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Background: Although measures to reduce and treat the postoperative surgical drain output are discussed, along with the increased interest in causative factors related to the prevention and treatment reported by many studies, these are still controversial. Methods: A retrospective study was conducted on a consecutive series of 217 patients who had underwent ACCF between January 2016 and March 2017. Patients were categorized based on normal or increased total drain output. These two groups were compared for demographic distribution and clinical data to investigate the predictive factors of increased drain output by multivariate analysis. Results: The overall incidence rate of increased drain output after ACCF was 16.6%. There are no significant differences in sex, BMI, history of taking aspirin, and ASA classification between the two groups (P >0.05). Of the patients with increased drain output, a significantly higher proportion of patients have OPLL in the surgical level, 18 (50.0%) versus 33 (18.2%) (P = 0.000). The mean age was 60.67 ± 8.18 years versus 54.41 ± 10.05 years (P = 0.001). Number of discs involved was 2.42 ± 0.50 versus 2.02 ± 0.65 (P =0.001). Operation time was 112.22 ± 16.49 min versus 105.21 ± 17.89 min (P = 0.031). Intraoperative blood loss was 109.86±62.02 mL versus 87.83 ±56.40 mL (P = 0. 036). Logistic regression analysis showed that age (OR, 1.075; p = 0.003), history of smoking (OR, 2.792; p = 0.021), OPLL in surgical level (OR, 2.107; p = 0.001), and number of discs involved (OR, 2.764; p = 0.003) maintained its significance in predicting likelihood of increased surgical drain output. Conclusions: The occurrence of increased drain output after ACCF is most likely multifactorial and is related to age, history of smoking, OPLL in surgical level, and number of discs involved. [ABSTRACT FROM AUTHOR]

Osteosarcoma is a prevalent type of cancer and has a high metastatic ability, particularly for metastasis to the lungs. Effective treatment strategies have improved, however, the detailed molecular mechanism underlying the onset of this malignancy remains to be fully elucidated. The current study investigated the role of the tripartite motif (TRIM) family protein TRIM59 in osteosarcoma growth and metastasis. It was identified that TRIM59 was overexpressed in clinical osteosarcoma tissues and cultured osteosarcoma cell lines. In addition, the MTT assay demonstrated that in U2OS and MG63 cells, knockdown of TRIM59 by specific siRNA inhibited proliferation, whereas overexpression of TRIM59 promoted cell proliferation. Furthermore, overexpression of TRIM59 significantly increased the U2OS cell migrative and invasive abilities in a Transwell chamber assay. In addition, TRIM59 was able to negatively regulate the protein levels of P53 without significantly affecting the mRNA levels in U2OS and MG63 cells. These data suggest the oncogenic abilities of TRIM59 in osteosarcoma, which promote osteosarcoma cell proliferation, migration and invasion. [ABSTRACT FROM AUTHOR]

Objective: To identify risk factors for postoperative complications associated with growing rod surgery for early-onset scoliosis (EOS). Methods: A total of 55 consecutive patients underwent growing rod surgery for EOS were examined from database. Data included age at initial surgeries, sex, diagnosis, body mass index (BMI), duration of follow-up, initial and final measure of major curve, T2-5, T5-12, T10-L2, and T12-S1 kyphosis angles, levels and type of instrumentation, total number of surgeries, number of rods inserted, number of lengthenings, lengthening intervals and rod location were studied. Risk factors for postoperative complications were analyzed using binomial multiple logistic regression analysis. Results: Postoperative complications were associated with 37 of 272 procedures (14%) and affected 23 patients (42%). Complications included 25 implant-related failures (66%), 4 alignment complications (11%), 4 infections (11%), 1 neurological impairment (3%), 3 respiratory problems, 2 gastrointestinal problems, 1 urinary problem, and 1 dural tear. The most frequent implant-related failure was dislodged implant (76%) and 92% of the dislodgements occurred at the proximal foundation. Binomial multiple logistic regression analysis demonstrated that curve magnitude in last follow-up (OR: 1.042; P = 0.036), duration between growing-rod lengthening procedures (OR: 1.121; P = 0.003) and duration of follow-up (OR: 1.079; P = 0.001) maintained its significance in predicting likelihood of postoperative complications. Conclusion: The occurrence of postoperative complications in growing rod surgery for EOS is most likely multifactorial and is related to curve magnitude in last follow-up and duration between growing-rod lengthening procedures. [ABSTRACT FROM AUTHOR]

Background Although measures to reduce and treat degenerative changes after fusion are discussed, these are still controversial. Methods A retrospective study was conducted on a consecutive series of 3,799 patients who underwent posterior lumbar fusion for degenerative lumbar disease between January 1999 and January 2009. A total of 28 patients with symptomatic adjacent segment degeneration surgery were identified. Another group of 56 matched patients with degenerative lumbar disease without symptomatic adjacent segment degeneration after spinal fusion were marked as the control group. These two groups were compared for demographic distribution and clinical and radiographic data to investigate the predictive factors of symptomatic adjacent segment degeneration surgery by logistic regression. Results The overall incidence rate of symptomatic adjacent segment degeneration surgery was 0.74%. Strong risk factors for the development of a symptomatic adjacent segment degeneration requiring surgery were preoperative distance from L1 to S1 sagittal plumb line (p = 0.031), preoperative lumbar lordosis (p = 0.005), and preoperative adjacent disc height (p = 0.003). Mean postoperative lumbar lordosis was smaller (p = 0.000) in symptomatic adjacent segment degeneration surgery (SASDS) group compared with in the control group (33.3° vs. 39.8°). Postoperative adjacent disc height was also significantly lower in the former group compared with the latter group (p = 0.002). Logistic regression analysis showed that body mass index (BMI) (OR: 1.75; p = 0.006), preoperative adjacent disc degeneration (ADD) on MRI (OR: 13.52; p = 0.027), and disc bulge in preoperative CT examination (OR: 390.4; p = 0.000) maintained their significance in predicting likelihood of symptomatic adjacent segment degeneration surgery. Conclusions The occurrence of a symptomatic adjacent segment degeneration surgery is most likely multifactorial and is related to BMI, preoperative ADD on MRI, and disc bulge in preoperative CT examination. [ABSTRACT FROM AUTHOR]

Study Design: Meta-analysis to collect all the relevant studies to date to further investigate whether or not the rs11190870 polymorphism is associated with susceptibility to adolescent idiopathic scoliosis (AIS) in East Asian population.Objective: To investigate whether or not the rs11190870 polymorphism is associated with susceptibility to AIS in East Asian population.Summary Of Background Data: To date, the single nucleotide polymorphism rs11190870 was identified as the most significant common variant in Japanese females. Three association studies conducted in Chinese Han population from Hong Kong, Yangtze River region, and Southern region of mainland China replicated the association between AIS and rs1190870. However, there is limited published data about the association of rs11190870 with AIS in East Asian population.Methods: A systematic search of all relevant studies published through August 2013 was conducted using the MEDLINE, EMBASE, OVID, and ScienceDirect. Single nucleotide polymorphism of rs11190870 was evaluated. The included studies were assessed in the analysis of the following allele model: T allele versus C allele for the allele-level comparison; (b) TC + TT versus CC for dominant model of T allele; (c) TT versus TC + CC for recessive model of T allele, and (d) TT versus CC for extreme genotype.Results: Four studies with 8415 total participants (2889 patients with AIS and 5526 controls), who were all East Asian population, were eligible for inclusion. We searched for genotypes T allele versus C allele, TT versus TC + CC, TC + TT versus CC, and TT versus CC in a fixed/random-effects model. The effect summary odds ratios and 95 % confidence intervals were obtained, which shows significant association between rs11190870 and AIS in East Asian populations (all genetic models P < 0.001). Subgroup analyses were conducted according to sex. The results showed a significant association between rs11190870 and AIS in female (all genetic models, P < 0.001) but not in male (all genetic models, P > 0.05).Conclusion: The present meta-analysis demonstrated that the T allele of single nucleotide polymorphism rs11190870 may be a major susceptibility locus in the East Asian population with AIS, especially in female.Level Of Evidence: 1. [ABSTRACT FROM AUTHOR]

Hyperleptinemia is implicated in obesity-associated lumbar disc degeneration. Nevertheless, the effect of leptin on the intracellular signaling of nucleus pulposus cells is not clear. The current study sought to delineate the possible involvement of the RhoA/ROCK pathway in leptin-mediated cytoskeleton reorganization in nucleus pulposus cells. Nucleus pulposus cells isolated from scoliosis patients were treated with 10 ng/mL of leptin. Fluorescent resonance energy transfer analysis was used to determine the activation of RhoA signaling in nucleus pulposus cells. The protein expression of LIMK1 and cofilin-2 were analyzed by western blot analysis. F-actin cytoskeletal reorganization was assessed by rhodamine-conjugated phalloidin immunoprecipitation. Leptin induced F-actin reorganization and stress fiber formation in nucleus pulposus cells, accompanied by localized RhoA activation and phosphorylation of LIMK1 and cofilin. The RhoA inhibitor C3 exoenzyme or the ROCK inhibitor Y-27632 potently attenuated the effects of leptin on F-actin reorganization and stress fiber formation. Both inhibitors also prevented leptin-induced phosphorylation of LIMK1 and cofilin-2. Our study demonstrated that leptin activated the RhoA/ROCK/LIMK/cofilin-2 cascade to induce cytoskeleton reorganization in nucleus pulposus cells. These findings may provide novel insights into the pathogenic mechanism of obesity-associated lumbar disc degeneration. [ABSTRACT FROM AUTHOR]

Leptin affects a number of cell signaling pathways, at present, the mechanism(s) by which leptin affects the cartilage cells in OA patient is not well understood. The current study seeks to elucidate whether leptin induces cytoskeletal remodeling in chondrocytes and the possible involvement of the RhoA/ROCK pathway and its downstream mediators in this process. Fluorescent resonance energy transfer (FRET) and western analysis were used to determine the activations of the key proteins in the RhoA/LIMK1/Cofilin pathway. Accompanying cytoskeletal remodeling was elucidated. Upon leptin stimulation, a substantial increase of RhoA activity localized at one end of the cell was observed from 2 to 30 min post-stimulation. The results of Western blot showed leptin significantly increased LIMK1 and cofilin-2 phosphorylation in a time-dependent manner with maximal stimulation attained 60 min and 24 h post-stimulation, respectively. Chondrocytes stimulated with leptin exhibited an epithelioid morphology with increased cellular spreading. F-actin in leptin-stimulated chondrocytes also showed more intense cytoplasmic staining with occasional localization along filamentous structures. The results indicate that leptin activates the RhoA/ROCK/LIMK/cofilin pathway, which results in cytoskeletal reorganization in chondrocytes. These findings provide novel evidence supporting the possible involvement of leptin and the RhoA pathway in the pathogenesis of OA. © 2010 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 29:369-374, 2011 [ABSTRACT FROM AUTHOR]

Background: Both patients with Chiari-I malformation (CIM) with syringomyelia and those with idiopathic syringomyelia (ISm) have a syrinx and can have scoliosis as well. However, there is no literature regarding differences between CIM and ISm in terms of radiographic outcomes and surgical complications after posterior fusion, to our knowledge. The aim of the present study was to compare radiographic features, clinical outcomes, and surgical complications after posterior spinal fusion between patients with CIM-associated scoliosis and those with ISm-associated scoliosis.Methods: One hundred and twenty patients with syringomyelia-associated scoliosis were retrospectively analyzed. Twenty-one patients with scoliosis secondary to CIM were enrolled and matched by sex, age, and the Cobb angle of the scoliotic curve with 21 patients with scoliosis secondary to ISm. All patients underwent 1-stage posterior fusion surgery. Coronal and sagittal radiographic parameters were evaluated before surgery, immediately after surgery, and at the final follow-up (at least 2 years). We also collected data regarding syringeal features, neurological deficits, intraoperative neuromonitoring, and complications.Results: Sex, age, preoperative coronal/sagittal scoliosis parameters, and neurological deficits were similar between the matched CIM and ISm groups. On average, the CIM group had a longer syrinx (12.3 ± 3.6 versus 8.9 ± 4.5 vertebral levels, p = 0.010) than the ISm group. The CIM and ISm groups showed similar correction rates for primary curves (70.9% ± 10.6% versus 69.5% ± 16.3%, p = 0.739). There were no significant differences in coronal/sagittal correction, intraoperative neuromonitoring abnormalities, surgical complications, or Scoliosis Research Society-22 questionnaire scores between the 2 groups.Conclusions: Despite matched demographic and scoliotic coronal parameters, patients with CIM had longer syrinxes compared with patients with ISm. One-stage posterior fusion achieved comparable clinical and radiographic outcomes for both CIM- and ISm-associated scoliosis without significant differences in neurological complications.Level Of Evidence: Prognostic Level III. See Instructions for Authors for a complete description of levels of evidence. [ABSTRACT FROM AUTHOR]

Study Design: Retrospective study.Objective: To compare syrinx characteristics, scoliotic parameters, and neurological deficits between Chiari I malformation (CIM) and idiopathic syringomyelia (IS) in the scoliotic population.Summary Of Background Data: CIM and IS are common in neuromuscular scoliosis patients; however, differences in syrinx characteristics, scoliotic parameters, and neurological deficits between CIM and IS are unclear.Methods: Thirty-six patients with scoliosis secondary to CIM were enrolled retrospectively and matched with 36 IS patients for sex, age, scoliosis classification, and Cobb angle. Information on radiographic features of scoliosis and syrinx and neurological deficits was systematically collected.Results: Sex, age, and coronal, and sagittal scoliosis parameters did not differ between the CIM and IS groups. The CIM group had a longer syrinx (12.9 ± 4.0 vertebral levels vs. 8.7 ± 5.5 vertebral levels, P < 0.001), a higher cranial extent (3.6 ± 2.2 vs. 5.2 ± 3.5, P = 0.027), and a lower caudal extent (15.6 ± 2.9 vs. 13.0 ± 4.6, P = 0.006) than the IS group, despite no differences in syrinx/cord (S/C) ratio or syrinx classification. No differences in neurological deficits were identified between the CIM and IS patients.Conclusion: With demographic and scoliotic coronal parameters matched, the CIM patients had a longer syrinx, located at a higher cranial and lower caudal level, compared with the IS group. No significant differences in syrinx S/C ratio, sagittal features of scoliosis, or neurological deficits were detected between the two groups.Level Of Evidence: 3. [ABSTRACT FROM AUTHOR]

Increasing evidence suggests that obesity and aberrant proliferation of nucleus pulposus (NP) cells are associated with intervertebral disc degeneration. Leptin, a hormone with increased circulating level in obesity, has been shown to stimulate cell proliferation in a tissue-dependent manner. Nevertheless, the effect of leptin on the proliferation of human NP cells has not yet been demonstrated. Here, we show that leptin induced the proliferation of primary cultured human NP cells, which expressed the leptin receptors OBRa and OBRb. Induction of NP cell proliferation was confirmed by CCK8 assay and immunocytochemistry and Real-time PCR for PCNA and Ki-67. Mechanistically, leptin induced the phosphorylation of STAT3, Akt and ERK1/2 accompanied by the upregulation of cyclin D1. Pharmacological inhibition of JAK/STAT3, PI3K/Akt or MEK/ERK signaling by AG490, Wortmannin or U0126, respectively, reduced leptin-induced cyclin D1 expression and NP cell proliferation. These experiments also revealed an intricate crosstalk among these signaling pathways in mediating the action of leptin. Taken together, we show that leptin induces human NP cell cyclin D1 expression and proliferation via activation of JAK/STAT3, PI3K/Akt or MEK/ERK signaling. Our findings may provide a novel molecular mechanism that explains the association between obesity and intervertebral disc degeneration. [ABSTRACT FROM AUTHOR]

Most cases of congenital spinal deformities were sporadic and without strong evidence of heritability. The etiology of congenital spinal deformities is still elusive and assumed to be multi-factorial. The current study seeks to elucidate the effect of maternal vitamin A deficiency and the production of congenital spinal deformities in the offsping. Thirty two female rats were randomized into two groups: control group, which was fed a normal diet; vitamin A deficient group, which were given vitamin A-deficient diet from at least 2 weeks before mating till delivery. Three random neonatal rats from each group were killed the next day of parturition. Female rats were fed an AIN-93G diet sufficient in vitamin A to feed the rest of neonates for two weeks until euthanasia. Serum levels of vitamin A were assessed in the adult and filial rats. Anteroposterior (AP) spine radiographs were obtained at week 2 after delivery to evaluate the presence of the skeletal abnormalities especially of spinal deformities. Liver and vertebral body expression of retinaldehyde dehydrogenase (RALDHs) and RARs mRNA was assessed by reverse transcription-real time PCR. VAD neonates displayed many skeletal malformations in the cervical, thoracic, the pelvic and sacral and limbs regions. The incidence of congenital scoliosis was 13.79% (8/58) in the filial rats of vitamin A deficiency group and 0% in the control group. Furthermore, vitamin A deficiency negatively regulate the liver and verterbral body mRNA levels of RALDH1, RALDH2, RALDH3, RAR-α, RAR-β and RAR-γ. Vitamin A deficiency in pregnancy may induce congenital spinal deformities in the postnatal rats. The decreases of RALDHs and RARs mRNA expression induced by vitamin A deprivation suggest that vertebral birth defects may be caused by a defect in RA signaling pathway during somitogenesis. [ABSTRACT FROM AUTHOR]

Kaposiform hemangioendothelioma (KHE) is a rare locally aggressive vascular tumor that usually presents as a superficial or deep soft tissue mass with associated cutaneous lesions. We report a unique spinal KHE with painless thoracic scoliosis in a 14-year-old girl. She underwent simultaneous tumor biopsy, spinal deformity correction and fusion. At 3 years follow-up, the patient's MRI showed no significant deterioration of process without any therapy. KHE presenting as scoliosis is rare and to our knowledge this is the first recognized case in the reported world literature. [ABSTRACT FROM AUTHOR]