• Journal of Chest Surgery
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• v.31 no.12
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• pp.1119-1126
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• 1998

Background: In this study, we investigated the early time course of expression of the major histocompatibility(MHC) antigens, intercellular adhesion molecule-1(ICAM-1), vascular cell adhesion molecule-1(VCAM-1), interleukin-6 and the histopathological changes in the coronary arteries of cardiac allografts exchanged between inbred mice strains that differ in one loci of class I major histocompatibility antigen (B10.BR to B10.A). Material and Method: No immunosuppressive therapy was used. Both allografts and the hearts of the recipients were harvested at 7(group 1, n=6), 15(group 2, n=6), 21(group 3, n=6), and 30(group 4, n=6) days after transplantation. They were examined by immunohistochemistry, microscopy and morphometry. All allografts had contractions at the time of harvest. Result: A strong MHC class I antigen expression was present on the endothelial and medial cells of the coronary arteries in group 1 and remained unchanged in the rest of the groups. However, MHC class II reactivity was none or very little at any time. Mild to moderate ICAM-1 expression was observed on the endothelial cells, but not on the medial cells at any time by 30 days. VCAM-1 expression was strong both on the endothelial and medial cells at any time. Moderate degree expression of interleukin-6 was observed from 7 to 30 day specimens. Histopathologically, percentage of affected vessels(vessels with intimal thickening) was less than 10 % in 7 day group and increased up to 50 % at 30 days. Mean percent narrowing of the lumen of the affected vessels revealed less than 20 % at 7 days and 40 % at 30 days. The area occupied by tropomyosin positive cells in the intimal lesion, graded from 0 to 3, showed gradual increase but remained between grade 0 to 1 by 30 days. Medial integrity was also well preserved at any time. Moderate perivascular mononuclear cell infiltration was observed at 7 days and it was progressively increased upto 30 days. Recipients' heart revealed no positive immunopathologic findings. Conclusion: In this study, the early time course of progression of the transplantation vasculopathy was demonstrated in the murine heterotopic heart transplant model.

• Journal of the Korean Chemical Society
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• v.40 no.1
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• pp.28-36
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• 1996

The pentanuclear complexes have been obtained by the reactions of molybdenum(VI) and tungsten(VI) polynuclear complexes with molybdenum(O) and tungsten(O) dinitrosyl mononuclear complexes, and methylthioamidoxime. The prepared complexes (n-Bu4N)2[Mo4O12Mo(NO)2{CH3SCH2C(NH2)NHO}2{CH3SCH2C(NH)NO}2](1), (n-Bu4N)2[W4O12Mo(NO)2{CH3SCH2C(NH2)NHO}2{CH3SCH2C(NH)NO}2](2), (n-Bu4N)2[Mo4O12W (NO)2{CH3SCH2C(NH2)NHO}2{CH3SCH2C(NH)NO}2] (3) have been characterized by elemental analysis, infrared, UV-visible and 1H NMR spectra. The complexes are elucidated the cis-{M(NO)2}2+(M = Mo, W) unit and a slight delocalization by spectroscopy. The structure of (n-Bu4N)2[W4O12Mo(NO) 2{CH3SCH2C(NH2)NHO}2{CH3SCH2C(NH)NO}2] was determined by X-ray single crystal diffraction. Crystal data are follows: Monoclinic, $P21}a$, a = 22.14(2) $\AA$, b = 14.93(1) $\AA$, c = 23.20(1) $\AA$, $\beta$ = 111.08(6) $\AA$, V = 7155(9) $\AA$, Z = 4, final R = 0.072 for 6191(I > $3\sigma(I)).$ The structure of complex forms two dinuclear [W2O5{CH3SCH2C(NH2)NHO}{CH3SCH2C(NH)NO}] and a central {Mo(NO)2} 2+ core. The geometric structure of the {Mo(NO)2} 2+unit is the formally cistype and C2v symmetry.

• Journal of Life Science
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• v.20 no.10
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• pp.1556-1562
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• 2010

This study examined the histopathologic and electron microscopic findings of aborted fetuses from pregnant dairy cows naturally infected with Neospora caninum (N. caninum) at four farms in Gongju city and Yeonki gun of Choongnam province. Systemic subcutaneous edema was observed in the aborted fetuses. The necropsy revealed considerable serosanguinous fluid in the body cavity of the aborted fetuses. Light microscopy showed the infiltration of many inflammatory cells consisting of macrophages, lymphocytes and mononuclear cells, accompanied by congestion, hemorrhage and necrosis of myocardiac cells and hepatocytes in the liver and heart of the aborted fetuses. In the liver, clusters of tachyzoites were formed in the cytoplasm of hepatocytes and the interstitial tissue. In the brain, many tissue cysts of various sizes were observed in the nerve cells and their adjacent areas. Tissue cysts had a round shape and contained a large amount of bradyzoite. In addition, there was diffuse gliosis accompanied by congestion and hemorrhage and focal necrosis in the brain. Infiltration of microglial cells were observed at the periphery of the focal necrosis and perivascular area in the brain. Electron microscopy showed that the tissue cyst wall had a thickness of approximately 1 ${\mu}m$ with an irregular shape. On the interior side, more than 100 bradyzoites with lengths of 2-5 ${\mu}m$ and widths of 1-2 ${\mu}m$ were observed. The nucleus of in the bradyzoites was located approximately 1-1.5 ${\mu}m$ anterior to the posterior tip of the zoite. In the cytoplasm between the nucleus and the posterior tip, there were many amylopectin granules, electron-dense small-sized and electron-thin large-sized round granules, homogeneously electron-dense rhoptries and micronemes oriented perpendicularly to the zoite pellicle. To summarize, tissue cysts were identified on electron microscopy from the aborted fetus from N. caninum seropositive pregnant cow by the ELISA. This led to the confirmed presence of N. caninum.

• Tuberculosis and Respiratory Diseases
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• v.41 no.1
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• pp.11-19
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• 1994

Background: Mycobacterium tuberculosis is a facultative intracellular pathogen which persists and multiplies within macrophage. Competent cell mediated immunity by cooperation of both T lymphocyte and macrophage of the host is required to kill the Mycobacterium tuberculosis. But a precise understanding of the pathogenesis of tuberculosis infection in pulmonary alveolar macrophage has not been achived. Research on the macrophage's basic microbicidal mechanism has elucidated the importance of oxygen-dependent or oxygen-independent components. Oxygen dependent processing begins with the reduction of oxygen by NADPH oxidase and generation of superoxide. In this study, the oxidative metabolic status of blood monocyte and pulmonary alveolar macrophage in patients with active pulmonary tuberculosis was accessed and compared with that of healthy control subjects to know whether there was a basic difference in superoxide generation by mononuclear cells between two groups. Methods: Pulmonary alveolar macrophage was purified after performing BAL(bronchoalveolar lavage) through the bronchi of infected lesion by plastic adhesion method. Blood monocyte was purified by Ficoll-Hypaque method. Superoxide generation by blood monocyte and pulmonary alveolar macrophage was measured by ferricytochrome-C reduction method after either stimulated with PMA(phorbol myristate acerate) or non-stimulated states. We also measured the effect of pulmonary tuberculosis patient's serum on superoxide generation by monocyte. Results: 1) Generation of superoxide by alveolar macrophage obtained from patients with pulmonary tuberculosis was little higher than those of controls, and PMA enhanced the generation of 2) Generation of superoxide by blood monocyte obtained from patients with pulmonary tuberculosis was little higher than those of control(p>0.05), and PMA more enhanced the generation of superoxide in patientswith pulmonary tuberculosis than those in controls(p<0.02). 3) Patient's serum enhanced the generation of superoxide by blood monocyte obtained from patients with pulmonary tuberculosis and controls, but not in the case of PMA stimulated blood monocyte. Conclusion: The present study suggest that the phenomenon of M.tuberculosis escape the microbicidal action of macrophage was not result of suppressed superoxide generation by blood monocyte and pulmonary alveolar macrophage, rather there might be a factor to stimulate the generation of superoxide by blood monocyte in pulmonary tuberculosis patient serum, but the comparision with effect of control's serum on superoxide generation needs further elucidation.

• Journal of Periodontal and Implant Science
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• v.37 no.sup2
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• pp.353-369
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• 2007

Gingival tissue samples were obtained during periodontal surgery or tooth extraction. According to the patient's systemic condition & clinical criteria of gingiva, each gingival sample was divided into three groups. Group 1 (n=8) is clinically healthy gingiva without bleeding and no evidence of bone resorption or periodontal pockets, obtained from systemically healthy 8 patients. Group 2 (n=8) is inflamed gingiva from patients with chronic periodontitis. Group 3 (n=8) is inflamed gingiva from patients with chronic periodontitis associated with type 2 diabetes. Tissue samples were prepared and analyzed by Western blotting. The quantification of $IL-1{\beta}$, MMP-13 and TIMP-1 were performed using a densitometer and statistically analyzed by one-way ANOVA followed by Tukey test. 1. The expressions of MMP-13 and TIMP-1 showed increasing tendency in group 2 & 3 compared to group 1. 2. The expressions of $IL-1{\beta}$ & MMP-13 were showed increasing tendency in group 3 compared to group 2. 3. As $IL-1{\beta}$ levels were increasing, MMP-13 showed increasing tendency in group 3, and although $IL-1{\beta}$ , MMP-13 levels were increasing, TIMP-1 levels were similar expressed comparing to group 2. In conclusion, this study demonstrated that the expression levels of MMP-13 and TIMP-1 had increasing tendency in inflamed tissue. It can be assumed that $IL-1{\beta}$ and MMP-13 may be partly involved in the progression of periodontal inflammation associated to type 2 DM.

• 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.

• Radiation Oncology Journal
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• v.14 no.4
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• pp.281-290
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• 1996

Purpose : Chest irradiation leads to a significant cardiac injury in a number of patients. To prevent, or to reduce the risk of radiation-induced cardiac injury, pentoxifylline(PTX), a haemorrheologic agent that improves the blood flow through small blood capillaries has been employed. Materials and Methods : One hundred and eighty ICR mice were divided into three study groups: control, radiation alone, and radiation-pentoxifylline. Each group was subdivided into 12 subgroups: 1 3, 6 and 10 days and 2, 3, 4, 6, 8, 12, 16 and 20 weeks by observation Period after irradiation. The total 15Gy of radiation was delivered in a single fraction through anterior mediastinal port. Pentoxifylline was injected subcutaneously daily 50mg/kg to the back of the mice from the first day of irradiation throughout the observation period. The mice of each group after a certain observation period were sacrificed and sectioned for histopathologic examination of the heart. Result : The findings of acute radiation-induced carditis i.e., heterophilic infiltration and vacuolization and ballooning of endothelial cells were observed upto 6 weeks and reduced sharply afterwards. The late radiation effects including pericarditis with mononuclear cell infiltration, pericardial fibrosis, endothelial cell changes, myocardial degeneration and fibrosis present from 4 weeks onwards after irradiation but with various degree of severity. The overall process of pathologic changes of radiation-pentoxifylline group was similar to those of radiation alone group but the duration of acute stage was relatively short and the severity of late cardiac toxicity was much lesser compared with those of radiation alone group. Conclusion : Pentoxifylline can effectively reduce the late radiation-induced cardiac injury and reslve the acute effects relatively rapidly.

• Tuberculosis and Respiratory Diseases
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• v.46 no.1
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• pp.44-52
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• 1999

Background : Airway infiltration by inflammatory cells, particularly of eosinophils, is one of the characteristic features of asthma. Several mechanisms for the recruitment of eosinophil is focused on the CD4+ T lymphocyte for the preferential production of Th2-c1erived cytokines. Interleukin-10(IL-10) is identified cytokine with potent antiinflammatory activity. This molecule has been shown to inhibit the release of cytokine from inflammatory cells including Th2 cell, and also to inhibit eosinophil survival. We therefore attempted to determine whether decreased synthesis of IL-10 in the lung of bronchial asthma may contribute to inflammation that is characteristics of this dease. Method: Subjects were patients with bronchial asthma(n=23) and normal controls(n=11). IL-10 produced from peripheral mononuclear cell(PBMC) and in bronchoalveolar lavage(BAL) fluid was measured by ELISA method. Degree of bronchial inflammation was assessed by total cell counts and eosinophil percents in BAL fluid, eosinophil infiltration on bronchial biopsy tissue and $PC_{20}$ for methacholine. Results: The IL-10 level produced by PBMC and in BAL fluid from patient with bronchial asthma were not different with normal controls(respectively, $901.6\pm220.4$ pg/ml, $810.9\pm290.8$ pg/ml for PBMC, $24.5\pm9.5$ pg/mL $30.5\pm13.5$ pg/ml for BAL fluid p>0.05). There were significant negative correlation between IL-10 in BAL fluid and eosinophil percents in BAL fluid or degree of eosinophil infiltration in bronchial biopsy (respectively r=-0.522, r=-0.4486 p<0.05). However there was no difference of IL-10 level according to $PC_{20}$ for methacholine. There were no correlation between IL-10 production by PBMC and peripheral blood eosinophil counts or serum eosinophilic cationic protein levels(respectively r=0.1146, r=0.0769 p>0.05). Conclusion: These observation suggest that IL-10 may participate but not acts the crucial role in regulation of the airway inflammation in bronchial asthma.

• Tuberculosis and Respiratory Diseases
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• v.59 no.4
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• pp.397-405
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• 2005

Background : Laminin-1 is known to have regular functions in the development and course of differentiation of the lungs. The morphogenesis and distribution of laminin-1 still remains as a mystery and its distribution and changes in the molecular structure of laminin-1 in the pathogenesis of the lung still is a subject of great controversy. In this study, experiments were done to delineate the distribution and changes in the amount of laminin-1 after inducing inflammation of the lungs by exposing experimental animals to CS gas and especially, to find compositions of laminin-1 within type II pneumocytes. Materials and Methods : The experimental subjects of study were newborn rats and the extracted tissue from the experimental rats were viewed under light microscope and electron microscope after the sections were treated with immunohistochemical methods and immunogold reaction methods using bounded gold particles. Results : 1) Lymphocytes and mononuclear phagocytes invaded the alveolar septa in the 2 day group rats after CS gas exposure and intense interstitial inflammation was seen in the 3 day group. 2) Laminin immunoreactions decreased to a moderate degree in the 2 and 3 day group rats after CS gas exposure and strong laminin immunoreactions were seen again in the 5 and 7 day group rats. 3) Gold particles in basal lamina of the lung blood-air barrier decreased and in the type I pneumocytes decreased in the 2 and 3 day group rats after CS gas exposure. 4) Gold particles were seen only on the surface of the cell membranes of type II pneumocytes of the 1 and 2 day group rats after CS gas exposure. 5) Few gold particles around the lamellar bodies and cytoplasm of type II pneumocytes in the control rat group and at 12 hours after CS gas exposure. Gold particles are seen only on the surface of type II pneumocytes of the 1 and 2 day group rats after CS gas exposure and are evenly distributed in small amounts in the cells of the 3 day group after CS gas exposure. Conclusion : CS gas exposure in the rats caused inflammation of lung alveolar septa and also induced a decrease in laminin-1 in basal lamina and loss of laminin-1 in the cytoplasm of type II pneumonocytes. As the inflammatory cells disappeared, an increase in the distribution of laminin-1 occurred. This reflects tissue regeneration functions of laminin-1 in the pneumocytes of rats and the distribution of laminin-1 in type II pneumocytes can be seen through the electron microscope using immunogold methods.

• Microbiology and Biotechnology Letters
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• v.38 no.1
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• pp.93-104
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• 2010

In this study, we investigated the effects of frankincense essential oil (BSEO) on the immune cell change in the lung, BALF and PBMC using a mouse model of asthma. BALB/c mice after intraperitoneal OVA sensitization (day 1) were challenged intratracheally with OVA on day 14. Then, the asthma was induced by repeated OVA inhalation challenged. The asthma induced mice group inhaled 0.3% BSEO for 30 minutes per trial, three times a week, for 8 weeks using the nebulizer. After 12 weeks from the experiment, the mice was killed and the lung, bronchoalveolar lavage fluid (BALF) and peripheral blood mononuclear cell (PBMC) were obtained. Next, the change of immune cells inside the separated tissues was observed to identity the effects of BSEO on the allergic asthma mice. In conclusion, the hypersensitive reaction of airway to the bronchoconstrictor in the allergic asthma induced mice was effectively suppressed in Frankincense group, in Bermagot, Eucalyptus, Chamomile, Marjoram and Frankincense groups, the natural aromatic essential oil groups. Furthermore, it was also confirmed that the weight of lung, total number of alveolus cells and the number of BALF, MNL and DLN increased after inducing allergic asthma were reduced. BSEO suppressed the percentage of $CD3e^+/CD19^-$, $B220^+/CD23^+$ and $CD11b^+/Gr-1^+$ cells in the lung tissue of allergic asthma mice. Moreover, BSEO also reduced the percentage of $CD4^+/CD8^-$, $B220^+/CD23^+$ and $CD3^+/CCR3^+$ cells in BALF. In addition, the percentage of $CD3e^+/CD19^-$, $CD3^+/CD69^+$ and $B220^+/CD23^+$ cells in PBMC was reduced. The results of this study indicate that BSEO would be effective to treat allergic asthma by the immune control suppressing the activity of immune cells in each tissue.