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find Author "MAXinlong" 3 results
  • RISK FACTORS FOR INCIDENTAL DUROTOMY DURING LUMBAR SURGERY

    ObjectiveTo evaluate the risk factors for incidental durotomy (ID) during lumbar surgery. MethodsEighty-six patients with ID and 86 patients with no ID (who were matched 1∶1 in surgeons and surgery time) were selected from 2 235 patients who underwent lumbar surgery between January 2010 and December 2012. The gender, age, body mass index, history of smoking, alcoholism, nonsteroidal drug use, the etiology, lumbar surgery history, revision surgery, surgical approach, osteoporosis, diabetes, and surgical procedure were compared between 2 groups. Logistic regression analysis was applied to analyze the risk factors for ID. ResultsThere was significant difference (P<0.05) in etiology, surgical approach, revision surgery, lumbar surgery history, and surgical procedure between patients with ID and patients with no ID, which were then included in multivariate analysis. Logistic regression analysis demonstrated that lumbar surgery history, revision surgery, and minimal invasive surgery were risk factors for ID during lumbar surgery (P<0.05). ConclusionLumbar surgery history, revision surgery, and minimal invasive surgery were risk factors for ID during lumbar surgery, thus surgery for patients with the above histories should be carefully performed to prevent ID.

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  • INDUCTING DIFFERENTIATION EFFECT OF SCIATIC NERVE EXTRACTS ON RABBIT ADIPOSE-DERIVED STEM CELLS IN VITRO

    ObjectiveTo study the inducting differentiation effect of the sciatic nerve extracts on rabbit adipose-derived stem cells (ADSCs) in vitro. MethodsThe ADSCs were isolated from 2 healthy 4-month-old New Zealand rabbits (weighing, 2.0-2.5 kg) and cultured to passage 3, which were pretreated with 10 ng/mL basic fibroblast growth factor (bFGF) for 24 hours before induction. Then the induction media containing the extracts of normal sciatic nerve (group B) and injured sciatic nerve at 3, 7, and 14 days (group C, group D, and group E) were used, and D-Hank was used in group A as blank control group. The morphological changes of the cells were observed. At 7 days of induction, the gene expressions of neuron-specific enolase (NSE), nestin (NES), and S-100 were detected by real-time fluorescent quantitative PCR. The S-100 protein expression was tested by immunocytochemical staining. ResultsAt 4 days after induction, some ADSCs of groups C, D, and E showed the morphology of Schwann-like cells or neuron-like cells, the change of group D was more obvious; and the ADSCs of group A and B had no obvious change, which were still spindle. The S-100 immunocytochemical staining showed positive expression in groups C, D, and E (more obvious in group D) and negative expression in groups A and B. The gene expression of S-100 displayed time-dependent increases in groups C and D, which was significantly higher than that of groups A, B, and E (P<0.05), but no significant difference was found between groups C and D (P>0.05). The gene expression of NSE showed the same tendency to S-100, which reached the peak in group D; the gene expression of NSE in groups D and E was significantly higher than that of groups A, B, and C (P<0.05), and groups D and E showed significant difference (P<0.05). However, the gene expression of Nestin showed no significant difference among different groups (P>0.05). ConclusionThe ADSCs can be induced to differentiate into Schwann-like cells or neuron-like cells with sciatic nerve extracts; and the early stage (3-7 days) after injury is the best time for stem cell transplantation.

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  • EXPERIMENTAL STUDY ON EFFECT OF NICOTINE INTAKE ON IMPACT OF BONE MICROSTRUCTURE AND OXIDATIVE STRESS IN RATS

    ObjectiveTo evaluate the influence of nicotine intake on bone microstructure, bone biomechanics, and oxidative stress state in rats. MethodsThirty-six 6-week-old male Sprague Dawley rats (weight, 160-180 g) were randomly divided into control group, low dose group, and high dose group, 12 rats each group. The rats in high dose group and low dose group were given respectively 6.0 mg/kg and 0.4 mg/kg nicotine gavage intervention for 12 months; no intervention was made in the control group. The survival of rats was observed during experiment, and the weight of rats was measured every month. At 12 months after modeling, the L1 vertebral body was harvested to measure the bone mineral density (BMD), bone volume fraction (BVF), trabecular thickness (TT), trabecular number (TN), and trabecular spacing (TS) by Micro-CT three-dimensional reconstruction; the left femur was harvested for biomechanical tests of maximal load, stiffness, and the maximal fracture energy; and arterial blood was extracted to measure the malonyldialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and cotinine. ResultsDuring the experiment, two rats and one rat were added in the high dose group and the low dose group because of death, and no death in the control group. The body weight of the rats in the high and low dose groups gradually decreased with time when compared with one in the control group, and significant difference was found between two dose groups and the control group at 8-12 months (P < 0.05); the body weight of the high dose group was significantly lower than that of the low dose group at 11 and 12 months (P < 0.05). At 12 months after modeling, BMD, BVF, TT, and TN were significantly lower in the high dose group than the control group and the low dose group, but TS was significantly increased (P < 0.05). Difference in BVF, TN, and TS was significant between the low dose group and the control group (P < 0.05). The maximal load, stiffness, and maximal fracture energy of femoral shaft were significantly lower in the high dose group than the control group and the low dose group, and in the low dose group than the control group (P < 0.05). Compared with the control group, the levels of cotinine and MDA were significantly increased, and the levels of CAT and SOD were significantly decreased in the high and low dose groups (P < 0.05), and there were significant differences between the high and low dose groups (P < 0.05). ConclusionNicotine intake can cause micro-structural changes of the bone, decreased bone mechanical properties, and imbalance of oxidation-antioxidant levels in rats. High-dose nicotine intake may be one of the causes of osteoporosis.

    Release date:2016-12-12 09:20 Export PDF Favorites Scan
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