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Objective Exploring the effect of spinal cord decellularized scaffold on spinal cord defects and observing the behavior and regeneration of rats after operation. Methods The spinal cords of 30 SD rats were treated with 3% Triton X-100 and 2% sodium deoxycholate on oscillator. The cell residue and the spatial structure of the tissue were compared before and after treatment, in order to understand the tissue structure of the stent itself. 90 SD rats were randomly divided into control group, simple injury group and stent transplantation group. Excision of the spinal cord 9-10 segments in the simple injury group and the stent graft group the acellular scaffold was transplanted to the stent graft group. Behavioral scores were observed postoperatively. At 4, 8, and 12 weeks, the spinal cords of the injured part of the rats were taken for HE staining and immunofluorescence detection of nerve regeneration-related proteins. Results After decellularization of the spinal cord, the nerve cells and axons were completely removed, and the extracellular matrix of the spinal cord was preserved. Scanning electron microscopy revealed that the scaffold retained a certain porous network scaffold structure. In the experiment of decellularized scaffold in vivo, the Basso-Beattie-Bresnahan(BBB) score showed that the recovery of hindlimb motor function in rats with decellularized scaffolds was better than that in rats with simple injury. HE staining showed that the decellularized scaffold could fill the defect of the spinal cord segment and accelerate the repair process of the injured spinal cord. Immunofluorescence showed that there was a certain axonal regeneration in the injured part of the stent transplantation group. Conclusion The spinal cord decellularized scaffold retains the extracellular matrix and has a certain spatial structure, which can accelerate the process of spinal cord defect repair to a certain extent, and has a certain promoting effect on nerve regeneration.
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<p><b>OBJECTIVE</b>To compare the clinical efficacy of minimally invasive percutaneous plate osteosynthesis(MIPPO)and open reduction and internal fixation (ORIF) in treating senile NEER IIproximal humerus fractures.</p><p><b>METHODS</b>From March 2014 to March 2016, 46 elderly patients with Neer II proximal humerus fractures were retrospectively reviewed. Among them, 20 patients in MIPPO group included 9 males and 11 females with an average age of (70.4±4.4) years old; while 26 patients in ORIF group included 11 males and 15 females with an average age of (70.9±4.0) years old. The length of hospital stay, times of fluoroscopy, beginning time of function rehabilitation, healing time of fracture, Constant Murley score of the shoulder joint at 3, 6, 12 months after operation and complications were observed and compared.</p><p><b>RESULTS</b>All patients were followed up for 12 to 24 months with an average of 16.8±3.7. The healing time of fracture, beginning time of function rehabilitation in MIPPO group were(13.0±0.8) weeks, (3.0±0.9) days respectively and shorter than those in ORIF group which were (13.8±1.4) weeks and(6.8±1.3) days. The times of fluoroscopy in MIPPO group was 19.2±3.7 and more than that in ORIF group which was 12.1±3.4. At 3 and 6 months after operation, Constant Murley score in MIPPO group were 81.3±3.9, 86.6±5.4 and more than that in ORIF group which were 69.5±6.6, 80.5±6.7. There were no differences between two groups in the length of hospital stay, Constant Murley score at 12 months after operation and grading at the final follow-up. There was one fracture redisplacement in each group. And 1 case of axillary nerve injury in MIPPO group, 2 cases of delayed union in ORIF group. No incision infection, screw loosening or plate break was found.</p><p><b>CONCLUSIONS</b>MIPPO and ORIF are both effective in treating Neer II proximal humeral fractures. MIPPO technique has the advantages of faster recovery, earlier rehabilitative exercise and better shoulder function. The disadvantages are more exposure to radiationd and the possibility of axillary nerve injure.</p>
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The effects of magnetic stimulation on spinal cord injury-induced migration of white matter astrocytes were studied using an established animal model. Ethidium bromide was injected into the dorsal spinal cord funiculus of adult Sprague-Dawley rats on the left side at T10-11. Animals then received 1.52 Tesla-pulsed magnetic stimulation for 5 min at different frequencies (0-20 Hz) for 14 consecutive days. Selected animals received the non-competitive MEK1/2 inhibitor U0126 (10 μM), prior to stimulation at 10 Hz. Lesion volumes were measured in hematoxylin/eosin-stained sections. Expression of glial fibrillary acidic protein (GFAP), microtubule associated protein-2 (MAP-2) and extra-cellular signal-regulated kinase1/2 (ERK1/2) near the epicenter of injury was examined by Western blotting with quantification using an image analysis system. Lesion volumes decreased and GFAP and p-ERK1/2 expression increased with increasing magnetic stimulation frequency (0-10 Hz). MAP-2 expression was not affected at any frequency. Pretreatment with U0126 reduced GFAP and ERK1/2 expression and increased lesion volumes in response to stimulation at 10 Hz. It is concluded that magnetic stimulation increases the migration of astrocytes to spinal cord lesions. Activation of the ERK1/2 signaling pathway is proposed to mediate astrocyte migration and glial scar formation in response to spinal cord injury.