BACKGROUND: This study attempts to prove a cause and effect relationship between spine immobilization following posterior fixation for unstable burst fractures and degeneration observed following hardware removal. METHODS: We enrolled 57 patients (259 intervertebral discs [IVDs]) who underwent only posterior instrumentation without fusion for thoracolumbar and lumbar unstable burst fractures. We arbitrarily named the IVD that has an endplate fracture after immobilization using pedicle screws as the fractured endplate and immobilized disc (FEID), the IVD that has no endplate fracture after immobilization using pedicle screws as the nonfractured endplate and immobilized disc (NFEID), and the IVD that has no endplate fracture and no immobilization instrumentation as the normal disc (ND). At 2 years after implant removal, magnetic resonance imaging (MRI) was performed again for comparison. The extent of disc degeneration was classified using the Pfirrmann classification system. RESULTS: FEIDs were present in 67 levels, NFEIDs in 78 levels, and NDs in 114 levels. According to the Pfirrmann classification, 7.9% of the NDs, 32.1% of the NFEIDs, and 43.3% of the FEIDs were more degenerated at 2 years after implant removal. The FEIDs and NFEIDs were more degenerated than the NDs and the FEIDs were more degenerated than the NFEIDs at statistically significant levels (p < 0.001 for both). CONCLUSIONS: Spine immobilization with transpedicular screws has a significant influence on disc degeneration, and an endplate fracture accelerates the degeneration process.
Classification ; Humans ; Immobilization ; Intervertebral Disc ; Intervertebral Disc Degeneration ; Magnetic Resonance Imaging ; Pedicle Screws ; Spine

Previously, we reported that glucose-deprived astrocytes are more vulnerable to the cytotoxicity of peroxynitrite, the reaction product of nitric oxide and superoxide anion. The augmented vulnerability of glucose-deprived astrocytes to peroxynitrite cytotoxicity was dependent on their proliferation rate. Inhibition of cell cycle progression has been shown to inhibit the apoptotic cell death occurring in cerebral ischemia-reperfusion. In the present study, we demonstrate that the increased death of glucose-deprived astrocytes by peroxynitrte was largely blocked by the cell cycle phase G2/M transition blocker etoposide. However, the cytoprotective effect of etoposide was not associated with its inhibition of cell cycle progression. Instead, etoposide effectively scavenged peroxynitrite. However, etoposide did not scavenge individual nitric oxide and superoxide anion and it did not prevent the hydrogen peroxide-induced cytotoxicity. The present results indicate that etoposide prevents the toxicity of peroxynitrite in astrocytes by directly scavenging peroxynitrite, not by inhibiting cell cycle progression.
Astrocytes ; Cell Cycle ; Cell Death ; Etoposide ; Hydrogen ; Nitric Oxide ; Peroxynitrous Acid ; Superoxides

BACKGROUND: There is a well recognized interlaboratory variation in the results using the polymerase chain reaction(PCR) to detect the IS6110 sequence. The clinical utility of a commercially developed PCR test(Amplicor) in bronchial washings for detecting pulmonary tuberculosis in smear negative patients was evaluated. The sensitivity and specificity of Amplicor was compared with that of an in-house PCR test used for detecting the IS6110 sequence of Mycobacterium tuberculosis(M.tbc) in the bronchial washing fluid. METHODS: 66 patients whose sputum smear for M.tbc were negative or who could not produce any sputum were recruited from January 1999 to July 1999. They all had a bronchoscopy performed to determine if there were signs of hemoptysis, patients who could not cough up sputum, lung lesion that exclude pulmonary tuberculosis. Pulmonary tuberculosis was diagnosed on the basis of a positive culture or a response to anti-tuberculosis therapy. RESULTS: 19 patients with tuberculosis were identified and samples from 16 patients were later confirmed by culture. Bronchial washing for Amplicor PCR revealed a sensitivity, specificity, positive and negative predictive values of 94.7%, 97.9%, 94.7%, 97.9%, respectively. Using IS6110 based PCR, the sensitivity, specificity, positive and negative predictive values were of 73.7%, 87.2%, 70%, 89.1% respectively. CONCLUSION: Bronchial washing for Amplicor PCR proved to be more useful than IS6110 based PCR in rapidly diagnosing smear negative pulmonary pulmoary tuberculosis in patients where tuberculosis was likely to be differential and rapid diagnosis was essential for optimal treatment.
Bronchoscopy ; Cough ; Diagnosis* ; Hemoptysis ; Humans ; Lung ; Mycobacterium ; Polymerase Chain Reaction* ; Sensitivity and Specificity ; Sputum ; Tuberculosis ; Tuberculosis, Pulmonary*

N-methyl-D-aspartate (NMDA) receptor-mediated excitotoxicity is one of the major causes for neuronal cell death during cerebral ischemic insult. Previously, we reported that the final product of lipid membrane peroxidation 4-hydroxy-2E-nonenal (HNE) synergistically increased NMDA receptor-mediated excitotoxicity (J Neurochem., 2006). In this study, we investigated the mechanism involved in the synergistic neuronal cell death induced by co-treatment with HNE and NMDA. Although neither HNE (1 microM) nor NMDA (2 microM) alone induced the death of cortical neurons, simultaneous treatment of neuronal cells with HNE and NMDA synergistically evoked the death of the cells. However, the synergistic effect on neuronal death was observed only in the presence of calcium. HNE neither increased the cytosolic calcium level ([Ca2+]i) nor altered the NMDA-induced intracellular calcium influx. However, HNE together with NMDA elevated the mitochondrial calcium level and depolarized the mitochondrial transmembrane potential. Furthermore, HNE evoked damage of isolated mitochondria at the cytosolic calcium level (200 nM), which is maximally induced by 2 microM NMDA. Consistently, ATP was depleted in neurons when treated with both HNE and NMDA together. Ciclopirox, a potent inhibitor of mitochondrial permeability transition pore opening (Br. J. Pharmacol., 2005), largely prevented the synergistic damage of mitochondria and death of cortical neurons. Therefore, although low concentrations of HNE and NMDA cannot individually induce neuronal cell death, they can evoke the neuronal cell death by synergistically accelerating mitochondrial dysfunction.
Adenosine Triphosphate ; Calcium ; Cell Death ; Cytosol ; Membrane Potentials ; Membranes ; Mitochondria ; Mitochondrial Membrane Transport Proteins ; N-Methylaspartate ; Neurons ; Permeability ; Pyridones

OBJECTIVE: This study evaluated the cost for occupational health and safety in manufacturing factories in Korea according to the factory's size and the industrial classification. METHODS: The costs to prevent occupational injuries and promote the general health of the workers were calculated by using the data of The Occupational Safety and Health Survey in Korea in the year of 2005 and the data of the Industrial Accident Compensation Insurance (IACI) premiums at the same factories for the year of 2004. RESULTS: The mean cost per one worker was as follows: 990,000 won for the factory with 5~49 workers, 869,000 won for the factory with 50~299 workers and 1,773,000 won for the factory with more than 300 workers. In the factories with 5~49 workers and 50~299 workers, the premium for the IACI was the largest portion of the cost (62.8% and 52.8%, respectively) and the cost for gear to protect workers from dangerous machineries was the next biggest portion of the cost (20.1% and 19.1%, respectively). The largest portion of the cost in the factories with more than 300 workers was the premium for the IACI (37.5%). CONCLUSIONS: The investment costs to prevent occupational injuries and to promote the general health of the workers were very diverse according to the size of the factories and the industrial classification. To reduce the occupational injuries and to promote the general health of the workers, systematic and continuous approaches to evaluate the investment costs for the occupational health and safety are required.
Accidents, Occupational ; Compensation and Redress ; Health Surveys ; Insurance ; Investments ; Korea ; Occupational Health ; Occupational Injuries ; Occupations

OBJECTIVE: This study evaluated the cost for occupational health and safety in manufacturing factories in Korea according to the factory's size and the industrial classification. METHODS: The costs to prevent occupational injuries and promote the general health of the workers were calculated by using the data of The Occupational Safety and Health Survey in Korea in the year of 2005 and the data of the Industrial Accident Compensation Insurance (IACI) premiums at the same factories for the year of 2004. RESULTS: The mean cost per one worker was as follows: 990,000 won for the factory with 5~49 workers, 869,000 won for the factory with 50~299 workers and 1,773,000 won for the factory with more than 300 workers. In the factories with 5~49 workers and 50~299 workers, the premium for the IACI was the largest portion of the cost (62.8% and 52.8%, respectively) and the cost for gear to protect workers from dangerous machineries was the next biggest portion of the cost (20.1% and 19.1%, respectively). The largest portion of the cost in the factories with more than 300 workers was the premium for the IACI (37.5%). CONCLUSIONS: The investment costs to prevent occupational injuries and to promote the general health of the workers were very diverse according to the size of the factories and the industrial classification. To reduce the occupational injuries and to promote the general health of the workers, systematic and continuous approaches to evaluate the investment costs for the occupational health and safety are required.
Accidents, Occupational ; Compensation and Redress ; Health Surveys ; Insurance ; Investments ; Korea ; Occupational Health ; Occupational Injuries ; Occupations

OBJECTIVES: This study was performed to investigate the effect of drink containing sodium benzoate on the change of urinary hippuric acid (UHA) and methyl hippuric acid (UMHA) excretion among workers coexposed to low toluene and xylene. METHODS: Study subjects were 55 male shipbuilders who were divided into 3 groups; nonexposed group (n=10, who were not exposed to organic solvent and had drunk sodium benzoate), exposed A group (n=24, who were coexposed to toluene and xylene, and had drunk sodium benzoate), and exposed B group (n=21, who were coexposed to toluene and xylene, and had not drunk sodium benzoate). The study methodology consisted of questionnaire survey, urinary analysis for metabolites of toluene and xylene before and after drinking with or without sodium benzoate, and personal air sampling of toluene and xylene. RESULTS: Before drinking, there was no significant difference in UHA or UMHA between the exposed A and B groups. After 1.5 hour of drinking, UHA of the exposed A group was significantly higher than that of the exposed B group. After 3 hours, however, UHA of the exposed A group was decreased to the level of the exposed B group, regardless of the ambient toluene level. UMHA exhibited no significant difference between the exposed A and B groups regardless of time and ambient toluene level. The regression model showed that drinking of sodium benzoate was positively correlated with UHA after 1.5 hours of drinking, but not after 3 hours. In addition, sodium benzoate didn't affect UMHA. CONCLUSIONS: This study showed that sodium benzoate initially increased UHA temporally but that its effect disappeared after 3 hours. In the medical examination of toluene exposure workers, the ingestion of drink containing sodium benzoate should be forbidden during the 3 hours prior to urinary sampling.
Drinking ; Eating ; Humans ; Male ; Questionnaires ; Sodium Benzoate* ; Sodium* ; Toluene* ; Xylenes*

To investigate a specific mechanism of apoptosis induced by sonication, we applied 20 kHz ultrasound to leukemia cell line HL-60 with different intensities (0-60 W/cm2) and time durations (0-100 sec). In accordance with previous reports, ultrasound treatment in HL-60 cells induced immediate cell death and delayed cell death which are associated with cell lysis and apoptosis, respectively. Delayed cell death of HL-60 was also detected 5 hours after sonication in our experiment. Detection of caspase activation by Western blot and sub-G1 accumulation by flow cytometry confirmed that apoptosis plays a role in delayed cell death induced by sonication in HL-60 cells. In addition, we found that decrease in lysosomes of HL-60 cells after sonication suggesting lysosomal rupture is involved in the mechanism of cell death induced by sonication.
Apoptosis* ; Blotting, Western ; Cell Death ; Cell Line ; Flow Cytometry ; HL-60 Cells* ; Humans ; Leukemia ; Lysosomes ; Rupture ; Sonication* ; Ultrasonic Therapy ; Ultrasonography

Recently, we reported that the A3 adenosine receptor (A3AR) agonist LJ529 (2-chloro-N6-(3-iodobnzyl)-5'-N-methylcarbamoyl-4'-thioadenosine) reduces cerebral ischemic injury via inhibition of recruitment of peripheral inflammatory cells into ischemic brain lesion. A3AR agonists, however, are known to possess anti-platelet activity, which may deter the combination therapy with tissue plasminogen activator for the therapy of cerebral ischemic stroke. Thus, the present study investigates the neuroprotective/anti-ischemic effect of a synthetic seco-nucleoside, LMT497 ((S)-2-((R)-1-(2-chloro-6-(3-iodobenzylamino)-9H-purin-9-yl)-2-hydroxyethoxy)-3-hydroxy-N-methylpropanamide) with little anti-platelet activity. LMT497 neither showed A3AR binding activity nor anti-platelet activity. In our present study LMT497 significantly attenuated the injury/death of cortical neurons exposed to oxygen-glucose deprivation (OGD) followed by re-oxygenation (R). LMT497 significantly reduced the ascending cellular level of reactive oxygen species under ischemic conditions by increasing the superoxide dismutase (SOD) levels. LMT497 also inhibited the migration of microglia which mediates inflammatory responses in ischemia. In rats subjected to middle cerebral artery occlusion (MCAO, 1.5 h) followed by reperfusion, LMT497 largely reduced brain infarction volume, and edema, and improved neurological score. Therapeutic efficacy of LMT497 was obtained by twice treatments even at 10 h and 18 h after the onset of ischemia. Collectively, LMT497 could be a therapeutic drug candidate with a wide therapeutic time window for the treatment of cerebral ischemic stroke.
Animals ; Brain ; Brain Infarction ; Brain Ischemia ; Edema ; Infarction, Middle Cerebral Artery ; Inflammation ; Ischemia ; Microglia ; Neurons ; Oxidative Stress ; Rats ; Reactive Oxygen Species ; Receptors, Purinergic P1 ; Reperfusion ; Stroke ; Superoxide Dismutase ; Tissue Plasminogen Activator

Recently developed cDNA microarray or DNA chip technology allows expression monitoring of expression of hundreds and thousands of genes simultaneously and provides a format for identifying genes as well as changes in their activity. In order to search for changes in gene expression after X irradiation in HL60 cells, cDNA microarray technique was done. In this study, expression of 588 human genes (including oncogenes, tumor suppressor genes, cell cycle regulator genes, intracellular signal transduction modulator genes, apoptosis related genes, transcription factor genes, growth factors and receptor genes, cytokine genes, etc) were analyzed. For cDNA microarray analysis mRNAs were extracted from control and 8 Gy-irradiated HL60 cells. As a result the changes in expression of several genes were observed. This alteration of gene expression was confirmed by reverse transcription-polymerase chain reaction. The expression of heat shock 60 KD protein, c-jun, erythroid differentiation factor, CPP32, myeloid cell nuclear differentiation antigen, MAP kinase-activated protein kinase, interleukin-8, monocyte chemotactic peptide 1 and RANTES genes was increased, but the expression of p55CDC gene was decreased after X irradiation.
Apoptosis ; Cell Cycle ; Chemokine CCL5 ; DNA, Complementary* ; Gene Expression ; Genes, Regulator ; Genes, Tumor Suppressor ; HL-60 Cells* ; Hot Temperature ; Humans ; Intercellular Signaling Peptides and Proteins ; Interleukin-8 ; Monocytes ; Myeloid Cells ; Oligonucleotide Array Sequence Analysis* ; Oncogenes ; Protein Kinases ; RNA, Messenger ; Shock ; Signal Transduction ; Transcription Factors