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Keun Su Kim, S. Tim Yoon, Jin Soo Park, Jun Li, Moon Soo Park, and William C. Hutton

Object. Systemic nicotine has been hypothesized to cause degeneration of the intervertebral disc which in turn decreases vascular supply to the disc through a cholinergic receptor—mediated process. Another possible mechanism may be through direct regulatory effects on disc cells. In this study, the authors tested the hypothesis that nicotine adversely affects nucleus pulposus cells by directly inhibiting proteoglycan synthesis and gene expression of type II collagen (Phase I study). They also assessed the hypothesis that nicotine inhibits the bone morphogenetic protein (BMP)—2-induced upregulation of extracellular matrix (Phase II study).

Methods. Cells were isolated from nucleus pulposus obtained in rat lumbar discs and cultured on a monolayer. Media were treated with nicotine and/or recombinant human (rh)BMP-2 for 7 days. Sulfated glycosaminoglycan (SO4-GAG) in media was quantified using 1,9-dimethylmethylene blue (DMMB) assay. Gene assay of types I and II collagen, Sox9, and glyceraldehyde-3-phosphate dehydrogenase were quantified using reverse transcriptase—polymerase chain reaction (RT-PCR) and real time PCR. In the Phase I study, nicotine-treated (100 µg/ml) and nontreated cells were compared. The s-GAG production and messenger RNA (mRNA) of type II collagen and Sox9 decreased significantly in the nicotine-treated group. In the Phase II study, five groups were compared: 1) nontreatment; 2) rhBMP-2 only (100 ng/ml); and 3–5) with rhBMP-2 (100 ng/ml) and increasing doses of nicotine (1 [third group], 10, [fourth group], 100 [fifth group] µg/ml). The SO4-GAG production and mRNA of type II collagen and Sox9 decreased significantly in the groups treated with rhBMP-2 combined with 10 and 100 µg/ml of nicotine compared with the group treated with rhBMP-2.

Conclusions. The results of this study raise the possibility that nicotine may contribute to the process of disc degeneration by a direct effect on the nucleus pulposus cells, possibly by antagonizing the effect of BMP-2.

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Kotaro Jimbo, Jin Soo Park, Kimiaki Yokosuka, Kimiaki Sato, and Kensei Nagata

Object. Interleukin-1β (IL-1β) induces neurological symptoms in intervertebral disc herniation (IDH). Recently, the existence of a positive feedback loop of IL-1β, which encourages an inflammatory reaction or degeneration in the cells of tendon, has been reported. The authors hypothesized that there is a positive feedback loop of IL-1β in the cells of IDH.

Methods. Eight human intervertebral disc specimens were harvested during spinal surgery for lumbar disc herniation. The cells were stimulated in serum-free medium with or without exogenous IL-1β. The messenger RNA (mRNA) was extracted for reverse-transcription polymerase chain reaction (PCR) and real-time PCR to quantify the mRNA of endogenous IL-1β, IL-6, cyclooxygenase-2 (COX-2), and matrix metalloproteinases (MMPs). The cells were then stimulated in serum-free medium with or without exogenous IL-1β, and then exogenous IL-1β was removed. After 2, 4, and 6 days, the medium was collected, and enzyme-linked immunosorbent assay was used to measure the protein concentration of endogenous IL-1β. The mRNA expressions of endogenous IL-1β, IL-6, COX-2, and MMPs were increased significantly depending on the concentration of exogenous IL-1β. The protein concentration of endogenous IL-1β was increased over time.

Conclusions. There was a positive feedback loop of IL-1β in the cells of IDH. Furthermore, the productions of IL-6, COX-2, MMP-1, and MMP-3 were upregulated as a result of the increasing concentration of IL-1β in a positive feedback loop of IL-1β. The authors concluded that this positive feedback loop of IL-1β upregulated the production of mediators and thus can cause cessation of symptoms in IDH.

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Jeong-Yub Kim, Jongsun Lee, Jae-Soo Koh, Myung-Jin Park, and Ung-Kyu Chang

OBJECTIVE

Chordoma is a rare bone tumor of the axial skeleton believed to originate from the remnants of the embryonic notochord. The available tumor cells are characteristically physaliferous and express brachyury, a transcription factor critical for mesoderm specification. Although chordomas are histologically not malignant, treatments remain challenging because they are resistant to radiation therapy and because wide resection is impossible in most cases. Therefore, a better understanding of the biology of chordomas using established cell lines may lead to the advancement of effective treatment strategies. The authors undertook a study to obtain this insight.

METHODS

Chordoma cells were isolated from the tissue of a patient with dedifferentiated-type chordoma (DTC) that had recurred. Cells were cultured with DMEM/F12 containing 10% fetal bovine serum and antibiotics (penicillin and streptomycin). Cell proliferation rate was measured by MTS assay. Cell-cycle distribution and cell surface expression of proteins were analyzed by fluorescence-activated cell sorting (FACS) analysis. Expression of proteins was analyzed by Western blot and immunocytochemistry. Radiation resistance was measured by clonogenic survival assay. Tumor formation was examined by injection of chordoma cells at hindlimb of nude mice.

RESULTS

The putative (DTC) cells were polygonal and did not have the conventional physaliferous characteristic seen in the U-CH1 cell line. The DTC cells exhibited similar growth rate and cell-cycle distribution, but they exhibited higher clonogenic activity in soft agar than U-CH1 cells. The DTC cells expressed high levels of platelet-derived growth factor receptor–β and a low level of brachyury and cytokeratins; they showed higher expression of stemness-related and epithelial to mesenchymal transition–related proteins than the U-CH1 cells. Intriguingly, FACS analysis revealed that DTC cells exhibited marginal surface expression of CD24 and CD44 and high surface expression of CXCR4 in comparison to U-CH1 cells. In addition, blockade of CXCR4 with its antagonist AMD3100 effectively suppressed the growth of both cell lines. The DTC cells were more resistant to paclitaxel, cisplatin, etoposide, and ionizing radiation than the U-CH1 cells. Injection of DTC cells into the hindlimb region of nude mice resulted in the efficient formation of tumors, and the histology of xenograft tumors was very similar to that of the original patient tumor.

CONCLUSIONS

The use of the established DTC cells along with preestablished cell lines of chordoma may help bring about greater understanding of the mechanisms underlying the chordoma that will lead to therapeutic strategies targeting chordomas.

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Jin Soo Park, Isao Shirachi, Kimiaki Sato, Noriyuki Ando, and Kensei Nagata

✓ The authors present the case of a 60-year-old woman with a neck lipoma that developed dumb-bell extradural extension, causing radiculopathy. To the best of the authors' knowledge, this is the first report of a lipoma originating in the neck with dumb-bell extradural extension through the intervertebral foramen and into the spinal canal. The lipoma was first excised from the foramen via a posterior approach to allow decompression of the nerve roots. The remaining lipomatous tissue was then resected via an anterior approach to avoid the region around the vertebral artery.

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Hyun Ho Jung, Jong Hee Chang, Kum Whang, Jin Soo Pyen, Jin Woo Chang, and Yong Gou Park

Object

The purpose of this study was to assess the efficacy of Gamma Knife surgery (GKS) for treating cavernous sinus dural arteriovenous fistulas (CSDAVFs).

Methods

Of the 4123 GKSs performed between May 1992 and March 2009, 890 procedures were undertaken to treat vascular lesions. In 24 cases, the vascular lesion that was treated was a dural arteriovenous fistula, and in 6 of these cases, the lesion involved the cavernous sinus. One of these 6 cases was lost to follow-up, leaving the other 5 cases (4 women and 1 man) to comprise the subjects of this study. All 5 patients had more than 1 ocular symptom, such as ptosis, chemosis, proptosis, and extraocular movement palsy. In all patients, CSDAVF was confirmed by conventional angiography. Three patients were treated by GKS alone and 2 patients were treated by GKS combined with transarterial embolization. The median follow-up period after GKS in these 5 cases was 30 months (range 9–59 months).

Results

All patients experienced clinical improvement, and their improvement in ocular symptoms was noticed at a mean of 17.6 weeks after GKS (range 4–24 weeks). Two patients received embolization prior to GKS but did not display improvement in ocular symptoms. An average of 20 weeks (range 12–24 weeks) was needed for complete improvement in clinical symptoms. There were no treatment-related complications during the follow-up period.

Conclusions

Gamma Knife surgery should be considered as a primary, combined, or additional treatment option for CSDAVF in selected cases, such as when the lesion is a low-flow shunt without cortical venous drainage. For those selected cases, GKS alone may suffice as the primary treatment method when combined with close monitoring of ocular symptoms and intraocular pressure.

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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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Seung-Chyul Hong, Kwan-Soo Kang, Dae Won Seo, Seung Bong Hong, Munhyang Lee, Do-Hyun Nam, Jung-Il Lee, Jong Soo Kim, Hyung-Jin Shin, Kwan Park, Whan Eoh, Yeon-Lim Suh, and Jong-Hyun Kim

Object. Surgical treatment of cortical dysplasia (CD) together with intractable seizures is challenging because both visualization and localization of the lesion are difficult, correlation with seizure foci requires comprehensive study, and the surgical outcomes reported thus far are unsatisfactory. The authors report their experience in the surgical treatment of CD classified according to a surgical point of view.

Methods. The definition of CD used in this study was a dysplastic lesion visible on magnetic resonance (MR) images or a lesion that, although not visible on MR images, was diagnosed as moderate-to-severe dysplasia by using pathological analysis. During the last 4.5 years, the authors treated 36 patients with intractable epilepsy accompanied by CD. They divided the 36 cases of CD into four characteristic groups: Group A, diffuse bilateral hemispheric dysplasia; Group B, diffuse lobar dysplasia; Group C, focal dysplasia; and Group D, a moderate to severe degree of CD with a normal appearance on MR images. All but one patient in Group C were monitored in the epilepsy monitoring unit by using subdural electrodes for seizure localization and functional mapping.

The incidence of CD among a cohort of 291 patients who had undergone epilepsy surgery at the authors' center during the study period was 12.4%. The mean age of the 36 patients was 21.3 years and the mean age at seizure onset was 8.5 years. The mean follow-up period was 26 months. Twenty-six patients (72.2%) belonged to Engel Class I or II (20 and six, respectively). There were five cases in Group A, nine in Group B, nine in Group C, and 13 in Group D. Patients in Groups A and B were significantly younger at seizure onset and had significantly poorer surgical outcomes compared with patients in Groups C and D (p < 0.05). If outcome is compared on the basis of the extent of removal of CD, patients in whom CD was completely removed had significantly better outcomes than those in whom CD was only partially removed (p < 0.001).

Conclusions. The authors conclude that intractable epilepsy accompanied by CD can be treated surgically using comprehensive preoperative approaches. Deliberate resective procedures aimed at complete removal of dysplastic tissue ensure excellent seizure control without permanent neurological deficit.

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Jung-Il Lee, Do-Hyun Nam, Jong Soo Kim, Seung-Chyul Hong, Hyung-Jin Shin, Kwan Park, Whan Eoh, Yeon-Lim Suh, and Jong Hyun Kim

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Young-Soo Kim, Ho-Yeol Zhang, Byung-Jin Moon, Kyung-Woo Park, Kyu-Yeul Ji, Won-Chang Lee, Kyu-Sung Oh, Gwon-Ui Ryu, and Daniel H. Kim

Object

The purpose of this study was to analyze the usefulness of the BioFlex, a Nitinol spring rod dynamic stabilization system, and the Nitinol shape memory loop (KIMPF-DI Fixing System) as a posterior dynamic stabilization system in surgery for low-back pain.

Methods

The 103 patients who underwent treatment with the BioFlex system were divided into two groups: Group 1, dynamic stabilization with or without posterior lumbar interbody fusion (PLIF); and Group 2, rigid fixation (PLIF + BioFlex system only). A total of 66 segments were treated with only the BioFlex system; in these the preoperative range of motion (ROM) was 10.0 ± 4.3°, which changed to 4.1 ± 1.9° after surgery. Adjacent-segment ROM changed from 8.4 ± 3.4° to 10.7 ± 3.2° in Group 1 and from 6.5 ± 3.2° to 10.5 ± 4.6° in Group 2 postoperatively. A total of 110 segments received both BioFlex and PLIF, with a fusion rate of 90.0%. The visual analog scale score for back pain improved from 7.3 ± 3.1 to 1.4 ± 1.8 in Group 1 and from 7.4 ± 2.4 to 2.1 ± 2.3 in Group 2. The Oswestry Disability Index improved from 35.2 ± 6.4 to 12.1 ± 4.5 in Group 1 and from 37.8 ± 5.7 to 13.6 ± 4.2 in Group 2. (The ROM and assessment scores expressed are the mean ± standard deviation.)

The 194 patients in whom Nitinol memory loops were implanted were analyzed based on the preoperative and 1-year postoperative ROM of each lumbar segment. The change of ROM in looped segments treated with PLIF was significantly reduced, but the change of ROM in looped segments without PLIF was not significant. The change of ROM at the segment adjacent to the loop was not significant, and the change of kyphosis reflected a slight recovery.

Conclusions

The Nitinol BioFlex dynamic stabilization system can achieve stabilization and simultaneously allow physiological movement, which can in turn decrease the degeneration of adjacent segments. When used with PLIF, the fusion rate can be expected to increase. The flexible Nitinol shape memory loop, a posterior dynamic stabilization device, is an adequate tension band that displays strength similar to the posterior ligamentous structures. In combination with PLIF at the main lesion, the BioFlex system or the Nitinol memory loop can provide posterior dynamic stabilization to the transitional upper or lower segments, enhance the fusion rate, reduce the adjacent-segment degeneration, and provide dynamic stabilization of the spine.

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Kimiaki Yokosuka, Jin Soo Park, Kotaro Jimbo, Kei Yamada, Kimiaki Sato, Michiyo Tsuru, Masayoshi Takeuchi, Sho-Ichi Yamagishi, and Kensei Nagata

Object

The authors sought to clarify the role, if any, of advanced glycation end-products (AGEs) in disc degeneration.

Methods

Intervertebral discs were analyzed for the presence of AGEs and of their receptor (RAGE) by immunohistochemical analysis. Reverse transcriptase polymerase chain reaction (RT-PCR) was performed to detect any RAGE gene expression, and real-time PCR was used to quantify messenger RNA (mRNA) levels of aggrecan and collagen types I and II in nucleus pulposus cells treated with AGEs. Aggrecan protein concentration was determined by enzyme-linked immunosorbent assay.

Immunohistochemical analysis revealed that AGEs and RAGE were localized in the nucleus pulposus of the intervertebral disc. Advanced glycation end-products were found to significantly suppress the expression of aggrecan at both mRNA and protein levels in a dose- and time-dependent manner. The levels of collagen types I and II remained unchanged after treatments with AGEs.

Conclusions

These results suggest that the accumulation of AGEs and their interaction with their receptor in the nucleus pulposus might result in the downregulation of aggrecan production responsible for disc degeneration.