• 제목/요약/키워드: STAT2

검색결과 368건 처리시간 0.026초

금속 염 첨가 방법을 이용하여 사출성형된 텅스텐 중합금의 소결거동 (Sintering Behavior of the Injection Molded W-Ni-Fe Heavy Alloy by Addition of Metallic Stat)

  • 김대건;류성수;김은표;이정근;김영도;문인형
    • 한국분말재료학회지
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    • 제6권4호
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    • pp.294-300
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    • 1999
  • This study was carried out to investigate the possibility whether Metal Injection Molding (MIM) process could be applied to 95wt.%W-3.5wt.%Ni-1.5wt.%Fe heavy alloy in order to obtain an intricate shape. Methylcellulose was used in the injection molding for binder. $FeCl_2-4H_2O$ was added in solvent substituting Fe powder and $FeCl_2$ was doped on W-Ni premixed powder. When $FeCl_2-4H_2O$ was added in solvent, the binder separation occurred for injection molding so that the matrix content was changed. Such problem was solved when $FeCl_2$ was doped. In this study. the debinding process did not affect residual carbon content. The sintered microsouctures as addition methods of Fe element and the sintering temperature from $1420^{\circ}C$ to $1470^{\circ}C$, which are around the temperature of liquid phase formation, were observed.

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Nucleopolyhedrovirus Induces Suppressor of Cytokine Signaling in the Beet Armyworm, Spodoptera exigua

  • Noh Mi-Young;Jo Yong-Hun;Kim Seon-Am;Lee Yong-Seok;Bang In-Seok;Kim Seon-Gon;Park Jong-Dae;Chun Jae-Sun;Seo Sook-Jae;Han Man-Deuk;Kim Ik-Soo;Han Yeon-Soo
    • International Journal of Industrial Entomology and Biomaterials
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    • 제12권2호
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    • pp.63-67
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    • 2006
  • Suppressor of cytokine signaling (SOCS) is known to playa key role as a negative feedback regulator in JAK/STAT signaling cascade in innate immunity. Our laboratory has recently been interested in elucidating the interactions between Spodoptera exigua (Se) and SeNPV. This context leads us to clone and characterize SeSOCS that may have important functions in response to SeNPV infection. Using the RT-PCR and TA cloning approach, we found a partial fragment (416 bp) of SeSOCS. Blast search and multiple alignment data showed that it has a homology to various insects such as Anopheles gambiae (78%), Aedes aegypti (75%), Drosophila melanogastar (77%), Mus musculus (69%), and Homo sapiens (69%). Temporal induction patterns of SeSOCS were analysed after being immune-challenged with either NPV or laminarin. It showed that the level of SeSOCS mRNA was strongly induced in a biphasic manner in response to SeNPV and laminarin, respectively. It seems that SOCS, a negative regulator of JAK/STAT signaling system is also present in S. exigua and may playa role in innate immunity albeit its precise role should be further elucidated at the molecular and cellular level in the early phase of SeNPV infection in larvae.

연교(連翹) 에탄올 추출물의 대식세포의 염증성 사이토카인 합성과 신호전달에 대한 조절 (Effect of Forsythiae Fructus ethanol extract on inflammatory cytokine production and cellular signaling pathways in mouse macrophages)

  • 남정범;이미화;최호영;손낙원;강희
    • 대한본초학회지
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    • 제27권1호
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    • pp.59-64
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    • 2012
  • Objective : This study was performed to evaluate the effect of Forsythiae Fructus (FF) ethanol extract on inflammatory cytokine production and its underlying mechanisms in mouse macrophages. Methods : Peritoneal macrophages from thioglycollate medium-injected mice were cultured and stimulated with lipopolysaccharide(LPS) or LPS/interferon(IFN)-${\gamma}$ for cytokine measurement and cellular signaling molecule analysis. Results : FF ethanol extract decreased the levels of secreted tumor necrosis factor(TNF)-${\alpha}$ and interleukin(IL)-6 in IFN-${\gamma}$/LPS-stimulated cells in a concentration-dependent manner. FF extract reduced IFN-${\gamma}$/LPS-induced STAT1 phosphorylation and LPS-induced p38 and JNK activation, but not ERK1/2 activity. The extract also inhibited LPS-induced $I{\kappa}B{\alpha}$ degradation through suppression of $I{\kappa}B{\alpha}$ kinase. Conclusions : These results suggest that FF ethanol extract affects the production of TNF-${\alpha}$ and IL-6 through inhibition of activation of STAT-1, $I{\kappa}B{\alpha}$, p38, and JNK.

Effect of KH-BaRoKer-SeongJangTang based on traditional medicine theory on longitudinal bone growth

  • Kim, Min-Ho;Jeong, Hyeonseok;Park, Myungduek;Moon, Phil-Dong
    • 셀메드
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    • 제4권2호
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    • pp.14.1-14.6
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    • 2014
  • KH-BaRoKer-SeongJangTang (KBS) is a recently developed formulation by using traditional drugs considering traditional medical theory of Oriental books such as ShinNongBonChoGyeong and JuRye, which has been used to improve the growth of child in Korea. Although KBS is usually prescribed to many children who are in retard for their age, its pharmacological effects have not been fully understood in experimental models. The aim of this study was to evaluate the effects of KBS on bone growth. Growth plate thickness and bone parameters such as bone volume/tissue volume (BV/TV), trabecular thickness (Tb.Th), trabecular number (Tb.N), connection density (Conn.D), and total porosity were analyzed by means of microcomputed tomography. Serum insulin-like growth factor-I (IGF-I) levels were measured by enzyme-linked immunosorbent assay. Hepatic IGF-I mRNA expression was analyzed by real-time polymerase chain reaction. Phosphorylation of signal transducer and activator of transcription5 (STAT5) was investigated using Western blot analysis and immunohistochemistry. The thickness of growth plate was increased by KBS. BV/TV, Tb.Th, TbN, Conn.D, and total porosity were improved by KBS. Hepatic IGF-I mRNA and serum IGF-I levels were elevated by KBS. Phosphorylation of STAT5 was increased with administration of KBS. These results suggest that KBS would be helpful to children who are in retard for their age through the elevation of IGF-I.

HaCaT 각질형성세포에서 개똥쑥(Artemisia annua L) 유래 성분인 Artemisinic acid의 Macrophage-derived Chemokine 억제 효과 (Inhibitory Effect of Artemisinic Acid Isolated from Artemisia Annua L on the MDC in HaCaT Keratinocytes)

  • 강경진;강나진;한상철;구동환;김영수;이진혁;김상철;박덕훈;이종성;강희경;유은숙
    • 생약학회지
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    • 제43권3호
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    • pp.217-223
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    • 2012
  • In the present study, we investigated anti-inflammatory activity of artemisinic acid in HaCaT cells and RAW264.7 cells. Artemisinic acid showed inhibitory activity on macrophage-derived chemokines (MDC) expression, a factor related with atopic dermatitis (AD), in interferon (IFN)-${\gamma}$ and tumor necrosis factor (TNF)-${\alpha}$-stimulated HaCaT cells. In the study on action mechanism, pretreated artemisinic acid reduced the phosphorylation of STAT1 and p38 and the degradation of $I{\kappa}B$ by IFN-${\gamma}$ and TNF-${\alpha}$ stimulations. However, artemisinic acid didn't show the inhibitory activity on LPS-induced inflammatory mediators (NO, $PGE_2$, IL-6) in RAW264.7 cell. These results indicate that artemisinic acid inhibits IFN-${\gamma}$ and TNF-${\alpha}$-induced MDC expression through inhibition of signal factors, STAT1, NF-${\kappa}B$, and p38, in HaCaT keratinocytes.

WD Repeat Domain 1 Deficiency Inhibits Neointima Formation in Mice Carotid Artery by Modulation of Smooth Muscle Cell Migration and Proliferation

  • Hu, JiSheng;Pi, ShangJing;Xiong, MingRui;Liu, ZhongYing;Huang, Xia;An, Ran;Zhang, TongCun;Yuan, BaiYin
    • Molecules and Cells
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    • 제43권8호
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    • pp.749-762
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    • 2020
  • The migration, dedifferentiation, and proliferation of vascular smooth muscle cells (VSMCs) are responsible for intimal hyperplasia, but the mechanism of this process has not been elucidated. WD repeat domain 1 (WDR1) promotes actin-depolymerizing factor (ADF)/cofilin-mediated depolymerization of actin filaments (F-actin). The role of WDR1 in neointima formation and progression is still unknown. A model of intimal thickening was constructed by ligating the left common carotid artery in Wdr1 deletion mice, and H&E staining showed that Wdr1 deficiency significantly inhibits neointima formation. We also report that STAT3 promotes the proliferation and migration of VSMCs by directly promoting WDR1 transcription. Mechanistically, we clarified that WDR1 promotes the proliferation and migration of VSMCs and neointima formation is regulated by the activation of the JAK2/STAT3/WDR1 axis.

Hycanthone Inhibits Inflammasome Activation and Neuroinflammation-Induced Depression-Like Behaviors in Mice

  • Kyung-Jun, Boo;Edson Luck, Gonzales;Chilly Gay, Remonde;Jae Young, Seong;Se Jin, Jeon;Yeong-Min, Park;Byung-Joo, Ham;Chan Young, Shin
    • Biomolecules & Therapeutics
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    • 제31권2호
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    • pp.161-167
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    • 2023
  • Despite the various medications used in clinics, the efforts to develop more effective treatments for depression continue to increase in the past decades mainly because of the treatment-resistant population, and the testing of several hypotheses- and target-based treatments. Undesirable side effects and unresponsiveness to current medications fuel the drive to solve this top global health problem. In this study, we focused on neuroinflammatory response-mediated depression which represents a cluster of depression etiology both in animal models and humans. Several meta-analyses reported that proinflammatory cytokines such as interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α) were increased in major depressive disorder patients. Inflammatory mediators implicated in depression include type-I interferon and inflammasome pathways. To elucidate the molecular mechanisms of neuroinflammatory cascades underlying the pathophysiology of depression, we introduced hycanthone, an antischistosomal drug, to check whether it can counteract depressive-like behaviors in vivo and normalize the inflammation-induced changes in vitro. Lipopolysaccharide (LPS) treatment increased proinflammatory cytokine expression in the murine microglial cells as well as the stimulation of type I interferon-related pathways that are directly or indirectly regulated by Janus kinase-signal transducer and activator of transcription (JAK-STAT) activation. Hycanthone treatment attenuated those changes possibly by inhibiting the JAK-STAT pathway and inflammasome activation. Hycanthone also ameliorated depressive-like behaviors by LPS. Taken together, we suggest that the inhibitory action of hycanthone against the interferon pathway leading to attenuation of depressive-like behaviors can be a novel therapeutic mechanism for treating depression.

IL-34 Aggravates Steroid-Induced Osteonecrosis of the Femoral Head via Promoting Osteoclast Differentiation

  • Feng Wang;Hong Sung Min;Haojie Shan;Fuli Yin;Chaolai Jiang;Yang Zong;Xin Ma;Yiwei Lin;Zubin Zhou;Xiaowei Yu
    • IMMUNE NETWORK
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    • 제22권3호
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    • pp.25.1-25.11
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    • 2022
  • IL-34 can promote osteoclast differentiation and activation, which may contribute to steroid-induced osteonecrosis of the femoral head (ONFH). Animal model was constructed in both BALB/c and IL-34 deficient mice to detect the relative expression of inflammation cytokines. Micro-CT was utilized to reveal the internal structure. In vitro differentiated osteoclast was induced by culturing bone marrow-derived macrophages with IL-34 conditioned medium or M-CSF. The relative expression of pro-inflammation cytokines, osteoclast marker genes, and relevant pathways molecules was detected with quantitative real-time RT-PCR, ELISA, and Western blot. Up-regulated IL-34 expression could be detected in the serum of ONFH patients and femoral heads of ONFH mice. IL-34 deficient mice showed the resistance to ONFH induction with the up-regulated trabecular number, trabecular thickness, bone value fraction, and down-regulated trabecular separation. On the other hand, inflammatory cytokines, such as TNF-α, IFN-γ, IL-6, IL-12, IL-2, and IL-17A, showed diminished expression in IL-34 deficient ONFH induced mice. IL-34 alone or works in coordination with M-CSF to promote osteoclastogenesis and activate ERK, STAT3, and non-canonical NF-κB pathways. These data demonstrate that IL-34 can promote the differentiation of osteoclast through ERK, STAT3, and non-canonical NF-κB pathways to aggravate steroid-induced ONFH, and IL-34 can be considered as a treatment target.

2원 분할표의 소표본 검증법 (Small sample tests for two-way contingency tables)

  • 허명회
    • 응용통계연구
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    • 제10권2호
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    • pp.339-352
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    • 1997
  • 소표본으로부터 형성되는 2원 분할표에는 빈도가 작은 칸들이 적지 않기 때문에 대표본이론에 근거한 카이제곱 검증 등 기존 통계적 방법의 적용이 적절하지 않응 수가 있다. 이런 경우에 한 대안으로서 정확검증법(exact tests)이 개발되어 있으나 이것이 너무 많은 계산을 요구하므로 사용하기가 쉽지 않다. 본 연구는 소표본 2원 분할표에서, 단순한 몬테칼로 알로리즘에 의한 행 균일성 가설의 카이제곱 임의화 검증법(randomization test)을 제안하고 튜키(Tukey) 형의 행간 다중비교법을 제안한다. 아울러 열 범주가 순서형인 2원 분할표에 대하여도 유사한 방법론을 적용할 수 있음을 밝힌다.

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The Gene Expression Profile of LPS-stimulated Microglial Cells

  • Sohn, Sung-Hwa;Ko, Eun-Jung;Kim, Sung-Hoon;Kim, Yang-Seok;Shin, Min-Kyu;Hong, Moo-Chang;Bae, Hyun-Su
    • Molecular & Cellular Toxicology
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    • 제5권2호
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    • pp.147-152
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    • 2009
  • This study was conducted to evaluate the inflammatory mechanisms of LPS-stimulated BV-2 microglial cells. The inflammation mechanism was evaluated in BV-2 cells with or without LPS treated using the Affymetrix microarray analysis system. The microarray analysis revealed that B cell receptor signaling pathway, cytokine-cytokine receptor interaction, Jak-STAT signaling pathway, MAPK signaling pathway, Neuro-active ligand-receptor interaction, TLR signaling path-way, and T cell receptor signaling pathway-related genes were up-regulated in LPS stimulated BV-2 cells. Selected genes were validated using real time RTPCR. These results can help an effective therapeutic approach to alleviating the progression of neuro-in-flammatory diseases.