http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
오목한 반구면의 Jet Impingement/Effusion Hole 주변 유동 특성에 대한 실험과 시뮬레이션의 비교
윤성지,서희림,염은섭 한국가시화정보학회 2022 한국가시화정보학회지 Vol.20 No.2
Flow characteristics of jet impingement over concave hemispherical surface with effusion cooling holes is relatively more complex than that of a flat surface, so the experimental validation for computational fluid dynamics (CFD) results is important. In this study, experimental results were compared with simulation results obtained by assuming different turbulence models. The vortex was observed in the region between the central jets where the recirculation structure appeared. The different patterns of vorticity distributions were observed for each turbulence models due to different interaction of the injected jet flow. Among them, the transition k-kl-ω model predicted similarly not only the jet potential core region with higher velocity, but also the recirculation region between the central jets. From the validation, it may be helpful to accurately predict heat and mass transfer in jet impingement/effusion hole system.
윤성지(Sung Ji Yoon),안윤주(Youn Joo An) 大韓環境工學會 2012 대한환경공학회지 Vol.34 No.4
나노산업의 발달로 인해 나노제품의 제조, 소비, 폐기 과정에서 나노물질이 직·간접적인 경로를 통해 수생태 및 토양 생태계로 유입되고 있다. 나노물질은 벌크물질과는 다른 특성을 가지고 있으며 나노물질의 다양한 물리화학적 변화는 환경내 나노물질의 거동 및 무생물적·생물적 상호작용에 영향을 미친다. 나노물질의 생태 독성 연구는 꾸준하게 증가하는 추세이며 특히 나노물질의 마이크로코즘 연구가 최근 보고되고 있다. 마이크로코즘(Microcosm)은 통제된 실험 조건 하에서 생태계의 일부분을 모사하여 자연 현상을 연구하기 위한 기법으로서, 마이크로코즘 연구는 생태계 내 나노물질의 거동과 통합적인 독성영향 평가를 가능하게 한다. 본 연구는 수생태 및 토양생태계에서 나노물질을 이용한 마이크로코즘 및 메조코즘(Mesocosm) 선행연구를 국제 학술 논문을 중심으로 조사하였다. 현재까지 마이크로코즘 연구는 총 12건의 논문이 발표되었고 단 1건의 메조코즘 연구가 보고되었는데, 대부분의 연구들이 미생물 군집 수준에서 나노물질의 영향을 제한적으로 평가하였다. 나노물질의 통합적 독성 영향을 평가하기 위해서 좀 더 다양한 생물종을 대상으로 그들의 상호작용을 연구할 필요가 있다. 본 연구에서는 수생태 및 토양생태계에서 나노물질의 마이크로코즘 연구동향을 분석하고 중금속, 유기물질과 같은 일반 화학물질 이용한 마이크로코즘 독성 연구를 바탕으로 향후 나노물질의 마이크로코즘 연구방향을 제시하였다. The current growth of nano-industries has resulted in released nanoparticles entering into water and soil ecosystems via various direct or indirect routes. Physicochemical properties of nanoparticles differ from bulk materials, and nanomaterials influence the fates of nanoparticles and the interactions of living or non-living things in the environment. Microcosm analysis is a research methodology for revealing natural phenomena by mimicking part of an ecosystem under controlled conditions. Microcosm study allows for the integrated analysis of toxic effects and fates of nanoparticles in the ecosystem. Ecotoxicity studies of nanomaterials are steadily increasing, and microcosm studies of nanomaterials are currently beginning to surface. In this study, microcosm studies of nanomaterials in water and soil ecosystems were extensively investigated based on SCI (E) papers. We found that the microcosm studies have been reported in 12 instances, and mesocosm studies have been reported in only once until now. Advanced research was mostly evaluated at the microorganism level. But integrated analysis of nanotoxicity is required to research the interactions based of various species. Thus, our studies analysed the trend of microcosm studies on nanomaterials in water and soil ecosystems and suggested future directions of microcosm research of nanomaterials.
Molecular Events of Insulin Action Occur at Lipid Raft/Caveolae in Adipocytes
배순식,윤성지,김은경,김치대,최장현,서판길,Bae, Sun-Sik,Yun, Sung-Ji,Kim, Eun-Kyung,Kim, Chi-Dae,Choi, Jang-Hyun,Suh, Pann-Ghill Korean Society of Life Science 2007 생명과학회지 Vol.17 No.1
인슐린은 지방세포 또는 근육세포에서 포도당 흡수 조절 통로단백질이 함유되어 있는 소포제를 세포막으로의 이동을 촉진시킨다. 우리는 여기서 지방세포로의 분화는 인슐린에 의한 포도당 흡수에 대한 반응이 증가됨을 보였다. 반면에 지방세포로의 분화는 PDGF에 의한 포도당 흡수 반응이 감소됨을 보였다. 인슐린 수용체나 caveolae는 지방세포로의 분화과정 동안 발현이 증가된다. 또한 지방세포로의 분화는 인슐린에 의한 Akt의 활성을 증가시켰다. 하지만 PDGF에 의한 Akt의 활성은 크게 감소하였다. 하지만 인슐린은 지방세포 또는 섬유아 전구세포에서 ERK의 활성을 유도하지 않았다. PDGF에 의한 ERK 활성 또한 지방세포로의 분화과정에 따라 감소하였다. P13K의 저해제인 LY294002는 지방세포 뿐만 아니라 섬유아 전구세포에서 인슐린에 의한 포도당 흡수를 저해하였다. 마지막으로 인슐린 수용체, Akt, SHIP2, p85등이 lipid raft/caveolae에 존재함을 확인하였고 인슐린에 의해 이런 단백질들이 lipid raft/caveolae로 이동함을 관찰하였다. 이런 결과를 토대로 lipid raft는 포도당 홉수를 위한 인슐린의 기능적 작용을 하는데 매우 중요한 환경을 제공함을 주장한다. Insulin stimulates the fusion of intracellular vesicles containing glucose transporter 4 (GLUT4) with plasma membrane in adipocytes and muscle cells. Here we show that adipocyte differentiation results in enhanced insulin sensitivity of glucose uptake. On the other hand, glucose uptake in response to platelet-derived growth factor (PDGF) stimulation was markedly reduced by adipocyte differentiation. Expression level of insulin receptor and caveolin-1 was dramatically increased during adipocyte differentiation. Adipocyte differentiation caused :ilightly enhanced activation of acutely transforming retrovirus AKT8 in rodent T cell lymphoma (Akt) by insulin stimulation. However, activation of Akt by PDGF stimulation was largely reduced. Activation of ERK was not detected in both fibroblasts and adipocytes after stimulation with insulin. PDGF-dependent activation of ERK was reduced by adipocyte differentiation. Insulin-dependent glucose uptake was abrogated by LY294002, a phosphatidylinositol 3-kinase (PI3K) inhibitor, in both fibroblasts and adipocytes. Also disassembly of caveolae structure by $methyl-\beta-cyclodextrin$ caused impairment of Akt activation and glucose uptake. Finally, insulin receptor, Akt, SH2-domain-containing inositol 5-phosphatase 2 (SHIP2), and regulatory subunit of PI3K are localized at lipid raft domain and the translocation was facilitated upon insulin stimulation. Given these results, we suggest that lipid raft provide proper site for insulin action for glucose uptake.
Lysophosphatidic acid induces cell migration through the selective activation of Akt1
김은경,윤성지,도기헌,김민성,조몽,서동수,김치대,김재호,Morris J. Birnbaum,배순식 생화학분자생물학회 2008 Experimental and molecular medicine Vol.40 No.4
Akt plays pivotal roles in many physiological responses including growth, proliferation, survival, metabolism, and migration. In the current studies, we have evaluated the isoform-specific role of akt in lysophosphatidic acid (LPA)-induced cell migration. Ascites from ovarian cancer patients (AOCP) induced mouse embryo fibroblast (MEF) cell migration in a dose-dependent manner. On the other hand, ascites from liver cirrhosis patients (ALCP) did not induce MEF cell migration. AOCP-induced MEF cell migration was completely blocked by pre-treatment of cells with LPA receptor antagonist, Ki16425. Both LPA- and AOCP-induced MEF cell migration was completely attenuated by PI3K inhibitor, LY294002. Furthermore, cells lacking Akt1 displayed defect in LPA-induced cell migration. Re-expression of Akt1 in DKO (Akt1-/-Akt2-/-) cells restored LPA-induced cell migration, whereas re-expression of Akt2 in DKO cells could not restore the LPA-induced cell migration. Finally, Akt1 was selectively phosphorylated by LPA and AOCP stimulation. These results suggest that LPA is a major factor responsible for AOCP-induced cell migration and signaling specificity of Akt1 may dictate LPA-induced cell migration.