• Title/Summary/Keyword: fluid infiltration

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Bio-Inspired Surface Modification of 3-Dimensional Polycaprolactone Scaffold for Enhanced Cellular Behaviors

  • Jo, Seon-Ae;Gang, Seong-Min;Park, Su-A;Lee, Hae-Shin
    • Proceedings of the Korean Vacuum Society Conference
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    • 2011.08a
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    • pp.202-202
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    • 2011
  • The research of 3-dimensional (3-D) scaffold for tissue engineering has been widely investigated as the importance of the 3-D scaffold increased. 3-D scaffold is needed to support for cells to proliferate and maintain their biological functions. Furthermore, its architecture defines the shape of the new bone and cartilage growth. Polycaprolactone (PCL) has been one of the most promising materials for fabricating 3-D scaffold owing to its excellent mechanical property and biocompatibility. However, there are practical problems for using it, in vitro and in vivo; extracellular matrix components and nutrients cannot penetrate into the inner space of scaffold, due to its hydrophobic property, and thus cell seeding and attachment onto the inner surface remain as a challenge. Thus, the surface modification strategy of 3-D PCL scaffold is prerequisite for successful tissue engineering. Herein, we utilized a mussel-inspired approach for surface modification of 3-D PCL scaffold. Modification of 3-D PCL scaffolds was carried out by simple immersion of scaffolds into the dopamine solution and stimulated body fluid, and as a result, hydroxyapatite-immobilized 3-D PCL scaffolds were obtained. After surface modification, the wettability of 3-D PCL scaffold was considerably changed, and infiltration of the pre-osteoblastic cells into the 3-D scaffold followed by the attachment onto the surface was successfully achieved.

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Genome-Wide Transcriptional Response During the Development of Bleomycin-Induced Pulmonary Fibrosis in Sprague-Dawley Rats

  • Park, Han-Jin;Yang, Mi-Jin;Oh, Jung-Hwa;Yang, Young-Su;Kwon, Myung-Sang;Song, Chang-Woo;Yoon, Seok-Joo
    • Toxicological Research
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    • v.26 no.2
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    • pp.137-147
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    • 2010
  • Pulmonary fibrosis is a common consequence of many lung diseases and a leading cause of morbidity and mortality. The molecular mechanisms underlying the development of pulmonary fibrosis remain poorly understood. One model used successfully to study pulmonary fibrosis over the past few decades is the bleomycin-induced pulmonary fibrosis model. We aimed to identify the genes associated with fibrogenesis using an Affymetrix GeneChip system in a bleomycin-induced rat model for pulmonary fibrosis. To confirm fibrosis development, several analyses were performed, including cellular evaluations using bronchoalveolar lavage fluid, measurement of lactate dehydrogenase activity, and histopathological examinations. Common aspects of pulmonary fibrosis such as prolonged inflammation, immune cell infiltration, emergence of fibroblasts, and deposition of extracellular matrix and connective tissue elements were observed. Global gene expression analysis revealed significantly altered expression of genes ($\geq$ 1.5-fold, p < 0.05.) in a time-dependent manner during the development of pulmonary fibrosis. Our results are consistent with previous results of well-documented gene expression. Interestingly, the expression of triggering receptor expressed on myeloid cells 2 (Trem2), secreted phosphoprotein 1 (Spp1), and several proteases such as Tpsab1, Mcpt1, and Cma1 was considerably induced in the lung after bleomycin treatment, despite little evidence that they are involved in pulmonary fibrogenesis. These data will aid in our understanding of fibrogenic mechanisms and contribute to the identification of candidate biomarkers of fibrotic disease development.

Numerical analyses using CFD on the pressure losses of the grout flow with variation of joint roughness and grout features (전산유동역학을 이용한 절리 거칠기 및 주입재 특성에 따른 그라우트 주입 시 압력 손실 해석)

  • Sagong, Myung;Ryu, Sung-ha
    • Journal of Korean Tunnelling and Underground Space Association
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    • v.20 no.6
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    • pp.989-1002
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    • 2018
  • Grouting for the rock joint is to strengthen the rock strata by infiltrating cement grout materials into the rock joints. Grouting is one of a field of study which is difficult to develop deterministic and quantitative design approach because of multiphase behaviors of grout materials and 3 dimensional features of rock joints. Therefore, GIN (Grouting Intensity Number) can be a good index with appropriate monitoring of pressure and volume of grout. In this paper, we investigate the effects of joint roughness (JRC) and rheology of cement material during the infiltration of cement grout material into rock joint through CFD (computational fluid dynamics) analyses. With rough joint surface and increase of WC ratio, the frictional resistance during the grouting increases. The results have been summarized with polynomial correlations.

HemoHIM, A herbal preparation, alleviates airway inflammation caused by cigarette smoke and lipopolysaccharide

  • Shin, Na-Rae;Kim, Sung-Ho;Ko, Je-Won;Park, Sung-Hyeuk;Lee, In-Chul;Ryu, Jung-Min;Kim, Jong-Choon;Shin, In-Sik
    • Laboraroty Animal Research
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    • v.33 no.1
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    • pp.40-47
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    • 2017
  • HemoHIM, herbal preparation has designed for immune system recovery. We investigated the anti-inflammatory effect of HemoHIM on cigarette smoke (CS) and lipopolysaccharide (LPS) induced chronic obstructive pulmonary disease (COPD) mouse model. To induce COPD, C57BL/6 mice were exposed to CS for 1 h per day (eight cigarettes per day) for 4 weeks and intranasally received LPS on day 26. HemoHIM was administrated to mice at a dose of 50 or 100 mg/kg 1h before CS exposure. HemoHIM reduced the inflammatory cell count and levels of tumor necrosis factor receptor (TNF)-${\alpha}$, interleukin (IL)-6 and IL-$1{\beta}$ in the broncho-alveolar lavage fluid (BALF) induced by CS+LPS exposure. HemoHIM decreased the inflammatory cell infiltration in the airway and inhibited the expression of iNOS and MMP-9 and phosphorylation of Erk in lung tissue exposed to CS+LPS. In summary, our results indicate that HemoHIM inhibited a reduction in the lung inflammatory response on CS and LPS induced lung inflammation via the Erk pathway. Therefore, we suggest that HemoHIM has the potential to treat pulmonary inflammatory disease such as COPD.

Antiasthmatic effects on Pinellia ternate Breitenbach(PTB) water extracts against airway inflammation and hyperresponsiveness induced by diesel exhaust particles with ovalbumin sensitization in BALB/c mice (생쥐에서 ovalbumin과 디젤배기가스 입자로 유도된 기도염증과 기도 과민성에 대한 반하 물 추출물의 항천식 효과)

  • Kim, Seung Hyung;Lim, Heung Bin
    • The Korea Journal of Herbology
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    • v.28 no.1
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    • pp.65-71
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    • 2013
  • Objectives : Asthma is a chronic, complex respiratory disease, caused by airway obstruction, airway eosinophilic inflammation(AEI), and airway hyperresponsiveness(AHR). This study was conducted to determine whether oral administration of crude water extracts of Pinellia ternate Breitenbach(PTB) has an antiasthmatic potential in the treatment of asthma in mice. Methods : Asthmatic AEI and AHR were induced by systemic sensitization to ovalbumin(OVA) by intratracheal instillation with 0.1 mg/mL suspension of diesel exhaust particles(DEP) once a week for 10 weeks in BALB/c mice. Crude PTB water extracts(50 mg/kg and 200 mg/kg) were orally administered 5 times a week for 10 weeks. Cyclosporin(10 mg/kg) was administrered the same manner as a positive control. Results : Long-term treatment with crude PTB water extracts suppressed the infiltration of inflammatory cells, including eosinophils, into airways from blood. It also reduced asthmatic AEI and AHR by attenuating the increase in the levels of cytokines such as interleukin(IL)-4, IL-5 and IL-13 in bronchoalveolar lavage fluid(BALF), as well as the levels of histamine and OVA-specific IgE in blood. However, the effect of crude PTB water extracts(200 mg/kg) was not likely to be stronger than that of cyclosporin(10 mg/kg). Conclusion : These results suggest that crude PTB water extracts have inhibitory effects on AEI and AHR in a mouse model of asthma and may act as a potential Th2 cytokine antagonist, and have a therapeutic effect on allergic asthma.

Ante-Mortem Diagnosis of an Atypical Mixed Form of Feline Infectious Peritonitis through Pericardial Effusion Analysis in a Cat

  • Junyoung Kim;Yebeen Kim;Jihye Choi;Junghee Yoon
    • Journal of Veterinary Clinics
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    • v.40 no.4
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    • pp.308-313
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    • 2023
  • A 1-year-old castrated male Korean Shorthair cat presented with dyspnea, anorexia, lethargy, and seizures. Physical examination revealed salivation, right forelimb hemiparesis, and rapid breathing. No abnormalities were detected on auscultation. Laboratory findings revealed increased levels of bilirubin, aspartate aminotransferase (AST), globulin, glucose, and a decreased albumin-to-globulin (A:G) ratio. Both N-terminal pro-B-type natriuretic peptide (NT-proBNP) and feline serum amyloid A (fSAA) levels were significantly elevated. Thoracic radiography revealed mild cardiomegaly and diffuse increased interstitial infiltration with soft tissue opacity in the periphery of the right caudal pleural space. Echocardiography and lung ultrasonography were performed to investigate the cause of mild cardiomegaly and soft tissue opacity in the pleural space. Echocardiography revealed a mild amount of echogenic pericardial effusion, and lung ultrasonography showed an echogenic soft tissue mass with no blood signal in the right caudal pleural space, suggestive of a granulomatous lesion. After obtaining 5 mL of pericardial fluid through pericardiocentesis, cytology of the pericardial effusion sample revealed marked neutrophils and macrophages with no bacteria. IDEXX feline infectious peritonitis (FIP) virus real-time reverse transcriptase polymerase chain reaction (RT-PCR) confirmed the presence of the FIP virus biotype in the sample. This case presents a rarely reported atypical mixed form of FIP in a cat diagnosed ante-mortem using pericardial effusion analysis. In this case, ultrasound examination played a crucial role in the definitive diagnosis of FIP by PCR biotyping through pericardiocentesis. Ultrasonography can be highly beneficial in guiding the diagnosis and evaluation of cats with suspected FIP.

Bronchoscopic Findings of Pulmonary Paragonimiasis

  • Jeon, Kyeongman;Song, Jae-Uk;Um, Sang-Won;Koh, Won-Jung;Suh, Gee Young;Chung, Man Pyo;Kwon, O Jung;Han, Joungho;Kim, Hojoong
    • Tuberculosis and Respiratory Diseases
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    • v.67 no.6
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    • pp.512-516
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    • 2009
  • Background: Pulmonary paragonimiasis is a subacute to chronic inflammatory disease of the lung caused by lung flukes that result in prolonged inflammation and mechanical injury to the bronchi. However, there are few reports on the bronchoscopic findings of pulmonary paragonimiasis. This report describes the bronchoscopic findings of pulmonary paragonimiasis. Methods: The bronchosocpic findings of 30 patients (20 males, median age 50 years) with pulmonary paragonimiasis between May 1995 and December 2007 were reviewed retrospectively. Results: The diagnoses were based on a positive serologic test results for Paragonimus-specific antibodies in 13 patients (43%), or the detection of Paragonimus eggs in the sputum, bronchial washing fluid, or lung biopsy specimens in 17 patients (57%). The bronchoscopic examinations revealed endobronchial lesions in 17 patients (57%), which were located within the segmental bronchi in 10 patients (59%), lobar bronchi in 6 patients (35%) and main bronchi in 1 patient (6%). The bronchoscopic characteristics of endobronchial lesions were edematous swelling of the mucosa (16/17, 94%) and mucosal nodularity (4/17, 24%), accompanied by bronchial stenosis in 16 patients (94%). Paragonimus eggs were detected in the bronchial washing fluid of 9 out of the 17 patients with endobronchial lesions. The bronchial mucosal biopsy specimens showed evidence of chronic inflammation with eosinophilic infiltration in 6 out of 11 patients (55%). However, no adult fluke or ova were found in the bronchial tissue. Conclusion: Bronchial stenosis with mucosal changes including edematous swelling and mucosal nodularity is the most common bronchoscopic finding of pulmonary paragonimiasis.

Apios americana Medik Extract Alleviates Lung Inflammation in Influenza Virus H1N1- and Endotoxin-Induced Acute Lung Injury

  • Sohn, Sung-Hwa;Lee, Sang-Yeon;Cui, Jun;Jang, Ho Hee;Kang, Tae-Hoon;Kim, Jong-Keun;Kim, In-Kyoung;Lee, Deuk-Ki;Choi, Seulgi;Yoon, Il-Sub;Chung, Ji-Woo;Nam, Jae-Hwan
    • Journal of Microbiology and Biotechnology
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    • v.25 no.12
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    • pp.2146-2152
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    • 2015
  • Apios americana Medik (hereinafter Apios) has been reported to treat diseases, including cancer, hypertension, obesity, and diabetes. The therapeutic effect of Apios is likely to be associated with its anti-inflammatory activity. This study was conducted to evaluate the protective effects of Apios in animal models of acute lung injury induced by lipopolysaccharide (LPS) or pandemic H1N1 2009 influenza A virus (H1N1). Mice were exposed to LPS or H1N1 for 2-4 days to induce acute lung injury. The treatment groups were administered Apios extracts via oral injection for 8 weeks before LPS treatment or H1N1 infection. To investigate the effects of Apios, we assessed the mice for in vivo effects of Apios on immune cell infiltration and the level of pro-inflammatory cytokines in the bronchoalveolar lavage (BAL) fluid, and histopathological changes in the lung. After induction of acute lung injury, the numbers of neutrophils and total cells were lower in the Apios-treated groups than in the non-Apios-treated LPS and H1N1 groups. The Apios groups tended to have lower levels of tumor necrosis factor-a and interleukin-6 in BAL fluid. In addition, the histopathological changes in the lungs were markedly reduced in the Apios-treated groups. These data suggest that Apios treatment reduces LPS- and H1N1-induced lung inflammation. These protective effects of Apios suggest that it may have therapeutic potential in acute lung injury.

Effect of the Inhibition of PLA2 on Oxidative Lung Injury Induced by $Interleukin-1{\alpha}$

  • Lee, Young-Man;Cho, Hyun-Gug;Park, Yoon-Yub;Kim, Jong-Ki;Lee, Yoon-Jeong;Park, Won-Hark;Kim, Teo-An
    • The Korean Journal of Physiology and Pharmacology
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    • v.2 no.5
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    • pp.617-628
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    • 1998
  • In order to understand the pathogenetic mechanism of adult respiratory distress syndrome (ARDS), the role of phospholipase A2 (PLA2) in association with oxidative stress was investigated in rats. $Interleukin-1{\alpha}\;(IL-1,\;50\;{\mu}g/rat)$ was used to induce acute lung injury by neutrophilic respiratory burst. Five hours after IL-1 insufflation into trachea, microvascular integrity was disrupted, and protein leakage into the alveolar lumen was followed. An infiltration of neutrophils was clearly observed after IL-1 treatment. It was the origin of the generation of oxygen radicals causing oxidative stress in the lung. IL-1 increased tumor necrosis factor (TNF) and cytokine-induced neutrophil chemoattractant (CINC) in the bronchoalveolar lavage fluid, but mepacrine, a PLA2 inhibitor, did not change the levels of these cytokines. Although IL-1 increased PLA2 activity time-dependently, mepacrine inhibited the activity almost completely. Activation of PLA2 elevated leukotriene C4 and B4 (LTC4 and LTB4), and 6-keto-prostaglandin $F2{\alpha}\;(6-keto-PGF2{\alpha})$ was consumed completely by respiratory burst induced by IL-1. Mepacrine did not alter these changes in the contents of lipid mediators. To estimate the functional changes of alveolar barrier during the oxidative stress, quantitative changes of pulmonary surfactant, activity of gamma glutamyltransferase (GGT), and ultrastructural changes were examined. IL-1 increased the level of phospholipid in the bronchoalveolar lavage (BAL) fluid, which seemed to be caused by abnormal, pathological release of lamellar bodies into the alveolar lumen. Mepacrine recovered the amount of surfactant up to control level. IL-1 decreased GGT activity, while mepacrine restored it. In ultrastructural study, when treated with IL-1, marked necroses of endothelial cells and type II pneumocytes were observed, while mepacrine inhibited these pathological changes. In histochemical electron microscopy, increased generation of oxidants was identified around neutrophils and in the cytoplasm of type II pneumocytes. Mepacrine reduced the generation of oxidants in the tissue produced by neutrophilic respiratory burst. In immunoelectron microscopic study, PLA2 was identified in the cytoplasm of the type II pneumocytes after IL-1 treatment, but mepacrine diminished PLA2 particles in the cytoplasm of the type II pneumocyte. Based on these experimental results, it is suggested that PLA2 plays a pivotal role in inducing acute lung injury mediated by IL-1 through the oxidative stress by neutrophils. By causing endothelial damage, functional changes of pulmonary surfactant and alveolar type I pneumocyte, oxidative stress disrupts microvascular integrity and alveolar barrier.

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Hu.4-1BB-Fc fusion protein inhibits allergic inflammation and airway hyperresponsiveness in a murine model of asthma

  • Kim, Byoung-Ju;Kwon, Ji-Won;Seo, Ju-Hee;Choi, Won-Ah;Kim, Young-Jun;Kang, Mi-Jin;Yu, Jin-Ho;Hong, Soo-Jong
    • Clinical and Experimental Pediatrics
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    • v.54 no.9
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    • pp.373-379
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    • 2011
  • Purpose: 4-1BB (CD 137) is a costimulatory molecule expressed on activated T-cells. Repression by 4-1BB is thought to attenuate Th2-mediated allergic reactions. The aim of this study was to investigate the effect of 4-1BB on allergic airway inflammation in a murine asthma model. Methods: BALB/c mice were sensitized to and challenged with ovalbumin (OVA). Hu.4-1BB-Fc was administered 1 day before the first OVA sensitization or 1 day after the second OVA sensitization. Following antigen challenge, airway responsiveness to methacholine was assessed and bronchoalveolar lavage (BAL) fluid was analyzed. Total immunoglobulin (Ig) E, OVA-specific IgE, $IgG_1$, and $IgG_{2a}$ levels in sera were measured by enzyme-linked immunosorbent assay. Lung pathology was also evaluated. Results: In mice treated with Hu.4-1BB-Fc before the first OVA sensitization, there was a marked decrease in airway hyperresponsiveness, total cell count, and eosinophil count in the BAL fluid. In addition, Hu.4-1BB-Fc treatment decreased serum OVA-specific $IgG_1$ levels and increased serum $IgG_{2a}$ level significantly compared with the corresponding levels in mice sensitized to and challenged with OVA. Hu.4-1BB-Fc-treated mice also showed suppressed peribronchial and perivascular inflammatory cell infiltration. In contrast, treatment with Hu.4-1BB-Fc 1 day after sensitization had no effect on airway hyperresponsiveness and showed less suppression of inflammation in lung tissue. Conclusion: Administration of Hu.4-1BB-Fc can attenuate airway inflammation and hyperreactivity in a mouse model of allergic airway inflammation. In addition, administration before sensitization may be more effective. These findings suggest that 4-1BB may be a useful therapeutic molecule against asthma.