• Korean Journal of Clinical Laboratory Science
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• v.48 no.2
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• pp.102-108
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• 2016

Der p 2 is the major allergen of the house dust mite (HDM) associated with the development of allergic diseases. The pathogenic mechanism of the allergy is related to cytokine release of lymphocytes and constitutive apoptosis of neutrophils. In the present study, we examined whether Der p 2 induces cytokine release of lymphocytes, which is involved in regulation of neutrophil apoptosis. In normal and allergic subjects, Der p 2 enhanced the secretion of IL-6, IL-8, MCP-1, and GM-CSF in a time-dependent manner. Although Der p 2 was weakly effective against neutrophil apoptosis, conditioned media collected from normal and allergic lymphocytes after Der p 2 treatment inhibited the apoptosis of normal and allergic neutrophils. Der p 2 showed stronger inhibition of apoptosis of allergic neutrophils cocultured with allergic lymphocytes than normal neutrophils cocultured with normal lymphocytes. These findings improve our understanding of the role of Der p 2 in regulation of lymphocytes and neutrophils and will enable elucidation of allergy pathogenesis.

• The Journal of the Korean Society for Microbiology
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• v.35 no.2
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• pp.159-169
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• 2000

Scrub typhus is caused by Orientia tsutsugamushi characterized by fever, headache, lymphadenopathy and eschar formation. Infiltration of inflammatory cells around blood vessels and within the affected organs isS known to be pathologic hallmark of the scrub typhus. Recently, expression of adhesion molecules on vascular endothelial cells was implicated as an important pathogenic mechanism in rickettsial disease. This study was performed to examine the expression of adhesion molecules and to investigate its role in the pathogenesis of O. tsutsugamushi infection. The expression of adhesion molecules on human umbilical vein endothelial cells (HUVEC) was measured by flow cytometry and indirect immunofluorescence. Expression of E-selectin, ICAM-1 and VCAM-1 was significantly increased 4 hours after the infection and persisted at least for 24 hours. Expression of those molecules was not induced by killed O. tsutsugamushi. Adhesion of polymorphonuclear cells and mononuclear cells to HUVEC was increased after the infection with O. tsutsugamushi. In conclusion, adhesion molecules are expressed on HUVEC during the infection of live O. tsutsugamushi and those molecules can contribute to the infiltration of inflammatory cells during the infection.

• Journal of Trauma and Injury
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• v.31 no.2
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• pp.51-57
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• 2018

Purpose: Patients with diffuse axonal injury experience various disabilities and have a high cost of treatment. Recent researches have revealed the underlying mechanism and pathogenesis of diffuse axonal injury. This study aimed to investigate the correlation between the radiological grading of diffuse axonal injury and the clinical outcomes of patients. Methods: From January 2011 to December 2016, among 294 patients with traumatic brain injury, 44 patients underwent magnetic resonance imaging (MRI). A total of 18 patients were enrolled in this study except for other cerebral injuries, such as cerebral hemorrhage or hypoxic brain damage. Demographic data, clinical data, and radiological findings were retrospectively reviewed. The grading of diffuse axonal injury was analyzed based on patient's MRI findings. Results: For the most severe diffuse axonal injury patients, prolonged intensive care unit (ICU) stay (p=0.035), hospital stay (p=0.012), and prolonged mechanical ventilation (p=0.030) were observed. However, there was no significant difference in healthcare-associated infection rates between MRI grading (p=0.123). Massive transfusion, initial hemoglobin and lactate levels, and MRI gradings were found to be highly significant in predicting the duration of unconsciousness. Conclusions: This study showed that patients with high grade diffuse axonal injury have prolonged ICU stays and significantly longer hospital stays. Deteriorated mental patients with high energy injuries should be evaluated to identify diffuse axonal injuries by using an appropriate imaging tool, such as MRI. It will be important to predict the duration of consciousness recovery using MRI scans.

• Biomolecules & Therapeutics
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• v.16 no.4
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• pp.394-402
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• 2008

Atopic dermatitis (AD) is an inflammatory skin disease commonly characterized by infiltration of inflammatory cells into skin lesions. Keratinocytes produce many chemokines that are involved in the pathogenesis of skin disorders. In particular, macrophage-derived chemokine (MDC/CCL22) and thymus and activationregulated chemokine (TARC/CCL17) are Th2-type cytokines. Serum MDC and TARC levels are increased in AD patients. In this study, we investigated the anti-inflammatory effect and mechanism of action of the active fraction from Prunus yedoensis bark. We evaluated their inhibitory effects on the AD-like inflammatory markers (MDC and TARC) and JAK-STAT pathway (STAT1) in HaCaT keratinocytes. The EtOAc fraction of the crude extract (80% EtOH) and the E5 sub-fraction potently inhibited the induction of MDC and TARC mRNA and protein at 50 ${\mu}g$/mL in HaCaT cells. In addition, the E5 sub-fraction inhibited the phosphorylation of STAT1 protein associated with IFN-$\gamma$ signaling transduction in a dose-dependent manner. Thus, P. yedoensis may have antiatopic activity by suppressing the inflammatory chemokines (MDC and TARC).

• Journal of Chest Surgery
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• v.44 no.2
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• pp.123-130
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• 2011

Background: The aim of the present study was to identify chromosomal loci that contribute to the pathogenesis of aortic dissection (AD) in a Korean population using array comparative genomic hybridization (CGH) and to confirm the results using real-time polymerase chain reaction (PCR). Materials and Methods: Eighteen patients with ADs were enrolled in this study. Genomic DNA was extracted from individual blood samples, and array CGH analyses were performed. Four corresponding genes with obvious genomic changes were analyzed using real-time PCR in order to assess the level of genomic imbalance identified by array CGH. Results: Genomic gains were most frequently detected at 8q24.3 (56%), followed by regions 7q35, 11q12.2, and 15q25.2 (50%). Genomic losses were most frequently observed at 4q35.2 (56%). Real-time PCR confirmed the results of the array CGH studies of the COL6A2, DGCR14, PCSK6, and SDHA genes. Conclusion: This is the first study to identify candidate regions by array CGH in patients with ADs. The identification of genes that may predispose an individual to AD may lead to a better understanding of the mechanism of AD formation. Further multicenter studies comparing cohorts of patients of different ethnicities are warranted.

• Journal of Microbiology
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• v.44 no.4
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• pp.375-382
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• 2006

From its initial colonization to causation of disease, Streptococcus pneumoniae has evolved strategies to cope with a number of stressful in vivo environmental conditions. In order to analyze a global view of this organism's response to heat shock, we established a 2-D electrophoresis proteome map of the S. pneumoniae D39 soluble proteins under in vitro culture conditions and performed the comparative proteome analysis to a 37 to $42^{\circ}C$ temperature up-shift in S. pneumoniae. When the temperature of an exponentially growing S. pneumoniae D39 culture was raised to $42^{\circ}C$, the expression level of 25 proteins showed changes when compared to the control. Among these 25 proteins, 12 were identified by MALDI-TOF and LC-coupled ESI MS/MS. The identified proteins were shown to be involved in the general stress response, energy metabolism, nucleotide biosynthesis pathways, and purine metabolism. These results provide clues for understanding the mechanism of adaptation to heat shock by S. pneumoniae and may facilitate the assessment of a possible role for these proteins in the physiology and pathogenesis of this pathogen.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.4
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• pp.479-491
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• 1998

In order to know the pathogenesis of adult respiratory distress syndrome (ARDS) in association with the oxidative stress by neutrophils, the role of platelet activating factor (1-0-alkyl-2-acetyl-snglycero-3-phosphocholine, PAF) was investigated during acute lung injury induced by interleukin- $1{\alpha}$ (IL-1) in rats. An insufflation of IL-1 into the rat's trachea increased the acetyltransferase activity in the lung and the increase of PAF content was followed. As evidences of acute lung injury by neutrophilic respiratory burst, lung leak index, myeloperoxidase activity, numbers of neutrophils in the bronchoalveolar lavage fluid, neutrophilic adhesions to endothelial cells and NBT positive neutrophils were increased after IL-1 treatment. In addition, a direct instillation of PAF into the trachea caused acute lung leak and the experimental results showed a similar pattern in comparison with IL-1 induced acute lung injury. For the confirmation of oxidative stress during acute lung leak by IL-1 and PAF, a histochemical electron microscopy was performed. In IL-1 and PAF treated lungs of rats, the deposits of cerrous perhydroxide were found. To elucidate the role of PAF, an intravenous injection of PAF receptor antagonist, WEB 2086 was given immediately after IL-1 or PAF treatment. WEB 2086 decreased the production of hydrogen peroxide and the acute lung leak. In ultrastructural study, WEB 2086 mitigated the pathological changes induced by IL-1 or PAF. The nuclear factor kappa B (NFkB) was activated by PAF and this activation was inhibited by WEB 2086 almost completely. Based on these experimental results, it is suggested that the PAF produced in response to IL-1 through the remodeling pathway has the major role for acute lung injury by neutrophilic respiratory burst. In an additional experiment, we can also come to conclude that the activation of the NFkB by PAF is thought to be the fundamental mechanism to initiate the oxidative stress by neutrophils causing release of proinflammatory cytokines and activation of phospholipase $A_2$.

• Journal of Life Science
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• v.16 no.6
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• pp.1066-1070
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• 2006

Smooth muscle cell (SMC) proliferation is important in the pathogenesis of vascular proliferative disorders. Understanding of the molecular mechanism underlying SMC growth after arterial injury would have therapeutic implications. Here we report that receptor activator of $NF-{\kappa}B$ ligand (RANKL), a member of tumor necrosis factor (TNF) family, promotes the proliferation of SMC, leading to decreased expression of p21 and enhancement of SMC growth. ERK and p38 phosphorylation was enhanced after RANKL treatment in SMC. Inhibition of ERK/p38 MAPK activity by PD98059/SB203580 completely abolished RANKL-induced proliferation of SMC, indicating ERK and p38 MAPK are essential for RANKL-induced SMC proliferation. Taken together, our findings demonstrate that RANK-RANKL-ERK/p38 pathway is important for proliferation of SMC and that these molecules may be the new therapeutic targets for the prevention of vascular diseases.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.10 no.1
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• pp.159-184
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• 1997

A Literature study on the language disturbance, the results are as follows; 1. Utterance was closely concerned not only the vocal organs(pharynx, larynx, epiglottis, lips, tongue, vocal cord etc,) but also five viscera{especially heart, lung, kidney etc.) in The Yellow Emperor's Canon of Internal Medicine. It is very like the vocal mechanism in Medical science. 2. In the language disturbance, It is classified with dysarthria and dysphasia in Medical science. But in Oriental medicine, it is expressed the language disturbance as coma-speech lessness, stiff tongue-speechlessness, frightening-speechlessness etc. Especially in Oriental medicine, Non-utterance is called aphasia in literature study. 3. In the concern of the language disturbance and five viscera, $Heart{\cdot}Lung{\cdot}Kidney$ are counted of first importence. In differential diagnosis, It is divided sthenia-syndrome and asthenia-syndrome. Sthenia-syndrome is classified with wind-cold, fire-evil, adverseness of vital energy, stagnation of phlegm, is easy to cure. Asthenia-syndrome is classified with sexual desire, anxiety-meditation, fear, is hard to cure. 4. The pathogenesis of dysphasia originated from two factors; The first internal damages are consumption of body fluid caused by lung-dryness and yin-dificiency of lung & kidney. The second disease caused by exogenous evjls is sluggishness of lung-energy. 5. In many using points of acupuncture of the language disturbance, the order is LI-4(合谷), H-7(神門), K-l(湧泉), L-3(太衝), K-3(太谿), S-6(三陰交), H-5(通里), G-15(아門), C-23(廉泉), S-40(豊降), K-6(照海), L-7(列缺), S-36(足三里) etc.

• The Journal of Korean Medicine
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• v.26 no.1 s.61
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• pp.26-36
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• 2005

Objective : Many traditional herbal remedies exhibit several beneficial effects including anti-inflammation. Euonymus alatus (Thunb.) Sieb (EA), known as Gui jun woo in Korea, has long been used in folk medicine to regulate Qi (bodily energy) and blood circulation, relieve pain, eliminate stagnant blood, and treat dysmenorrhea in oriental countries. The exact mechanism of the anti-inflammatory action of Euonymus alatus (Thunb.) Sieb (EA), however, has not been determined. Methods: Since there is increasing evidence that nitric oxide (NO) plays a crucial role in the pathogenesis of inflammatory diseases, this study was undertaken to address whether the methanol (MeOH) extract and its fractions of the bark of EA could modulate the expression of inducible NO synthase (iNOS) in thioglycollate-elicited murine peritoneal macrophages and murine macrophage cell line, RA W264.7 cells. Results: Stimulation of the peritoneal macrophages and RAW264.7 cells with $interferon-\gamma\;(IFN-\gamma)$ and lipopolysaccharide (LPS) resulted in increased production of NO in the medium. However, the butanol (BuOH) fraction of the MeOH extract of EA barks showed marked inhibition of NO synthesis in a dose-dependent manner. The inhibition of NO synthesis was reflected in the decreased amount of iNOS protein, as determined by Western blotting. The BuOH fraction did not affect the viability of RA W264.7 cells, as assessed by methylthiazol-2-yl-2, 5-diphenyl tetrazolium bromide (MTT) assay; rather, it reduced endogenous NO-induced apoptotic cell death via inhibition of NO synthesis in RAW264.7 cells. On the other hand, the MeOH and BuOH fraction showed no inhibitory effect on the synthesis of NO by RAW264.7 cells, when iNOS was already expressed by the stimulation with $IFN-\gamma$ and LPS. Conclusion: Collectively, these results demonstrate that the MeOH and BuOH fraction inhibits NO synthesis by inhibition of the induction of iNOS in murine macrophages.