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Lee, Kyung Sun,Park, Seoung Ju,Kim, So Ri,Min, Kyung Hoon,Jin, Sun Mi,Lee, Hern Ku,Lee, Yong Chul American Association of Immunologists 2006 Journal of Immunology Vol.177 No.8
<P>Toluene diisocyanate (TDI) is a leading cause of occupational asthma. Although considerable controversy remains regarding its pathogenesis, TDI-induced asthma is an inflammatory disease of the airways characterized by airway remodeling. Peroxisome proliferator-activated receptor gamma (PPARgamma) has been shown to play a critical role in the control of airway inflammatory responses. However, no data are available on the role of PPARgamma in TDI-induced asthma. We have used a mouse model for TDI-induced asthma to determine the effect of PPARgamma agonist, rosiglitazone, or pioglitazone, and PPARgamma on TDI-induced bronchial inflammation and airway remodeling. This study with the TDI-induced model of asthma revealed the following typical pathophysiological features: increased numbers of inflammatory cells of the airways, airway hyperresponsiveness, increased levels of Th2 cytokines (IL-4, IL-5, and IL-13), adhesion molecules (ICAM-1 and VCAM-1), chemokines (RANTES and eotaxin), TGF-beta1, and NF-kappaB in nuclear protein extracts. In addition, the mice exposed to TDI developed features of airway remodeling, including thickening of the peribronchial smooth muscle layer, subepithelial collagen deposition, and increased airway mucus production. Administration of PPARgamma agonists or adenovirus carrying PPARgamma2 cDNA reduced the pathophysiological symptoms of asthma and decreased the increased levels of Th2 cytokines, adhesion molecules, chemokines, TGF-beta1, and NF-kappaB in nuclear protein extracts after TDI inhalation. In addition, inhibition of NF-kappaB activation decreased the increased levels of Th2 cytokines, adhesion molecules, chemokines, and TGF-beta1 after TDI inhalation. These findings demonstrate a protective role of PPARgamma in the pathogenesis of the TDI-induced asthma phenotype.</P>
Hydrogen Peroxide Induces Vascular Permeability via Regulation of Vascular Endothelial Growth Factor
Lee, Kyung Sun,Kim, So Ri,Park, Seoung Ju,Park, Hee Sun,Min, Kyung Hoon,Lee, Min Hee,Jin, Sun Mi,Jin, Gong Yong,Yoo, Wan Hee,Lee, Yong Chul American Thoracic Society 2006 AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR Vol.35 No.2
<P>Oxidative stress plays critical roles in initiation and/or worsening of respiratory disease process. Although reactive oxygen species (ROS) are shown to cause vascular leakage, the mechanisms by which ROS induce an increase in vascular permeability are not clearly understood. In this study, we have used a murine model to evaluate the effect of hydrogen peroxide (H(2)O(2)) to examine roles of ROS and the molecular mechanism in vascular permeability. The results have revealed that ROS levels, vascular endothelial growth factor (VEGF) expression, hypoxia-inducible factor-1alpha protein level, airway hyperresponsiveness, and vascular permeability are increased after inhalation of H(2)O(2). Administration of antioxidants markedly reduced plasma extravasation and VEGF levels in lungs treated with H(2)O(2). These results indicate that ROS may modulate vascular permeability via upregulation of VEGF expression.</P>
Lee, Kyung Sun,Kim, So Ri,Park, Seoung Ju,Lee, Ho Kyung,Park, Hee Sun,Min, Kyung Hoon,Jin, Sun Mi,Lee, Yong Chul American Society for PharmacologyExperimental Ther 2006 Molecular pharmacology Vol.69 No.6
<P>Vascular endothelial growth factor (VEGF) plays a pivotal role in the pathogenesis of bronchial asthma. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) has been implicated in regulating cell survival signaling through the phosphoinositide 3-kinase (PI3K)/Akt pathway. The key role of PI3K in VEGF-mediated signal transduction is established. However, the effects of PTEN on VEGF-mediated signaling in asthma are unknown. This study aimed to determine the effect of PI3K inhibitors and PTEN on VEGF expression in allergen-induced airway inflammation. We have used a female C57BL/6 mouse model for asthma to determine the role of PTEN in allergen-induced airway inflammation, specifically in the expression of VEGF. Allergen-induced airway inflammation leads to increased activity of PI3K in lung tissue. These mice develop the following typical pathophysiological features of asthma in the lungs: increased numbers of inflammatory cells of the airways; airway hyper-responsiveness; increased expression of interleukin (IL)-4, IL-5, IL-13, intercellular adhesion molecule 1, vascular cell adhesion molecule 1, regulated on activation normal T cell expressed and secreted (RANTES), and eotaxin; increased vascular permeability; and increased levels of VEGF. Administration of PI3K inhibitors or adenoviruses carrying PTEN cDNA reduced the symptoms of asthma and decreased the increased levels of plasma extravasation and VEGF in allergen-induced asthmatic lungs. These results indicate that PTEN reduces VEGF expression in allergen-induced airway inflammation.</P>
Ju Ri Lee,Seung Wan Suh,Ji Won Han,Seonjeong Byun,Soon Jai Kwon,Kyoung Hwan Lee,Kyung Phil Kwak,Bong Jo Kim,김신겸,김정란,Tae Hui Kim,Seung-Ho Ryu,Seok Woo Moon,Joon Hyuk Park,Dong Woo Lee,Jong Chul Youn,D 대한신경정신의학회 2019 PSYCHIATRY INVESTIGATION Vol.16 No.8
Objective We investigated the impact of depressed mood (dysphoria) and loss of interest or pleasure (anhedonia)on the risk of dementia in cognitively-normal elderly individuals. Methods This study included 2,685 cognitively-normal elderly individuals who completed the baseline and 4-year follow-up assessments of the Korean Longitudinal Study on Cognitive Aging and Dementia. We ascertained the presence of dysphoria and anhedonia using the Mini International Neuropsychiatric Inventory. We defined subjective cognitive decline as the presence of subjective cognitive complaints without objective cognitive impairments. We analyzed the association of dysphoria and anhedonia with the risk of cognitive disorders using multinomial logistic regression analysis adjusted for age, sex, education, Cumulative Illness Rating Scale score, Apolipoprotein E genotype, and neuropsychological test performance. Results During the 4-year follow-up period, anhedonia was associated with an approximately twofold higher risk of mild cognitive impairment (OR=2.09, 95% CI=1.20–3.64, p=0.008) and fivefold higher risk of dementia (OR=5.07, 95% CI=1.44–17.92, p=0.012) but was not associated with the risk of subjective cognitive decline. In contrast, dysphoria was associated with an approximately twofold higher risk of subjective cognitive decline (OR=2.06, 95% CI=1.33–3.19, p=0.001) and 1.7-fold higher risk of mild cognitive impairment (OR=1.75, 95% CI=1.00–3.05, p=0.048) but was not associated with the risk of dementia. Conclusion Anhedonia, but not dysphoria, is a risk factor of dementia in cognitively-normal elderly individuals.
( Ju-ri Jeong ),( Ju Hee Han ),( Ji-eun Cho ),( Wan-hee Lee ) 물리치료재활과학회 2016 Physical therapy rehabilitation science Vol.5 No.3
Objective: This study aimed to investigate the reliability and validity of a personal computer-based muscle viewer (PC-BMW) compared with that of a portable ultrasound (P-US) for measuring upper trapezius (UT) and transversus abdominis (TrA) muscle thickness at rest and during contraction. Design: Observational inter-rater reliability study. Methods: Fifty-five healthy participants (25 men, 30 women) participated in this study. PC-BMW and P-US were randomly measured at the UT and TrA muscles. Two examiners randomly obtained the images of all participants in 3 test sessions lasting 2 days. Intra-class correlation coefficients (ICCs), standard error of measurement, contraction ratio, and correlation were used to estimate reliability and validity. Pearson`s correlation coefficients were used to analyze the relationship between muscle thickness measures taken from PC-BMW and P-US. Results: The intra-rater reliability ICCs of UT and TrA muscle thickness for the PC-BMW were >0.995, indicating excellent reliability. Inter-rater reliability ICCs for the PC-BMW ranged from 0.963 to 0.987. The P-US also exhibited high reliability. A high correlation was found between the measurements of the two muscles in PC-BMW and P-US (p<0.01). Conclusions: PC-BMW provides clear and excellent images, is pocket-sized and less expensive than a conventional ultrasound imaging system. PC-BMW can be utilized variously and has the advantage of rehabilitative ultrasound imaging. More research is needed to evaluate the utility of PC-BMW for rehabilitation.
Ju-Ri Woo,Doo-Ho Choi,Muhammed Taofiq Hamza,Kyung-Oh Doh,Chang-Yoon Lee,Yeon-Sik Choo,Sangman Lee,Jong-Guk Kim,Heeyoun Bunch,Young-Bae Seu 한국균학회 2022 Mycobiology Vol.50 No.5
Regulation of proper gene expression is important for cellular and organismal survival, main- tenance, and growth. Abnormal gene expression, even for a single critical gene, can thwart cellular integrity and normal physiology to cause diseases, aging, and death. Therefore, gene expression profiling serves as a powerful tool to understand the pathology of diseases and to cure them. In this study, the difference in gene expression in Flammulina velutipes was compared between the wild type (WT) mushroom and the mutant one with clogging phe- nomenon. Differentially expressed transcripts were screened to identify the candidate genes responsible for the mutant phenotype using the DNA microarray analysis. A total of 88 genes including 60 upregulated and 28 downregulated genes were validated using the real- time quantitative PCR analysis. In addition, proteomic differences between the WT and mutant mushroom were analyzed using two–dimensional gel electrophoresis and matrix- assisted laser desorption/ionization-time of flight (MALDI-TOF). Interestingly, the genes iden- tified by these genomic and proteomic analyses were involved in stress response, transla- tion, and energy/sugar metabolism, including HSP70, elongation factor 2, and pyruvate kinase. Together, our data suggest that the aberrant expression of these genes attributes to the mutant clogging phenotype. We propose that these genes can be targeted to foster normal growth in F. velutipes.
Lee, Min Ju,Suh, Chae Ri,Shin, Jeong Hee,Lee, Jee Hyun,Lee, Yoon,Eun, Baik-Lin,Yoo, Kee Hwan,Shim, Jung Ok The Korean Society of Pediatric Gastroenterology 2019 Pediatric gastroenterology, hepatology & nutrition Vol.22 No.6
Arthrogryposis-renal dysfunction-cholestasis (ARC) syndrome is a rare autosomal recessive multisystemic disease that is associated with the liver, kidney, skin, and central nervous and musculoskeletal systems. ARC occurs as a result of mutations in the VPS33B (Vacuolar protein sorting 33 homolog B) or VIPAR (VPS33B interacting protein, apical-basolateral polarity regulator) genes. A female infant presented with neonatal cholestasis with a severe clinical outcome. She was diagnosed with ARC syndrome using targeted exome sequencing (TES). Exome sequencing revealed compound heterozygous mutations, c.707A>T and c.239+5G>A, in VPS33B, where c.707A>T was a novel variant; the resultant functional protein defects were predicted via in silico analysis. c.239+5G>A, a pathogenic mutation that affects splicing, is found in less than 0.1% of the general population. Invasive techniques, such as liver biopsies, did not contribute to a differential diagnosis of ARC syndrome; thus, early TES together with clinical presentations constituted an apparently accurate diagnostic procedure.
A FIXED POINT APPROACH FOR THE APPROXIMATION OF JORDAN TRIPLE LINEAR DERIVATIONS IN BANACH ALGEBRAS
Ju ri Lee,Eun young Son,Ick Soon Chang 충청수학회 2009 충청수학회지 Vol.22 No.2
We adopt the idea of C˘adariu and Radu to prove the stability of Jordan triple linear derivations and we take account of the Jacobson radical range problem for linear derivations.
Lee, Kyung Sun,Kim, So Ri,Park, Seoung Ju,Park, Hee Sun,Min, Kyung Hoon,Jin, Sun Mi,Lee, Moon Kyu,Kim, Uh Hyun,Lee, Yong Chul Elsevier 2006 The journal of allergy and clinical immunology Vol.118 No.1
<P><B>Background</B></P><P>Reactive oxygen species (ROSs) play a crucial role in the pathogenesis of airway inflammation. Peroxisome proliferator activated receptor (PPAR)-γ is also involved in airway inflammation. We have demonstrated that the administration of PPARγ agonists or adenovirus carrying PPARγ cDNA (AdPPARγ) reduced bronchial inflammation and airway hyperresponsiveness. However, the effects of PPARγ on ROS generation in conditions associated with airway inflammation have not been clarified.</P><P><B>Objective</B></P><P>This study aimed to investigate the effects of the PPARγ on ROS generation in allergic airway disease of mice.</P><P><B>Methods</B></P><P>We have used a female C57BL/6 mouse model for allergic airway disease to determine the role of PPARγ.</P><P><B>Results</B></P><P>In this study with an ovalbumin-induced murine model of allergic airway disease, the increased ROS generation and the increased expression of T<SUB>H</SUB>2 cell cytokines, adhesion molecules, chemokines, and vascular endothelial growth factor in lungs after ovalbumin inhalation were significantly reduced by the administration of PPARγ agonists or AdPPARγ. We also showed that the increased nuclear factor-κB and hypoxia-inducible factor 1α levels in nuclear protein extracts of lung tissues after ovalbumin inhalation were decreased by the administration of PPARγ agonists or AdPPARγ.</P><P><B>Conclusion</B></P><P>These results indicate that the effects of PPARγ are mediated by the modulation of ROS generation and activation of redox-sensitive transcription factor nuclear factor-κB and HIF-1α in allergic airway disease of mice.</P><P><B>Clinical implications</B></P><P>Thus, these findings provide a pivotal molecular mechanism for the use of PPARγ agonists to prevent and/or treat asthma and other airway inflammatory disorders.</P>