• 대한토목학회논문집
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• 제13권5호
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• pp.173-181
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• 1993

자연하천에 대한 합리적인 하천개수계획수립 및 유로의 유지관리면에서 반드시 규명되어야 할 유로만곡부에서의 정량적인 해석은 여러가지 접근방법이 있으며, 사행하천의 유로이동에 대한 예측은 도로, 교량 등의 위치선정과 기존하천구조물의 방재에 필수적이다. 하상계수가 큰 우리나라의 하천에 유로이동 예측모형을 적용할 때 유량은 기간별-지배유량을 고려하는 것이 타당할 것으로 사료되며, 본 연구대상 유역에 대한 침식계수, 유로이동에 대한 평균오차량, 하상세굴계수 등을 비교검토한 결과 유로이동을 지배하는 유량이 존재함을 알 수 있으며, 연구대상유역에서 유로이동에 대한 지배유량은 재현기간 4년에 해당하는 6,000CMS 이상으로 사료된다. 유로이동모형을 실측값이 있는 남한강의 연구대상유로에 적용하여 침식계수를 구하였으며, 계산된 침식계수를 이용하여 그 유로에서의 2000년에 대한 유로이동을 예측하였다.

• BMB Reports
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• 제55권5호
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• pp.244-249
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• 2022

Characterized by abnormal proliferation and migration of vascular smooth muscle cells (VSMCs), neointima hyperplasia is a hallmark of vascular restenosis after percutaneous vascular interventions. Vaccinia-related kinase 1 (VRK1) is a stress adaption-associated ser/thr protein kinase that can induce the proliferation of various types of cells. However, the role of VRK1 in the proliferation and migration of VSMCs and neointima hyperplasia after vascular injury remains unknown. We observed increased expression of VRK1 in VSMCs subjected to platelet-derived growth factor (PDGF)-BB by western blotting. Silencing VRK1 by shVrk1 reduced the number of Ki-67-positive VSMCs and attenuated the migration of VSMCs. Mechanistically, we found that relative expression levels of β-catenin and effectors of mTOR complex 1 (mTORC1) such as phospho (p)-mammalian target of rapamycin (mTOR), p-S6, and p-4EBP1 were decreased after silencing VRK1. Restoration of β-catenin expression by SKL2001 and re-activation of mTORC1 by Tuberous sclerosis 1 siRNA (siTsc1) both abolished shVrk1-mediated inhibitory effect on VSMC proliferation and migration. siTsc1 also rescued the reduced expression of β-catenin caused by VRK1 inhibition. Furthermore, mTORC1 re-activation failed to recover the attenuated proliferation and migration of VSMC resulting from shVrk1 after silencing β-catenin. We also found that the vascular expression of VRK1 was increased after injury. VRK1 inactivation in vivo inhibited vascular injury-induced neointima hyperplasia in a β-catenin-dependent manner. These results demonstrate that inhibition of VRK1 can suppress the proliferation and migration of VSMC and neointima hyperplasia after vascular injury via mTORC1/β-catenin pathway.

• 한국세라믹학회지
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• 제28권11호
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• pp.878-884
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• 1991

The mobility and diffusivity in an edge dislocation in an FCC crystal formed by the removal of one half of a (100) plane were evaluated in an applied field by analyzing a vacancy tight binding model using Stark's matrix technique. A model of an edge dislocation in an FCC crystal was constructed for a [100] Burgers vector where vacancy transport along the edge dislocation in an FCC crystal was constructed for a [100] Burgers vector where vacancy transport along the edge of the extrac half plane of ions was considered. The model considered a tight binding approximation of the vacancy to the compressed region of the core and carried the calculation to the limit of an infinite length of dislocation. The diffusivity and the ratio of mobility to diffusivity were found to increase without bounds in the limit where the correlation factor becomes zero. In contrast, as the correlation factor became unity, the diffusivity became zero and the ratio of mobility to diffusivity became unity associated with the uncorrelated limit of 1/kT. This implied that the phenomenon was not unique to the crystal structure but was unique to edge dislocations with vacancy tight binding.

• Asian Pacific Journal of Cancer Prevention
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• 제13권5호
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• pp.1737-1744
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• 2012

Macrophage migration inhibitory factor (MIF) is a pluripotent cytokine which plays roles in inflammation, immune responses and cancer development. It assists macrophages in carrying out functions like phagocytosis, adherence and motility. Of late, MIF is implicated in almost all stages of neoplasia and expression is a feature of most types of cancer. The presence of MIF in almost all tumors and all stages of cancer makes it an interesting candidate for cancer therapy. This review explores the roles of MIF in neoplasia.

• Molecules and Cells
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• 제28권1호
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• pp.1-5
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• 2009

Vascular endothelial growth factor (VEGF) is essential for many angiogenic processes both in normal and pathological conditions. However, the signaling pathways involved in VEGF-induced angiogenesis are incompletely understood. The protein kinase D1 (PKD1), a newly described calcium/calmodulin-dependent serine/threonine kinase, has been implicated in cell migration, proliferation and membrane trafficking. Increasing evidence suggests critical roles for PKD1-mediated signaling pathways in endothelial cells, particularly in the regulation of VEGF-induced angiogenesis. Recent studies show that class IIa histone deacetylases (HDACs) are PKD1 substrates and VEGF signal-responsive repressors of myocyte enhancer factor-2 (MEF2) transcriptional activation in endothelial cells. This review provides a guide to PKD1 signaling pathways and the direct downstream targets of PKD1 in VEGF signaling, and suggests important functions of PKD1 in angiogenesis.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2003년도 추계학술대회
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• pp.142-142
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• 2003

Transforming growth factor (TGF)-${\beta}$, a hormonally active polypeptide found in normal and transformed tissue, is a potent regulator of cell growth and differentiation. In this study, we examined the effect of TGF-${\beta}$ on invasion and motility of MCF10A human breast epithelial cells. TGF-${\beta}$ induced migration and invasive phenotype of the parental MCF10A cells in a dose-dependent manner.(omitted)

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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• pp.165.1-165.1
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• 2003

Transforming growth factor (TGF)-$\beta$, a hormonally active polypeptide found in normal and transformed tissue, is a potent regulator of cell growth and differentiation. In this study, we examined the effect of TGF-$\beta$ on invasion and motility of MCF10A human breast epithelial cells. TGF-$\beta$-induced migration and invasive phenotype of the parental MCF10A cells in a dose-dependent manner. Activity of MMP-2 promoter was increased by TGF-b, suggesting that the TGF-$\beta$-induced invasive phenotype may possibly be mediated by MMP-2 rather than MMP-9. (omitted)

• 한국균학회지
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• 제15권1호
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• pp.1-8
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• 1987

화학주성인자를 선택하기 위하여 chemotactic factor로 영지추출액(靈芝抽出液), 대장균 배양액, N-fMLP 및 TC-199 medium을 사용하였으며 modified Boyden chamber와 Nuclepore membrane filter를 이용하여 백혈구의 유주능을 측정한 바 다음과 같은 결과를 얻었다. 1. 화학주성인자로 TC-199 medium과 N-fMLP 그리고 대장균 배양액을 사용하였을때, N-fMLP에서 백혈구의 유주능이 우수하었으나 대장균 배양액도 그에 못지않게 우수하였다. 2. 영지추출액(靈芝抽出液)을 PBS로 1.00%, 0.10%, 0.01%로 희석 조제하여 화학주성인자로 사용하였을때 비교적 저농도인 0.01%에서 우수하였다. 3. 영지추출액(靈芝抽出液)의 각 희석액 (1.00%, 0.10%, 0.01%)로 백혈구를 처리한 후 유주능을 실험(實驗)한 결과 0.01%에서 매우 우수하였다. 따라서 영지(靈芝) 추출액(抽出液)은 0.01%에서 우수한 유주능을 나타낸다는 사실을 알았다.

• Journal of Acupuncture Research
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• 제22권2호
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• pp.171-180
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• 2005

Background & Objective : Angiogenesis consists of the proliferation, migration, and differentiation of endothelial cells, and angiogenic factors and matrix protein interactions modulate this process. The aim of this study was to determine whether Puerariae radix could induce angiogenic activity in human umbilical vein endothelial cells (HUVECs). Methods: The angiogenic activity of Puerariae radix were evaluated by using BrdU assay, chemotactic migration assay, tube formation assay, measurement of bFGF in HUVECs, and Matrigel plug assay in mice. Results : Puerariae radix significantly increased HUVECs proliferation in a dose-dependent manner. In addition, Puerariae radix increased migration and tube-like formation in HUVECs. Interestingly,the expression of basic fibroblast growth factor (bFGF), an angiogenesis-stimulating growth factor, was dose-dependently increased by Puerariae radix. The angiogenic activity of Puerariae radix was confirmed using an in vivo Matrigel angiogenesis model, showing promotion of blood vessel formation. Conclusion : Puerariae radix significantly induces angiogenesis in vitro and in vivo. These results suggest that Puerariae radix is a potent angiogenic agent, and a promising drug, for the induction of neovascularization.

• Journal of the Korean Society for Industrial and Applied Mathematics
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• 제17권2호
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• pp.129-138
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• 2013

A spatio-temporal models as systems of ODE which describe two-species Beddington - DeAngelis type predator-prey system living in a habitat of two identical patches linked by migration is investigated. It is assumed in the model that the per capita migration rate of each species is influenced not only by its own but also by the other one's density, i.e. there is cross diffusion present. We show that a standard (self-diffusion) system may be either stable or unstable, a cross-diffusion response can stabilize an unstable standard system and destabilize a stable standard system. For the diffusively stable model, numerical studies show that at a critical value of the bifurcation parameter the system undergoes a Turing bifurcation and the cross migration response is an important factor that should not be ignored when pattern emerges.