• Journal of Gastric Cancer
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• v.4 no.3
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• pp.156-163
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• 2004

Purpose: While E-cadherin in normal cells induces calciumdependent cell-cell adhesion, in malignant cell, it plays a role in invasion and metastasis with a reduction of adhesion. Serum soluble E-cadherin is a result of the reduction of the cellular E-cadherin molecule and is found in the circulation of normal individuals, but it is particularly known to be increased in patients with malignancies. Accordingly, through checking the level of serum soluble E-cadherin in patients with gastric cancer and analyzing it in the view of clinicopathology, we investigated whether serum soluble E-cadherin could be translated into a clinicopathologic esult and used as a tumor marker. Materials and Methods: The investigation targeted 88 patients who had been diagnosed as having gastric cancer by the Department of Surgery, St. Mary's Hospital, from October 1, 2002, to July 30, 2003, and who had under gone performed surgery. We measured the level of preoperative serum E-cadherin in the 88 patients by unsing ELISA. Among them, we collected gastric cancer tissues from 54 patients and executed immunohistochemistry for E-cadherin. The samples were compared with normal tissues in terms of both serum E-cadherin level and immunohistochemistry level, as well as with other clinicopathologic factors. Result: The mean serum E-cadherin level of the 88 patients was 4368.7 ng/ml and was significantly higher than the level in 12 normal control patients, 3335.5 ng/ml (P=0.016). In terms of clinicopathology, the serum level of E-cadherin was significantly correlated with increasing age (P=0.0006) and was higher in positive venous invasion patients (P=0.0005). When the E-cadherin immunohistochemical stain was compared with the serum E-cadherin level in 54 patients, no significant statistically meaningful result was obtained (P=0.2881). However, 4 patients with serum E-cadherin levels about 6000 ng/ml were classified into the lower expression group ($<80\%$ of E-cadherin immunohistochemicals stain. In the analysis for 36 patients who were early gastric cancer patients, the serum E-cadherin level in lymph-node-metastatic patients was higher than it was in the other patients (P=0.0442). Conclusion: The serum E-cadherin level in gastric cancer patients was higher than the level in normal control patients. In advanced gastric cancer patients, that the difference was increased. Also, since the E-cadherin level correlated with the serum E-cadherin level with venous invasion, it can be used as an effective tumor marker for gastric cancer. Particularly, in that the serum E-cadherin level correlated with lymph node metastasis in early gastic cancer, it can be used when a therapeutic method for early gastric cancer is selected.

• Journal of Gastric Cancer
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• v.9 no.4
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• pp.172-176
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• 2009

Purpose: The rapid urease test is a rapid and reliable method for diagnosing Helicobacter pylori infection. However it requires gastric mucosal biopsies during endoscopy, and the test is not covered by national health insurance for patients with gastric cancer. So, we introduced an alternative method for a rapid urease test using back-table gastric mucosal biopsies from gastrectomy specimen. Materials and Methods: Ninety gastric cancer patients underwent an anti H. pylori IgG ELISA test and gastrectomy. Just after gastrectomy, two gastric mucosal biopsies from the prepyloric antrum and lower body of the gastrectomy specimen were taken from the back table in the operative room, and these were fixed immediately with the rapid urease test kit, and the color change was monitored for up to 24 hours. In this study, H. pylori infection was defined as positive when the serology or rapid urease test showed positive results. Results: The positive rate of the rapid urease test and serology was 91.1% and 77.8%, respectively. The sensitivity, specificity, positive predictive value and negative predictive value of the rapid urease test and serology were 94.3 and 80.5%, 100 and 100%, 100 and 100%, and 37.5 and 15%, respectively. The accuracy of the rapid urease test was higher than that of serology (94.4 vs. 81.1%, respectively). The rapid urease test showed a higher rate of detecting H. pylori infection than that of serology (McNemar's test, P=0.019). Conclusion: The result of the rapid urease test using back-table gastric mucosal biopsies from a gastrectomy specimen is comparable to the reference data of the conventional rapid urease test using gastric mucosal endoscopic biopsies. Therefore, it can be an alternative diagnostic method for H. pylori infection.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.32 no.3
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• pp.218-228
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• 2010

Components of dental resin-based restorative materials are reported to leach from the filling materials even after polymerization. Hydroquinone (HQ) is one of the major monomers used in the dental resin and is known as a carcinogen. Thus, carcinogenic risk of HQ leaching from the dental resin becomes a public health concern. The present study attempted to examine the carcinogenic potentials of HQ on the human epithelial cell, which is the target cell origin of the most of oral cancers. Cytotoxicity of HQ was observed above 50${\mu}M$ as measured by LDH assay, indicating a relatively low toxicity of this substance in human epithelial cells. The parameters of neoplastic cellular transformation such as cell saturation density, soft agar colony formation and cell aggregation were analyzed to examine the carcinogenic potential of HQ. The study showed that 2-week exposure of HQ showed the tendency of increase in the saturation density and the significant enhancement of soft agar colony formation at the highest dose, 50 ${\mu}M$ only. It is suggested that HQ has a weak potential of carcinogenicity. When cells were treated with HQ and TPA, a well-known tumor promoter, the parameters of neoplastic cellular transformation was significantly increased. This result indicates that the potential risk of carcinogenicity from HQ is largely dependent upon the presence of promoter. Exposure of 50 ${\mu}M$ HQ increased the time-dependent apoptosis as measured by the ELISA kit. This concentration coincides with a dose of neoplastic transformation, indicating a possible link between apoptosis and HQ-induced cellular transformation. Hydroquinone generated Reactive Oxygen Species (ROS) which was evidenced by the treatment of antioxidants such as trolox and N-acetyl cysteine and the GSH depleting agent, BSO. Antioxidants blocked the generation of ROS and the GSH depleting agent, BSO dramatically increased the ROS production. Since HQ is known to increase ROS production thru activation of transcriptional factor such as c-Myb and Pim-1, it is speculated that ROS generation by HQ plays a role in the activation of oncogene, which may lead to neoplastic transformation. In addition, ROS is involved in the alteration of signal transduction, which regulates the apoptosis in many cellular systems. Thus, ROS-mediated apoptosis may be involved in the HQ-induced carcinogenic processes. Protein kinase C (PKC) is known to play pivotal roles in neoplastic transformation of cells and its high expression is often found in a variety of types of tumors including oral cancer. PKC translocation of PKC-${\alpha}$ was observed following HQ exposure. Altered signaling system may also play a role in the transformation process. Taken together, HQ leached from the dental resin does not pose a significant threat as a cancer causing agent, but its carcinogenic potential can be significantly elevated in the presence of promoter. The mechanism of HQ-induced carcinogenesis involved ROS generation, apoptosis and altered signaling pathway. The present study will provide a valuable data to estimate the potential risk of HQ as a carcinogen and understand mechanism of HQ-induced carcinogenesis in human epithelial cells.

• Journal of the Korean Society of Food Science and Nutrition
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• v.43 no.10
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• pp.1510-1518
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• 2014

This study investigated the effects of calcium citrate on papain-induced osteoarthritis in C57BL/6J mice. Osteoarthritis was induced by injecting $6{\mu}L$ of papain into the knee joints of mice. Calcium citrate was made by crushing the centrifuged precipitate after reacting 0.5 M citric acid with 1 kg of oyster shell extract. The mice were divided into five groups (n=8). The normal group was untreated, whereas the papain group was induced to have osteoarthritis and treated with $200{\mu}L$ of water per day. The papain+DS group was treated with diclofenac sodium. The papain+calcium citrate groups were treated with calcium citrate at 150 and 300 mg/kg/bw for 28 days. Proteoglycan contents in articular cartilages were measured by safranin O/fast green staining and hematoxylin & eosin staining. Histopathological changes in cartilages were analyzed by the Rudolphi score approach. Contents of pro-inflammatory cytokines including TNF-${\alpha}$, IL-$1{\beta}$ and IL-6 in plasma, were measured by the ELISA method. Body weights among the treated groups were not significantly different compared with that of the normal group. Cartilage loss and joint instability in the calcium citrate group improved significantly (P<0.05) in a dose-dependent manner compared with the papain group. Further, proteoglycan content of the calcium citrate group was considerably (P<0.05) higher than that of the papain group. Osteoarthritis scores in the calcium citrate group were considerably (P<0.05) reduced compared with the papain group. In the group treated with calcium citrate, contents of TNF-${\alpha}$, IL-$1{\beta}$ and IL-6 in plasma were significantly (P<0.05) reduced in a dose-dependent manner in comparison with the normal group. Based on these results, we suggest that calcium citrate is effective for treatment of osteoarthritis.

• Journal of Gastric Cancer
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• v.5 no.4 s.20
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• pp.238-245
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• 2005

Purpose: Ghrelin, produced primarily in the gastrointestinal tract, including the stomach, has been reported to reflect nutritional status and to control homeostasis by influencing food intake and adiposity. The purpose of this study is to evaluate nutritional status, as well as plasma and gastric tissue ghrelin levels, in patients with gastric cancer who underwent a gastrectomy. Materials and Methods: Eighty patients were analyzed by the degree of weight loss $(weight\;loss{\geq}5%\;or\;<5%)$ and the extent of gastrectomy (subtotal or total gastrectomy). Blood samples were collected from all patients preoperatively and postoperatively especially at seven days. Gastric tissues, including tumor and normal tissues, were obtained from the resected stomach. levels of plasma and tissue ghrelin were measured with a commercial ELISA kit. Results: There were no significant differences in the clinical characteristics and ghrelin levels of plasma, gastric tumor tissue and normal tissue by the degree of weight loss. The ghrelin levels in plasma and tumor tissue showed no correlations with each other while the ghrelin level in tumor tissue was significantly lower than that in normal tissue. The degree of cellular differentiation also had an association with ghrelin production. A gastrectomy proved to decrease significantly plasma ghrelin levels, body mass index, and biochemical markers, regardless of the extent of gastric resection. Conclusion: These results show that gastric cancer affects the production of ghrelin in the gastric mucosa and that ghrelin is mainly produced in stomach even though it could be partially covered by endogenous ghrelin from other organs following a gastrectomy. However, we should further investigate which other factors have an impact on energy consumption, ghrelin secretion, and changes in ghrelin levels after a gastrectomy.

• Tuberculosis and Respiratory Diseases
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• v.52 no.4
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• pp.338-345
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• 2002

Background : Coal workers' pneumoconiosis(CWP) is a fibrotic lung disease resulting from the chronic inhalation of coal dust. Various cytokines and growth factors secreted from macrophages and monocytes play a key role in the pathogenesis of pneumoconiosis. The platelet-derived growth factor (PDGF)-BB and the insulin-like growth factor(IGF)-1 secreated from the macrophages and monocytes are believed to stimulate the accumulation of mesenchymal cells and fibrosis of the lower respiratory tract that is observed in fibrotic lung disease. The serum concentraion of PDGF-BB and IGF-1 in 30 CWP patients and 10 healthy controls were measured in order to determine if PDGF-BB and IGF-1 can be used as sensitive biomarkers in CWP. Method : Serum was collected from 30 patients with CWP(13 with simple CWP and 17 with complicated CWP) and 10 healthy controls. The serum concentrations of PDGF-BB and IGF-1 were measured using ELISA (R&D system, Minneapolis, MN). Results : The serum PDGF-BB concentration in patients with complicated CWP($10083.76{\pm}639.07pg/mL$) was significantly higher than in the patients with simple CWP ($8493.88{\pm}848.51pg/mL$) and the healthy controls ($3726.17{\pm}292.20pg/mL$) (p<0.05). Compared to the healthy controls ($413.40{\pm}1.94ng/mL$), there was no significant difference in the serum IGF-1 concentration in patients with simple ($366.77{\pm}183.67ng/mL$) and complicated CWP ($403.18{\pm}15.39ng/mL$) (p>0.05). Conclusion : These results show the important role of the PDGF-BB mediated pathways in the pathogenesis of CWP. These data suggests that the PDGF-BB serum concentration is a useful biomarkers of the fibrotic extent in CWP patients.

• Tuberculosis and Respiratory Diseases
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• v.60 no.3
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• pp.297-303
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• 2006

Background : Pulmonary tuberculosis is frequently accompanied with complications such as bronchiectasis, cavities, fibrosis and a deterioration of the lung function. However, there is little information available on the pathogenesis of these complications in pulmonary tuberculosis. Among the many factors involving in tissue remodeling, transforming growth factor-${\beta}1$ ($TGF-{\beta}1$) is a potent stimulus of the extracellular matrix fomation and a mediator of potential relevance for airway wall remodeling. Therefore, this study examined the relationship between the radiological changes and the $TGF-{\beta}1$ level in patients with pulmonary tuberculosis. Methods : Serum and bronchoalveolar lavage fluid (BALF) were collected from total of 35 patients before treating them for active pulmonary tuberculosis, and the $TGF-{\beta}1$ levels were measured using an enzyme-linked immunosorbent assay (ELISA). The BALF levels were recalculated as the epithelial lining fluid (ELF) levels using the albumin method. pulmonary function test (PFT) and high resolution computed tomography (HRCT) were performed before and after treatment. Results : There was a strong correlation between the serum $TGF-{\beta}1$ level and the presence of cavities (r=0.404, p=0.006), even though the BAL $TGF-{\beta}1$ level showed a weak correlation with complications. In addition, there was no correlation between the $TGF-{\beta}1$ levels before treatment and the changes in the PFT and HRCT during treatment. Conclusion : There is a correlation between the serum $TGF-{\beta}1$ level and cavity formation in pulmonary tuberculosis before treatment. However, further study will be needed to confirm this.

• Tuberculosis and Respiratory Diseases
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• v.60 no.3
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• pp.330-336
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• 2006

Background : Aquaporins (AQPs) may play a role in the pathogenesis of pulmonary inflammation and edema. This study investigated the role ofAQPs in acute lung injury following bleomycin inhalation in rats. Methods : Sprague-Dawley rats were treated via inhalation with 10 U/kg bleomycin hydrochloride dissolved in 5 ml of normal saline. The control rats were treated with 5 ml normal saline. The animals (n = 6-8 rats per group) were sacrificed at 4, 7, and 14 d. The changes in AQP1, AQP4, and AQP5 expression levels over time were analyzed by Western blotting. The nitrate and nitrite concentrations in the bronchoalveolar lavage fluid (BALF) were measured using a modified Griess reaction. ELISA was used to check cytokines. Results : The respiration rates were significantly higher 4 and 7 days after the bleomycin treatment compared with those of the control rats. The tidal volume was lower in rats at 4 days after the bleomycin treatment, and the wet/dry weights of the lung were significantly higher than those of the control group. The nitrite and nitrate concentrations in the BALF from the rats at 4 days after exposure to bleomycin were greater than those from the saline-treated rats. Immunoblotting studies demonstrated that the AQP1 and AQP4 expression levels were lower in the rats at 4 days. However, the AQP4 expression level was higher at 7 days. The AQP5 expression level increased at 4, 7 and 14 days after the bleomycin treatment. Conclusion : This study demonstrates that AQPs are expressed differently in bleomycin-induced pulmonary edema.

• Tuberculosis and Respiratory Diseases
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• v.66 no.6
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• pp.451-456
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• 2009

Paragonimiasis is a parasitic infection that occurs following the ingestion of infectious Paragonimus metacercariae, which occurs as a result of eating raw or undercooked freshwater crabs or crayfish. Pulmonary paragonimiasis is the most common clinical manifestation of this infection. Human paragonimiasis occurs sporadically. We experienced a case of pulmonary paragonimiasis in a 35-year-old woman with left lower chest pain. The patient had hypereosinophilia and a pleural effusion. The diagnosis was confirmed by positive ELISA (Enzyme-linked immunosorbent assay) that detected Paragonimiasis westermani antibody in the serum. We treated the patient with praziquantel for two days at a daily dosage of 75 mg/kg. Left pleuritic pain and pleural effusion improved after treatment. However, similar symptoms and pleural effusion developed recurrently for the first 3 courses of treatment with praziquantel. Upon the fourth round of treatment, the patient made a full recovery.

• Tuberculosis and Respiratory Diseases
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• v.66 no.6
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• pp.444-450
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• 2009

Background: Biomarkers for cancer have several potential clinical uses, including the following: early cancer detection, monitoring for recurrence prognostication, and risk stratification. However, no biomarker has been shown to have adequate sensitivity and specificity. Many investigators have tried to validate biomarkers for the early detection and recurrence of lung cancer. To evaluate plasma G-CSF as such a biomarker, protein levels were measured and were found to correlate with the clinicopathological features of primary lung tumors. Methods: Between December 2006 and May 2008, 100 patients with histologically-validated primary lung cancer were enrolled into this study. To serve as controls, 127 healthy volunteers were enrolled into this study. Plasma G-CSF levels were measured in lung cancer patients using the sandwich ELISA system (R & D inc.) prior to treatment. Results: The mean plasma G-CSF levels were 12.2$\pm$0.3 pg/mL and 46.0$\pm$3.8 pg/mL (mean$\pm$SE) in the normal and in the cancer groups, respectively. In addition, plasma G-CSF levels were higher in patients with early lung cancer than in healthy volunteers (p<.001). Plasma G-CSF levels were higher in patients who were under 65 years old or smokers. Within the cancer group, plasma G-CSF levels were higher in patients with non small cell lung cancer than in patients with small cell lung cancer (p<.05). Overall, plasma G-CSF levels were shown to increase dependent upon the type of lung cancer diagnsosed. In the order from highest to lowest, the levels of plasma G-CSF tended to decrease in the following order: large cell carcinoma, squamous cell carcinoma, adenocarcinoma, and bronchioloalveolar carcinoma. Plasma G-CSF levels tended to be higher in patients with advanced TNM stage than in localized TNM stage (I, II