Closed reduction and internal fixation versus total hip arthroplasty for displaced femoral neck fracture

【Abstract】Objective:To compare the clinical effects between closed reduction and internal fixation (CRIF) and total hip arthroplasty (THA) for displaced femoral neck fracture. Methods:In this prospective randomized study, 285 patients aged above 65 years with hip fractures (Garden III or IV) were included from January 2001 to December 2005. The cases were randomly allocated to either the CRIF group or THA group. Patients with pathological fractures (bone tumors or metabolic bone disease), preoperative avascular necrosis of the femoral head, osteoarthritis, rheumatoid arthritis, hemiplegia, long-term bed rest and complications affecting hip functions were excluded. Results:During the 5-year follow-up, CRIF group had significantly higher rates of complication in hip Chin J Traumatol 2014;17(2):63-68 Closed reduction and internal fixation versus total hip arthroplasty for displaced femoral neck fracture Cao Liehu, Wang Bin, Li Ming, Song Shaojun, Weng Weizong, Li Haihang, Su Jiacan* joint, general complication and reoperation than THA group (38.3% vs. 12.7%, P<0.01; 45.3% vs. 21.7%, P<0.01; 33.6% vs. 10.2%, P<0.05 respectively). There was no difference in mortality between the two groups. Postoperative function of the hip joint in THA group recovered favorably with higher Harris scores. Conclusion:For displaced fractures of the femoral neck in elderly patients, THA can achieve a lower rate of complication and reoperation, as well as better postoperative recovery of hip joint function compared with CRIF

A Matrine Derivative M54 Suppresses Osteoclastogenesis and Prevents Ovariectomy-Induced Bone Loss by Targeting Ribosomal Protein S5

Post-menopausal osteoporosis (PMOP) is a metabolic bone disorder characterized by low bone mass and micro-architectural deterioration of bone tissue. The over-activated osteoclastogenesis, which plays an important role in osteoporosis, has become an important therapeutic target. M54 was a bioactive derivative of the Chinese traditional herb matrine. We found that M54 could suppress RANKL-induced osteoclastogenesis in bone marrow mononuclear cells and RAW264.7 cells through suppressing NF-κB, PI3K/AKT, and MAPKs pathways activity in vitro, and prevent ovariectomy-induced bone loss in vivo. Our previous study has proved that ribosomal protein S5 (RPS5) was a direct target of M19, based on which M54 was synthesized. Thus we deduced that M54 also targeted RPS5. During osteoclastogenesis, the RPS5 level in RAW264.7 cells was significantly down-regulated while M54 could maintain its level. After RPS5 was silenced, the inhibitory effects of M54 on osteoclastogenesis were partially compromised, indicating that M54 took effects through targeting RPS5. In summary, M54 was a potential clinical medicine for post-menopause osteoporosis treatment, and RPS5 is a possible key protein in PMOP

A Comparative Study of Bioartificial Bone Tissue Poly-L-lactic Acid/Polycaprolactone and PLLA Scaffolds Applied in Bone Regeneration

Bioartificial bone tissue engineering is an increasingly popular technique to repair bone defect caused by injury or disease. This study aimed to investigate the feasibility of PLLA/PCL (poly-L-lactic acid/polycaprolactone) by a comparison study of PLLA/PCL and PLLA scaffolds applied in bone regeneration. Thirty healthy mature New Zealand rabbits on which 15 mm distal ulna defect model had been established were selected and then were divided into three groups randomly: group A (repaired with PLLA scaffold), group B (repaired with PLLA/PCL scaffold), and group C (no scaffold) to evaluate the bone-remodeling ability of the implants. Micro-CT examination revealed the prime bone regeneration ability of group B in three groups. Bone mineral density of surgical site in group B was higher than group A but lower than group C. Meanwhile, the bone regeneration in both groups A and B proceeded with signs of inflammation for the initial fast degradation of scaffolds. As a whole, PLLA/PCL scaffolds in vivo initially degrade fast and were better suited to repair bone defect than PLLA in New Zealand rabbits. Furthermore, for the low mineral density of new bone and rapid degradation of the scaffolds, more researches were necessary to optimize the composite for bone regeneration

Inhalation of Hydrogen of Different Concentrations Ameliorates Spinal Cord Injury in Mice by Protecting Spinal Cord Neurons from Apoptosis, Oxidative Injury and Mitochondrial Structure Damages

Background/Aims: Hydrogen selectively neutralizes reactive oxygen species (ROS) and ameliorates various ROS-induced injuries. Spinal cord injury (SCI) is a serious injury to the central nervous system, and secondary SCI is closely related to excessive ROS generation. We hypothesized that hydrogen inhalation ameliorates SCI, and the mechanism of action may be related to the protective effects of hydrogen against oxidative stress, apoptosis, and mitochondrial damage. Methods: Mechanically injured spinal cord neurons were incubated with different concentrations of hydrogen in vitro. Immunofluorescence staining and transmission electron microscopy were used to confirm the protective effects of hydrogen. ROS and related proteins were detected with dihydroethidium fluorescence staining, enzyme-linked immunosorbent assays, and western blotting. Terminal deoxynucleotidyl transferase dUTP nick end labeling assays, flow cytometry, and western blotting were used to detect neuronal apoptosis. ATP concentrations, Janus Green B staining, and mitochondrial permeability transition pore (mPTP) status were assessed to investigate mitochondrial damage. RNA sequencing was performed to screen potential target genes of hydrogen application. Hydrogen was administered to mice after spinal cord contusion injury was established for 42 days. The Basso Mouse Scale (BMS) and footprint analyses were used to assess locomotor functions, and immunofluorescence staining of the injured spinal cord segments was performed to detect oxidative stress status. Results: Spinal cord neurons were preserved by hydrogen administration after mechanical injury in a dose-dependent manner. ROS generation, oxidative stress injury-related markers, and the number of apoptotic neurons were significantly reduced after hydrogen treatment. The ATP production and mPTP function in injured neurons were preserved by hydrogen incubation. The expression levels of Cox8b, Cox6a2, Cox7a1, Hspb7, and Atp2a1 were inhibited by hydrogen treatment. BMS scores and the footprint assessment of mice with SCI were improved by hydrogen inhalation. Conclusions: Hydrogen inhalation (75%) ameliorated SCI in vivo and attenuated neuronal mechanical injuries in vitro, and its protective effect on spinal cord neurons was exerted in a dose-dependent manner. The underlying mechanisms included reducing ROS generation and oxidative stress, inhibiting neuronal apoptosis, and restoring mitochondrial construction and function. Cox8b, Cox6a2, Cox7a1, Hspb7, and Atp2a1 were identified as potential target genes of hydrogen treatment

Représentations sociales des handicaps en Belgique Francophone. Handicaps, attitudes et représentations sociales.

Hypertrophic scars, characterized by excessive cell proliferation, disordered cell growth, and aberrant deposition of collagens, could cause significant clinical problems. Herein, aligned carbon nanotubes (ACNTs) were synthesized <i>via</i> chemical vapor deposition, and bulk ACNTs were pulled out from the arrays. The capacity of the ACNTs to reduce hypertrophic scar formation was evaluated both <i>in vitro</i> and <i>in vivo</i>. The results demonstrated that the ACNTs suppressed the overproliferation of fibroblast cells, directed their growth, and inhibited collagen expression <i>in vitro</i> without cell cytotoxicity. Moreover, <i>in vivo</i> evaluation in a rabbit ear model indicated relieved scar hypertrophy after the ACNTs treatment. The gene expression microarray was further used to understand the mechanism, which showed that ACNTs could inhibit the TGFβ pathway to alter the components in the extracellular matrix, cell proliferation, cell cytoskeleton, and cell motility. These findings may provide a potent strategy of using carbon nanotubes in the bioengineering field

Aligned Carbon Nanotubes Reduce Hypertrophic Scar <i>via</i> Regulating Cell Behavior

Hypertrophic scars, characterized by excessive cell proliferation, disordered cell growth, and aberrant deposition of collagens, could cause significant clinical problems. Herein, aligned carbon nanotubes (ACNTs) were synthesized <i>via</i> chemical vapor deposition, and bulk ACNTs were pulled out from the arrays. The capacity of the ACNTs to reduce hypertrophic scar formation was evaluated both <i>in vitro</i> and <i>in vivo</i>. The results demonstrated that the ACNTs suppressed the overproliferation of fibroblast cells, directed their growth, and inhibited collagen expression <i>in vitro</i> without cell cytotoxicity. Moreover, <i>in vivo</i> evaluation in a rabbit ear model indicated relieved scar hypertrophy after the ACNTs treatment. The gene expression microarray was further used to understand the mechanism, which showed that ACNTs could inhibit the TGFβ pathway to alter the components in the extracellular matrix, cell proliferation, cell cytoskeleton, and cell motility. These findings may provide a potent strategy of using carbon nanotubes in the bioengineering field

Aligned Carbon Nanotubes Reduce Hypertrophic Scar <i>via</i> Regulating Cell Behavior

Hypertrophic scars, characterized by excessive cell proliferation, disordered cell growth, and aberrant deposition of collagens, could cause significant clinical problems. Herein, aligned carbon nanotubes (ACNTs) were synthesized <i>via</i> chemical vapor deposition, and bulk ACNTs were pulled out from the arrays. The capacity of the ACNTs to reduce hypertrophic scar formation was evaluated both <i>in vitro</i> and <i>in vivo</i>. The results demonstrated that the ACNTs suppressed the overproliferation of fibroblast cells, directed their growth, and inhibited collagen expression <i>in vitro</i> without cell cytotoxicity. Moreover, <i>in vivo</i> evaluation in a rabbit ear model indicated relieved scar hypertrophy after the ACNTs treatment. The gene expression microarray was further used to understand the mechanism, which showed that ACNTs could inhibit the TGFβ pathway to alter the components in the extracellular matrix, cell proliferation, cell cytoskeleton, and cell motility. These findings may provide a potent strategy of using carbon nanotubes in the bioengineering field