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Identification of Orfamide A as an Insecticidal Metabolite Produced by Pseudomonas protegens F6
Jang, Ja Yeong,Yang, Si Young,Kim, Young Cheol,Lee, Chul Won,Park, Myung Soo,Kim, Jin Cheol,Kim, In Seon American Chemical Society 2013 Journal of agricultural and food chemistry Vol.61 No.28
<P>The use of biosurfactants for agricultural crop protection has been gaining interest because they are generally biodegradable and environmentally friendly. In the present study, we identified an insecticidal biosurfactant produced by Pseudomonas protegens F6 (F6) and examined its use for aphid control. The growth of F6 was accompanied by increased aphid mortality and decreased water surface tension. Bioassay-guided chromatography coupled with instrumental analyses, nuclear magnetic resonance (NMR), and time-of-flight mass spectrometer (TOF MS) identified orfamide A as a major metabolite that showed insecticidal activity against green peach aphid (Myzus persicae). Orfamide A revealed a dose-dependent mortality against aphids, producing a LC<SUB>50</SUB> value at 34.5 μg/mL, and caused a considerable decrease in the surface tension value of water, giving about 35.7 mN/m at 10 μg/mL. Laboratory and greenhouse mortality bioassays suggested that orfamide A may be applicable to control aphids in organic agriculture. This is the first report of orfamide A as an insecticidal metabolite against Myzus persicae.</P><P><B>Graphic Abstract</B> <IMG SRC='http://pubs.acs.org/appl/literatum/publisher/achs/journals/content/jafcau/2013/jafcau.2013.61.issue-28/jf401218w/production/images/medium/jf-2013-01218w_0006.gif'></P><P><A href='http://pubs.acs.org/doi/suppl/10.1021/jf401218w'>ACS Electronic Supporting Info</A></P>
Pertussis Toxin Inhibits Colchicine-Induced DNA Synthesis in Human Fibroblast
Jang, Won-Hee,Rhee, In-Ja The Pharmaceutical Society of Korea 1994 Archives of Pharmacal Research Vol.17 No.3
Several lines evidence indicate that microtubule depolymerization initiates DNA synthesis or enhances the effects of serum or purified growth factors in many types of fibroblasts. Yet little is known about the intracellular events responsible for the mitogenic effect of microtubule disrupting agents. The effects of antitubulin agents on DNA synthesis in sparse and dense cultures in the presence or absence of serum and possible involvement of G-proteins in their mitotic action were examined. In these studies, colchicine by itself appeared to be mitogenic only for confluent quiesecent human lung fibroblasts. In sparse culture, however, colchicine inhibited serum-stimulated DNA synthesis. Colcemid, another antitubulin agent, showed similar effects of growth inhibition and stimulation in sparse and confluent cultures while lumicolhicine, inactive colchicine, did not. The mitogenic effect of two antitubulin agents, colchicine and colcemid, was partially inhibited by pertussis toxin. These data suggest that microtubular integrity is associated with the expression of either negative or positive control on DNA synthesis and mitogenic effect of antitubulin agents may be partially mediated by pertussis toxin-sensitive G protein.
Hydrogenated Amorphous Silicon Gate Driver Made of Thin-Film Transistors
Ja Hun Koo,Jin Jang,Eung Bum Kim,H. Uchiike,Jae Won Choi,Moon Hyo Kang,S.W. Lee,Se Hwan Kim,Young Seoung Kim 한국물리학회 2007 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.50 No.4
We developed a hydrogenated amorphous silicon thin-film transistor (a-Si:H TFT) gate driver having a long operation. The gate driver, composed of 9 a-Si:H TFTs including two pull-down transistors and one capacitor, was demonstrated in the present work. The pull-down transistors, under an AC bias during operation, prevent the floating of the gate line. The bias-stress effect of the fabricated a-Si:H TFTs was studied with various bias conditions to study the lifetime. The simulation results based on the experimental results indicate that the lifetime of the proposed a-Si:H gate driver can be over 5 years.
Jang-Won Lee,Hyung Bae Kim,Hea Ja Baek 한국발생생물학회 2016 발생과 생식 Vol.20 No.3
The objective of the current study was to determine acute plasma stress responses in two size groups of juvenile Epinephelus akaara (average body weight: 8.4±2.1 and 3.3±0.6 g; 150 and 120 days after hatch, respectively) exposed to abrupt salinity drops (from 34 practical salinity unit, PSU seawater to 18, 10 PSU (experiment 1) or 26, 18, 10 PSU (experiment 2), respectively). Plasma glucose, glutamic oxalate transaminase, glutamic pyruvate transaminase, red blood cell counts, and gill histology were determined during 72 h exposure. Significantly increased plasma glucose, glutamic oxalate transaminase levels, and red blood cell counts were observed in fish exposed to 18 or 10 PSU. Histological changes, such as hyperplasia and lifting of epithelium in the gill secondary lamellae, were also observed in fish exposed to 18 or 10 PSU at 72 h post-drop. E. akaara exposed to sudden salinity drops to 18 or 10 PSU still seems to undergo the primary adjustment phase before fish reaches a new homeostasis, whereas fish exposed to 26 PSU seems to mount osmotic changes. Therefore, the no observed adverse effect levels for 72 h acute salinity challenge was 26 PSU in our study, and salinity drop to 18 PSU and below can possibly cause acute adverse effect, in which fish could be vulnerable to additional stresses such as a temperature changes or handling stress.
Won, Cheolhee,Kim, Byung‐,Hak,Yi, Eun Hee,Choi, Kyung‐,Ju,Kim, Eun‐,Kyung,Jeong, Jong‐,Min,Lee, Jae‐,Ho,Jang, Ja‐,June,Yoon, Jung‐,Hwan,Jeong, Won‐,Il,P John Wiley and Sons Inc. 2015 Hepatology Vol.62 No.4
<P>Enhanced expression of the cancer stem cell (CSC) marker, CD133, is closely associated with a higher rate of tumor formation and poor prognosis in hepatocellular carcinoma (HCC) patients. Despite its clinical significance, the molecular mechanism underlying the deregulation of CD133 during tumor progression remains to be clarified. Here, we report on a novel mechanism by which interleukin‐6/signal transducer and activator of transcription 3 (IL‐6/STAT3) signaling up‐regulates expression of CD133 and promotes HCC progression. STAT3 activated by IL‐6 rapidly bound to CD133 promoter and increased protein levels of CD133 in HCC cells. Reversely, in hypoxic conditions, RNA interference silencing of STAT3 resulted in decrease of CD133 levels, even in the presence of IL‐6, with a concomitant decrease of hypoxia‐inducible factor 1 alpha (HIF‐1α) expression. Active STAT3 interacted with nuclear factor kappa B (NF‐κB) p65 subunit to positively regulate the transcription of HIF‐1α providing a mechanistic explanation on how those three oncogenes work together to increase the activity of CD133 in a hypoxic liver microenvironment. Activation of STAT3 and its consequent induction of HIF‐1α and CD133 expression were not observed in Toll‐like receptor 4/IL‐6 double‐knockout mice. Long‐term silencing of CD133 by a lentiviral‐based approach inhibited cancer cell‐cycle progression and suppressed <I>in vivo</I> tumorigenicity by down‐regulating expression of cytokinesis‐related genes, such as TACC1, ACF7, and CKAP5. We also found that sorafenib and STAT3 inhibitor nifuroxazide inhibit HCC xenograft formation by blocking activation of STAT3 and expression of CD133 and HIF‐1α proteins. <I>Conclusion</I>: IL‐6/STAT3 signaling induces expression of CD133 through functional cooperation with NF‐κB and HIF‐1α during liver carcinogenesis. Targeting STAT3‐mediated CD133 up‐regulation may represent a novel, effective treatment by eradicating the liver tumor microenvironment. (H<SMALL>EPATOLOGY</SMALL> 2015;62:1160‐1173)</P>
Won Kyung Kwon,Suhee Kim,Ja-Hyun Jang,Jong-Won Kim 대한의학유전학회 2020 대한의학유전학회지 Vol.17 No.1
Since the American College of Medical Genetics and Genomics and Association of Molecular Pathology published their guidelines in 2015, most interpretations of genetic tests have followed them. However, all variants have only limited evidence along 28 interpretation standards, especially de novo variants. When de novo variants, which are classified as variants of uncertain signiἀcance (VUS) due to lack of evidence, are detected, segregation in the affected family could provide an impor-tant key to clarifying the variants. Autosomal dominant polycystic kidney disease is the most common inherited kidney dis-order with pathogenic variants in the PKD1 or PKD2 genes. We detected a novel in-frame deletion variant in the PKD1 gene, c.7575_7577del (p.(Cys2526del)), which was interpreted as a VUS. We analyzed this variant in a Korean family to decide for segregation. Here, we report the variant as a likely pathogenic variant based on the evidence of segregation in three affected relatives and two unaffected members.
Jang, Won-Hee,Rhee, In-Ja The Pharmaceutical Society of Korea 1995 Archives of Pharmacal Research Vol.18 No.6
Monocyte adhesion involves specific cell surface receptors, integrins and results in cell differentiation. We have studied expression and regulation of integrin .${\alpha}_5{\beta}_1$ during differntiation of U937 as in vitro model. To determine expression of integrin ${\alpha}_5{\beta}_1$ during differentiation of U937 as in vitro model. To determine expression of integrin ${\alpha}_5{\beta}_1$ genes by RT-PCR (reverse transcription and polymerase chain reaction) method. We determined expression of integrin ${\alpha}_5{\beta}_1$ genes by RT-PCE (reverse transcription and polymerase chain reaction) method. We found that expression of integrin .alpha.5.betha.1 was greatly increased during PMA-induced differentiation of U937 cells and also found that PMA-induced expression of integrin ${\alpha}_5{\beta}_1$ was inhibited by colchicine, microtubule depoly merizing agent. These results indicate that microtubular integrity is associated with expression of integrin. ${\alpha}_5{\beta}_1$ during PMA-induced differentiation of U937 cells.