No abstract available.
Blister* ; Thoracotomy*

No abstract available.

PURPOSE: To evaluate the outcome of ductal carcinoma in situ (DCIS) patients who underwent surgery followed by radiation therapy (RT). MATERIALS AND METHODS: We retrospectively reviewed 106 DCIS patients who underwent surgery followed by postoperative RT between 1994 and 2006. Ninety-four patients underwent breast-conserving surgery, and mastectomy was performed in 12 patients due to extensive DCIS. Postoperative RT was delivered to whole breast with 50.4 Gy/28 fx. Tumor bed boost was offered to 7 patients (6.6%). Patients with hormonal receptor-positive tumors were treated with hormonal therapy. RESULTS: The median follow-up duration was 83.4 months (range, 33.4 to 191.5 months) and the median age was 47.8 years. Ten patients (9.4%) had resection margin <1 mm and high-grade and estrogen receptor-negative tumors were observed in 39 (36.8%) and 20 (18.9%) patients, respectively. The 7-year ipsilateral breast tumor recurrence (IBTR)-free survival rate was 95.3%. Resection margin (<1 or > or =1 mm) was the significant prognostic factor for IBTR in univariate and multivariate analyses (p < 0.001 and p = 0.016, respectively). CONCLUSION: Postoperative RT for DCIS can achieve favorable treatment outcome. Resection margin was the important prognostic factor for IBTR in the DCIS patients who underwent postoperative RT.
Breast ; Breast Neoplasms ; Carcinoma, Ductal* ; Carcinoma, Intraductal, Noninfiltrating* ; Estrogens ; Follow-Up Studies ; Humans ; Mastectomy ; Mastectomy, Segmental ; Multivariate Analysis ; Recurrence ; Retrospective Studies ; Survival Rate ; Treatment Outcome*

OBJECTIVES: Numerous studies have revealed the adverse health effects of acute and chronic exposure to particulate matter less than 10 mum in aerodynamic diameter (PM10). The aim of the present study was to examine the spatial distribution of PM10 concentrations and cardiovascular mortality and to investigate the spatial correlation between PM10 and cardiovascular mortality using spatial scan statistic (SaTScan) and a regression model. METHODS: From 2008 to 2010, the spatial distribution of PM10 in the Seoul metropolitan area was examined via kriging. In addition, a group of cardiovascular mortality cases was analyzed using SaTScan-based cluster exploration. Geographically weighted regression (GWR) was applied to investigate the correlation between PM10 concentrations and cardiovascular mortality. RESULTS: An examination of the regional distribution of the cardiovascular mortality was higher in provincial districts (gu) belonging to Incheon and the northern part of Gyeonggido than in other regions. In a comparison of PM10 concentrations and mortality cluster (MC) regions, all those belonging to MC 1 and MC 2 were found to belong to particulate matter (PM) 1 and PM 2 with high concentrations of air pollutants. In addition, the GWR showed that PM10 has a statistically significant relation to cardiovascular mortality. CONCLUSIONS: To investigate the relation between air pollution and health impact, spatial analyses can be utilized based on kriging, cluster exploration, and GWR for a more systematic and quantitative analysis. It has been proven that cardiovascular mortality is spatially related to the concentration of PM10.
Air Pollutants ; Air Pollution ; Gyeonggi-do ; Incheon ; Mortality* ; Particulate Matter ; Seoul ; Spatial Analysis*

OBJECTIVE: Malignant meningiomas are rare and have worse prognosis than benign meningiomas. We report our experience of a malignant meningioma and review relevant literature in an attempt to investigate the clinical features, treatment, and prognosis of these tumors. METHODS: Fifteen patients underwent surgical treatment for intracranial malignant meningiomas between year 1990 and 2012 in our institution. Anaplastic meningiomas were diagnosed in thirteen cases and papillary meningiomas in two. Fourteen patients (93.3%) received radiotherapy after surgical resection. All patients were followed regularly including clinical-neurological follow-up as well as magnetic resonance imaging. Progression was determined radiographically when there was more than 10% of mass volume increase or when there were onset or worsening of neurological symptoms not attributable to other causes. RESULTS: Six patients were male and nine were women, and their mean age was 56.9 years (range 36-78). The median follow-up was 54 months (range 3-246). According to our study result, the 5-year progression free survival rate of malignant meningiomas was 53.6%. There were 2 cases (13.3%) of postoperative complications. Recurrences were confirmed in 4 patients (26.7%) during follow-up, the median recurrence time was 35 months (range 12-61), and further procedures were performed. Two of the recurred patients were treated with radiosurgery after secondary tumor resection, and other two patients were treated with radiosurgery alone. There was no more recurred disease patients in the follow-up period after then. CONCLUSION: We report the outcomes of the aggressive surgery with radiation of malignant meningiomas. Although the data is limited, we found that radiosurgery treatment had favorable tumor control on recurred patients from our experience.
Disease-Free Survival ; Female ; Follow-Up Studies ; Humans ; Magnetic Resonance Imaging ; Male ; Meningioma* ; Postoperative Complications ; Prognosis ; Radiosurgery ; Radiotherapy ; Recurrence

As a cause of spinal cord compression, intramedullary spinal tuberculoma with central nervous system (CNS) involvement is rare. Aurthors report a 66-year-old female presented with multiple CNS tuberculomas including spinal intramedullary tuberculoma manifesting paraparesis and urinary dysfunction. We review the clinical menifestation and experiences of previous reported literature.
Aged ; Central Nervous System ; Female ; Humans ; Paraparesis ; Spinal Cord Compression ; Tuberculoma ; Tuberculoma, Intracranial ; Tuberculosis

BACKGROUND: Although an oxidants and antioxidants imbalane has been considered in the pathogenesis of chronic obstructive pulmonary disease (COPD), there is a paucity of reports focussing on the smoking-induced changes of oxidants and antioxidants in COPD. METHOD: The concentration of antioxidants (ascorbic acid, uric acid, retinol, and α- &γ-tocopherol) was measured in the serum and induced sputum of 30 healthy controls and 34 stable COPD patients using high performance liquid chromatography (HPLC). The inhibition of lipid peroxidation as an index of antioxidant capacity was measured in the serum by a TBA assay. RESULTS: The serum concentration of ascorbic acid, α-tocopherol, and retinol were significantly lower in the patients with COPD than in healthy controls (484.8±473.3 vs 1497.8±819.2 pmol/L, p<0.001, 48.38±17.34 vs 73.96±26.29 pmol/L, p<0.001, and 9.51±8.33 vs 15.01±5.88 pmol/L, p<0.05, respectively, mean±SD). However, there were little differences in the ascorbic acid and uric acid concentrations in the induced sputum between the COPD patients and the controls. The induced sputum to serum ratio of ascorbic acid was significantly higher in COPD patients compared with healthy control (0.375 vs 0.085, p<0.05). In the normal controls, the serum ascorbic acid concentration was lower in smokers than in nonsmokers (1073±536 vs 1757±845 pmol/L, p<0.05), but the level was still higher than that of the COPD patients (p<0.05). The serum retinol levels were correlated with FEV1 in COPD patients (r=0.58, p<0.05). The products of lipid peroxidation were increased in normal smokers and COPD compared with normal nonsmokers (115.56±19.93 and 120.02±24.56 vs 91.87±20.71 µmol/µmol Pi of liposome, p<0.05). CONCLUSION: Cigarette smoking may induce the depletion of serum antioxidants and this depletion of antioxidants is suggested to play a role in the pathogenesis of COPD.
Antioxidants* ; Ascorbic Acid ; Chromatography, Liquid ; Humans ; Lipid Peroxidation ; Liposomes ; Oxidants ; Pulmonary Disease, Chronic Obstructive* ; Smoking ; Sputum* ; Uric Acid ; Vitamin A

To examine the impact of lactate dehydrogenase (LDH) as an early marker of ventilator-induced lung injury (VILI) and the effect of prone position during the VILI, we ventilated 28 normal white rabbits (10 supine, 10 prone, 8 controls) for 6 hr or until PaO2/FIO2 ratio was<200 mmHg. We applied an identical injurious ventilatory pattern (peak inspiratory pressure of 35 cmH2O with a PEEP of 3 cmH2O, I:E ratio of 1:2, and FIO2 of 0.40) in the supine and prone group. VILI was assessed by oxygenation, gravimetric analysis and histologic grading. Serum levels of LDH progressively increased significantly during the VILI (supine and prone groups) as compared with controls. There was a significant negative correlation between oxygenation and LDH levels (r=-0.619, p<0.001). Wet weight/dry weight ratios (WW/DW) and histologic scores for dependent regions were significantly higher in the supine than the prone group. There were no differences in WW/DW and histologic scores for nondependent regions between the supine and prone group. These findings suggest that serum LDH levels might be an early marker of severity of lung injury. The prone position resulted in a less severe and more homogenous distribution of VILI.
Animals ; Blood Pressure ; L-Lactate Dehydrogenase/*blood ; Lung/metabolism/pathology ; Oxygen/blood ; Prone Position ; Rabbits ; Respiration, Artificial/*adverse effects ; Respiratory Distress Syndrome, Adult/*blood/*etiology/pathology ; Support, Non-U.S. Gov't

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.

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.