragment was synthesized and cloned into the expression vector of pGenesil-1.The constructed Rhon-siRNA DNA plasmid was stably transfected into HerG2 cells by lipofectamine,and then HepG2 cells were divided into the HepG2/RhoA-siRNA group (HepG2 cells were transfected with pGenesil-1-RhoA-siRNA),HepG2/control group(HepG2 cells were transfected with control plasmid) and HepG2 group (without plasmid transfection).The inbibitory effect of RhoA-siRNA on RhoA protein expression was shown by Western blot.The proliferation,migration,growth potentiality and cell cycle of transfected HepG2 cells were evaluated by MTT assay,wounded healing,the plate cloning formation test and flow cytometry,respectively.All data were analyzed by one-way analysis of variance (ANOVA) and chi-square test.Results The expression of RhoA protein in the HepG2/RhoA-siRNA group was,significantly decreased compared with that in the other two groups (F=178.19,P<0.05).Scratched cells were healed within 48 hours in the HepG2/control group and HepG2 group,but not in the HepG2/RhoA-siRNA group.The clone formation rates in the HepG2/RhoA-siRNA group,HepG2 group and HepG2/control group were 39%±3%,67%±5%and 70%±6%,respectively,with a significant difference among the three groups(χ2=33.34,38.69,P<0.05).Flow cytometry showed that the number of cells transfected with RhoA-siRNA was highest in the G0/G1 phase and lowest in the S phase(F=70.46,76.57.P<0.05).Conclusion The RhoA-siRNA expression vector can effectively suppress the proliferation and migration of HepG2 cells,which may provide a novel gene therapy for hepatocellular carcinoma.     

ShRNA-mediated gene silencing of β-catenin inhibits growth of human colon cancer cell Colo205 in vitro

Objective To observe the gene silencing and disruption of WNT pathway mediated by the specific shRNA targeted against β-catenin and its effect on cell proliferation of the human colon cancer cell line Colo205. Methods The shRNA plasmid vectors against β-catenin were constructed and transfected into Colo205 ceils with LipofectamineTM 2000. The expression of β-catenin was detected by RT-PCR and Western blot. Immunofluorescence staining was also performed to detect the β-catenin protein expression in cells. The cell proliferation inhibition was determined by MTT assay and soft agar colony formation assay. Results The shRNA vectors targeted against β-catenin were successfully constructed and efficiently suppressed the expression of β-catenin mRNA and protein (P<0.05). The expression inhibition rates were 47.89% and 45.26% at the mRNA and protein level respectively. Immunofluorescence microscopy also demonstrated the inhibition of β-catenin protein induced by these specific shRNAs. The MTT assay indicated that the specific shRNA resulted in significant inhibition of cell growth on the culture plates in time-dependent manner. At 72 h post-transfection, the cell viability of CAT group was 48.5%, which was significantly different as compared with that of blank control group's 91.3%(P<0.05). In the soft agar, there were 9, 46, 43 cell colonies in the CAT, blank, and negative control groups respectively, which were significantly different (P<0.05). Conclusions The specific shRNAs targeted against β-catenin has a gene silencing effect and blocks the WNT signaling pathway, which can inhibit the growth of Colo205 cells.     

ShRNA-mediated gene silencing of β-catenin inhibits growth of human colon cancer cell Colo205 in vitro

Objective To observe the gene silencing and disruption of WNT pathway mediated by the specific shRNA targeted against β-catenin and its effect on cell proliferation of the human colon cancer cell line Colo205. Methods The shRNA plasmid vectors against β-catenin were constructed and transfected into Colo205 ceils with LipofectamineTM 2000. The expression of β-catenin was detected by RT-PCR and Western blot. Immunofluorescence staining was also performed to detect the β-catenin protein expression in cells. The cell proliferation inhibition was determined by MTT assay and soft agar colony formation assay. Results The shRNA vectors targeted against β-catenin were successfully constructed and efficiently suppressed the expression of β-catenin mRNA and protein (P<0.05). The expression inhibition rates were 47.89% and 45.26% at the mRNA and protein level respectively. Immunofluorescence microscopy also demonstrated the inhibition of β-catenin protein induced by these specific shRNAs. The MTT assay indicated that the specific shRNA resulted in significant inhibition of cell growth on the culture plates in time-dependent manner. At 72 h post-transfection, the cell viability of CAT group was 48.5%, which was significantly different as compared with that of blank control group's 91.3%(P<0.05). In the soft agar, there were 9, 46, 43 cell colonies in the CAT, blank, and negative control groups respectively, which were significantly different (P<0.05). Conclusions The specific shRNAs targeted against β-catenin has a gene silencing effect and blocks the WNT signaling pathway, which can inhibit the growth of Colo205 cells.     

ShRNA-mediated gene silencing of β-catenin inhibits growth of human colon cancer cell Colo205 in vitro

Objective To observe the gene silencing and disruption of WNT pathway mediated by the specific shRNA targeted against β-catenin and its effect on cell proliferation of the human colon cancer cell line Colo205. Methods The shRNA plasmid vectors against β-catenin were constructed and transfected into Colo205 ceils with LipofectamineTM 2000. The expression of β-catenin was detected by RT-PCR and Western blot. Immunofluorescence staining was also performed to detect the β-catenin protein expression in cells. The cell proliferation inhibition was determined by MTT assay and soft agar colony formation assay. Results The shRNA vectors targeted against β-catenin were successfully constructed and efficiently suppressed the expression of β-catenin mRNA and protein (P<0.05). The expression inhibition rates were 47.89% and 45.26% at the mRNA and protein level respectively. Immunofluorescence microscopy also demonstrated the inhibition of β-catenin protein induced by these specific shRNAs. The MTT assay indicated that the specific shRNA resulted in significant inhibition of cell growth on the culture plates in time-dependent manner. At 72 h post-transfection, the cell viability of CAT group was 48.5%, which was significantly different as compared with that of blank control group's 91.3%(P<0.05). In the soft agar, there were 9, 46, 43 cell colonies in the CAT, blank, and negative control groups respectively, which were significantly different (P<0.05). Conclusions The specific shRNAs targeted against β-catenin has a gene silencing effect and blocks the WNT signaling pathway, which can inhibit the growth of Colo205 cells.     

ShRNA-mediated gene silencing of β-catenin inhibits growth of human colon cancer cell Colo205 in vitro

Objective To observe the gene silencing and disruption of WNT pathway mediated by the specific shRNA targeted against β-catenin and its effect on cell proliferation of the human colon cancer cell line Colo205. Methods The shRNA plasmid vectors against β-catenin were constructed and transfected into Colo205 ceils with LipofectamineTM 2000. The expression of β-catenin was detected by RT-PCR and Western blot. Immunofluorescence staining was also performed to detect the β-catenin protein expression in cells. The cell proliferation inhibition was determined by MTT assay and soft agar colony formation assay. Results The shRNA vectors targeted against β-catenin were successfully constructed and efficiently suppressed the expression of β-catenin mRNA and protein (P<0.05). The expression inhibition rates were 47.89% and 45.26% at the mRNA and protein level respectively. Immunofluorescence microscopy also demonstrated the inhibition of β-catenin protein induced by these specific shRNAs. The MTT assay indicated that the specific shRNA resulted in significant inhibition of cell growth on the culture plates in time-dependent manner. At 72 h post-transfection, the cell viability of CAT group was 48.5%, which was significantly different as compared with that of blank control group's 91.3%(P<0.05). In the soft agar, there were 9, 46, 43 cell colonies in the CAT, blank, and negative control groups respectively, which were significantly different (P<0.05). Conclusions The specific shRNAs targeted against β-catenin has a gene silencing effect and blocks the WNT signaling pathway, which can inhibit the growth of Colo205 cells.     

膝关节后交叉韧带断裂治疗临床分析

目的 对35例膝关节后交叉韧带断裂治疗进行临床分析,重点探讨了有关交叉韧带断裂的治疗问题。方法 经明确诊断后,分析采用胫骨附着处撕脱骨折复位固定手术治疗26例、早期髌韧带中1／3移植重建3例、单纯长腿石膏固定6例。结果 本组病例全部进行随访,随访时间13个月－5年,胫骨附着处撕脱骨折复位固定及髋韧带中1／3移植重建29例为优良、单纯长腿石膏固定6例为差。结论 后交叉韧带断裂后应该及时给予手术修复;膝后外侧手术入路,操作简单,暴露充分;少于3个月的陈旧性病例仍适应手术治疗。     

不同方法重建指尖离断静脉回流的疗效分析

目的：探讨不同方法重建指尖离断静脉回流的疗效。方法：2008年3月-2013年2月收治指尖离断患者80例,38例吻合指侧方静脉重建回流,术中吻合动静脉比例1：1或1：2或2：2,平均1：2;22例吻合指腹静脉重建回流,术中吻合动静脉比例1：1;20例未吻合静脉,术中仅吻合1条动脉,行侧切口或甲床放血。观察各组治疗效果。结果：吻合指侧方静脉组手指全部成活,无一例发生回流障碍;吻合指腹静脉组19例发生静脉危象,其中4例手指坏死;未吻合静脉组20例均发生回流障碍,其中6例手指坏死。58例获随访,随访时间6~28个月。吻合指侧方静脉组32例,指尖外形佳、指腹饱满;吻合指腹静脉组14例,指体轻度萎缩,指甲生长不平整;未吻合静脉组12例,指体萎缩明显。吻合指侧方静脉组指甲生长近平整,长度长于其他两组[（14.4±3.2）mm比（12.5±2.3）mm和（12.2±2.2）mm],远侧指间关节活动度大于其他两组[（63±5）°比（48±3）°和（45±7）°],两点分辨觉小于其他两组[（4.6±0.4）mm比（7.1±1.2）mm和（7.3±0.6）mm],感觉级别高于其他两组[S（3.45±0.39）级比S（2.57±0.42）级和S（2.55±0.49）级],差异均具有显著性（P〈0.05）。吻合指腹静脉组和未吻合静脉组在指甲长度、运动和感觉方面差异无统计学意义（P〉0.05）。结论：吻合指侧方静脉能有效解决指尖再植静脉回流问题,可避免回流障碍,成活率高,促进指甲生长,可恢复 DIPJ 活动度及感觉。     

胫骨干骨折的手术治疗对策

目的：明确不同固定器械在胫骨干不同骨折类型固定中的特点，以指导临床应用。方法：68例胫骨干骨折，行加压钢板螺钉、交锁髓内钉、单侧外固定架固定后，作临床疗效分析。结果：加压钢板固定组42例，感染5例，骨不连1例，平均愈合时间3．8个月；交锁髓内钉固定组13例，无感染及骨不连，平均愈合时间5．4个月；单侧外固定架组13例，骨不连1例，踝关节背伸受限3例，平均愈合时间4．5个月。结论：胫骨骨折交锁髓内钉固定并发症少，功能恢复好，适用范围广，但要注意及时进行动力加压。加压钢板及外固定架固定应选择各自的最佳适应证，以达到理想的疗效。