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.
Background: Effect of sulfur dioxide($SO_2$) exposure on airway is well known but little about the effect of $SO_2$ exposure on lung parenchyme. This study is to determine if short tenn exposure to $SO_2$ in concentration commonly found in industrialized environment cause potentially harmful effect on the lung parenchyme, and to evaluate the exposure time-response relationship between short tenn exposure to $SO_2$ and the inflammatory response in mouse lung. Method: 5ppm $SO_2$ gas was used and 48 mice were grouped into control(10), 30(9), 60(11), and 120 minute exposure(18) group. In each group, bronchoalveolar lavage(BAL) was done immediately after and at 1,2,3 days after exposure. Histological examination was performed in control and 120 minute exposure group. Results: 1) Cell response in bronchoalveolar lavage fluid. In 30 and 60 minute exposure group, compared to the control group, lymphocyte count has significantly increased(p<0.05) at 1 day after exposure but did not differ at 2 days after exposure. In 120 minute exposure group, also compared to the control group, there was significant increase in total cell, macrophage, and lymphocyte count at 1 day after exposure, (p<0.05) which lasted for 2 days but did not significantly differ at 3 days after exposure. 2) Histological findings in 120 minute exposure group. In the airway, mild epithelial cell damage and ciliary loss were noted but there was no evidence of inflammatory cell infiltration. Interstitial inflammatory infiltration was noted at 1 day after exposure, which lasted for 3 days after exposure and there was no evidence of edema or fibrosis in the interstitium Conclusions: These data indicate potentially noxious effect of $SO_2$ on the lung parenchyme as well as the airway at exposure level that are regarded as relatively safe, and the duration of injury depends on the exposure time.
Park, Seong-Hee;Kwon, Sung-Tack;Hee Sagong;Cheong, Chang-Sik
Proceedings of the Mineralogical Society of Korea Conference
/
2001.06a
/
pp.75-75
/
2001
We report Sr, Nd and Pb isotope data of clinopyroxene separates from ultramafic xenoliths and their host basaltic rocks in Jeju Island, Baekryeong Island, Boeun and Ganseong, Korea. The isotopic data of the xenoliths and host basalts are distinctly different from those of Korean basement rocks. Except for two xenoliths from Ganseong, all samples in this study have isotopic ratios within the combined range of MORB-OIB data. All basaltic rocks have Nd-Sr-Pb isotope compositions different from those of xenoliths, indicating that the host basaltic magma did not derive from the lithospheric mantle where the xenoliths originated. The range of isotopic composition of xenoliths is much greater than that observed in host basalts, which reflects small-scale heterogeneity of the lithospheric mantle. The greater isotopic heterogeneity of the lithospheric mantle probably reflects its long-term stability. The spinel peridotite xenolith data of Jeju Island, Baekryeong Island and Boeun display mixing hyperbolas between DMM and EM II end members. Since Jeju basalts have EM II-like isotopic signature, the mixing relationship shown by the isotopic data of the Jeju xenoliths can be interpreted as the result of infiltration of metasomatic fluid or melt derived from basaltic magma into DMM-like lithospheric mantle. In contrast to other xenolith sites, the Ganseong xenoliths are dominantly clinopyroxene megacryst and pyroxenite. Clinopyroxene megacrysts have different isotopic ratios from their host basalt, reflecting its exotic origin. Two Ganseong xenoliths (wherlite and clinopyroxenite) have much enriched Sr and Nd isotopic ratios and Nd model ages of 2.5-2.9 Ga, and plot in an array away from the MORB-OIB field. The mantle xenoliths from Korean Peninsula have similar $\^$87/Sr/$\^$86/Sr,$\^$143/Nd/$\^$144/Nd and $\^$207/Pb/$\^$204/Pb ratios to, but higher $\^$208/Pb/$\^$204/Pb ratios than, those from eastern China, indicating that Korean xenoliths are derived from the lithospheric mantle with higher Th/U ratio compared with Chinese ones. The isotopic data of xenolith-bearing basalts of Baekryeong Island and Ganseong, along with Ulreung and Dok Islands, show a mixing trend betlveen DMM and EM I in Sr-Nd-Pb isotopic correlation diagrams, which is also observed in tile northeastern Chinese basalts. However, the Jeju volcanic rocks show an EM II signature that is observed in southeastern Chinese basalts. The isotopic variations in volcanic rocks from the northern and southern portions of the East Asia reflect a large-scale isotopic heterogeneity in their source mantle.
Kim, Dong-Goo;Bae, Gi-Sang;Choi, Sun Bok;Jo, Il-Joo;Shin, Joon-Yeon;Lee, Sung-Kon;Kim, Myoung-Jin;Kim, Min-Jun;Choo, Gab-Chul;Song, Ho-Joon;Park, Sung-Joo
The Korea Journal of Herbology
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v.29
no.6
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pp.15-20
/
2014
Objectives : Commiphora myrrha (CM) has been used in traditional medicine for treating disease such as obesity, hyperlipidemia, atherosclerosis, diabetes and osteoarthritis. However, the protective effects of CM on acute pancreatitis (AP) has not been reported. Thus, the aim of this study was to evaluate the protective effects of CM water extract on cerulein-induced AP. Methods : AP was induced in mice via intraperitoneal injection of supramaximal concentrations of the stable cholecystokinin analogue cerulein ($50{\mu}g/kg$) every hour for 6 times. Water extract of CM (0.1, 0.2, or 0.5 g/kg) was administrated intraperitoneally 1 h prior to the first injection of cerulein. The mice were killed at 6 h after the final cerulein injection. Pancreas was rapidly removed for morphologic and histochemical examination, myeloperoxidase (MPO) assay. Blood samples were taken to determine serum amylase and lipase activities. Results : Administration of CM significantly inhibited pancreatic weight/body weight ratio, pancreas histological injury. And CM administration inhibited the serum digestive enzyme elevation such as amylase and lipase on cerulein-induced pancreatitis. In addition, Pancreas MPO activity which indicates neutrophil infiltration was inhibited by CM extract on cerulein-induced pancreatitis. Conclusions : In conclusion, our results could suggest that pre-treatment of CM reduces the severity of cerulein-induced AP. Therefore, CM could be used as a protective agent against AP. Also, this study could give a clinical basis that CM could be a drug or agent to prevent AP.
Didecyldimethylammonium chloride (DDAC) is used in many types of biocidal products including tableware, carpets, humidifiers, and swimming pools, etc. In spite of increased chances of DDAC exposure through inhalation, studies on the inhalation toxicity of DDAC are not common even though the toxicity of DDAC might be significantly higher if it were to be administered through routes other than the respiratory system. DDAC aerosols were exposed to Sprague-Dawley rats in whole body exposure chambers for a duration of 13 weeks. The Mass Median Aerodynamic Diameters of the DDAC aerosol were $0.63{\mu}m$, $0.81{\mu}m$, and $1.65{\mu}m$, and the geometric standard deviations were 1.62, 1.65, and 1.65 in the low ($0.11{\pm}0.06mg/m^3$), the middle ($0.36{\pm}0.20mg/m^3$) and the high ($1.41{\pm}0.71mg/m^3$) exposure groups, respectively. Body weight was confirmed to be clearly influenced by exposure to DDAC and mean body weight was approximately 35% lower in the high ($1.41{\pm}0.71mg/m^3$) male group and 15% lower in the high ($1.41{\pm}0.71mg/m^3$) female group compared to that of the control group. In the bronchoalveolar lavage fluid assay, the levels of albumin and lactate dehydrogenase had no effect on DDAC exposure. The lung weight increased for the middle ($0.36{\pm}0.20mg/m^3$) and the high ($1.41{\pm}0.71mg/m^3$) concentrations of the DDAC exposure group, and inflammatory cell infiltration and interstitial pneumonia were partially observed in the lungs of the middle ($0.36{\pm}0.20mg/m^3$) and the high ($1.41{\pm}0.71mg/m^3$) exposure groups. However, severe histopathological symptoms, including proteinosis and/or fibrosis, were not found. Based on the results of the changes in the body weight and lung weight, it is considered that the NOAEL (no-observed adverse effect) level for the 13-week exposure duration is $0.11mg/m^3$.
Giant cell interstitial pneumonia. a synonym for hard metal pneumoconiosis, is a unique form of pulmonary fibrosis resulting from an exposure to hard metal dust. A case of biopsy-proved giant cell interstitial pneumonia in the absence of appropriate history of exposure to hard metal dust is reported. The patient presented with clinical features of chronic interstitial lung disease or idiopathic pulmonary fibrosis. He worked in a chemical laboratory at a fertilizer plant, where he had been exposed to various chemicals such as benzene and toluene. He denied having any other hobby in his house or job at work, which may have exposed him hard metal dust. High-resolution CT scan revealed multi-lobar distribution of ground glass opacity with peripheral and basal lung predominance. The retrieved fluid of bronchoalveolar lavage contained asbestos fiber and showed neutrotphil predominance. Surgical lung biopsy was performed for a definite diagnosis. Lung specimen showed alveolar infiltration of numerous multinucleated giant cells with mild interstitial fibrosis. Upon detailed examination of the lung tissue, one asbestos body was found. An analysis for mineral contents in lung tissue was performed. Compared with the control specimen, the amount of cobalt and several hard metal components in the lung tissue of this patient was ten times higher. We speculated that the inconsistency between occupational history and the findings of pathologic and mineralogical analyses could be explained by the difference in individual immunologic reactivity to hard metal dust despite the relatively small amount of unrecognized environmental exposure(ED: It's hard to understand what this phrase is trying to say).
Background: Idiopathic pulmonary fibrosis is a common interstitial lung disease; it is a chronic, progressive, and fatal lung disease of unknown etiology. Over the last two decades, knowledge about the underlying mechanisms of pulmonary fibrosis has improved markedly and facilitated the identification of potential targets for novel therapies. However, despite the large number of antifibrotic drugs being described in experimental pre-clinical studies, the translation of these findings into clinical practices has not been accomplished yet. NADH:quinone oxidoreductase 1 (NQO1) is a homodimeric enzyme that catalyzes the oxidation of NADH to $NAD^+$ by various quinones and thereby elevates the intracellular $NAD^+$ levels. In this study, we examined the effect of increase in cellular $NAD^+$ levels on bleomycin-induced lung fibrosis in mice. Methods: C57BL/6 mice were treated with intratracheal instillation of bleomycin. The mice were orally administered with ${\beta}$-lapachone from 3 days before exposure to bleomycin to 1-3 weeks after exposure to bleomycin. Bronchoalveolar lavage fluid (BALF) was collected for analyzing the infiltration of immune cells. In vitro, A549 cells were treated with transforming growth factor ${\beta}1$ (TGF-${\beta}1$) and ${\beta}$-lapachone to analyze the extracellular matrix (ECM) and epithelial-mesenchymal transition (EMT). Results: ${\beta}$-Lapachone strongly attenuated bleomycin-induced lung inflammation and fibrosis, characterized by histological staining, infiltrated immune cells in BALF, inflammatory cytokines, fibrotic score, and TGF-${\beta}1$, ${\alpha}$-smooth muscle actin accumulation. In addition, ${\beta}$-lapachone showed a protective role in TGF-${\beta}1$-induced ECM expression and EMT in A549 cells. Conclusion: Our results suggest that ${\beta}$-lapachone can protect against bleomycin-induced lung inflammation and fibrosis in mice and TGF-${\beta}1$-induced EMT in vitro, by elevating the $NAD^+$/NADH ratio through NQO1 activation.
Kim, Hye-Young;Kang, Hyun Kyu;Cho, Joon;Jung, In Duk;Yoon, Gun Young;Lee, Min-Goo;Shin, Sung Jae;Park, Won Sun;Park, Jong-Hwan;Ryu, Seung-Wook;Park, Yeong-Min;You, Ji Chang
BMB Reports
/
v.48
no.3
/
pp.178-183
/
2015
Dendritic cells play an important role in determining whether na${\ddot{i}}$ve T cells mature into either Th1 or Th2 cells. We determined whether heat-shock protein X (HspX) purified from Mycobacterium tuberculosis regulates the Th1/Th2 immune response in an ovalbumin (OVA)-induced murine model of asthma. HspX increased interferon-gamma, IL-17A, -12 and transforming growth factor (TGF)-${\beta}$ production and T-bet gene expression but reduced IL-13 production and GATA-3 gene expression. HspX also inhibited asthmatic reactions as demonstrated by an increase in the number of eosinophils in bronchoalveolar lavage fluid, inflammatory cell infiltration in lung tissues, airway luminal narrowing, and airway hyper-responsiveness. Furthermore, HspX enhanced OVA-induced decrease of regulatory T cells in the mediastinal lymph nodes. This study provides evidence that HspX plays critical roles in the amelioration of asthmatic inflammation in mice. These findings provide new insights into the immunotherapeutic role of HspX with respect to its effects on a murine model of asthma.
Proceedings of the Korean Society of Soil and Groundwater Environment Conference
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2004.04a
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pp.473-476
/
2004
In this study, hydrochemical studies of thermal waters in the Bugok and Magumsan areas showing geothermal anomalies were carried, and the applicability of ion seothermometers and multiple mineral equilibrium approach was examined to estimate their potential deep reservoir temperatures. Typical thermal waters of the two areas are clearly grouped into two major types, according to water chemistry: Na-Cl type (group A) and Na-SO4 type (group D). Compared to group A, group B and C waters show some modifications in chemistry. Group E waters show the modified chemistry from group D. Geothermal waters from the two areas showed some different chemical characteristics. The thermal waters of group A and B in Magumsan area are typically neutral to alkaline (pH=6.7 to 8.1) and Cl-rich (up to 446.1 mg/L), while the waters of group D and E in Bugok area are alkaline (pH=7.6 to 10.0) and SO$_4$-rich (up to 188.0 mg/L). The group A (Na-Cl type) and group D (Na-SO$_4$ type) waters correspond to mature or partially immature water, whereas the other types are immature water. The genesis of geothermal waters are considered as follows: group A and B waters were formed by seawater infiltration into reservoir rocks along faults and fracture zones and possibly affected by fossil connate waters in lithologic units through which deep hot waters circulate; on the other hand, group D and E waters were formed by the oxidation of sulfide minerals (mainly pyrite) in surrounding sedimentary rocks and/or hydrothermal veins occurring along restricted fracture channels and were possibly affected by the input and subsequent oxidation of S-bearing gases (e.g. H2S) from deep thermal reservoir (probably, cooling pluton). The application of quartz, Na-K, K-Mg geothermometers to the chemistry of representative group A and D waters yielded a reasonable temperature estimate (99-147$^{\circ}C$ and 90-142$^{\circ}C$) for deep geothermal reservoir. Aqueous liquid-rich fluid inclusions in fracture calcites obtained from drillcores in Bugok area have an average homogenization temperature of 128$^{\circ}C$, which corresponds to the results from ion geothermometers. The multiple mineral equilibrium approach yielded a similar temperature estimate (105-135$^{\circ}C$ and 100-14$0^{\circ}C$). We consider that deep reservoir temperatures of thermal waters in the Magumsan and Bugok areas can be estimated by the chemistry of typical Na-Cl and Na-SO$_4$ type waters and possibly approach 105-135$^{\circ}C$ and 100-14$0^{\circ}C$.
In asthma, T helper 2 (TH2)-type cytokines such as interleukin (IL)-4, IL-5, and IL-13 are produced by activated $CD^{4+}$ T cells. Dendritic cells played an important role in determining the fate of naive T cells into either $T_H1$ or $T_H2$ cells. We determined whether RG-II regulates the $T_H1/T_H2$ immune response by using an ovalbumin-induced murine model of asthma. RG-II reduced IL-4 production but increased interferon-gamma production, and inhibited GATA-3 gene expression. RG-II also inhibited asthmatic reactions including an increase in the number of eosinophils in bronchoalveolar lavage fluid, an increase in inflammatory cell infiltration in lung tissues, airway luminal narrowing, and airway hyperresponsiveness. This study provides evidence that RG-II plays a critical role in ameliorating the pathogenic process of asthmatic inflammation in mice. These findings provide new insights into the immunotherapeutic role of RG-II in terms of its effects in a murine model of asthma.
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