OBJECTIVE: The retrospective study is undertaken to report clinical results of anterior cervical interbody fusion with an intradiscal cage with an integrated plate (PCB cervical plating system). METHODS: 38 patients underwent anterior cervical interbody fusion with PCB cervical plating system and followed 6~24 months. The authors investigated overall surgical results; clinical outcome, fusion rate, change of interspace height & lordotic angle, and complications. RESULTS: No complication was observed during the operation. Clinical improvement was identified in 34 cases (89.5%). Bone fusion observed in 44 out of 49 sites (90.7%). After operation, the interspace height increased from 5.4+/-1.3 mm to 7.8+/-1.5 mm and maintained 7.4+/-1.1 mm and, interspace angle went up from 4.2+/-0.7 degrees to 4.8+/-1.1 degrees and maintained 4.6+/-0.9 degrees. The loosening of screw was observed in 6 cases, one of which had reoperation because of the expulsion of the device accompanied. CONCLUSION: PCB cervical plating system could restore interbody height and lordosis in anterior cervical interbody fusion. But, if the insertion of the spacer is not precise, the frequencies of hardware failure are relatively high. It is considered necessary for the operator to be careful in the procedure.
Animals ; Humans ; Lordosis ; Reoperation ; Retrospective Studies

PURPOSE: We wanted to evaluate the effective methods that are appropriate for an endemic area of thyroid disease and to compare the differences of cytologic diagnostic rates with and without using a peculiar smear technique. MATERIALS AND METHODS: We analyzed the incidence rate of insufficient results, complications and the total procedure times of 1,126 thyroid nodules in 776 patients who underwent US-FNAB (ultrasonography-guided fine-needle aspiration biopsy) from January to December 2005. We compared the diagnostic rate between the two groups; the groups' tests were performed with a peculiar smear technique (Group A, n = 313) or with a conventional smear technique (Group B, n = 250). RESULTS: According to the size of the thyroid nodule, the incidence rate of an insufficient result on US-FNAB and the mean total procedure time for 1126 thyroid nodules in 776 patients were measured as 16.9% (52/308) and 208 seconds for nodules under 0.5 cm, 9.8% (30/306) and 160 seconds for nodules between 0.5 cm-1.0 cm, and 6.0% (30/504) and 134 seconds for nodules over 1.0 cm. These 776 patients showed no significant complications, except for mild pain. In Group A, the incidence rate of an insufficient result was calculated as 15.1% (14/93) for the group with nodules under 0.5 cm, 5.3% (5/95) for the group with nodules between 0.5 cm-1.0 cm, 4.8% (6/125) for the group with nodules over 1.0 cm, and 8.0% (25/313) for the total A Group. In Group B, the incidence rate of an insufficient result was measured as 33.3% (15/45) for the group with nodules under 0.5 cm, 28.1% (25/89) for the group with nodules between 0.5 cm-1.0 cm, 21.4% (24/112) for the group with nodules over 1.0 cm, and 25.7% (63/245) for the total B group. There was a statistically significant correlation between the rate of an insufficient result and the peculiar smear technique or the size of the thyroid nodule. CONCLUSION: We consider that US-FNAB is very simple, safe and accurate diagnostic method for thyroid nodules, and US-FNAB with a peculiar smear technique is able to increase the diagnostic rate for thyroid nodules.
Biopsy, Fine-Needle* ; Humans ; Incidence ; Thyroid Diseases ; Thyroid Gland* ; Thyroid Nodule*

No abstract available.
Humans

BACKGROUND: Mad1 protein is known to repress Myc target genes and antagonize Myc function. We underwent this study to investigate the clinical implication of Mad1 expression in human breast cancer. MATERIALS AND METHODS: We performed immunohistochemical assay for Mad1 protein together with Myc in human brest cancer, along with tissues from normal and benign diseases. The data from protein assay were merged with clinical and biologic parameters of the patients. RESULTS: Of 66 patients with invasive ductal cancer, Mad1 expression was detected in 22(33.3%). Intensity and area of Mad1 expression significantly decreased in DCIS and invasive cancers while high levels of Mad1 expression were persistent in benign breast lesions. Mad1 expression was significantly reduced in poorly differentiated tumors(P<0.001). Expression of Mad1 was not associated with tumor size, lymph node status, and stage of the disease. We could not observe any correlation between S-phase and expression status of Myc or Mad1. Mad1 expression was closely linked to differentiation of the cancer cells and inversely correlated with Myc expression(P=0.042). In survival analysis, Mad1 possessed a prognostic significance to predict recurrence of the disease but not overall survival after CMF chemotherapy. CONCLUSIONS: In human breast cancer cells, expression of Mad1 seems to be downregulated while expression of Myc is amplified. Altered expression of Mad1 may play a role in malignant transformation of human mammary epithelial cells and represent an aggressive phenotype in human breast cancer.
Breast Neoplasms* ; Breast* ; Carcinoma, Intraductal, Noninfiltrating ; Drug Therapy ; Epithelial Cells ; Humans* ; Lymph Nodes ; Phenotype ; Prognosis ; Recurrence

BACKGROUND AND OBJECTIVES: Identification of coronary sites susceptible to progression or nonprogression might provide additional information to select medical or surgical treatment and furthermore for appropriate timing for percutaneous transluminal coronary angioplasty or coronary artery bypass graft. METHODS: We reviewed serial coronary arteriograms of 50 patients with coronary artery disease retrospectively. Patients were managed with standard treatment including anti-hypertensives, antiplatelets, lipid-lowering agents and other risk factor management by attending physician's decision. Patients who received percutaneous transluminal angioplasty, coronary artery bypass graft or thrombolysis were excluded. Cononary arteriographies were undertaken with average 33 months interval. Criteria for the progression and regression were the changes of the luminal diameter narrowing of the arterial segment by 20% or more reduction or increase, respectively. Results: Patients show progressive change, regressive change or no significant interval change in 50%, 12% and 30% of total 50 patients, respectively. Male gender, angiographic interval were the significant predictor of progressive change. In terms of coronary segment, stable segments are most frequent 52.2% (72/138) and progression in 40.2% (74/184), regression in 27.5% (38/138). Initial coronary lesions with low grade stenosis (less than 50%) have a tendency to progress than that of high grade stenosis (70% or more) Percentage diameter stenosis of new lesion are not related linearly with the interval between two sequential angiographies. CONCLUSION: Number of patients with progressive coronary arteriogram are more frequent than the patients with regressive change or no interval change. Progression and regression are frequent finding of serial coronary arteriography in usual clinical practice. Progression and regression are found frequently in the same patient at different coronary branches (16 patients). It suggested that the local factors may play an important role in the pathogenesis of coronary artery disease as well as systemic risk factors.
Angiography* ; Angioplasty ; Angioplasty, Balloon, Coronary ; Antihypertensive Agents ; Constriction, Pathologic ; Coronary Artery Bypass ; Coronary Artery Disease ; Humans ; Male ; Phenobarbital ; Retrospective Studies ; Risk Factors ; Transplants

The aim of the present study was to investigate the physiological role of nicotinamide phosphoribosyltransferase (NAMPT) associated with odontogenic differentiation during tooth development in mice. Mouse dental papilla cell-23 (MDPC-23) cells cultured in differentiation media were stimulated with the specific NAMPT inhibitor, FK866, and Visfatin (NAMPT) for up to 10 days. The cells were evaluated after 0, 4, 7, and 10 days. Cell viability was measured using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The mineralization assay was performed by staining MDPC-23 cells with Alizarin Red S solution. After cultivation, MDPC-23 cells were harvested for quantitative PCR or Western blotting. Analysis of variance was performed using StatView 5.0 software (SAS Institute Inc., Cary, NC, USA). Statistical significance was set at p < 0.05. The expression of NAMPT increased during the differentiation of murine odontoblast-like MDPC-23 cells. Furthermore, the up-regulation of NAMPT promoted odontogenic differentiation and accelerated mineralization through an increase in representative odontoblastic biomarkers, such as dentin sialophosphoprotein, dentin matrix protein-1, and alkaline phosphatase in MDPC-23 cells. However, treatment of the cells with the NAMPT inhibitor, FK866, attenuated odontogenic differentiation, as evidenced by the suppression of odontoblastic biomarkers. These data indicate that NAMPT regulated odontoblastic differentiation through the regulation of odontoblastic biomarkers. The increase in NAMPT expression in odontoblasts was closely related to the formation of the extracellular matrix and dentin via the Runx signaling pathway. Therefore, these data suggest that NAMPT is a critical regulator of odontoblast differentiation during tooth development.

Demethoxycurcumin (DMC), which is a curcuminoid found in turmeric, has anti-proliferative effects on cancer cells. However, the effect of DMC on osteosarcoma has not been established. The aim of this study was to examine the effects of DMC on cell growth and apoptosis induction in MG-63 human osteosarcoma cells. This study was investigated using 3-[4, 5-dimethylthiazol-2-yl]-2, 5 diphenyl tetrazolium bromid assay, Live/Dead cell assay, 4’, 6-diamidino-2-phenylindole staining, and immunoblotting in MG-63 cells. DMC induced MG-63 cell death in a dosedependent manner, with an estimated IC50 value of 54.4 μM. DMC treatment resulted in nuclear condensation in MG-63 cells. DMC-induced apoptosis in MG-63 cells was mediated by the expression of Fas and activation of caspase-8, caspase-3, and poly (ADP-ribose) polymerase. Immunoblotting results showed that Bcl-2 and Bcl-xL were downregulated, while Bax and Bad were upregulated by DMC in MG-63 cells. These results indicated that DMC inhibits cell proliferation and induces apoptotic cell death in MG-63 human osteosarcoma cells via the death receptormediated extrinsic apoptotic pathway and mitochondria-mediated intrinsic apoptotic pathway.

Demethoxycurcumin (DMC), which is a curcuminoid found in turmeric, has anti-proliferative effects on cancer cells. However, the effect of DMC on osteosarcoma has not been established. The aim of this study was to examine the effects of DMC on cell growth and apoptosis induction in MG-63 human osteosarcoma cells. This study was investigated using 3-[4, 5-dimethylthiazol-2-yl]-2, 5 diphenyl tetrazolium bromid assay, Live/Dead cell assay, 4’, 6-diamidino-2-phenylindole staining, and immunoblotting in MG-63 cells. DMC induced MG-63 cell death in a dosedependent manner, with an estimated IC50 value of 54.4 μM. DMC treatment resulted in nuclear condensation in MG-63 cells. DMC-induced apoptosis in MG-63 cells was mediated by the expression of Fas and activation of caspase-8, caspase-3, and poly (ADP-ribose) polymerase. Immunoblotting results showed that Bcl-2 and Bcl-xL were downregulated, while Bax and Bad were upregulated by DMC in MG-63 cells. These results indicated that DMC inhibits cell proliferation and induces apoptotic cell death in MG-63 human osteosarcoma cells via the death receptormediated extrinsic apoptotic pathway and mitochondria-mediated intrinsic apoptotic pathway.

The present study was carried out to investigate the effect of Arctigenin on cell growth and the mechanism of cell death elicited by Arctigenin were examined in FaDu human pharyngeal carcinoma cells. To determine the apoptotic activity of Arctigenin in FaDu human pharyngeal carcinoma cells, cell viability assay, DAPI staining, caspase activation analysis, and immunoblotting were performed. Arctigenin inhibited the growth of cells in a dose-dependent manner and induced nuclear condensation and fragmentation. Arctigenin-treated cells showed caspase-3/7 activation and increased apoptosis versus control cells. FasL, a death ligand associated with extrinsic apoptotic signaling pathways, was up-regulated by Arctigenin treatment. Moreover, caspase-8, a part of the extrinsic apoptotic pathway, was activated by Arctigenin treatments. Expressions of anti-apoptotic factors such as Bcl-2 and Bcl-xL, components of the mitochondria-dependent intrinsic apoptosis pathway, significantly decreased following Arctigenin treatment. The expressions of pro-apoptotic factors such as BAX, BAD and caspase-9, and tumor suppressor -53 increased by Arctigenin treatments. In addition, Arctigenin activated caspase-3 and poly (ADP-ribose) polymerase (PARP) induced cell death. Arctigenin also inhibited the proliferation of FaDu cells by the suppression of p38, NF-κB, and Akt signaling pathways. These results suggest that Arctigenin may inhibit cell proliferation and induce apoptotic cell death in FaDu human pharyngeal carcinoma cells through both the mitochondria-mediated intrinsic pathway and the death receptormediated extrinsic pathway.

Alpha-lipoic acid (ALA) is a naturally occurring antioxidant and has been previously used to treat diabetes and cardiovascular disease. However, the autophagy effects of ALA against oxidative stress-induced dopaminergic neuronal cell injury remain unclear. The aim of this study was to investigate the role of ALA in autophagy and apoptosis against oxidative stress in the SH-SY5Y human dopaminergic neuronal cell line. We examined SH-SY5Y phenotypes using the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assay (cell viability/proliferation), 4′,6-diamidino-2-phenylindole dihydrochloride nuclear staining, Live/Dead cell assay, cellular reactive oxygen species (ROS) assay, immunoblotting, and immunocytochemistry. Our data showed ALA attenuated hydrogen peroxide (H2O2)-induced ROS generation and cell death. ALA effectively suppressed Bax up-regulation and Bcl-2 and BclxL down-regulation. Furthermore, ALA increased the expression of the antioxidant enzyme, heme oxygenase-1. Moreover, the expression of Beclin-1 and LC-3 autophagy biomarkers was decreased by ALA in our cell model. Combined, these data suggest ALA protects human dopaminergic neuronal cells against H2O2-induced cell injury by inhibiting autophagy and apoptosis.