• 제목/요약/키워드: Tor

검색결과 492건 처리시간 0.028초

Glucosamine increases macrophage lipid accumulation by regulating the mammalian target of rapamycin signaling pathway

  • Sang-Min Kim;Dong Yeol Kim;Jiwon Park;Young-Ah Moon;Inn-Oc Han
    • BMB Reports
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    • 제57권2호
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    • pp.92-97
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    • 2024
  • Elevated blood glucose is associated with an increased risk of atherosclerosis. Data from the current study showed that glucosamine (GlcN), a normal glucose metabolite of the hexosamine biosynthetic pathway (HBP), promoted lipid accumulation in RAW264.7 macrophage cells. Oleic acid- and lipopolysaccharide (LPS)-induced lipid accumulation was further enhanced by GlcN in RAW264.7 cells, although there was no a significant change in the rate of fatty acid uptake. GlcN increased acetyl CoA carboxylase (ACC), fatty acid synthase (FAS), scavenger receptor class A, liver X receptor, and sterol regulatory element-binding protein-1c (SREBP-1c) mRNA expression, and; conversely, suppressed ATP-binding cassette transporter A1 (ABCA-1) and ABCG-1 expression. Additionally, GlcN promoted O-GlcNAcylation of nuclear SREBP-1 but did not affect its DNA binding activity. GlcN stimulated phosphorylation of mammalian target of rapamycin (mTOR) and S6 kinase. Rapamycin, a mTOR-specific inhibitor, suppressed GlcN-induced lipid accumulation in RAW264.7 cells. The GlcN-mediated increase in ACC and FAS mRNA was suppressed, while the decrease in ABCA-1 and ABCG-1 by GlcN was not significantly altered by rapamycin. Together, our results highlight the importance of the mTOR signaling pathway in GlcN-induced macrophage lipid accumulation and further support a potential link between mTOR and HBP signaling in lipogenesis.

철 환원 박테리아를 이용한 자철석 합성 (Microbial Synthesis of Magnetite Powder by Iron Reducing Bacteria)

  • Yul Roh;Hi-Soo Moon
    • 한국광물학회지
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    • 제13권2호
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    • pp.65-72
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    • 2000
  • 미생물을 이용한 광물 합성은 현재 초기 연구단계에 있으나 신소재 개발측면에서 다야한 활용성을 보인다. 본 연구의 목적은 철환원 박테리아를 이용한 자철석 합성에 있어 미치는 환경조건들을 알아보는데 있다. 본 연구를 위해 지하 3-km 코아 시료에서 분리한 호열성 철 환원 박테리아인 TOR-39을 이용하였다. TOR-39은 $65^{\circ}C$에서 12시간이내에 비정질 철수화물을 환원시켜 자철석을 형성한다. 25일 동안 배양하여 형성된 자철석은 정육각형 모양으로 입자 크기는 50-100 나노미터이다. TOR-39을 이용한 자철석 합성시 적절한 조건은 pH는 7.9-8.5, Eh는 -200 mV 이하, 배양기간은 3-25일 그리고 온도는 $45-75^{\circ}C$이다. 미생물에 의한 자철석 합성은 나노미터 크기의 광물을 직접 합성하므로, 산업적으로 많은 이용 가치를 가질 것으로 본다.

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파라과이와 한국 EIA 제도 비교 분석 (Comparative Analysis of EIA System between Paraguay and South Korea)

  • ;홍상표
    • 환경영향평가
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    • 제20권6호
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    • pp.823-831
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    • 2011
  • 파라과이와 한국의 환경영향평가에 관련된 제도와 법률은 환경영향평가 대상사업, 실행방법 및 사후감시 등에서 상이하다. 양국의 환경영향평가 제도 중에는 전혀 관련 없는 것도 있는데, 경제적, 사회적, 문화적, 역사적 그리고 지연조건이 상이하여 양국의 환경영향평가 제도에 영향을 주는 것으로 분석된다. 파라과이에서는 스코핑이 Term of References (TOR)가 준비되는 단계이다. TOR은 환경부에 의해 준비된 특정의 환경영향평가의 요구조건을 포함한다. 파라과이에서는 스코핑 단계에서 환경부의 주도로 주민참여가 진행된다. Environmental Impact Relatorio (RIMA)가 개발사업으로 인해 영향을 받는 지역사회에 시행되고, 간결하고 이해하기 쉬운 표현으로 작성된다. 파라과이에서는 EIS가 승인되기 전에 RIMA를 지역사회에 공개한다.

Analysis of corrugated board panels under compression load

  • Biancolini, M.E.;Brutti, C.;Porziani, S.
    • Steel and Composite Structures
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    • 제9권1호
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    • pp.1-17
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    • 2009
  • This paper is focused on the buckling and post buckling behaviour of rectangular corrugated board panels simply supported and subjected to compression load. The aim of the work is to understand the failure mechanism of investigated structure in order to quantify the effect of design parameters on the strength of a panel of given geometry. Two numerical models were developed adopting the finite element method. In the first one the corrugated board is represented by means of shell elements adopting an equivalent material, in the second the local structure is described in full detail modelling both straight and corrugated layers by means of shell elements and representing the connection between layers by special interface elements. The model correctness was checked by the comparison between out of plane central displacement predicted by the models and the experimental values found in literature. For the same case the effect of panel planarity error was evaluated. Finally a parametric analysis to investigate the effect of design parameters was carried out.

A parametric analysis of the flutter instability for long span suspension bridges

  • Como, M.;Ferraro, S. Del;Grimaldi, A.
    • Wind and Structures
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    • 제8권1호
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    • pp.1-12
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    • 2005
  • A simplified analysis able to point out the most relevant geometrical and aerodynamic parameters that can influence the flutter of long span modern bridges is the aim of the paper. With this goal, by using a continuous model of the suspension bridge and by a quasi stationary approach, a simple formula of the combined vertical/torsional flutter wind speed is given. A good agreement is obtained comparing the predictions from the proposed formula with the flutter speeds of three modern suspension or cable stayed bridges: the Great Belt East Bridge, the Akashi and Normandie bridges. The paper ends with some comments and comparisons with the well known Selberg formula.

Neuroprotective Effect of Duloxetine on Chronic Cerebral Hypoperfusion-Induced Hippocampal Neuronal Damage

  • Park, Jin-A;Lee, Choong-Hyun
    • Biomolecules & Therapeutics
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    • 제26권2호
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    • pp.115-120
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    • 2018
  • Chronic cerebral hypoperfusion (CCH), which is associated with onset of vascular dementia, causes cognitive impairment and neuropathological alterations in the brain. In the present study, we examined the neuroprotective effect of duloxetine (DXT), a potent and balanced serotonin/norepinephrine reuptake inhibitor, on CCH-induced neuronal damage in the hippocampal CA1 region using a rat model of permanent bilateral common carotid arteries occlusion. We found that treatment with 20 mg/kg DXT could attenuate the neuronal damage, the reduction of phosphorylations of mTOR and p70S6K as well as the elevations of $TNF-{\alpha}$ and $IL-1{\beta}$ levels in the hippocampal CA1 region at 28 days following CCH. These results indicate that DXT displays the neuroprotective effect against CCH-induced hippocampal neuronal death, and that neuroprotective effect of DXT may be closely related with the attenuations of CCH-induced decrease of mTOR/p70S6K signaling pathway as well as CCH-induced neuroinflammatory process.

A CONJECTURE OF GROSS AND ZAGIER: CASE E(ℚ)tor ≅ ℤ/2ℤ OR ℤ/4ℤ

  • Dongho Byeon;Taekyung Kim;Donggeon Yhee
    • 대한수학회지
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    • 제60권5호
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    • pp.1087-1107
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    • 2023
  • Let E be an elliptic curve defined over ℚ of conductor N, c the Manin constant of E, and m the product of Tamagawa numbers of E at prime divisors of N. Let K be an imaginary quadratic field where all prime divisors of N split in K, PK the Heegner point in E(K), and III(E/K) the Shafarevich-Tate group of E over K. Let 2uK be the number of roots of unity contained in K. Gross and Zagier conjectured that if PK has infinite order in E(K), then the integer c · m · uK · |III(E/K)| $\frac{1}{2}$ is divisible by |E(ℚ)tor|. In this paper, we prove that this conjecture is true if E(ℚ)tor ≅ ℤ/2ℤ or ℤ/4ℤ except for two explicit families of curves. Further, we show these exceptions can be removed under Stein-Watkins conjecture.

Hep3B 간암세포에서 개똥쑥추출물로부터 Akt-mTOR-GSK3β 신호경로에 의한 apoptosis 효과 (Apoptotic Effect of Extract from Artemisia annua Linné by Akt/mTOR/GSK-3β Signal Pathway in Hep3B Human Hepatoma Cells)

  • 김은지;김근태;김보민;임은경;하성호;김상용;김영민
    • 생명과학회지
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    • 제26권7호
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    • pp.764-771
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    • 2016
  • 개똥쑥 추출물은 항박테리아, 항바이러스 그리고 항산화효과를 포함한 다양한 기능을 가지고 있는 것으로 잘 알려져 있다. 그러나, 개똥쑥 항증식 작용기전은 알려지지 않았다. 따라서, 우리는 Hep3B 간암 세포에서 AAE추출물의 apoptotic 효과를 알아보고자 한다. 본 연구의 목적은 AAE가 인체 간암 세포주(Hep3B)의 증식에 미치는 효과를 분석하고 이에 대한 apoptosis의 효과를 조사하는데 있다. 인산화에 의해 활성화된 Akt는 TSC2, mTOR 그리고 GSK-3β의 인산화를 유도하여 세포증식을 유도한다. 본 연구에서, 우리는 AAE가Akt-mTOR-GSK3β 신호 경로와 mitochondria를 매개하는 apoptotic 단백질을 통한 암세포의 apoptosis 유도할 것이라고 추측하였다. 이를 위해, 먼저 AAE가 처리농도에 따라 세포증식에 미치는 효과를 분석하였다. AAE처리는 세포증식을 억제시켰을 뿐만 아니라 젖산 탈수소 효소의 방출을 유도하였다. 이러한 결과는 MTT assay, LDH assay로 확인하였다. 또한 Hoechst 33342 staining, Annexin Ⅴ- PI staining, JC-1 staining 그리고 Western blotting을 통해 apoptosis 효과를 확인하였다. 본 연구에서는 간암세포에 AAE의 처리가 Akt, TSC2, GSK-3β-phosphorylated, Bim, Bcl-2, pro-caspase 3의 억제와 Bak, Bax 활성을 유도한다는 것을 확인하였다. 이러한 결과는 AAE가 Akt-mTOR-GSK-3β 신호 경로를 통해 intrinsic apoptosis를 유도한다는 것을 나타낸다.

Modulated Gene Expression of Toxoplasma gondii Infected Retinal Pigment Epithelial Cell Line (ARPE-19) via PI3K/Akt or mTOR Signal Pathway

  • Zhou, Wei;Quan, Juan-Hua;Gao, Fei-Fei;Ismail, Hassan Ahmed Hassan Ahmed;Lee, Young-Ha;Cha, Guang-Ho
    • Parasites, Hosts and Diseases
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    • 제56권2호
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    • pp.135-145
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    • 2018
  • Due to the critical location and physiological activities of the retinal pigment epithelial (RPE) cell, it is constantly subjected to contact with various infectious agents and inflammatory mediators. However, little is known about the signaling events in RPE involved in Toxoplasma gondii infection and development. The aim of the study is to screen the host mRNA transcriptional change of 3 inflammation-related gene categories, PI3K/Akt pathway regulatory components, blood vessel development factors and ROS regulators, to prove that PI3K/Akt or mTOR signaling pathway play an essential role in regulating the selected inflammation-related genes. The selected genes include PH domain and leucine- rich-repeat protein phosphatases (PHLPP), casein kinase2 (CK2), vascular endothelial growth factor (VEGF), pigment epithelium-derived factor (PEDF), glutamate-cysteine ligase (GCL), glutathione S-transferase (GST), and NAD(P)H: quinone oxidoreductase (NQO1). Using reverse transcription polymerase chain reaction (RT-PCR) and quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR), we found that T. gondii up-regulates PHLPP2, $CK2{\beta}$, VEGF, GCL, GST and NQO1 gene expression levels, but down-regulates PHLPP1 and PEDF mRNA transcription levels. PI3K inhibition and mTOR inhibition by specific inhibitors showed that most of these host gene expression patterns were due to activation of PI3K/Akt or mTOR pathways with some exceptional cases. Taken together, our results reveal a new molecular mechanism of these gene expression change dependent on PI3K/Akt or mTOR pathways and highlight more systematical insight of how an intracellular T. gondii can manipulate host genes to avoid host defense.

Expression and secretion of CXCL12 are enhanced in autosomal dominant polycystic kidney disease

  • Kim, Hyunho;Sung, Jinmo;Kim, Hyunsuk;Ryu, Hyunjin;Park, Hayne Cho;Oh, Yun Kyu;Lee, Hyun-Seob;Oh, Kook-Hwan;Ahn, Curie
    • BMB Reports
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    • 제52권7호
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    • pp.463-468
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    • 2019
  • Autosomal dominant polycystic kidney disease (ADPKD), one of the most common human monogenic diseases (frequency of 1/1000-1/400), is characterized by numerous fluid-filled renal cysts (RCs). Inactivation of the PKD1 or PKD2 gene by germline and somatic mutations is necessary for cyst formation in ADPKD. To mechanistically understand cyst formation and growth, we isolated RCs from Korean patients with ADPKD and immortalized them with human telomerase reverse transcriptase (hTERT). Three hTERT-immortalized RC cell lines were characterized as proximal epithelial cells with germline and somatic PKD1 mutations. Thus, we first established hTERT-immortalized proximal cyst cells with somatic PKD1 mutations. Through transcriptome sequencing and Gene Ontology (GO) analysis, we found that upregulated genes were related to cell division and that downregulated genes were related to cell differentiation. We wondered whether the upregulated gene for the chemokine CXCL12 is related to the mTOR signaling pathway in cyst growth in ADPKD. CXCL12 mRNA expression and secretion were increased in RC cell lines. We then examined CXCL12 levels in RC fluids from patients with ADPKD and found increased CXCL12 levels. The CXCL12 receptor CXC chemokine receptor 4 (CXCR4) was upregulated, and the mTOR signaling pathway, which is downstream of the CXCL12/CXCR4 axis, was activated in ADPKD kidney tissue. To confirm activation of the mTOR signaling pathway by CXCL12 via CXCR4, we treated the RC cell lines with recombinant CXCL12 and the CXCR4 antagonist AMD3100; CXCL12 induced the mTOR signaling pathway, but the CXCR4 antagonist AMD3100 blocked the mTOR signaling pathway. Taken together, these results suggest that enhanced CXCL12 in RC fluids activates the mTOR signaling pathway via CXCR4 in ADPKD cyst growth.