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Objective:To explore the role of cytokine, interleukin-17(IL-17) in human degenerative disc disease.Methods:Through magnetic resonance imaging, human degenerative disc tissues were confirmed from the isolated nucleus pulposus cells, which were then cultured in vitro.The cells were cultured with and without different concentrations ofIL-17.2 ng/mL,5 ng/mL,10 ng/mL,15 ng/mL and20 ng/mLIL-17 concentrations were used for stimulation.After72 hours, the inhibition rate of proliferation was measured byMTS method.For48 and96 hours, the nucleus pulposus cells were cultured with and without the appropriateIL-17 concentrations.The mRNA and protein expression levels of the matrix macromolecules and degrading tissue genes were measured byReal-timePCR andWestern blot analysis.Results:It was noted that nucleus pulposus cell proliferation was inhibited after culturing in vitro withIL-17 stimulation, and it was further observed that the inhibition effect was significantly stronger with15 ng/mLIL-17 concentration.With the dosage of15 ng/mL,IL-17 stimulation induced multiple cellular responses, such as the significant increase in mRNA expression for both aggrecan(ACAN) and type Ⅰ collagen(COL1A1) genes(P<0.05), and the significant decrease in mRNA expression of both degrading tissue genes,MMP3 andTIMP3(P<0.05).Western blot results also showed that the protein level ofCOL1A1 was significantly decreased(t=3.199,P=0.006), while the protein level of one peptidases(ADAMTS5) significantly increased(t=2.667, P=0.021).Conclusions:These findings suggest thatIL-17 can inhibit proliferation and affect the metabolism of the cultured nucleus pulposus cells in vitro, and these findings could possibly contribute to the degenerative changes that occur inDDD through extracellular matrix synthesis inhibition, promoting nucleus pulposus extracellular matrix degradation and disrupting the metabolic balance.
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Objective:To determine the expression of miR-17-92 cluster in osteosarcoma tissue samples and explore its associa-tion with clinical significance. Methods: Quantitative polymerase chain reactiom analysis was used to examine the expression of miR-17-92 cluster in osteosarcoma tissues. Normal bone tissues from 63 patients were matched, and the relationships between the ex-pression of miR-17-92 cluster and the clinicopathological features and prognosis of osteosarcoma were explored. Results:The relative expression of miR-17-92 cluster in osteosarcoma tissues was significantly higher than those in adjacent normal tissues (P<0.05). The high expression of miR-17-92 had a significant correlation with reduced survival (P=0.027). Conclusion:The expression of miR-17-92 cluster closely correlates with the occurrence and progress of osteosarcoma and may be used as an indicator for osteosarcoma prognosis.
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Objective To discuss the technical feasibility and clinical effectiveness of using complex tissue flap pedicled with inferior gluteal artery perforator for repair giant sacrococcygeal pressure sore.Methods Thirty embalmed lower limbs of adult cadavers perfused with red latex were used for anatomical study,and the followings were observed:①The course,branche and distribution of gluteal artery.②The course and distribution of the posterior femoral cutaneous nerve.③Anastomosis between the posterior cutaneous branch of gluteal artery and nutrient vessels of the posterior femoral cutaneous nerve.8 cases aging from 17 years to 56 years were completed during May 2007 to July 2013,6 cases were males and 2 cases were females.The sizes of pressure sore with the depth to Ⅳ degree were ranged from 16 cm × 9 cm to 22 cm × 10 cm.The sizes of flaps were harvested from 32 cm × 10 cm to 25 cm × 9 cm.Results The gluteal artery crossed the edge of the piriformis,the main stem was (3.1 ± 0.4) mm in diameter and gave out 2-5 muscular branches to supply the gluteus maximus.The posterior femoral cutaneous nerve crossed the edge of gluteus maximus and descended between biceps femoris and semitendinosus.Perforating deep fascia point located was (5.9 ± 0.8) cm above the line between medial and lateral femoral epicondyle.The constant anastomosis were formed by the posterior cutaneous branch of gluteal artery,the obturator artery perforator and the direct popliteal artery perforator around the posterior femoral cutaneous nerve.The complex flap survived successfully in all patients.Sutures were removed at 14 days postoperatively and the wounds healed well.All supplied areas were closed by directly suturing.Recurrent sacrococcygeal pressure sore was not observed in all cases with satisfied appearance and normal color during the outpatient follow-up period from 5 months to 5 years.Conclusion The united flap of gluteal myocutaneous flap and the posterior femoral cutaneous neurovascular flap pedicled with inferior gluteal artery perforator can be used to primary repair giant sacrococcygeal pressure sore.Rich blood supply,simple operation technique and high rate survival rate was considered as advantages of the flap.The lower recurrence of pressure sore was due to nice wear resisting with rich layer of anatomical structure in the flap and strong ability of anti-infection.The clinical effect was satisfied.
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BACKGROUND:Studies have shown that the changes of extracellular matrix in degenerative intervertebral disc tissues mainly present as the decrease of col agen type Ⅱ and proteoglycan contents and the increase of col agen type Ⅰ content. OBJECTIVE:To explore the effect of adeno-associated virus-mediated bone morphogenetic protein 2 gene on nucleus pulposus Ⅰ and Ⅱ col agen levels in rabbit degenerative intervertebral disc tissues. METHODS:L 2-3 , L 3-4 , L 4-5 and L 5-6 lumbar discs of 12 New Zealand white rabbits were punctured to establish interverbral disc degeneration model. Subsequently, 12 rabbits were randomly divided into three groups, four rabbits in each group. The intervertebral discs in the adeno-associated virus-mediated bone morphogenetic protein 2 group were injected with the adeno-associated virus-mediated bone morphogenetic protein 2 gene, the intervertebral discs in the adeno-associated virus group were injected with adeno-associated virus only, while the discs in the normal saline group were injected with normal saline. Al rabbits were sacrificed after injected for 8 weeks, and the L 2-3 , L 3-4 , L 4-5 and L 5-6 lumbar discs of each rabbit were col ected, paraffin-embedded and sliced. The histological changes of nucleus pulposus were observed with hematoxylin-eosin staining, and the immunohistochemistry was used to detect the col agen type Ⅰ and Ⅱ expressions in nucleus pulposus. Semi-quantitative analysis was performed. RESULTS AND CONCLUSION:Hematoxylin-eosin staining showed that the nucleus pulposus in the intervertebral disc tissues was less in the adeno-associated virus-mediated bone morphogenetic protein 2 group, the nucleus pulposus was in single or clustered distribution with clear nucleus structure and without fibrous tissue fil ing. The tissue structures of nucleus pulposus were the same in the adeno-associated virus group and normal saline group, the cellnumber in nucleus pulposus was smal , the nucleus pulposus was shrunken and shriveled, and the cells were fil ed with fibrous tissue and arranged disorderly. Immunohistochemistry staining showed the expression of col age type Ⅰ in the intervertebral disc nucleus pulposus of adeno-associated virus-mediated bone morphogenetic protein 2 group was higher than that of the adeno-associated virus group and normal saline group (P<0.05);the expression of col age typeⅠ in the intervertebral disc nucleus pulposus of adeno-associated virus-mediated bone morphogenetic protein 2 group was lower than that of the adeno-associated virus group and normal saline group (P<0.05). The results indicate that adeno-associated virus-mediated bone morphogenetic protein 2 can inhibit the expression of col agen type Ⅰ in the intervertebral disc nucleus pulposus, promote the expression of col agen type Ⅱ. Maintaining the content of col agen in intervertebral disc can keep the histological structure and morphology of intervertebral disc, stabilize the environment for nucleus pulposus cellgrowth, and delay the intervertebral disc degeneration.