• 제목/요약/키워드: Signalling Effect

검색결과 74건 처리시간 0.042초

안전성 분석에 대한 사례 연구 (A Case Study for Safety Analysis)

  • Chang, Kwang-Chi;Lee, Key-Seo
    • 한국철도학회논문집
    • /
    • 제7권3호
    • /
    • pp.251-258
    • /
    • 2004
  • A systematic methodology to determine safety requirements for railway signalling system and safety requirement allocation into system are presented. THR concept is used for as an interface between Risk Analysis to be performed by railway operator and System Design Analysis by the supplier. This approach is based on Signalling Safety Standard EN50129 by CENELEC.

Photobiomodulation therapy activates YAP and triggers proliferation and dedifferentiation of Müller glia in mammalian retina

  • Seo-Yeon Kim;Myung-Jun Song;In-Beom Kim;Tae Kwan Park;Jungmook Lyu
    • BMB Reports
    • /
    • 제56권9호
    • /
    • pp.502-507
    • /
    • 2023
  • Photobiomodulation therapy has been proposed as a promising therapeutic approach for retinal degenerative diseases. However, its effect on the regenerative capacity in mammalian retina and its intracellular signalling mechanisms remain unknown. Here, we show that photobiomodulation with 670 nm light stimulates Müller glia cell cycle re-entry and dedifferentiation into a progenitor-like state in both the uninjured and injured retina. We also find that 670 nm light treatment inhibits the Hippo pathway, which is activated in Müller glia following NaIO3-induced retinal injury. YAP, a major downstream effector of the Hippo signalling pathway was translocated into the nucleus of Müller glia along with YAP dephosphorylation in retina treated with 670 nm light. Deficiency of YAP attenuated Müller glia cell cycle re-entry and dedifferentiation. Our data reveal that the Hippo-YAP signalling pathway is associated with the photostimulatory effect on regenerative response in mammalian retina, and suggest a potential therapeutic strategy for retinal degenerative diseases.

Modulation of L-type $Ca^{2+}$ Channel Currents by Various Protein Kinase Activators and Inhibitors in Rat Clonal Pituitary $GH_3$ Cell Line

  • Bae, Young-Min;Baek, Hye-Jung;Cho, Ha-Na;Earm, Yung-E;Ho, Won-Kyung
    • The Korean Journal of Physiology and Pharmacology
    • /
    • 제5권2호
    • /
    • pp.139-146
    • /
    • 2001
  • L-type $Ca^{2+}$ channels play an important role in regulating cytosolic $Ca^{2+}$ and thereby regulating hormone secretions in neuroendocrine cells. Since hormone secretions are also regulated by various kinds of protein kinases, we investigated the role of some kinase activators and inhibitors in the regulation of the L-type $Ca^{2+}$ channel currents in rat pituitary $GH_3$ cells using the patch-clamp technique. Phorbol 12,13-dibutyrate (PDBu), a protein kinase C (PKC) activator, and vanadate, a protein tyrosine phosphatase (PTP) inhibitor, increased the $Ba^{2+}$ current through the L-type $Ca^{2+}$ channels. In contrast, bisindolylmaleimide I (BIM I), a PKC inhibitor, and genistein, a protein tyrosine kinase (PTK) inhibitor, suppressed the $Ba^{2+}$ currents. Forskolin, an adenylate cyclase activator, and isobutyl methylxanthine (IBMX), a non-specific phosphodiesterase inhibitor, reduced $Ba^{2+}$ currents. The above results show that the L-type $Ca^{2+}$ channels are activated by PKC and PTK, and inhibited by elevation of cyclic nucleotides such as cAMP. From these results, it is suggested that the regulation of hormone secretion by various kinase activity in $GH_3$ cells may be attributable, at least in part, to their effect on L-type $Ca^{2+}$ channels.

  • PDF

배당공시이후 애널리스트 이익추정치 발표가 주가에 미치는영향 (The Effect of Analysts' Earnings Forecasts Following Dividend Announcements on Stock Returns)

  • 홍춘욱;이성효;김경일
    • 융합정보논문지
    • /
    • 제7권3호
    • /
    • pp.105-109
    • /
    • 2017
  • 본 연구는 기업의 배당공시 이후 애널리스트들의 이익 추정 수정치가 주가에 어떤 영향을 미치는지 살펴보았다. 우선, 배당공시 이후 발표된 애널리스트들의 이익 추정치에 대한 주가 반응을 추정한 결과, 이익 추정이 상향조정된 기업들은 그렇지 못한 기업들에 비해 통계적으로 유의한 양(+)의 누적초과수익률을 기록한 것으로 나타났다. 그리고 배당공시와 이익 추정치 발표의 상호관계에 있어서 '신호효과'와 '확증효과'를 검증하였다. 검증 결과, 확증효과가 우세한 것으로 나타났다. 이는 배당과 이익 수정이 동일한 방향일 때는 시장이 반응을 하지만, 서로 다른 방향일 때는 시장에 중요한 정보가 되지 못함을 의미한다.

β-Elemene Induces Apoptosis in Human Renal-cell Carcinoma 786-0 Cells through Inhibition of MAPK/ERK and PI3K/Akt/mTOR Signalling Pathways

  • Zhan, Yun-Hong;Liu, Jing;Qu, Xiu-Juan;Hou, Ke-Zuo;Wang, Ke-Feng;Liu, Yun-Peng;Wu, Bin
    • Asian Pacific Journal of Cancer Prevention
    • /
    • 제13권6호
    • /
    • pp.2739-2744
    • /
    • 2012
  • Background: Renal-cell carcinoma (RCC) is resistant to almost all chemotherapeutics and radiation therapy. ${\beta}$-Elemene, a promising anticancer drug extracted from a traditional Chinese medicine, has been shown to be effective against various tumors. In the present study, anti-tumor effects on RCC cells and the involved mechanisms were investigated. Methods: Human RCC 786-0 cells were treated with different concentrations of ${\beta}$-elemene, and cell viability and apoptosis were measured by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay and flow cytometry, respectively. Protein expression was assayed by western blotting. Autophagy was evaluated by transmission electron microscopy. Results: ${\beta}$-Elemene inhibited the viability of 786-0 cells in a dose- and time-dependent manner. The anti-tumor effect was associated with induction of apoptosis. Further study showed that ${\beta}$-elemene inhibited the MAPK/ERK as well as PI3K/Akt/mTOR signalling pathways. Moreover, robust autophagy was observed in cells treated with ${\beta}$-elemene. Combined treatment of ${\beta}$-elemene with autophagy inhibitors 3-methyladenine or chlorochine significantly enhanced the anti-tumor effects. Conclusions: Our data provide first evidence that ${\beta}$-elemene can inhibit the proliferation of RCC 786-0 cells by inducing apoptosis as well as protective autophagy. The anti-tumor effect was associated with the inhibition of MAPK/ERK and PI3K/Akt/mTOR signalling pathway. Inhibition of autophagy might be a useful way to enhance the anti-tumor effect of ${\beta}$-elemene on 786-0 cells.

Suppressive Effect of Maslinic Acid on PMA-induced Protein Kinase C in Human B-Lymphoblastoid Cells

  • Mooi, Lim Yang;Yew, Wong Teck;Hsum, Yap Wei;Soo, Khoo Kong;Hoon, Lim Saw;Chieng, Yeo Chew
    • Asian Pacific Journal of Cancer Prevention
    • /
    • 제13권4호
    • /
    • pp.1177-1182
    • /
    • 2012
  • Protein kinase C (PKC) has been implicated in carcinogenesis and displays variable expression profiles during cancer progression. Studies of dietary phytochemicals on cancer signalling pathway regulation have been conducted to search for potent signalling regulatory agents. The present study was designed to evaluate any suppressive effect of maslinic acid on PKC expression in human B-lymphoblastoid cells (Raji cells), and to identify the PKC isoforms expressed. Effects of maslinic acid on PKC activity were determined using a PepTag$^{(R)}$ assay for non-radioactive detection of PKC. The highest expression in Raji cells was obtained at 20 nM PMA induced for 6 hours. Suppressive effects of maslinic acid were compared with those of four PKC inhibitors (H-7, rottlerin, sphingosine, staurosporine) and two triterpenes (oleanolic acid and ursolic acid). The $IC_{50}$ values achieved for maslinic acid, staurosporine, H-7, sphingosine, rottlerin, ursolic acid and oleanolic acid were 11.52, 0.011, 0.767, 2.45, 5.46, 27.93 and $39.29\;{\mu}M$, respectively. Four PKC isoforms, PKC ${\beta}I$, ${\beta}II$, ${\delta}$, and ${\zeta}$, were identified in Raji cells via western blotting. Maslinic acid suppressed the expression of PKC ${\beta}I$, ${\delta}$, and ${\zeta}$ in a concentration-dependent manner. These preliminary results suggest promising suppressive effects of maslinic acid on PKC activity in Raji cells. Maslinic acid could be a potent cancer chemopreventive agent that may be involved in regulating many downstream signalling pathways that are activated through PKC receptors.

In vitro Study of the Antagonistic Effect of Low-dose Liquiritigenin on Gemcitabine-induced Capillary Leak Syndrome in Pancreatic Adenocarcinoma via Inhibiting ROS-Mediated Signalling Pathways

  • Wu, Wei;Xia, Qing;Luo, Rui-Jie;Lin, Zi-Qi;Xue, Ping
    • Asian Pacific Journal of Cancer Prevention
    • /
    • 제16권10호
    • /
    • pp.4369-4376
    • /
    • 2015
  • Background: To investigate in-vitro antagonistic effect of low-dose liquiritigenin on gemcitabine-induced capillary leak syndrome (CLS) in pancreatic adenocarcinoma via inhibiting reactive oxygen species (ROS)-mediated signalling pathways. Materials and Methods: Human pancreatic adenocarcinoma Panc-1 cells and human umbilical vein endothelial cells (HUVECs) were pre-treated using low-dose liquiritigenin for 24 h, then added into gemcitabine and incubated for 48 h. Cell viability, apoptosis rate and ROS levels of Panc-1 cells and HUVECs were respectively detected through methylthiazolyldiphenyl-tetrazoliumbromide (MTT) and flow cytometry. For HUVECs, transendothelial electrical resistance (TEER) and transcellular and paracellular leak were measured using transwell assays, then poly (ADP-ribose) polymerase 1 (PARP-1) and metal matrix proteinase-9 (MMP9) activity were assayed via kits, mRNA expressions of p53 and Rac-1 were determined through quantitative polymerase chain reaction (qPCR); The expressions of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and PARP-1 were measured via western blotting. Results: Low-dose liquiritigenin exerted no effect on gemcitabine-induced changes of cell viability, apoptosis rate and ROS levels in Panc-1 cells, but for HUVECs, liquiritigenin ($3{\mu}M$) could remarkably elevate gemcitabine-induced decrease of cell viability, transepithelial electrical resistance (TEER), pro-MMP9 level and expression of ICAM-1 and VCAM-1 (p<0.01). Meanwhile, it could also significantly decrease gemcitabine-induced increase of transcellular and paracellular leak, ROS level, PARP-1 activity, Act-MMP9 level, mRNA expressions of p53 and Rac-1, expression of PARP-1 and apoptosis rate (p<0.01). Conclusions: Low-dose liquiritigenin exerts an antagonistic effect on gemcitabine-induced leak across HUVECs via inhibiting ROS-mediated signalling pathways, but without affecting gemcitabine-induced Panc-1 cell apoptosis. Therefore, low-dose liquiritigenin might be beneficial to prevent the occurrence of gemcitabine-induced CLS in pancreatic adenocarcinoma.

전기철도에서의 통신선 유도전압에 대한 금속관 차폐효과 측정 (Measurement of Screening Effect by Metal Pipe on Induced Voltage to Communication Cable from Electric Railway)

  • 설일환;최규형;이상무
    • 한국산학기술학회논문지
    • /
    • 제15권4호
    • /
    • pp.2355-2362
    • /
    • 2014
  • 전기철도 선로변에 포설되어 있는 통신선에는 유도전압이 발생하여, 통신품질 저하와 기기 오작동 및 안전문제를 유발할 수 있다. 이와 같은 유도전압은 전차선과 통신선의 자계결합에 의해 유발되며, 구조물이나 레일 등의 금속물이 근처에 있을 경우 차폐영향을 받는다. 본 논문에서는 통신선 주변에 금속관이 매설되어 있을 경우에 발생하는 차폐효과를 실험을 통해 정량적으로 분석하였다. 고속철도 현장에서의 실험 결과, 금속관이 통신선으로부터 1~2m 거리에 병행매설되어 있을 경우, 금속관의 차폐효과는 20% 정도인 것으로 측정되었다. 또한, 이격거리가 4m 이상인 경우에는 차폐효과가 1% 이내로 미미하다는 것을 확인하였다. 이상의 결과는, 수도관이나 가스관, 구조물의 철근과 같은 금속 설치물의 차폐효과를 분석하는 데 활용할 수 있다.

전기철도 복선화 및 차폐 케이블 적용에 따른 통신선 유도장해 차폐 효과 (Screening Effects of Double-track Electric Railway and Shielded Cables on Communication-Line Inductive Interference)

  • 설일환;최규형
    • 한국산학기술학회논문지
    • /
    • 제14권10호
    • /
    • pp.5148-5155
    • /
    • 2013
  • 전기철도와 인접하여 병행 설치되어 있는 전기통신선에는 전자유도현상에 의한 유도전압이 발생하여 통신장애 및 안전사고가 발생할 수 있다. 이와 같은 유도장해를 경감시키고 통신신뢰성을 확보하기 위하여, 차폐케이블의 적용과 함께 최근 추진되고 있는 복선전철화에 따른 영향을 검토할 필요가 있다. 본 논문에서는 AT급전방식 전기철도에서 인근 통신선에 유기되는 유도전압에 영향을 미치는 각종 인수 및 산출식을 검토하고, 유도전압 발생 예측치를 시뮬레이션을 통하여 정량적으로 분석하였다. 시뮬레이션 결과, 복선철도에서는 단선철도에 비해 통신선 유도잡음 전압이 18[%] 정도 감소하여 타궤조 효과가 영향을 미치는 것으로 나타났다. 또한, 복선철도를 기준으로, 50% 차폐 통신케이블에서는 유도잡음전압이 1/8로 감소하였으며, 15% 차폐통신케이블에서는 1/15로 감소함에 따라 차폐효과가 크고 유도잡음전압 영향을 최소화할 수 있는 것으로 나타났다.