• Clinical and Experimental Pediatrics
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• v.49 no.11
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• pp.1186-1193
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• 2006

Purpose : Enterovirus infection is a type of viral infection that occurs relatively frequently in children during summer. It has clinical symptoms of non-specific fever, aseptic encephalomeningitis, gastrointestinal diseases, skin rash and, hand-foot-mouth disease. However, it can also occcaisionally, result in fatal symptoms like myocarditis, epicardial inflammation, transverse myelitis, quadriplegia and etc. There have been epidemic enterovirus studies, but not in the Chungnam area. Therefore, we undertook this study in order to comprehend the cause viruses in this area. Methods: We enlisted 157 children hospitalized with enteroviral infections at Soonchunhyang University hospital in Cheonan between May and August 2005. Cerebrospinal fluids or feces were collected during the acute phase after hospitalization, and observed the cytopathic effects caused by enterovirus and using reverse transcription polymerase chain reaction (RT-PCR). Results : The number of children hospitalized due to possible enteroviral infection during the period of study was 157. The number of children who tested positive with the reverse transcription polymerase chain reaction totalled 32 cases (20.4 percent). Among the children with entroviral diseases, 20 were male and 12 were female, thus the sex ratio of male to female was 1.67:1. Their clinical symptoms included fever most frequently (93.7 percent), was followed by headaches (90.0 percent), meningeal irritation signs (65.0 percent), and abdominal pain (30.0 percent). As for the type of isolated enterovirus, there were 17 cases of echovirus 18 and 6 cases of coxsackievirus B5. Furthermore, there were 2 cases of echovirus 9, 1 case of coxsackievirus A6 and coxsackievirus B3, respectively. But 5 cases were not determined by genotype. Conclusion : Echovirus 18 is circulating in Korea. We reported on identified enteroviruses, including echovirus 18, using RT-PCR in the Chungnam area during the summer of 2005.

• Tuberculosis and Respiratory Diseases
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• v.39 no.3
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• pp.219-227
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• 1992

Background: Acute and chronic airway inflammation are important in the pathogenesis of bronchial asthma. Corticosteroids have proved to be very effective in the management of asthma. Although the mechanism by which they produce this effect is still debated, suppression of the inflammatory response is thought to be the most likely. Although inhaled steroids are known to be safe and have less side effects than oral steroids, the extent which inhaled steroids have beneficial and the detrimental effects in the treatment of asthma has remained open to question. Budesonide is a recently developed corticosteroid for inhalation treatment with a strong local effect combined with rapid inactivation in the systemic circulation. We set out to look in more detail at the time course of change in bronchial reactivity, clinical symptoms and the effects on the adrenal function during 6 weeks of treatment with budesonide (800 ug per day). Methods: Clinical symptoms, pulmonary function test, histamine $PC_{20}$, serum ACTH and cortisol (8 AM and 4 PM) were measured in 23 allergic asthmatic patients before and after 6 weeks of treatment with budesonide. Results: 1) Pulmonary function test; PEFR, FEV1 and FVC after 6 weeks of treatment with budesonide were higher than those before treatment. 2) Clinical symptoms; Clinical symptoms were significantly improved after 3 weeks and 6 weeks of treatment with budesonide. 3) Histamine provocation; Histamine $PC_{20}$ after 6 weeks of treatment with budesonide was significantly higher than that before treatment. 4) Adrenal function; 6 weeks of budesonide therapy did not significantly affect the level of serum ACTH and cortisol. Conclusion: From these results, it is concluded that budesonide therapy improved the clinical symptoms, pulmonary function and bronchial hyperreactivity after 3 weeks of treatment and the improvement after 6 weeks of treatment was higher than that after 3 weeks of treatment. During 6 weeks of treatment with budesonide, the inhibitory effect on the adrenal function was not obvious.

• Journal of Gastric Cancer
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• v.2 no.2
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• pp.73-80
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• 2002

In spite the fact that H. pylori infection might be the causative organisms of acute and chronic gastritis, peptic ulcer diseases and the definition as the class I carcinogen by WHO IARC, still debates exist about the relationship between H. pylori and gastric carcinogenesis. Epidemiological and animal studies demonstrated a link between gastric cancer and chronic infection with H, pylori, but the exact mechanism responsible for the development of gastric cancer in H. pylori-infected patients still remain obscure. In order to declare the clear association, definate evidences like that decrement in the incidence of gastric cancer after the eradication of H. pylori in designated area compared to noneradicated region or the blockade of specific mechanism acting on the carcinogenesis by H. pylori infection. The other way is to identify the upregulating oncogenes or downregulating tumor suppressor genes specifically invovled in H. pylori-associated carcinogenesis. For that, we established the animal models using C57BL/6 mice strain. Already gastric carcinogenesis was developed in Mongolian gerbils infected with H. pylori, but there has been no development of gastric cancer in mice model infected with H. pylori after long-term evaluation. Significant changes such as atrophic gastritis were observed in mice model. However, we could observe the development of mucosal carcinoma in the stomach of transgenic mice featuring the loss of TGF-beta sig naling by the expressions of dominant negative forms of type II receptor specifically in the stomach. Moreover, the incidence of gastric adenocarcinoma was significantly increased in group administered with both MNU and H. pylori infection than MNU alone, signifying that H. pylori promoted the gastric carcinogenesis and there might be host susceptibility genes in H. pylori-associated gastric carcinogenesis. Based on the assumption that chronic, uncontrolled inflammation might predispose to carcinogenesis, there have been several evidences showing chronic atrophic gastritis predisposed to gastric carcinogenesis in H. pylori infection. Although definite outcome of chemoprevention was not drawn after the longterm administration of anti-inflammatory drug in H. pylori infection, the actual incidence of atrophic gastritis and molecular evidence of chemoprevention could be obtained. Selective COX-2 inhibitor was effective in decreasing the development of gastric carcinogenesis provoked by H. pylori infection and carcinogen like in chemoprevention of colon carcinogenesis.

• Tuberculosis and Respiratory Diseases
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• v.42 no.2
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• pp.184-205
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• 1995

Background: Pulmonary toxicity by bleomycin has multiple mechanisms including direct tissue toxicity due to oxygen-derived free radicals and indirect toxicity through amplification of pulmonary inflammation. To evaluate the effect of chelators or free radical scavenger to lung damage induced by bleomycin, penicillamine as a copper chelator, deferoxamine as an iron chelator and vitamin E as a free radical scavenger were administered. Methods: Two hundred Wistar rats were divided into five groups: Control, bleomycin treated, bleomycin-penicillamine treated, bleomycin-deferoxamine treated, and bleomycin-vitamin E treated groups. Rats sacrificed on day 1, day 3, day 4, day 7, day 14, and day 28 after treatment. Bronchoalveolar lavage, light microscopic and immunohistologic studies for type I, III, IV collagens, fibronectin, laminin and NBD phallicidin were evaluated. Results: There was a significant increase in the total cell counts of bronchoalveolar lavage on day 1 from all treated animals and vitamin treated group showed an abrupt decrease in total cell counts with decrease of neutrophils on day 3. Bleomycin-vitamin E treated group had the least histologic changes such as pulmonary fibrosis. The alveolar basement membranes were positive for type IV collegen and laminin. Basement membranes of bleomycin, bleomycin-penicillamine, or bleomycin-deferoxamine treated groups were disrupted and fragmented on day 4 or 7. The bleomycin-vitamin E treated group had intact basement membranes until day 28. Conclusion: Bleomycin-induced pulmonary fibrosis was related to the severity of acute injury to oxygen radicals or activation of neutrophils and disruption of basement membrane. Vitamin E seemed to be the most effective antioxidant in the inhibition of bleomycin-induced pulmonary injury and fibrosis.

• 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.

• Journal of Yeungnam Medical Science
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• v.15 no.1
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• pp.55-66
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• 1998

Pathophysiological mechanism of hemorrhagic fever with renal syndrome (HFRS) is not fully understood. Major clinical findings of HFRS patients are widespread hemorrhage, acute renal failure and shock. Basic lesion is vascular injury with microvascular hemorrhage and relatively little inflammation. According to autopsy findings, renal medulla shows focal hemorrhage, tubular necrosis and interstitial mononuclear infiltrates. The predominant cell type in the renal and pulmonary interstitium is a fibroblast and it participates in the healing process at the injury site by secreting a large amount of extracellular matrix proteins. Cultured human lung fibroblasts and Mongolian gerbil fibroblasts were known to be good host cells for the hantaan virus. It is possible that not only the endothelial cell but also the fibroblast is a target of Hantaan virus and the fibroblast might be involved in the pathogenesis and the healing process in HFRS. Integrins are adhesion molecules, and act as receptors for many extracellular matrix proteins. Recently, there are many reports that cell surface integrins influence on some viral infections or reversely viruses influence on the expression of integrins. The ${\alpha}_5{\beta}_1$ integrin is a major receptor for the fibronectin which is an important extracellular matrix protein secreted by fibroblasts. In this study, the role of ${\alpha}_5{\beta}_1$ integrin in the infection of Hantaan virus was examined by using anti-${\alpha}_5{\beta}_1$, integrin, anti-${\alpha}_5$ integrin and anti-${\beta}_1$, integrin antibodies in chicken embryo fibroblasts (CEF) and Mongolian gerbil fibroblasts(MGF). The treatment of anti-${\alpha}_5{\beta}_1$, integrin antibody in CEF reduced the virion titers 26.8% and the amount of nucleocapsid N protein 32.6% when compared with control CEF. When MGF were treated with anti-${\alpha}_5$, anti-${\beta}_1$ and anti-${\alpha}_5{\beta}_1$ integrin antibodies, virion titers were reduced by 26.5%, 29.4% and 28.7% and the amount of nucleocapsid N protein were reduced by 65.2%, 59.7% and 72.6%. These results suggested that ${\alpha}_5{\beta}_1$ integrin might act as a receptor for the Hantaan virus or blocking of ${\alpha}_5{\beta}_1$ integrin influences on the viral replication in CEF and MGF. It is also possible that the blocking of only one subunit of integrin represents similar results in that of whole molecule.

• Microbiology and Biotechnology Letters
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• v.43 no.1
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• pp.45-55
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• 2015

This study was carried out to demonstrate the anti-inflammatory effect of tuna oil (TO) using LPS-induced inflammation responses and mouse models. First, nitric oxide (NO) and pro-inflammatory cytokines levels were suppressed up to 50% with increasing concentrations of TO without causing any cytotoxicity. Also, the expression of a variety of proteins, such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and nuclear factor kappa B (NF-κB), was suppressed in a dosedependent manner by treatment with TO. Furthermore, TO also inhibited the phosphorylation of mitogen-activated protein kinases (MAPKs), including c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and p38 protein kinase (p38). Moreover, in in vivo testing the formation of ear edema was reduced at the highest dose tested compared to that in the control, and a reduction of ear thickness and the number of mast cells was observed in histological analysis. In acute toxicity test, no mortalities occurred in mice administrated 5,000 mg/kg body weight of TO over a two-week observation period. Our results suggest that TO has a considerable anti-inflammatory property through the suppression of inflammatory mediator productions and that it could prove to be useful as a potential anti-inflammatory therapeutic material.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.12 no.1
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• pp.23-34
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• 2012

Purpose: Acute symptomatic seizures are caused by structural changes, inflammation or metabolic changes of brain, such as tumor, stroke, meningitis, encephalitis and metabolic disorders. Inherited metabolic disorders that can cause seizures are organic acidopathies, lysosomal storage disorders, peroxisomal disorders and mineral disorders. We have done this study to find out the importance of organic acidopathies causing seizure disorders in Korean childhood and adolescent patients. Method: Retrograde analysis for 1,306 patients with seizure disorders whose clinical informations are available and have done urine organic acid analysis for 5 years period, between Jan. 1st 2007 to Dec. 31th 2011. Statistical analysis was done with Student's t test using SPSS. Result: Out of 1,306 patients, 665 patients (51%) showed abnormalities on urine organic acid analysis. The most frequent disease was mitochondrial respiratory chain disorders (394, 30.1%), followed by mandelic aciduria (127, 9.7%), ketolytic defects (81, 6.2%), 3-hydroxyisobutyric aciduria (19, 1.4%), glutaric aciduria type II (10, 0.8%), ethylmalonic aciduria (4), propionic aciduria (4), methylmalonic aciduria (3), glutaric aciduria type I (3), pyruvate dehydrogenase deficiency (3), pyruvate carboxylase deficiency (3), isovaleric aciduria (2), HMG-CoA lyase deficiency (2), 3-methylcrotonylglycinuria (2), fatty acid oxidation disorders (2), fumaric aciduria (1), citrullinemia (1), CPS deficiency (1), MCAD deficiency (1). Conclusion: On neonatal period, mandelic aciduria due to infection was found relatively frequently. Mitochondrial disorders are most frequent etiologic disease on all age group, followed by ketolytic defects and various organic acidopathies. The number and diversities of organic acidopathies emphasize meticulous evaluation of basic routine laboratory examinations and organic acid analysis with initial sample on every seizure patient.

• Journal of Food Hygiene and Safety
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• v.24 no.4
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• pp.352-356
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• 2009

The purpose of this study was to introduce the toxicological study review to evaluate the safety of PDMS on the 69th JECFA meeting. Polydimethylsiloxane is a polymer and its ADI was established at 23rd JECFA meeting in 1979. The ADI was maintained although the specification was expanded at its 26th, 29 th, 37 th meetings. Recently, it was reported that PDMS with low molecular weight and viscosity has high absorption rate and different toxicity, so it was submitted at 69th meeting. Toxicological studies of PDMS were submitted from the sponsor and additional information is collected from a document searching. The toxicological studies were reviewed in accordance with the 'Guidelines for the preparation of toxicological working papers for the Joint FAO/WHO Expert Committee on Food Additives'. In the available acute, sub-chronic and chronic toxicity studies on PDMS, dose-related increases in incidence and severity of ocular lesions(corneal crystal, inflammation of the corneal epithelium etc.) were consistently observed after oral dosing. It seems to be a local irritant effect, but the mechanism by which the ocular lesions arose is unclear, although the lack of absorption of PDMS indicates that it is unlikely to be a direct systemic effect. Consequently, the relevance of the ocular lesions for food use of PDMS could not be determined. The ADI of PDMS was re-established from 0-1.5 mg/kg bw/day to 0-0.8 mg/kg bw/day by applying additional safety factor 2 based on its ocular toxicity. The result of 0-0.8 mg/kg bw/day is a temporary ADI until further data are provided to 2010.

• Journal of the Korean Society of Food Science and Nutrition
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• v.44 no.11
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• pp.1612-1620
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• 2015

Inflammation is a complex process involving a variety of immune cells, which defend the body from harmful stimuli. However, pro-inflammatory cytokines and inflammatory mediators can also exacerbate diseases such as cancer. Onion peel contains several phenolic compounds, including quercetin at an amount 20 times greater in peel than edible flesh. Therefore, in this study, the anti-inflammatory effects of onion peel ethanol extract (OPEE) were investigated lipopolysaccharide-induced inflammatory response. In our results, NO production decreased in a dose-dependent manner. Secretion of IL-6, $TNF-{\alpha}$, and $IL-1{\beta}$ was suppressed by 44%, 53%, and 60% respectively, at $100{\mu}g/mL$. Moreover, OPEE also suppressed expression of COX-2, iNOS, $NF-{\kappa}B$, and MAPKs in a dose-dependent manner. Formation of mice ear edema was reduced at the highest dose tested compared to the control, and reduction of ear thickness was observed in the histological analysis as well. In the acute toxicity test, no morality was observed in mice administered 5,000 mg/kg body weight of OPEE over a 2-week observation period. These results suggest that OPEE may have significant effects on inflammatory factors and be a potential anti-inflammatory material.