Kenaf열기계펄프로부터 제조한 신문용지의 광학적 특성(제4회 산림과학 세미나)

Guo-Min Tan 忠北大學校 農業科學硏究所 1996 農業科學硏究 Vol.14 No.-

Let-7c Inhibits NSCLC Cell Proliferation by Targeting HOXA1

Zhan, Min,Qu, Qiang,Wang, Guo,Liu, Ying-Zi,Tan, Sheng-Lan,Lou, Xiao-Ya,Yu, Jing,Zhou, Hong-Hao Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.1

Objective: The aim of the present study was to explore mechanisms by which let-7c suppresses NSCLC cell proliferation. Methods: The expression level of let-7c was quantified by qRT-PCR. A549 and H1299 cells were transfected with let-7c mimics to restore the expression of let-7c. The effects of let-7c were then assessed by cell proliferation, colony formation and cell cycle assay. Mouse experiments were used to confirm the effect of let-7c on tumorigenicity in vivo. Luciferase reporter assays and Western blotting were performed to identify target genes for let-7c. Results: HOXA1 was identified as a novel target of let-7c. MTS, colony formation and flow cytometry assays demonstrated that forced expression of let-7c inhibited NSCLC cell proliferation by inducing G1 arrest in vitro, consistent with inhibitory effects induced by knockdown of HOXA1. Mouse experiments demonstrated that let-7c expression suppressed tumorigenesis. Furthermore, we found that let-7c could regulate the expression of HOXA1 downstream effectors CCND1, CDC25A and CDK2. Conclusions: Collectively, these results demonstrate let-7c inhibits NSCLC cell proliferation and tumorigenesis by partial direct targeting of the HOXA1 pathway, which suggests that restoration of let-7c expression may thus offer a potential therapeutic intervention strategy for NSCLC.

[Poster Presentation] THE EFFECT OF FORMATION OF PAPER FROM EUCALYPTUS CHEMIMECHANICAL PULP ON PRINTABILITY

Kai-Tang HU,Guo-Min TAN,Qi-Rong Fu,Nam-Soek Cho 한국펄프·종이공학회 1999 한국펄프종이학회 기타 간행물 Vol.- No.-

The relation between the paper formation analyzed by image process system and smoothness, compressibility, uniform of ink absorption is studied. The results indicate that the paper with bad formation has higher apparent bulk than the paper with good formation. The bad formation of paper results in the nonuniform calendering and decrease of the compressibility. The bad formation of paper also results in deformation and omission of printing dots, which affects the reproduction of the printing images.

Multi-objective Optimization for Time-Open Lambert Rendezvous Between Non-coplanar Orbits

Guan-Qun Wu,Li-Guo Tan,Xin Li,Shen-Min Song 한국항공우주학회 2020 International Journal of Aeronautical and Space Sc Vol.21 No.2

The problem of time-open Lambert multi-objective optimal rendezvous between non-coplanar orbits is studied in the paper. Based on the Lambert’s theorem, the descriptions of time-open Lambert rendezvous subjected to two-impulse and three-impulse are presented, and a universally applicable method for the solution of the transfer orbits is given. To deal with the multi-objective optimization subject to fuel consumption and flight time for rendezvous, an improved NSGA-II algorithm with a better performance is provided. Via the global optimization, Pareto set can be obtained by the improved NSGA-II for the multi-objective optimal rendezvous considering multi-constraints. Numerical simulations are conducted to validate the feasibility of the improved multi-objective optimization algorithm, and the results of the two-impulse and three-impulse multi-objective optimal rendezvous are shown.

IRS-2 Partially Compensates for the Insulin Signal Defects in IRS-1^-/- Mice Mediated by miR-33

Tang, Chen-Yi,Man, Xiao-Fei,Guo, Yue,Tang, Hao-Neng,Tang, Jun,Zhou, Ci-La,Tan, Shu-Wen,Wang, Min,Zhou, Hou-De Korean Society for Molecular and Cellular Biology 2017 Molecules and cells Vol.40 No.2

Insulin signaling is coordinated by insulin receptor substrates (IRSs). Many insulin responses, especially for blood glucose metabolism, are mediated primarily through Irs-1 and Irs-2. Irs-1 knockout mice show growth retardation and insulin signaling defects, which can be compensated by other IRSs in vivo; however, the underlying mechanism is not clear. Here, we presented an Irs-1 truncated mutated mouse ($Irs-1^{-/-}$) with growth retardation and subcutaneous adipocyte atrophy. $Irs-1^{-/-}$ mice exhibited mild insulin resistance, as demonstrated by the insulin tolerance test. Phosphatidylinositol 3-kinase (PI3K) activity and phosphorylated Protein Kinase B (PKB/AKT) expression were elevated in liver, skeletal muscle, and subcutaneous adipocytes in Irs-1 deficiency. In addition, the expression of IRS-2 and its phosphorylated version were clearly elevated in liver and skeletal muscle. With miRNA microarray analysis, we found miR-33 was down-regulated in bone marrow stromal cells (BMSCs) of $Irs-1^{-/-}$ mice, while its target gene Irs-2 was up-regulated in vitro studies. In addition, miR-33 was down-regulated in the presence of Irs-1 and which was up-regulated in fasting status. What's more, miR-33 restored its expression in re-feeding status. Meanwhile, miR-33 levels decreased and Irs-2 levels increased in liver, skeletal muscle, and subcutaneous adipocytes of $Irs-1^{-/-}$ mice. In primary cultured liver cells transfected with an miR-33 inhibitor, the expression of IRS-2, PI3K, and phosphorylated-AKT (p-AKT) increased while the opposite results were observed in the presence of an miR-33 mimic. Therefore, decreased miR-33 levels can up-regulate IRS-2 expression, which appears to compensate for the defects of the insulin signaling pathway in Irs-1 deficient mice.

IRS-2 Partially Compensates for the Insulin Signal Defects in IRS-1−/−Mice Mediated by miR-33

Chen-Yi Tang,Xiao-Fei Man,Yue Guo,Hao-Neng Tang,Jun Tang,Ci-La Zhou,Shu-Wen Tan,Min Wang,Hou-De Zhou 한국분자세포생물학회 2017 Molecules and cells Vol.40 No.2

Insulin signaling is coordinated by insulin receptor substrates (IRSs). Many insulin responses, especially for blood glucose metabolism, are mediated primarily through Irs-1 and Irs-2. Irs-1 knockout mice show growth retardation and insulin signaling defects, which can be compensated by other IRSs in vivo; however, the underlying mechanism is not clear. Here, we presented an Irs-1 truncated mutated mouse (Irs-1−/−) with growth retardation and subcutaneous adipocyte atrophy. Irs-1−/− mice exhibited mild insulin resistance, as demonstrat-ed by the insulin tolerance test. Phosphatidylino-sitol 3-kinase (PI3K) activity and phosphorylated Protein Kinase B (PKB/AKT) expression were elevated in liver, skeletal muscle, and subcu-taneous adipocytes in Irs-1 deficiency. In addition, the expression of IRS-2 and its phosphorylated version were clearly elevated in liver and skeletal muscle. With miRNA microarray analysis, we found miR-33 was down-regulated in bone marrow stromal cells (BMSCs) of Irs-1−/− mice, while its target gene Irs-2 was up-regulated in vitro studies. In addition, miR-33 was down-regulated in the presence of Irs-1 and which was up-regulated in fasting status. What’s more, miR-33 restored its expression in re-feeding status. Meanwhile, miR-33 levels decreased and Irs-2 levels increased in liver, skeletal muscle, and subcutaneous adipocytes of Irs-1−/− mice. In primary cultured liver cells transfected with an miR-33 inhibitor, the expression of IRS-2, PI3K, and phosphorylated-AKT (p-AKT) increased while the opposite results were observed in the presence of an miR-33 mimic. Therefore, decreased miR-33 levels can up-regulate IRS-2 expression, which appears to compensate for the defects of the insulin signaling pathway in Irs-1 deficient mice.

A sigma class glutathione S-transferase gene regulated by the CncC pathway is required for phytochemical tolerance in the red flour beetle, Tribolium castaneum

Gao Shan-shan,Li Dong-yu,Huo Zhuang-kun,Zhang Yong-lei,Cao Yi-zhuo,Tan Yue-yao,Guo Xin-long,Zhang Jia-hao,Zhang Kun-peng,Li Rui-min 한국응용곤충학회 2022 Journal of Asia-Pacific Entomology Vol.25 No.4

Insect glutathione S-transferases (GSTs) play a crucial role in the detoxification of exogenous compounds, especially insecticides and plant allelochemicals. A sigma class GST gene, TcGSTS7, mediates the response to eugenol in Tribolium castaneum. However, the mechanism underlying this effect remains largely unknown. In this study, TcGSTS7, which exhibits a structural motif and domain organization characteristic of GSTs, was cloned from the T. castaneum genome. Spatiotemporal expression analysis revealed that TcGSTS7 was most highly expressed at the late larva stage and was mainly expressed in the fat body and epidermis of larvae and adults, suggesting that TcGSTS7 may play a potential role in the protection against toxic xenobiotics in T. castaneum. Furthermore, the expression of TcGSTS7 was significantly induced after exposure to eugenol, while RNA inter ference (RNAi) targeting TcGSTS7 enhanced the sensitivity of the beetle to eugenol, indicating that TcGSTS7 is involved in the tolerance of T. castaneum to this insecticide. Interestingly, the depletion of TcCncC, which encodes a transcription factor of the CncC pathway that has been associated with the regulation of detoxification-related genes in insects, led to a reduction in the TcGSTS7 transcript level following exposure to eugenol, which suggests that TcGSTS7 acts downstream of the CncC pathway. Combined, these results indicated that TcGSTS7 partici pates in the tolerance of T. castaneum to phytochemicals in a CncC pathway-dependent manner. These findings have implications for the development of novel drugs for use in pest control.