• Asian Pacific Journal of Cancer Prevention
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• v.15 no.1
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• pp.467-474
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• 2014

Objective: To observe the effects of allogeneic and autologous transfusion on cellular immunity, humoral immunity and secretion of serum inflammatory factors and perforin during the perioperative period in patients with malignant tumors. Methods: A total of 80 patients (age: 38-69 years; body weight: 40-78 kg; ASA I - II) receiving radical operation for gastro-intestinal cancer under general anesthesia were selected. All the patients were divided into four groups based on the methods of infusion and blood transfusion: blank control group (Group C), allogeneic transfusion group (group A), hemodiluted autotransfusion Group (Group H) and hemodiluted autotransfusion + allogenic transfusion Group (A+H group). Venous blood was collected when entering into the surgery room ($T_0$), immediately after surgery ($T_1$) and 24h ($T_2$), 3d ($T_3$) and 7d ($T_4$) after surgery, respectively. Moreover, flow cytometry was applied to assess changes of peripheral blood T cell subpopulations and NK cells. Enzyme linked immunosorbent assays were performed to determine levels of IL-2, IL-10, TNF-${\alpha}$ and perforin. Immune turbidimetry was employed to determine the changes in serum immunoglobulin. Results: Both CD3+ and NK cells showed a decrease at $T_1$ and $T_2$ in each group, among which, in group A, CD3+ decreased significantly at $T_2$ (P<0.05) compared with other groups, and CD3+ and NK cell reduced obviously only in group A at $T_3$ and $T_4$ (P<0.05). CD4+ cells and the ratio of D4+/CD8+ were decreased in groups A, C and A+H at $T_1$ and $T_2$ (P<0.05). No significant intra- and inter-group differences were observed in CD8+ of the four groups (P<0.05). IL-2 declined in group C at $T_1$ and $T_2$ (P<0.05) and showed a decrease in group A at each time point (P<0.05). Moreover, IL-2 decreased in group A + H only at $T_1$. No significant difference was found in each group at $T_1$ (P<0.05). More significant decrease in group ?? at $T_2$, $T_3$ and $T_4$ compared with group A (P<0.05), and there were no significant differences among other groups (P>0.05). IL-10 increased at $T_1$ and $T_2$ in each group (P<0.05), in which it had an obvious increase in group A, and increase of IL-10 occurred only in group A at $T_3$ and $T_4$ (P<0.05). TNF-${\alpha}$ level rose at $T_1$ (P<0.05), no inter- and intra-group difference was found in perforin in all groups (P<0.05). Compared with the preoperation, both IgG and IgA level decreased at $T_1$ in each group (P<0.05), and they declined only in Group A at $T_2$ and $T_3$ (P<0.05), and these parameters were back to the preoperative levels in other groups. No significant differences were observed between preoperative and postoperative IgG and IgA levels in each group at $T_4$ (P>0.05). No obvious inter- and intra-group changes were found in IgM in the four groups (P>0.05). Conclusions: Allogeneic transfusion during the perioperative period could obviously decrease the number of T cell subpopulations and NK cells and the secretion of stimulating cytokines and increase the secretion of inhibiting cytokines in patients with malignant tumors, thus causing a Th1/Th2 imbalance and transient decreasing in the content of plasma immune globulin. Autologous transfusion has little impact and may even bring about some improvement oo postoperative immune function in patients with tumors. Therefore, cancer patients should receive active autologous transfusion during the perioperative period in place of allogeneic transfusion.

• Clinical and Experimental Pediatrics
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• v.46 no.3
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• pp.284-290
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• 2003

Purpose : A new airway inflammatory marker, exhaled nitric oxide(ENO) has been reported to correlate with bronchial hyperresponsiveness(BHR) and atopy. The purpose of this study was to analyze the relationship of ENO with BHR or atopy in patients with asthma and with allergic rhinitis. Methods : The subjects consisted of 55 children with asthma, 17 with allergic rhinitis, and 14 healthy controls. The asthma group was subdivided into the atopic asthma group(n=37) and the nonatopic asthma group(n=18) and the allergic rhinitis group into BHR group(n=7) and non-BHR group(n=10). All were investigated with spirometry and measurements of ENO concentration. The correlations between ENO concentration and both methacholine $PC_{20}$(provocative concentration causing a 20% decrease in forced expiratory volume in one second) and the number of allergen skin test positivity were analyzed. Results : ENO concentrations of both asthma and allergic rhinitis groups were significantly greater than that of control(P<0.01). ENO concentration of atopic asthma was significantly greater than that of nonatopic asthma(P<0.01). In allergic rhinitis, ENO concentration did not differ according to the presence or absence of BHR(P=0.50). ENO concentrations correlated significantly with the number of skin test positivity(r=0.32, P=0.02) or methacholine $PC_{20}$(r=-0.38, P<0.01) in asthma group, but not in the allergic rhinitis group(r=0.42, P=0.09; r=-0.06, P=0.83). Conclusion : In asthma patients, some pathogenetic mechanisms associated with atopy and BHR seem to influence ENO concentration. In allergic rhinitis patients, some factors other than BHR may be important in determining ENO concentration.

• Tuberculosis and Respiratory Diseases
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• v.62 no.4
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• pp.299-307
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• 2007

Background: High mobility group box 1 (HMGB1) is a novel, late mediator of inflammation. This study compared the pro-inflammatory effects of LPS and HMGB1. The transcriptional factors that play an important role in mediating the HMGB1-induced stimulation of IL-8 were also evaluated. Methods: RAW264.7 cells were stimulated with either LPS (100 ng/ml) or HMGB1 (500 ng/ml). The $TNF-{\alpha}$, MIP-2 and $IL-1{\beta}$ levels in the supernatant were evaluated by ELISA at 0, 2, 4, 8, 12 and 24h after stimulation. An acute lung injury was induced by an injection of LPS (5 mg/kg) or HMGB1 (2.5 mg/kg) into the peritoneum of the Balb/c mice. The lung cytokines and MPO activity were measured at 4h (for LPS) or 24h (for HMGB1) after the injection. The transcriptional factor binding sites for NF-IL6, $NF-{\kappa}B$ and AP-1 in the IL-8 promoter region were artificially mutated. Each mutant was ligated with pIL-6luc and transfected into the RAW264.7 cells. One hour after stimulation with HMGB1 (500 ng/ml), the cell lysate was analyzed for the luciferase activity. Results: The expression of MIP-2, which peaked at 8h with LPS stimulation, increased sequentially until 24h after HMGB1 stimulation. An intraperitoneal injection of HMGB1, which induced a minimal increased in $IL-1{\beta}$ expression, provoked the accumulation of neutrophils the lung. A mutation of AP-1 as well as $NF-{\kappa}B$ in the IL-8 promoter region resulted in a lower luciferase activity after HMGB1 stimulation. Conclusion: The proinflammatory effects of HMGB1, particularly on IL-8, are mediated by both $NF-{\kappa}B$ and AP-1.

• Clinical and Experimental Pediatrics
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• v.51 no.5
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• pp.492-499
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• 2008

Purpose : Helicobacter pylori infection is one of the most common gastrointestinal infections worldwide; it almost invariably causes chronic gastritis. Pediatric studies may provide important insights into the mucosal immune response of H. pylori-infection, as children are not submitted to environmental factors such as alcohol, tobacco and anti-inflammatory medication. The aim of the present study was to investigate the mucosal immune response against H. pylori in clinically well-defined groups: H. pylori-positive (divided into peptic ulcer disease and gastritis) and H. pylori-negative control. Methods : Antral biopsies were obtained from 45 children undergoing an upper GI endoscopy for dyspeptic symptoms. T cells (CD3+, CD4+, CD8+) and B cells (CD20+) were analyzed by quantitative immunohistochemistry. The correlation of lymphocyte subsets of gastric mucosa with histology was evaluated. Results : T cells (CD3+, CD4+, CD8+) and B cells (CD20+) were significantly increased in the lamina propria of H. pylori-positive group (P<0.01). CD8+ T cells were significantly increased in the lamina propria of the H. pylori-positive peptic ulcer disease (P<0.01). Within the epithelium, only CD4+ T cells were significantly increased in the H. pylori-positive group (P<0.01). Gastric histological parameters had a closer correlation with lymphocytes in the lamina propria than intraepithelial lymphocytes. Conclusion : This study suggests that both T cells and B cells in the lamina propria play important roles in the local immune response of H. pylori-infected children. Furthermore, it remains to be elucidated whether CD8+ T cells in the lamina propria may contribute to peptic ulcer formation in H. pylori-infected children.

• Journal of Life Science
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• v.17 no.8 s.88
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• pp.1090-1099
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• 2007

Myristicin, l-allyl-3,4-methylenedioxy-5-methoxybenzene, was one of the major essential oils of nutmeg. However, its anti-allergic effect in the Th1/Th2 immune response was poorly understood. Recently, it was shown that T-bet and GATA-3 was master Th1 and Th2 regulatory transcription factors. In this study, we have attempted to determine whether myristicin regulates Th1/Th2 cytokine production, T-bet and GATA-3 gene expression in ovalbumin (OVA)-induced asthma model mice. Myristicin reduced levels of IL-4, Th2 cytokine production in OVA-sensitized and challenged mice. In the other side, it increased $IFN-{\gamma}$, Th1 cytokine production in myristicin administrated mice. We also examined to ascertain whether myristicin could influence eosinophil peroxidase (EPO) activity. After being sensitized and challenged with ovalbumin (OVA) showed typical asthmatic reactions. These reactions included an increase in the number of eosinophils in bronchoalveolar lavage fluid, an increase in inflammatory cell infiltration into the lung tissue around blood vessels and airways, and the development of airway hyper-responsiveness (AHR). The administration of myristicin before the last airway OVA challenge resulted in a significant inhibition of all asthmatic reactions. Accordingly, these findings provide new insight into the immunopharmacological role of myristicin in terms of its effects in a murine model of asthma.

• Journal of Life Science
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• v.19 no.12
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• pp.1802-1807
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• 2009

Platycodin D, a major component of Platycodi radix, is known to have various activities including anti-inflammatory, anti-hyperlipidemic, anti-tumor activities and others. Recently, it was reported that platycodin D inhibits fat accumulation and adipogenesis. The aim of this study was to investigate whether various adipogenic regulators are modulated by platycodin D treatment during the adipogenesis of 3T3-L1 cells. mRNA levels of terminal markers of adipogenesis such as ADIPOQ (adiponectin) and GLUT (glucose transporter) 4, which were quantified by real time PCR, were decreased by platycodin D treatment. mRNA expression of PPAR (peroxisome proliferator-activated receptor) $\gamma$ and C/EBP (CCAAT/enhaner binding protein) $\alpha$, which are central transcription factors of adipogenesis, were also decreased by platycodin D treatment. To elucidate the detailed molecular mechanism of platycodin D-induced inhibition of adipogenesis, we analyzed mRNA expression of upstream regulators of PPAR$\gamma$ and C/EPB$\alpha$. mRNA levels of the pro-adipogenic regulators, KROX20 and KLF (Kruppel-like factor) 15 were markedly down-regulated by platycodin D treatment. On the other hand, mRNA expression of CHOP (C/EBP homologous protein), an anti-adipogenic regulator, was significantly up-regulated by platycodin D treatment. mRNA levels of other pro-adipogenic regulators, C/EBP$\beta$ and C/EPB$\delta$, were not affected by platycodin D treatment, and another anti-adipogenic regulator, C/EBP$\gamma$ was also not affected by platycodin D treatment. Taken together, these results suggest that platycodin D-induced inhibition of adipogenesis is mediated by gene interactions including the down-regulation of pro-adipogenic regulators, KROX20 and KLF15, and the up-regulation of an anti-adipogenic regulator, CHOP.

• Journal of the korean academy of Pediatric Dentistry
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• v.32 no.4
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• pp.628-633
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• 2005

Deep caries in primary molars without early intervention frequently induce a pulpal disease and consequent furcation lesion with fistulous openings Up to now, majority of the textbooks on pediatric dentistry and literatures have described that extraction of the inflicted teeth is indicated for these cases and in reality these teeth have usually been extracted in the dental clinics. However when we recognize the excellent capacity of bone regeneration in children and the presence of numerous accessory canals at furcation areas, the removal of infection source in pulp by pulpectomy and inflammatory granulation tissues at furcation areas by furcal curettage might open the possibility of rapid healing at the furcation regions. In this report, 10 cases of primary molars in 3 to 6-year-old children with fistulous openings and furcation lesions in moderate size of 2 to 4mm in depth radiolucency at furcation lesion have been chosen. After pulpectomy and furcal curettage, evident bone regeneration was detected radiographically in all cases. Through the cases, we came to realize that all the cases previously described are not the indications of extraction and this approach could make many cases with pulp and furca combined lesions survive and remain healthy in the children's dental arches. However, in order for this approach to acquire objective appropriateness, it is thought that more scrupulous evaluation is desirable on the various factors regarding the indication such as the extent of furcation lesions, absorption status of teeth, amount of covering bone on succeeding teeth and so on.

• Tuberculosis and Respiratory Diseases
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• v.50 no.2
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• pp.171-181
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• 2001

Background : Angiogenesis is an essential process for the growth and metastatic ability of solid tumors. One of the key factors known to be capable of stimulating tumor angiogenesis is the vascular endothelial growth factor (VEGF). The serum VEGF concentration has been shown to be a useful parameter related to the clinical features and prognosis of lung cancer and has been recently applied to a the malignant pleural effusion showing a correlation with the biochemical parameters. The VEGF has been shown to play a role in the inflammatory diseases, but rarely in the tuberculosis (TB). The serum and pleural fluid VEGF levels were measured in patients with lung cancer and TB. Their relationship with the clinical and laboratory parameters and repeated measurement 3 months after various anticancer treatments were evaluated to assess the utility of the VEGF as a tumor marker. Methods : Using a sandwich enzyme-linked immunosorbent assay, the VEGF conoentration was measured in both sera and pleural effusions collected from a total of 85 patients with lung cancer, 13 patients with TB and 20 healthy individuals. Results : The serum VEGF levels in patients with lung cancer ($619.9{\pm}722.8pg/ml$) were significantly higher than those of healthy controls ($215.9{\pm}191.1pg/ml$), However, there was no significant difference between the VEGF levels in the lung cancer and TB patients. The serum VEGF levels were higher in large cell and undifferentiated carcinoma than in squamous cell carcinoma and adenocarcinoma. The serum VEGF levels of lung cancer patients revealed no significant relationship with the various clinical parameters. The VEGF concentrations in the malignant effusion ($2,228.1{\pm}2,103.0pg/ml$) were significantly higher than those in the TB effusion ($897.6{\pm}978.8pg/ml$). In the malignant pleural effusion, the VEGF levels revealed significant correlation with the number of red blood cells (r=0.75), the lactate dehydrogenase (LDH)(r=0.70), and glucose concentration (r=-0.55) in the pleural fluid. Conclusion : The serum VEGF levels were higher in the lung cancer patients. The VEGF levels were more elevated in the malignant pleural effusion than in the tuberculous effusion. In addition, the VEGF levels in the pleural fluid were several times higher than the matched serum values suggesting a local activation and possible etiologic role of VEGF in the formation of malignant effusions. The pleural VEGF levels showed a significant correlation with the numbers of red blood cells, LDH and glucose concentrations in the pleural fluid, which may represent the tumor burden.

• Journal of the Korean Chemical Society
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• v.51 no.6
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• pp.536-542
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• 2007

Behcet's disease (BD) is a chronic inflammatory disorder, involving several organs. Inflammation in the disease is thought to be mediated by cytokines derived from T-helper type 1 (Th1) lymphocytes. Although the exact pathogenesis for BD is not completely understood, it has been suggested that the disease is triggered in genetically susceptible individuals by environmental factors, such as microbial agents. It is noted that multiple genes, including MHC (major histocompatibility complex) and non-MHC genes, are implicated in the pathogenesis of BD. This study tries to determine whether HLA-B51, IL-18, SLC11A1 and TNF-α polymorphisms are associated with susceptibility to Behcet's disease in Koreans. As a results, HLA-B51 was a genetic factor with the strongest association with BD. But it is still uncertain whether this HLA molecule is directly involved in the pathogenesis of BD. Although the IL-18 gene polymorphisms were not associated with a susceptibility to BD in the Korean population, the patients carrying the GG genotype at position 137 had a higher risk of developing the ocular lesions. This study suggests that the allele 3 and the genotype allele 3 / allele 3 of 5'-promoter (GT)n polymorphism in the SLC11A1 gene may have a protective effect for the development of BD in the Korean population. There were no evidences for genetic association conferred by the TNF-α gene with respect to susceptibility to BD.

• Korean Journal of Plant Resources
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• v.29 no.1
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• pp.1-10
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• 2016

Obesity is a pro-inflammatory state that contributes to the development of metabolic disorders such as hyperlipidemia, insulin resistance, type 2 diabetes, non-alcoholic fatty liver, and cardiovascular disease. In this study, we evaluated the inhibition of adipogenesis in 3T3-L1 cells and in high-fat diet (HFD)-induced obese mice by Peucedanum japonicum Thunberg L. water extract (PJT). Lipid accumulation measurement indicates that PJT markedly inhibited adipogenesis in a dose-dependent manner. RT-PCR results demonstrated that the mRNA expression of adipogenic transcription factors such as peroxisome proliferator-activated receptor-γ (PPARγ) and CCAAT/enhancer binding protein-α (C/EBPα) in 3T3-L1 cells were significantly down-regulated by PJT treatment. Oral administration of PJT (100, 300, and 500 ㎎/㎏, b.w/daily for 4 weeks) was conducted in high-fat diet induced obese mice and C57BL/6 mice. The PJT-administered group of HFD-induced mice had a lower body weight gain, along with decreased serum levels of glucose, triglycerides, and total cholesterol compared with the control mice, however, the HDL-cholesterol/total cholesterol ratio was increased. Furthermore, the elevated mRNA expression levels of adipogenesis related genes in the white adipose tissue of obese mice were significantly suppressed by PJT. These results indicate that PJT exhibits anti-obesity effects in obese mice by decreasing in serum lipid levels and lipogenesis related gene.