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Xia X.-P.,Traditional Chinese Medical Hospital of Nantong City | Chen H.-L.,Nantong University | Cheng H.-B.,Traditional Chinese Medical Hospital of Nantong City

STUDY DESIGN.: Systematic review of published prevalence of adjacent segment degeneration (ASD) after spine surgery. OBJECTIVE.: To evaluate the prevalence of ASD in patients after cervical and lumbar spine surgery. SUMMARY OF BACKGROUND DATA.: ASD is a common complication after spine surgery in long-term follow-up. A large body of literature has been reported on the topic, but no meta-analysis of the epidemiological data on ASD has been published METHODS.: We searched the MEDLINE until March 2012 published in English language that reported the prevalence of ASD after spine surgery. We determined the ASD rates by calculating proportions and 95% confidence interval (CI) for each study and then pooled the data to derive a pooled proportion and 95% CI. RESULTS.: A total of 94 studies with 34,716 patients from 19 countries were included. The occurrence of radiograph ASD ranged from 4.8% to 92.2%, and the pooled prevalence was 29.3% (95% CI, 22.7%-35.8%) by the random-effects model. The occurrence of symptoms ASD ranged from 0.0% to 30.3%, and the pooled prevalence was 7.4% (95% CI, 6.4%-8.5%). In cervical position, the occurrence of radiograph ASD and symptoms ASD was 32.8% (95% CI, 17.8%-47.9%) and 6.3% (95% CI, 4.8%-7.8%); in lumbar position, the occurrence of radiograph ASD and symptoms ASD was 26.6% (95% CI, 21.3%-31.9%) and 8.5% (95% CI, 6.4%-10.7%). In the 0.5- to 2- or less, more than 2- to 5- or less, and more than 5- to 20- or less year diagnosis time, the radiograph ASD prevalence was 21.8% (16.0%-27.6%), 33.6% (21.8%-45.4%), and 37.4% (10.7%-64.1%), respectively; and the symptoms ASD prevalence was 6.5% (4.8%-8.1%), 12.1% (8.2%-16.0%), and 3.2% (2.5%-4.0%), respectively. CONCLUSION.: Spine surgery is associated with significant risk of ASD. These figures may be useful in the estimation of the burden of the ASD after spine surgery. © 2013, Lippincott Williams & Wilkins. Source

Tao R.,Nantong University | Xu X.,Nantong University | Sun C.,Nantong University | Wang Y.,Nantong University | And 6 more authors.
Experimental and Molecular Pathology

Objective: Karyopherin alpha 2 (KPNA2) is a member of the importin α family, which acts as an adaptor to deliver P65 to the nucleus by recognizing the classic nuclear localization signal (NLS) of the cargo protein, and which has been reported as being involved in the pathogenesis of many diseases. This study was undertaken to determine the expression and possible functions of KPNA2 in osteoarthritis (OA). Methods: KPNA2 expression in cartilage tissues of OA patients and normal controls was detected by RT-PCR and immunohistochemistry. SW1353 cells were stimulated with IL-1β to establish the chondrocyte injury model in vitro. The expression of KPNA2 and catabolic genes in IL-1β-treated SW1353 cells were determined by Western blot. The interaction between KPNA2 and P65 was analyzed by co-immunoprecipitation, the subcellular distribution and transportation of P65 were detected by the subcellular fractionation followed by immunoblot analysis and immunofluorescence. Furthermore, we used RNA interference to analyze the role of KPNA2 in IL-1β-induced P65 nuclear importation and MMP13, ADAMTS-5 expression in SW1353 cells. Results: Cartilage expression of KPNA2 was higher in patients with OA compared with normal controls and mainly locating in chondrocytes. In IL-1β-treated SW1353 cells, up-regulation of KPNA2 was accompanied by the elevated expression of the catabolic marker protein levels, including MMP13 and ADAMTS-5, and increased NF-κB P65 nuclear importation. Knock-down of KPNA2 resulted in decreased catabolic marker protein levels in IL-1β-treated SW1353 cells. KPNA2 interacted with p65, and loss of KPNA2 caused decreased nuclear translocation of the active p50/p65 NF-κB complex. Conclusions: These findings suggested that KPNA2 may promote NF-κB activation via facilitating P65 nuclear transportation, and thus subsequently accelerate the catabolic events of osteoarthritis. © 2015 Elsevier Inc. Source

Wang L.,Nanjing University | Wang L.,Nantong University | Yuan D.,Nantong University | Zhang D.,Nantong University | And 5 more authors.
Cellular and Molecular Neurobiology

Exploring effective drugs that are capable of promoting nerve regeneration has gained much attention. Ginsenoside Re (Re) is the main ingredient of ginseng berries and roots. Research in the area has shown that ginsenoside Re exhibits multiple pharmacological activities via different mechanisms both in vivo and in vitro. But the potential therapeutic effects of Re on sciatic nerve crush injury (SNC) have been little investigated. Herein, we investigated the protect effect of Re on peripheral nerve regeneration in a rat SNC model. Walking track analysis revealed that Re treatment significantly promoted functional recovery of crushed sciatic nerve in rats. The expression of PCNA in rat sciatic nerve was up-regulated by Re treatment, and peaked when the concentration of Re was 2.0 mg/kg. Using immunofluorescent staining, we found that Re greatly increased the expression of GAP-43 and S100 in injured rat sciatic nerve. Furthermore, we evaluated the effects of Re on proliferation, differentiation, and migration of Schwann cells in SNC rat models. Our studies reveal that Re promotes nerve regeneration is depend on ERK1/2 and JNK1/2 signaling pathway. Elevated Oct-6 expression and featured morphological changes indicated that Re facilitated the differentiation of Schwann cells following SNC. Also, transwell and wound-healing assay demonstrated that the migration capabilities of Schwann cell were significantly enhanced after Re treatment. © 2015, Springer Science+Business Media New York. Source

Liu Z.,Nantong University | Zhang D.,Nantong University | Sun C.,Nantong University | Tao R.,Nantong University | And 5 more authors.

Karyopherin-α2 (KPNA2) functions as an adaptor that transports several proteins to the nucleus. We investigated the function and possible mechanisms of KPNA2 involved in rheumatoid arthritis (RA). Western blotting and immunohistochemistry showed the protein expression of KPNA2 increased in synovial tissue of RA patients compared with the healthy controls. Double immunofluorescent staining indicated that KPNA2 co-localized with T cells, macrophage-like synoviocytes, fibroblast-like synoviocytes, and neutrophils in synovial tissue of RA patients. Moreover, the expression of KPNA2 in SW982 cells was increased in a time-dependent manner in response to TNFα stimulation. Both Western blotting and immunofluorescent staining assay revealed the co-localization of KPNA2 and P65 and their translocation from cytoplasma in TNFα-treated SW982 cells. Furthermore, knocking down the expression of KPNA2 by siRNA inhibited TNFα-induced expression of IL-6, MMP-1, and MMP-13 and, more importantly, decreased the P65 phosphorylation in SW982 cells. We therefore suggested that KPNA2 may play a key role in the inflammation process of RA via NF-κB P65 signal transduction pathway. © 2015, Springer Science+Business Media New York. Source

Tao R.,Nantong University | Wang S.,Nantong University | Xia X.,Traditional Chinese Medical Hospital of Nantong City | Wang Y.,Nantong University | And 9 more authors.

Osteoarthritis (OA) is the most common arthritis and also one of the major causes of joint pain in elderly people. The aim of this study was to investigate the effects of pyrroloquinoline quinone (PQQ) on degenerated-related changes in osteoarthritis (OA). SW1353 cells were stimulated with IL-1β to establish the chondrocyte injury model in vitro. PQQ was administrated into SW1353 cultures 1 h before IL-1β treatment. Amounts of MMP-1, MMP-13, P65, IκBα, ERK, p-ERK, P38, and p-P38 were measured via western blot. The production of NO was determined by Griess reaction assay and reflected by the iNOS level. Meniscal-ligamentous injury (MLI) was performed on 8-week-old rats to establish the OA rat model. PQQ was injected intraperitoneally 3 days before MLI and consecutively until harvest, and the arthritis cartilage degeneration level was assessed. The expressions of MMP-1 and MMP-13 were significantly downregulated after PQQ treatment compared with that in IL-1β alone group. NO production and iNOS expression were decreased by PQQ treatment compared with control group. Amounts of nucleus P65 were upregulated in SW1353 after stimulated with IL-1β, while PQQ significantly inhibited the translocation. In rat OA model, treatment with PQQ markedly decelerated the degeneration of articular cartilage. These findings suggested that PQQ could inhibit OA-related catabolic proteins MMPs expression, NO production, and thus, slow down the articular cartilage degeneration and OA progression. Owing to its beneficial effects, PQQ is expected to be a novel pharmacological application in OA clinical prevention and treatment in the near future. © 2015, Springer Science+Business Media New York. Source

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