• 제목/요약/키워드: Human migration

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인적자원이 지역경제성장에 미치는 효과: 미국 카운티 데이터를 이용한 실증연구 (Effects of Human Capital on Regional Growth: Evidence from US County Data)

  • 김영배
    • 디지털융복합연구
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    • 제11권2호
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    • pp.71-78
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    • 2013
  • 본 논문에서는 인적자원과 노동시장환경이 경제성장과정에 있어서의 역할을 실증 분석하고자 하였다. 이를 위해 미국의 50개 주 전역의 3062개 카운티의 데이터를 활용하였다. 먼저, 실증분석 결과는 카운티들 간의 소득수렴을 보여주었다, 둘째, 인적자원은 경제성장 제고효과가 있는 반면, 교육지출은 경제성장을 저해하는 것으로 나타났다. 셋째, 실업률은 지역경제성장과 부정적인 상관관계가 있는 반면, 순이주율은 이와 반대로 긍정적인 관계가 있는 것을 밝혀졌다. 마지막으로 전체샘플 카운티들을 저소득 그룹과 고소득 그룹으로 양분된 뒤에도 위와 같은 주요 실증분석 결과는 대부분의 경우에서 변함없이 통계적으로 실효성이 있는 것으로 나타났다.

한국(韓國)의 급격(急激)한 이촌향도형(離村向都型) 인구이동(人口移動)과 농촌경제(農村經濟) (Rapid Rural-Urban Migration and the Rural Economy in Korea)

  • 이번송
    • KDI Journal of Economic Policy
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    • 제12권3호
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    • pp.27-45
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    • 1990
  • 이촌향도형(離村向都型) 인구이동(人口移動) 농촌지역경제(農村地域經濟)에 미치는 영향(影響)에 관해 두가지 상반(相反)된 견해(見解)가 있다. 신고전학파적(新古典學派的) 낙관론(樂觀論) 따르면 이농현상(離農現象)은 농촌지역(農村地域)의 소득(所得)이나 후생수준(厚生水準)을 저해(沮害)하지 않는다고 보는 반면 Lipton (1980)은 그 반대의 견해(見解)를 취하고 있다. 본고(本稿)에서는 비교역재(非交易財)(nontraded goods)에 대한 국제무역이론(國濟貿易理論)과 화란병(和蘭病)(Dutch Disease)의 이론(理論)을 원용하여 농촌(農村)에서 도시(都市)로의 인구이동모형을 개발했다. 이 모형은 이농인구이동(離農人口移動)이 농촌지역(農村地域)의 소득(所得)과 후생수준(厚生水準)을 저해(沮害)한다는 점에서는 Lipton의 견해(見解)와 일치하나 소득(所得)을 감소(減少)시키는 요인들은 Lipton의 모형(模型)에서 지적(指摘)된 것들과는 다르다. 본고(本稿)는 이농현상(離農現象)이 농촌소득(農村所得)을 감소(減少)시키는 이유가 농업생산성(農業生産性)의 하락(下落) 때문이 아니라 농촌노동 및 소비인구의 격감으로 인한 농업부문(農業部門)의 이윤감소(利潤減少)와 농촌(農村) 서비스부문(部門)와 쇠퇴(衰退)때문이라고 주장한다. 1966, 1970, 1975, 1980 및 1985년의 한국인구(韓國人口)센서스 통계자료(統計資料)를 이용하여 주요가설(主要假說)들에 대해 실증분석(實證分析)을 한 결과 신고전학파(新古典學派)의 주장(主張)이나 Lipton의 견해(見解)보다 본(本) 연구모형(硏究模型)의 설명력(說明力)이 더 높은 것으로 밝혀졌다.

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Auraptene Inhibits Migration and Invasion of Cervical and Ovarian Cancer Cells by Repression of Matrix Metalloproteinasas 2 and 9 Activity

  • Jamialahmadi, Khadijeh;Salari, Sofia;Alamolhodaei, Nafiseh Sadat;Avan, Amir;Gholami, Leila;Karimi, Gholamreza
    • 대한약침학회지
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    • 제21권3호
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    • pp.177-184
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    • 2018
  • Objectives: Auraptene, a natural citrus coumarin, found in plants of Rutaceae and Apiaceae families. In this study, we investigated the effects of auraptene on tumor migration, invasion and matrix metalloproteinase (MMP)-2 and -9 enzymes activity. Methods: The effects of auraptene on the viability of A2780 and Hela cell lines was evaluated by MTT assay. Wound healing migration assay and Boyden chamber assay were determined the effect of auraptene on migration and cell invasion, respectively. MMP-2 and MMP-9 activities were analyzed by gelatin zymography assay. Results: Auraptene reduced A2780 cell viability. The results showed that auraptene inhibited in vitro migration and invasion of both cells. Furthermore, cell invasion ability suppressed at $100{\mu}M$ auraptene in Hela cells and at 25, $50{\mu}M$ in A2780 cell line. Gelatin zymography showed that for Hela cell line, auraptene suppressed MMP-2 enzymatic activity in all concentrations and for MMP-9 at a concentration between 12.5 to $100{\mu}M$ in A2780 cell line. Conclusion: Auraptene inhibited migration and invasion of human cervical and ovarian cancer cells in vitro by possibly inhibitory effects on MMP-2 and MMP-9 activity.

혈관내피세포의 이동에 미치는 Hepatocyte Growth Factor의 영향 (Effect of Hepatocyte Growth Factor on the Migration of Human Umbilical Vein Endothelial Cells)

  • 오인숙;소상섭;김환규
    • KSBB Journal
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    • 제18권6호
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    • pp.485-489
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    • 2003
  • HGF는 내피세포의 증식 및 이동을 일으키는 강력한 혈관 신생 유도인자 및 생존인자로서 작용한다고 알려져 있다. 본 연구에서는 HUVECs 세포를 이용하여 내피세포의 이동 및 단백질분해효소의 분비에 미치는 HGF의 효과를 확인하였다. 그 곁과, HGF 처리 (10ng/$m\ell$)에 의해 HUVECs 세포의 이동이 약 3.3배 촉진되어, HGF가 HUVECs 세포에서 강력한 이동 유도인자라는 사실을 확인하였다. 내피세포의 이동에 관여할 것이라 여겨지는 MMPs, TIMPs 및 플라스민의 분비에 미치는 HGF의 효과를 관찰한 결과, HGF에 의해 MMP-2 및 MMP-3의 분비양이 각각 3.3배와 6.1배씩 증가되었다. HGF에 의한 TIMPs 분비효과를 관찰한 결과, TIMP-1은 대조군에 비해 약 1.8배 분비가 증가되었으나, TIMP-2는 대조군에 비해 약 3.1배 분비가 억제되었다. 또한, 광범위 MMPs-억제제인 BB-94 (20ng/$m\ell$) 및 플라스민 억제제인 $\alpha$$_2$-antiplasmin (100mU)을 처리했을 때, HGF에 의해 유도된 혈관내피세포의 이동이 거의 완벽하게 억제되었다. 결론적으로, HGF는 HUVECs 세포에서 MMP-2, MMP-3, MMP-9, TIMP-1 및 플라스민의 분비 증가를 일으켰으며, HGF에 의해 분비가 증가 된 단백질분해효소에 의해 세포외기질 및 기저막 단백질로의 혈관내피세포의 이동이 촉진되고, 결과적으로 혈관신생을 유도할 것이라 사료된다.

Effect of secretory leukocyte protease inhibitor on migration and invasion of human KB oral carcinoma cells

  • Wang, Guanlin;Lim, Do-Seon;Choi, Baik-Dong;Park, Jin-Ju;Jeong, Soon-Jeong;Kim, Jin-Soo;Kim, Jae-Duk;Park, Jung-Su;Kim, Eung-Kwon;Kim, Byung-Hoon;Ham, Joo-Hyun;Jeong, Moon-Jin
    • Animal cells and systems
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    • 제15권2호
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    • pp.139-146
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    • 2011
  • Secretory leukocyte protease inhibitor (SLPI) plays an important role in promoting the invasion and metastasis of a range of cancer cells. However, there are no reports of the expression and function of SLPI in oral carcinoma cells. In this study, the oral carcinoma cell line KB was used to determine whether SLPI affects the proliferation, migration and invasion of oral carcinoma cells. RT-PCR and Western blotting revealed high levels of endogenous SLPI expression in KB cells as well as a strong increase in SLPI secretion after wounding compared to immortalized normal oral keratinocytes (INOK). The wound healing assay revealed more migration of KB cells than INOK cells, and the SLPI treatment increased the migration of KB cells. KB cell proliferation was increased significantly by the SLPI protein but decreased by SLPI-siRNA. SLPI strongly increased the migration and invasion of KB cells. On the other hand, SLPI-siRNA decreased the migration and invasion of KB cells. This suggests that SLPI plays an important role in the metastasis of oral carcinoma cells.

Transforming Growth Factor-$\beta$ (TGF-$\beta$) Induces Invasion and Migration of MCF10A Human Breast Epithelial Cells

  • Kim, Eun-Sook;Kim, Mi-Sung;Aree Moon
    • 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)

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Retroviral Delivery of TIMP-2 Inhibits H-ras-induced Migration and Invasion in MCF10A Human Breast Epithelial Cells

  • Ahn, Seong-Min;Jeong, Seo-Jin;Kim, Yeon-Soon;Sohn, Yeo-Won;Moon, Aree
    • 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.168.3-169
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    • 2003
  • The matrix metalloproteases (MMPs) play important roles in invasion, metastasis and angiogenesis in various cell types. Tissue inhibitor of metalloprotease (TIMP)-2, an endogenopus inhibitor of MMP-2, has been shown to inhibit invasion and metastasis. We have previously shown that MMP-2 is responsible for the H-ras-induced invasive and migrative phenotypes in MCF10A human breast epithelial cells. Here, we investigated the effect of TlMP-2 overexpression on invasion and migration in H-ras MCF10A cells. (omitted)

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Transforming Growth Factor-$\beta$ (TGF)-$\beta$, Induces Invasion and Migration of MCF10A Human Breast Epithelial Cells

  • Kim, Eun-Sook;Kim, Mi-Sung;Moon, Aree
    • 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)

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ATM Signaling Pathway Is Implicated in the SMYD3-mediated Proliferation and Migration of Gastric Cancer Cells

  • Wang, Lei;Wang, Qiu-Tong;Liu, Yu-Peng;Dong, Qing-Qing;Hu, Hai-Jie;Miao, Zhi;Li, Shuang;Liu, Yong;Zhou, Hao;Zhang, Tong-Cun;Ma, Wen-Jian;Luo, Xue-Gang
    • Journal of Gastric Cancer
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    • 제17권4호
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    • pp.295-305
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    • 2017
  • Purpose: We previously found that the histone methyltransferase suppressor of variegation, enhancer of zeste, trithorax and myeloid-nervy-deformed epidermal autoregulatory factor-1 domain-containing protein 3 (SMYD3) is a potential independent predictive factor or prognostic factor for overall survival in gastric cancer patients, but its roles seem to differ from those in other cancers. Therefore, in this study, the detailed functions of SMYD3 in cell proliferation and migration in gastric cancer were examined. Materials and Methods: SMYD3 was overexpressed or suppressed by transfection with an expression plasmid or siRNA, and a wound healing migration assay and Transwell assay were performed to detect the migration and invasion ability of gastric cancer cells. Additionally, an MTT assay and clonogenic assay were performed to evaluate cell proliferation, and a cell cycle analysis was performed by propidium iodide staining. Furthermore, the expression of genes implicated in the ataxia telangiectasia mutated (ATM) pathway and proteins involved in cell cycle regulation were detected by polymerase chain reaction and western blot analyses. Results: Compared with control cells, gastric cancer cells transfected with si-SMYD3 showed lower migration and invasion abilities (P<0.05), and the absence of SMYD3 halted cells in G2/M phase and activated the ATM pathway. Furthermore, the opposite patterns were observed when SMYD3 was elevated in normal gastric cells. Conclusions: To the best of our knowledge, this study provides the first evidence that the absence of SMYD3 could inhibit the migration, invasion, and proliferation of gastric cancer cells and halt cells in G2/M phase via the ATM-CHK2/p53-Cdc25C pathway. These findings indicated that SMYD3 plays crucial roles in the proliferation, migration, and invasion of gastric cancer cells and may be a useful therapeutic target in human gastric carcinomas.

MicroRNA-21 promotes epithelial-mesenchymal transition and migration of human bronchial epithelial cells by targeting poly (ADP-ribose) polymerase-1 and activating PI3K/AKT signaling

  • Zhang, Shiqing;Sun, Peng;Xiao, Xinru;Hu, Yujie;Qian, Yan;Zhang, Qian
    • The Korean Journal of Physiology and Pharmacology
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    • 제26권4호
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    • pp.239-253
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    • 2022
  • Epithelial-mesenchymal transition (EMT) is known to be involved in airway remodeling and fibrosis of bronchial asthma. However, the molecular mechanisms leading to EMT have yet to be fully clarified. The current study was designed to reveal the potential mechanism of microRNA-21 (miR-21) and poly (ADP-ribose) polymerase-1 (PARP-1) affecting EMT through the PI3K/AKT signaling pathway. Human bronchial epithelial cells (16HBE cells) were transfected with miR-21 mimics/inhibitors and PARP-1 plasmid/small interfering RNA (siRNA). A dual luciferase reporter assay and biotin-labeled RNA pull-down experiments were conducted to verify the targeting relationship between miR-21 mimics and PARP-1. The migration ability of 16HBE cells was evaluated by Transwell assay. Quantitative real-time polymerase chain reaction and Western blotting experiments were applied to determine the expression of Snail, ZEB1, E-cadherin, N-cadherin, Vimentin, and PARP-1. The effects of the PI3K inhibitor LY294002 on the migration of 16HBE cells and EMT were investigated. Overexpression of miR-21 mimics induced migration and EMT of 16HBE cells, which was significantly inhibited by overexpression of PARP-1. Our findings showed that PARP-1 was a direct target of miR-21, and that miR-21 targeted PARP-1 to promote migration and EMT of 16HBE cells through the PI3K/AKT signaling pathway. Using LY294002 to block PI3K/AKT signaling pathway resulted in a significant reduction in the migration and EMT of 16HBE cells. These results suggest that miR-21 promotes EMT and migration of HBE cells by targeting PARP-1. Additionally, the PI3K/AKT signaling pathway might be involved in this mechanism, which could indicate its usefulness as a therapeutic target for asthma.