ObjectiveTo compare the effectiveness between micro-anchor repair and modified pull-out suture in the treatment of mallet fingers. MethodsBetween June 2010 and March 2011, 33 patients with mallet fingers were treated by micro-anchor repair method (n=18, group A) and by modified pull-out suture method in which the broken tendons were sutured with double metal needle Bunnell’s suture and a knot was tied palmarly (n=15, group B). There was no significant difference in age, gender, and disease duration between 2 groups (P gt; 0.05). ResultsThe operation time was (62.5 ± 3.1) minutes in group A and (65.0 ± 4.6) minutes in group B, showing no significant difference (t=1.85, P=0.07). The treatment expense in group A [(8 566.2 ± 135.0) yuan] was significantly higher than that in group B [(5 297.0 ± 183.5) yuan] (t=58.92, P=0.00). Incision infection occurred in 2 cases of group A and 1 case of group B; the other patients obtained healing of incision by first intention. Relapsed mallet finger was observed in 1 case of group B. All patients in 2 groups were followed up 12-21 months. According to the Crawford functional assessment system, the results were excellent in 5 cases, good in 10 cases, fair in 2 cases, and poor in 1 case at the last follow-up with an excellent and good rate of 83.3% in group A; the results were excellent in 4 cases, good in 9 cases, fair in 1 case, and poor in 1 case with an excellent and good rate of 86.7% in group B. There was no significant difference in the excellent and good rate between 2 groups (χ2=0.23, P=0.97). ConclusionBoth micro-anchor repair and modified pull-out suture are simple and effective methods in the treatment of mallet finger. But compared with micro-anchor repair, pull-out suture has lower expense.
ObjectiveTo explore the biological functions of Kip1 ubiquitylation-promoting complex 2 (KPC2) in the repair process of spinal cord injury (SCI) by studying the expression and cellular localization of KPC2 in rat SCI models. MethodsFifty-six adult Sprague-Dawley rats were randomly divided into 2 groups: in the control group (n=7), simple T9 laminectomy was performed;in the experimental group (n=49), the SCI model was established at T9, 7 rats were used to detect follow indexs at 6 hours, 12 hours, 1 day, 3 days, 5 days, 7 days, and 14 days after SCI. Western blot analysis was used to detect the protein expressions of P27kip1, KPC2, CyclinA and proliferating cell nuclear antigen (PCNA) after SCI. Immunohistochemistry was used to observed the cellular localization of KPC2 after SCI, double-labeling immunofluorescence staining to observe the co-localization of KPC2 with neuronal nuclei (NeuN), glial fibrillary acidic protein (GFAP) and PCNA. in vitro astrocytes proliferation model was used to further validate these results, Western blot to detect KPC2, P27kip1, and PCNA expressions. The interaction of P27kip1, KPC1, and KPC2 in cell proliferation was analyzed by co-immunoprecipitation. ResultsThe Western blot analysis showed a significant down-regulation of P27kip1 and a concomitant up-regulation of KPC2, CyclinA, and PCNA after SCI. Immunohistochemistry staining revealed a wide distribution of KPC2 positive signals in the gray matter and white matter of the spinal cord. The number of KPC2 positive cells in the experimental group was significantly higher than that in the control group (t=10.982, P=0.000). Double-labeling immunofluorescence staining revealed the number of KPC2/NeuN co-expression cells in the gray matter of spinal cord was (0.43±0.53)/visual field in the control group and (0.57±0.53)/visual field in the experimental group, showing no significant difference (t=0.548, P=0.604);in the white matter of spinal cord, the number of KPC2/PCNA co-expression cells was (3.86±0.90)/visual field in the control group and (0.71±0.49)/visual field in the experimental group, showing significant difference (t=7.778, P=0.000). And then, the number of KPC2/PCNA co-expression cells were (0.57±0.53)/visual field in the control group and (5.57±1.13)/visual field in the experimental group, showing significant difference (t=8.101, P=0.000). Concomitantly, there was a similar kinetic in proliferating astrocytes in vitro. The Western blot analysis showed a significant down-regulation of P27kip1 and a concomitant up-regulation of KPC2 and PCNA after serum stimulated. Co-immunoprecipitation demonstrated increased interactions between P27kip1, KPC1, and KPC2 after stimulation. ConclusionThe up-regulated expression of KPC2 after SCI is related to the down-regulation of P27kip1, this event may be involved in the proliferation of astrocytes after SCI.
Objective To investigate the impact of joint capsule repair and external rotators suture on the prognosis in primary total hip arthroplasty (THA) by posterolateral approach. Methods Between January 2006 and June 2009, 159 patients with femoral neck fracture underwent primary THA by posterolateral approach, and were divided into 4 groups according to different treatments: joint capsule repair and external rotators suture were given in group A (n=38), only joint capsule repair in group B (n=39), only external rotators suture in group C (n=41), and no joint capsule repair or external rotators suture in group D (n=41). There was no significant difference in gender, age, cause of injure, disease duration, type of fracture, combined medical disease, or prosthesis selection among 4 groups (P gt; 0.05). The bleeding volume, drainage, postoperative hip dislocation rate, hip Harris score, and the hip range of motion (ROM) in internal rotation and external rotation were compared. Results There was no significant difference in operative time, bleeding volume, or drainage among 4 groups (P gt; 0.05). Postoperative hip dislocation occurred in 0, 0, 4 (9.8%), and 4 (9.8%) cases of groups A, B, C, and D, respectively, showing significant difference in incidence of postoperative hip dislocation among 4 groups (χ2=7.910, P=0.048). The hip Harris scores were significantly improved after operation when compared with preoperative scores in 4 groups (P lt; 0.05). Significant differences were found in hip Harris score at 6 weeks and 6 months after operation among 4 groups (P lt; 0.05); group D was significantly lower than groups A, B, and C, and groups B and C were significantly lower than group A (P lt; 0.05). There was no significant difference in the hip ROM in internal rotation among 4 groups at 6 weeks and 6, 12 months after operation (P gt; 0.05); but the hip ROM in external rotation were significantly bigger in groups A and C than in groups B and D at 6 weeks and 6 months after operation (P lt; 0.05). Conclusion Joint capsule repair and external rotators suture in primary THA by posterolateral approach do not increase the bleeding volume and drainage, but can reduce the early postoperative hip dislocation risk, increase the Harris score, and recover the external rotation function of involved hip. So joint capsule and external rotators should be repaired in THA by posterolateral approach.
Objective To investigate the role and mechanism of S100 calcium binding protein B (S100B) in osteoarthritis (OA) cartilage damage repair. Methods Twenty New Zealand rabbits were randomly divided into control group and model group, with 10 rabbits in each group. Rabbits in the model group were injured by the right knee joint immobilization method to make the artilage injury model, while the control group did not deal with any injury. After 4 weeks, the levels of interleukin-1β (IL-1β) and tumor necrosis factor α (TNF-α) in synovial fluid were detected by ELISA method; the mRNA and protein expressions of S100B, fibroblast growth factor 2 (FGF-2), and FGF receptor 1 (FGFR1) in cartilage tissue were examined by real-time fluorescence quantitative PCR (qRT-PCR) and Western blot assay. Human synovial fibroblasts (SF) were isolated and cultured in vitro. The effects of S100B overexpression and knockdown on the levels of IL-1β and TNF-α (ELISA method) and the expressions of FGF-2 and FGFR1 gene (qRT-PCR) and protein (Western blot) were observed. Moreover, the effects of FGFR1 knockdown in above S100 overexpression system on the levels of IL-1β and TNF-α (ELISA method) and the expressions of FGF-2 and FGFR1 gene (qRT-PCR) and protein (Western blot) were observed. Results ELISA detection showed that the expressions of IL-1β and TNF-α in the synovial fluid of the model group were significantly higher than those of the control group (P<0.05); qRT-PCR and Western blot detection showed that the mRNA and protein expressions of S100B, FGF-2, and FGFR1 in cartilage tissue were significantly higher than those of the control group (P<0.05). Overexpression and knockdown S100 could respectively significantly increase and decrease lipopolysaccharides (LPS) induced IL-1β and TNF-α levels elevation and the mRNA and protein expressions of FGF-2 and FGFR1 (P<0.05); whereas FGFR1 knockdown could significantly decrease LPS induced IL-1β and TNF-α levels elevation and the mRNA and protein expressions of FGF-2 and FGFR1 (P<0.05). Conclusion S100B protein can regulate the inflammatory response of SF and may affect the repair of cartilage damage in OA, and the mechanism may be related to the activation of FGF-2/FGFR1 signaling pathway.
Objective To investigate the changes of autophagy after spinal cord injury (SCI) in rats and its relationship with multisite phosphorylation of B-cell lymphoma-2 (Bcl-2) protein. Methods Forty male Sprague-Dawley rats aged 8 weeks were used to prepare SCI models by modified Allen method, and the SCI model were prepared successfully in 36 rats. The 36 SCI models were randomly divided into SCI group, autophagy inhibitor group, and autophagy promoter group, with 12 rats in each group. Another 12 rats were selected as sham operation group with only laminectomy and no spinal cord injury. At the end of modeling, the autophagy inhibitor group and the autophagy promoter group were intrathecally injected with 20 μL of 600 nmol/L 3-methyladenine and 25 nmol/L rapamycin, respectively, once a day for 4 weeks. The sham operation group and the SCI group were injected with only 20 μL of normal saline at the same time point. The motor function of rat in each group was evaluated by the Basso-Beattie-Bresnahan (BBB) score at 1 day and 1, 2, 4 weeks after modeling. The rats in each group were sacrificed at 24 hours after the last injection and the spinal cord tissues were taken. ELISA assay was used to detect the levels of inflammatory factors in spinal cord tissues, including myeloperoxidase (MPO), tumor necrosis factor α (TNF-α), and interleukin 1β (IL-1β); the morphological changes of spinal cord were observed by HE staining; the autophagy of mitochondria in spinal cord tissues was observed by transmission electron microscopy; the expressions of Beclin1 and microtubule-associated protein light chain 3 (LC3) were detected by immunofluorescence staining; neuronal apoptosis in spinal cord tissues were observed by TUNEL staining; LC3/TUNEL positive cells were calculated by immunofluorescence double staining; the expressions of Bcl-2 associated X protein (Bax), Bcl-2, p-Bcl-2 (Ser87), and p-Bcl-2 (Ser70) were detected by Western blot. Results Compared with sham operation group, BBB score of SCI group decreased at each time point, while the levels of MPO, TNF-α, and IL-1β increased; peripheral space of nerve cells enlarged, cells swelled, vacuoles appeared, and autophagic bodies appeared in mitochondria; the positive rates of Beclin1 and LC3 proteins, and apoptotic rate of neurons significantly increased; the LC3/TUNEL positive cells significantly increased; the expressions of Bax, p-Bcl-2 (Ser87), and p-Bcl-2 (Ser70) proteins increased, while the expression of Bcl-2 protein decreased; all showing significant differences (P<0.05). Compared with SCI group, BBB score in autophagy inhibitor group decreased at each time point, while the levels of MPO, TNF-α, and IL-1β increased; a few autophagic vesicles appeared in mitochondria; the positive rates of Beclin1 and LC3 proteins decreased and the apoptotic rate of neurons increased significantly; the LC3 positive cells decreased and the TUNEL positive cells increased; the expressions of Bax, p-Bcl-2 (Ser87), and p-Bcl-2 (Ser70) proteins increased, while the expression of Bcl-2 protein decreased. The results of autophagy promoter group were opposite to those of autophagy inhibitor group; all showing significant differences between groups (P<0.05). Conclusion Induction of autophagy after SCI in rats can reduce neuronal apoptosis and protect spinal cord function, which may be related to the inhibition of Bcl-2 protein multisite phosphorylation.