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Yoon Ha, Young Soo Kim, Jin Mo Cho, Seung Hwan Yoon, So Ra Park, Do Heum Yoon, Eun Young Kim and Hyung Chun Park

Object. Granulocyte—macrophage colony—stimulating factor (GM-CSF) is a potent hemopoietic cytokine that stimulates stem cell proliferation in the bone marrow and inhibits apoptotic cell death in leukocytes. Its effects in the central nervous system, however, are still unclear. The present study was undertaken to determine if GM-CSF can rescue neuronal cells from apoptosis and improve neurological function in a spinal cord injury (SCI) model.

Methods. To study the effect of GM-CSF on apoptotic neuronal death, the authors used a staurosporine-induced neuronal death model in an N2A cell line (in vitro) and in a rat SCI model (in vivo). The N2A cells were preincubated with GM-CSF for 60 minutes before being exposed to staurosporine for 24 hours. To inhibit GM-CSF, N2A cells were pretreated with antibodies against the GM-CSF receptor for 60 minutes. Clip compression was used to induce SCI. Animals were treated with daily doses of GM-CSF (20 µg/day) for 5 days. The number of apoptotic cells in the spinal cord and neurological improvements were assessed.

Pretreatment with GM-CSF was found to protect N2A cells significantly from apoptosis, and neutralizing antibodies for the GM-CSF receptors inhibited the rescuing effect of GM-CSF on apoptosis. In the rat SCI model, neurological function improved significantly in the GM-CSF—treated group compared with controls treated with phosphate-buffered saline. Terminal deoxynucleotidyl transferase—mediated deoxyuridine triphosphate nick-end labeling staining showed that GM-CSF administration reduced apoptosis in the injured spinal cord.

Conclusions. Treatment of SCI with GM-CSF showed beneficial effects. Neuronal protection against apoptosis is viewed as a likely mechanism underlying the therapeutic effect of GM-CSF in SCI.

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Ji Yong Kim, Chang Hyun Oh, Xian Huang, Moon Hang Kim, Seung Hwan Yoon, Kil Hwan Kim, Hyeonseon Park, Hyung Chun Park, So Ra Park and Byung Hyune Choi


The aim in this study was to determine whether granulocyte-macrophage colony-stimulating factor (GM-CSF) leads to sensory improvement in rat spinal cord injury (SCI) models.


Thirty male Sprague-Dawley rats were included in this study: 10 in the sham group (laminectomy alone without SCI), 10 in the SCI group (SCI treated with phosphate-buffered saline), and 10 in the GM-CSF treatment group (SCI treated with GM-CSF). A locomotor function test and pain sensitivity test were conducted weekly for 9 weeks after SCI or sham injury. Spinal tissue samples from all rats were immunohistochemically examined for the expression of calcitonin gene-related peptide (CGRP) and abnormal sprouting at Week 9 post-SCI.


Granulocyte-macrophage colony-stimulating factor treatment improves functional recovery after SCI. In the tactile withdrawal threshold and frequency of the hindlimb paw, the GM-CSF group always responded with a statistically significant lower threshold than the SCI group 9 weeks after SCI (p < 0.05). The response of the forelimb and hindlimb paws to cold in the GM-CSF group always reflected a statistically significant lower threshold than in the SCI group 9 weeks after injury (p < 0.05). Decreased CGRP expression, observed by density and distribution area, was noted in the GM-CSF group (optical density 113.5 ± 20.4) compared with the SCI group (optical density 143.1 ± 18.7; p < 0.05).


Treatment with GM-CSF results in functional recovery, improving tactile and cold sense recovery in a rat SCI model. Granulocyte-macrophage colony-stimulating factor also minimizes abnormal sprouting of sensory nerves after SCI.

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Chang-Hyun Lee, Chun Kee Chung, Jee-Soo Jang, Sung-Min Kim, Dong-Kyu Chin, Jung-Kil Lee, Seung Hwan Yoon, Jae Taek Hong, Yoon Ha, Chi Heon Kim and Seung-Jae Hyun


As life expectancy continues to increase, primary degenerative sagittal imbalance (PDSI) is diagnosed in an increasing number of elderly people. Although corrective surgery for this sagittal deformity is becoming more popular, the effectiveness of the procedure remains unclear. The authors aimed to collate the available evidence on the effectiveness and complications of deformity-correction surgery in patients with PDSI.


The authors carried out a meta-analysis of clinical studies regarding deformity correction in patients with PDSI. The studies were identified through searches of the PubMed, Embase, Web of Science, and Cochrane databases. Surgery outcomes were evaluated and overall treatment effectiveness was assessed in terms of the minimum clinically important difference (MCID) in Oswestry Disability Index (ODI) values and pain levels according to visual analog scale (VAS) scores and in terms of restoration of spinopelvic parameters to within a normal range. Data are expressed as mean differences with 95% CIs.


Ten studies comprising 327 patients were included. The VAS and ODI values improved after deformity-correction surgery. The smallest treatment effect exceeded the MCID for VAS values (4.15 [95% CI 3.48–4.82]) but not for ODI values (18.11 [95% CI 10.99–25.23]). At the final follow-up visit, the mean lumbar lordosis angle (−38.60° [95% CI −44.19° to −33.01°]), thoracic kyphosis angle (31.10° [95% CI 24.67°–37.53°]), C-7 sagittal vertical axis (65.00 mm [95% CI 35.27–94.72 mm]), and pelvic tilt angle (30.82° [95% CI 24.41°–37.23°]) remained outside their normal ranges. Meta-regression analyses revealed a significant effect of ODI change in relation to lumbar lordosis change (p = 0.004). After a mean of 2 years after deformity correction, the mean lumbar lordosis angle and C-7 sagittal vertical axis decreased by 5.82° and 38.91 mm, respectively, and the mean thoracic kyphosis angle increased by 4.7°. The incidences of proximal junctional kyphosis and pseudarthrosis were 23.7% and 12.8%, respectively.


Deformity correction substantially relieves back pain for about 2 years in adult patients with PDSI. Sufficient surgical restoration of lumbar lordosis can lead to substantial improvement in patient disability and reduced decompensation. Deformity correction represents a viable therapeutic option for patients with PDSI, but further technical advancements are necessary to achieve sufficient lumbar lordosis and reduce complication rates.

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Seung-Hwan Yoon, Masashi Miyazaki, Soon-Woo Hong, Ben Tow, Yuichiro Morishita, Ming Hu, Sung-Joon Ahn and Jeffrey C. Wang


Appropriate animal models of disc degeneration are critical for the study of proposed interventions as well as to further delineate the degenerative process. The purpose of this study was to characterize a porcine model for disc degeneration confirmed on magnetic resonance (MR) imaging studies and histological analysis.


Twelve miniature pigs were used (weight 48–65 kg) to study degeneration in the lumbar spine. Under fluoroscopic guidance, the disc was percutaneously punctured with a 3.2-mm-diameter trephine to a 5-mm depth into the annulus fibrosus. Control and experimental levels were randomized among 6 levels in the lumbar spine. The unlesioned spinal levels were used as controls and were compared with lesioned levels. Magnetic resonance imaging grading and disc height were serially recorded preoperatively, and at 5, 8, 19, 32, and 39 weeks postoperatively. The animals were killed in groups of 3 at 7, 18, 32, and 41 weeks postinjury, and the discs were examined histopathologically.


Consistent, sequential, and progressive degeneration of the annular injury was observed on MR imaging and histopathological studies from the time of injury to the final time point. The disc height and the disc height index also sequentially decreased from the time of the injury in a consistent manner. The uninjured control levels did not show any progressive degeneration and maintained their normal state.


Based on MR imaging and histopathological findings, the authors demonstrated and characterized a reliable model of sequential disc degeneration in miniature pigs with percutaneous injury to the annulus fibrosus. In the early stages, as soon as 5 weeks after injury, significant disc degeneration was seen on MR imaging grading with decreases in disc height. This degeneration did not improve by the final time point of 39 weeks.