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        문장형 브랜드네임의 품질암시와 구체성이 구매의도에 미치는 영향 - 구매관여도의 조절 역할

        황인석 ( Insuk Hwang ),김희연 ( Heeyeon Kim ) 한국소비자학회 2017 소비자학연구 Vol.28 No.2

        본 연구는 문장형 브랜드네임을 구분하는 기준으로 품질암시와 구체성을 제안하고, 이 두 기준이 구매의도에 미치는 영향을 구매관여도의 조절효과 관점에서 고찰하고 있다. 여기서 문장형 브랜드네임이란 문장이 포함된 브랜드네임을 의미하며, 실제 마케팅 상황에서는 ‘문장 그 자체 혹은 수식절과 피수식어(주로 상품범주명)’ 형태의 브랜드네임이 주로 관찰된다. 품질암시나 구체성은 여타 비문장형 브랜드네임에도 적용될 수 있는 개념으로서, 문장형 브랜드네임이 상대적으로 풍부하게 표현되는 특성으로 말미암아 그 효과가 보다 확대되어 나타날 수 있다. 한편, 구매관여도는 기존의 관여도 개념을 구매라는 특정 상황과 연관지은 개념이다. 가설은 품질암시와 구체성의 상호작용 관점과 이 효과를 조절하는 소비자의 구매관여도 관점에서 제시되었다. 구체적으로 본 연구는 문장형 브랜드네임의 품질암시가 높을 경우 추상적인 정보가 유리하며, 낮을 경우 구체적인 정보가 유리하다고 가정한다. 나아가 전자의 효과는 소비자의 구매관여도가 낮을 경우 더 분명하게 나타나며, 후자의 효과는 구매관여도가 높을 경우 더 분명하게 나타날 것임을 가정한다. 이러한 가설들을 검정하기 위해 본 연구는 인쇄광고를 대상으로 2(브랜드네임의 품질암시: 고/저) X 2(브랜드네임의 구체성: 고/저) X 2(구매관여도: 고/저)의 실험설계를 이용하였다. 브랜드네임의 노출은 다른 상품정보의 제공없이 가상의 상품모습과 함께 설문지에 삽입되는 방식으로 이루어졌다. 다른 상품정보를 제공하지 않는 어색함을 완화하기 위해 실험상품은 평가속성 수가적은 생수를 선정하였다. 피험자는 194명의 대학생이었다. 연구결과 문장형 브랜드네임의 품질암시가 높을 경우 구체적인 정보가 추상적인 정보보다 브랜드 구매의도를 높이는 것으로 나타났다. 이 결과는 구매관여도가 낮은 소비자에게서 더 분명하게 나타났다. 반면, 품질암시가 낮을 경우 소비자의 구매관여도가 높을 경우에 한해 추상적인 정보가 구체적인 정보보다 브랜드 구매의도를 높이는 것으로 나타났다. 추가적으로 본 연구에서는 소비자의 구매관여도가 낮을 경우 품질암시 여부에 상관없이 구체적인 정보가 추상적인 정보보다 구매의도를 높이는 경향이 있는 것으로 나타났다. This study explores the effects of quality signaling and the concreteness of a sentence-form brand name on purchase intention, focusing on the moderating role of consumers’ purchase involvement, which has been rarely investigated by earlier works. The sentence-form brand name refers to a brand that includes any kind of sentence. Some brand names, such as “WeAretheSuperlativeConspiracy,” “I Can’t Believe. It’s Not Butter!,” and “行列のできる店のラ-メン” are representative examples. Quality signaling and concreteness have been considered important characteristics of product information, and are closely related to product evaluation in the field of consumer information processing. In addition, we expect consumers’ purchase involvement to moderate the effects of these characteristics on purchase intention. Based on prior studies, the following four hypotheses have been addressed in the study: High concreteness enhances purchase intention more than low concreteness when the quality signaling is high (H1), and low concreteness enhances purchase intention more than high concreteness when the quality signaling is low (H2). The effect predicted by H1 is more evident in the low purchase involvement condition (H3); and that predicted by H2 is more evident in the high purchase involvement condition (H4). Specifically, the ease of message processing, the effect of high diagnostic information on the evaluation (e.g., Chang and Wildt 1994; Herr, Kardes and Kim 1991; Zeithaml 1988), the cognitive miser theory (e.g., Fiske and Taylor 1984; Orbell and Dawes 1991), and the effect of consumer involvement on their message processing (e.g., Petty and Cacioppo 1981; Petty, Cacioppo, and Schumann 1983) were logical grounds for the hypotheses. A 2(quality signaling: high or low) by 2(concreteness: high or low) by 2(purchase involvement: high or low) between-subjects factorial design was employed for the study. In order to earn extra course credits, 194 undergraduate students belonging to the college of one of the authors participated in the study. The sample group was between 20 and 26 years of age, with an average of 22.3 years, and nearly 60 percent comprised males. In the questionnaire, the brand name was revealed to the participants along with a visual of the product, which was mineral water. The appearance was identical across experimental groups and only the brand name varied along the different brand name conditions. We conducted a pretest to select four brand names for each brand name condition. Twelve brand names were initially selected by the authors from a simple survey. Twenty undergraduate students who did not take part in the main experiment were asked to rank the level of quality signaling and concreteness, respectively, for twelve brand names. The pretests, “Spring Water Coming from Cheonji Lake, Baekdoo Mt. (high quality signaling and high concreteness),” “Spring Water Filled with Freshness (high quality signaling and low concreteness),” “Spring Water Coming with Shaking (low quality signaling and high concreteness),” and “Spring Water Filled with Sprit (low quality signaling and low concreteness),” were selected to be used in the main experiment. Prior to the experiment, participants were told that the purpose of the study was to analyze consumers’ responses to products sold in a convenience store. In order to manipulate the purchase involvement, we asked participants only in the high involvement group to imagine a situation where they would buy mineral water for a person they respected. Subsequent to watching the visual and the brand name of the product, participants were asked to answer questions pertaining to the items, measuring purchase intention for the product (two items on a seven-point scale, α = .87), the levels of the quality signaling (three items on a seven-point scale, α = .88), the concreteness of the brand name (three items on a seven-point scale, α = .78), the level of purchase involvement (three items on a seven-point scale, α = .80), as well as demographics. At the end of the class, all participants were given a debriefing questionnaire that asked them in an open-ended format to report what they believed to be the purpose of the study. None of the participants was aware of the true purpose of the study. The measurement of quality signaling revealed that the scores were 4.42 and 3.29 for the high and low quality signaling conditions, respectively (F(1,192) = 32.65 p < .001). In addition, as expected, participants rated the concreteness as higher in the high concreteness condition than in the low concreteness condition (4.36 vs. 2.83, F(1,192) = 113.47, p < .001). Likewise, participants in the high purchase involvement condition had a higher mean value than did participants in the low purchase involvement condition (5.18 vs. 4.24, F(1,192) = 43.08, p < .001). These results revealed that our manipulation was indeed successful. However, we should note that the absolute level of purchase involvement in the low purchase involvement condition that was achieved through the manipulation was marginally high. The results showed that high concreteness marginally enhanced the purchase intention when compared with low concreteness, when the quality signaling was high (H1, 3.84 vs. 3.50, t(92) = 1.70, p < .10) and when the quality signaling was low, low concreteness significantly enhanced the purchase intention more than high concreteness (H2, 3.56 vs. 2.91, t(98) = 2.26, p < .05). As expected, the effect predicted by H1 was more evident in the low purchase involvement condition (high purchase involvement condition, t(48) = .67, N.S.; low purchase involvement condition, t(42) = 1.98, p < .05), implying that H3 was supported. However, the effect predicted by H2 was observed only in the high purchase involvement condition (high purchase involvement condition, t(49) = 5.84, p < .001), and not in the low purchase involvement condition. We also found that when consumers were in the low purchase involvement condition, high concreteness, rather than low concreteness, tended to improve the purchase intention. The study has several limitations. First, our sample was limited to one population group, namely, college students. This decreases the generality of the study’s results. Further research should explore the effect by including other population groups and obtaining confirmatory results. Second, we performed the study in a restricted situation using nonprofessional advertisements. It is necessary for further studies to examine effects of sentence-form brand name in a real situation using professional advertisements to derive more practical implications. Third, this study used only one product category to examine the effects of sentence-form brand names. Further research should include other product categories to investigate the extent to which quality signaling and concreteness of sentence-form brand name substantively influence the purchase intention of the product. Finally, the study failed to ensure perfect homogeneity among fictitious brand names used in the experiment (e.g., one experimental brand name included a proper noun). Further research should select experimental brand names more carefully using one or more pretests.

      • Effects of olanzapine and haloperidol on mTORC1 signaling, dendritic outgrowth, and synaptic proteins in rat primary hippocampal neurons under toxic conditions

        Park, Sung Woo,Seo, Mi Kyoung,McIntyre, Roger S.,Mansur, Rodrigo B.,Lee, Yena,Lee, Jae-Hon,Park, Seon-Cheol,Huh, Lyang,Lee, Jung Goo Elsevier 2018 Neuroscience Letters Vol.686 No.-

        <P><B>Abstract</B></P> <P>Recent studies have demonstrated that antipsychotic drugs may activate mammalian target of rapamycin complex 1 (mTORC1) signaling in neurons. However, the relationship between mTORC1 signaling activation and currently prescribed antipsychotic drugs remains incompletely understood. The purpose of this study was to determine whether alterations in the level of mTORC1 signaling occur after rat primary hippocampal neurons are treated with olanzapine and haloperidol under toxic conditions. Additionally, we investigated whether these drugs affect dendritic outgrowth and synaptic protein expression through the mTORC1 signaling pathway. We measured changes in mTORC1-mediated and synaptic proteins by Western blotting assay under toxic conditions induced by B27 deprivation. Dendritic outgrowth was determined by a neurite assay. Olanzapine significantly increased the phosphorylated levels of mTORC1, its downstream effectors, and its upstream activators. The increased mTORC1 phosphorylation induced by olanzapine was significantly blocked by specific PI3K, MEK, or mTORC1 inhibitors. Olanzapine also increased dendritic outgrowth and synaptic proteins levels; all of these effects were blocked by rapamycin. However, haloperidol had none of these effects. We demonstrated that olanzapine, but not haloperidol, activated the mTORC1 signaling pathway and increased dendritic outgrowth and synaptic proteins by activating mTORC1 signaling in rat primary hippocampal neurons. These findings suggest that olanzapine affects neuroplasticity by activating mTORC1 signaling.</P> <P><B>Highlights</B></P> <P> <UL> <LI> B27 deprivation in hippocampal cultures decreases mTOR signaling activity. </LI> <LI> Olanzapine can actives the mTOR signaling pathway. </LI> <LI> Olanzapine increases synaptic plasticity through mTOR signaling. </LI> <LI> However, haloperidol has no such effects. </LI> </UL> </P>

      • KCI등재

        MtMKK5 inhibits nitrogen-fixing nodule development by enhancing defense signaling

        류호진 한국식물생명공학회 2022 JOURNAL OF PLANT BIOTECHNOLOGY Vol.49 No.4

        The mitogen-activated protein kinase (MAPK) signaling cascade is essential for a wide range of cellular responses in plants, including defense responses, responses to abiotic stress, hormone signaling, and developmental processes. Recent investigations have shown that the stress, ethylene, and MAPK signaling pathways negatively affect the formation of nitrogen-fixing nodules by directly modulating the symbiotic signaling components. However, the molecular mechanisms underlying the defense responses mediated by MAPK signaling in the organogenesis of nitrogen-fixing nodules remain unclear. In the present study, I demonstrate that the Medicago truncatula mitogenactivated protein kinase kinase 5 (MtMKK5)-Medicago truncatula mitogen-activated protein kinase 3/6 (MtMPK3/6) signaling module, expressed specifically in the symbiotic nodules, promotes defense signaling, but not ethylene signaling pathways, thereby inhibiting nodule development in M. truncatula. U0126 treatment resulted in increased cell division in the nodule meristem zone due to the inhibition of MAPK signaling. The phosphorylated TEY motif in the activation domain of MtMPK3/6 was the target domain associated with specific interactions with MtMKK5. I have confirmed the physical interactions between M. truncatula nodule inception (MtNIN) and MtMPK3/6. In the presence of high expression levels of the defense-related genes FRK1 and WRKY29, MtMKK5a overexpression significantly enhanced the defense responses of Arabidopsis against Pseudomonas syringae pv. tomato DC3000 (Pst DC3000). Overall, my data show that the negative regulation of symbiotic nitrogen-fixing nodule organogenesis by defense signaling pathways is mediated by the MtMKK5- MtMPK3/6 module.

      • KCI등재

        FGF signaling이 연골 형성에 미치는 영향

        박충제,이상원,남순현,김영진,류현모,김현정 大韓小兒齒科學會 2003 大韓小兒齒科學會誌 Vol.30 No.4

        막내골화와 연골내골화 등의 정상적인 골격 성장은 섬유아세포 성장인자 (FGF) 와 이들 수용체들 (FGFR) 에 의한 신호전달체계에 의해 조절된다. 또한 전사조절인자인 Runx2 (Cbfa1/Pebp2αA/AML3) 는 골아세포분화 뿐만 아니라 골형성에도 필수적인 유전자로 알려져 있다. FGF signaling이 mouse의 두 개관과 하악에서의 연골 형성에 어떤 영향을 미치고 있으며, 이 과정에서 Runx2의 연관성을 알아보고자 in vivo 및 in vitro 실험을 시행하여 다음과 같은 결과를 얻었다. 두 개관의 하악을 Alcian blue 염색한 결과 시상두개봉합부 연골은 태생16일부터, Meckel's 연골은 태생11일부터 형성되기 시작하였다. 이들 연골세포들의 성사을 알아보기위한 in situ hybridization 결과 시상두개봉합부 연골 및 Meckel's 연골 모두에서 type Ⅱ collagen은 발현되었으나, Type X collagen은 발현되지 않았다. Runx2 mRNA는 시상두개봉합부 연골과 Meckel's 연골 모두에서 발현되지 않았지만, 이들 연골들의 가장자리를 둘러싸고 있는 독특한 발현양상을 나타내었다. 두개 봉합부에서의 FGF2 protein의 국소적 적용은 두개봉합부 하방의 연골형성을 억제하였다. 또한 하악의 Meckel's 연골 발생부위에 FGF2 protein의 국소적 적용 역시 Meckel's 연골의 형성을 억제하였다. FGF2 protein은 시상두개봉합부상의 bead 주위로 Runx2의 발현을 유도하였다. 이 결과들을 종합해볼 때, FGF signaling은 골아세포와 연골아세포가 공존하고 있는 조직에서의 연골 형성을 억제하고 있음을 시사해 주고 있으며, 이 과정에서 FGF signaling은 부분적으로 Runx2 유전자의 발현을 조절하므로써 연골세포의 증식과 분화에 관여할 것으로 사료된다. Figroblast growth factor (FGF) / FGF receptor (FGFR) mediated signaling is required for skeletogenesis including intramembranous and endochondral ossifications. Runx2 (Cbfa1/Pebp2αA/AML3) is an essential transcription factor for osteoblast differentiation and bone formation. Murine calvaria and mandible are concurrently undergoing both intramembranous bone and cartilage formations in the early development stage. However the mechanism by which these cartilage formations are regulated remains unclear. To elucidate the effect of FGF signaling on development of cranial sutural catilage and Meckel's cartilage and to understand the role of Runx2 in these processs, we have done both in vivo and in vitro experiments. Alcian blue staining showed that cartilage formation in sagittal suture beings from embryonic state 16 (E16), Meckel's cartilage formation in mandible from E12. We analyzed by in situ hybridization the characteristics of cartilage cells that type Ⅱ collagen, not type X collagen, was expressed in sagittal sutural cartilage and Meckel's cartilage. In addition, Runx2 was not expressed in Meckel's cartialge as well as sagittal sutural cartilage, except specific expression pattern only surrounding both cartilages. FGF signaling pathway was further examined in vitro. Beads soaked in FGF2 placed on the sagittal suture and mandible inhibited both sutural and Meckel's cartilage formations. We next examined whether Runx2 gene lies in FGF siganling pathway during regulation of catilage formation. These results suggest that FGF signaling inhibits formations of sagittal sutural and Meckel's cartilages, also propose that FGF siganling is involved in the proliferation and differentiation of chondroblasts through regulating the transcription factor Runx2.

      • Distributed Coordination of Co-Channel Femtocells via Inter-Cell Signaling With Arbitrary Delay

        Ji-Hoon Yun,Shin, Kang G. IEEE 2015 IEEE journal on selected areas in communications Vol.33 No.6

        <P>To achieve high spatial reuse of spectrum resources with limited inter-layer/cell interference, co-channel femtocells must be coordinated with the underlying macro- and other femto-cells in using radio resources. While inter-cell signaling can coordinate femtocells by providing the status information of neighbor cells explicitly, signaling delay-which may result from a limited signaling rate to reduce the resulting overhead, network latency, etc.-and its impact on the behavior of distributed coordination has not been explored before. In this paper, we propose a new architecture for the distributed coordination of co-channel femtocells based on asynchronous inter-cell signaling, called asynchronous coordination of co-channel femtocells (ACoF). ACoF improves solutions iteratively; femtocells update radio resource usage based on the received information, which usually gets outdated due to delayed signaling and asynchronous update behavior. ACoF allows each femtocell to adjust its signaling rate depending on its local conditions for fine-grained cost minimization, but at the expense of higher degree of inconsistency of femtocells' knowledge. Despite such asynchrony and inconsistency, the solution yielded by ACoF is guaranteed to converge to a global optimum under a certain condition of configuration parameters, which we prove theoretically. We design the optimization method of per-cell signaling rate for both wired and over-the-air signaling. Finally, we present a joint muting and transmit power adjustment scheme designed for ACoF and evaluate its convergence behavior and performance gain.</P>

      • Transcriptional Properties of the BMP, TGF-B, RTK, Wnt, Hh, Notch, and JAK/STAT Signaling Molecules in Mouse Embryonic Stem Cells

        Jeung-Yon Rho,Gab-Yong Bae,Jung-Il Chae,Kweon Yu,Deog-Bon Koo,Kyung-Kwang Lee,Yong-Mahn Han 한국동물생명공학회(구 한국동물번식학회) 2006 Reproductive & developmental biology Vol.30 No.2

        Major characteristics of embryonic stem cells (ESCs) are sustaining of stemness and pluripotency by self-renewal. In this report, transcriptional profiles of the molecules in the developmentally important signaling pathways including Wnt, BMP4, TGF-β, RTK, Hh, Notch, and JAK/STAT signaling pathways were investigated to understand the self- renewal of mouse ESCs (mESCs), J1 line, and compared with the NIH3T3 cell line and mouse embryonic fibroblast (MEF) cells as controls. In the Wnt signaling pathway, the expression of Wnt3 was seen widely in mESCs, suggesting that the ligand may be an important regulator for self-renewal in mESCs. In the Hh signaling pathway, the expression of Gli and N-myc were observed extensively in mESCs, whereas the expression levels of in a Shh was low, suggesting that intracellular molecules may be essential for the self-renewal of mESCs. IGF-I, IGF-II, IGF-IR and IGF-IIR of RTK signaling showed a lower expression in mESCs, these molecules related to embryo development may be restrained in mESCs. The expression levels of the Delta and HES5 in Notch signaling were enriched in mESCs. The expression of the molecules related to BMP and JAK-STAT signaling pathways were similar or at a slightly lower level in mESCs compared to those in MEF and NIH3T3 cells. It is suggested that the observed differences in gene expression profiles among the signaling pathways may contribute to the self-renewal and differentiation of mESCs in a signaling-specific manner.

      • Transcriptional Properties of the BMP, $TGF-\beta$, RTK, Wnt, Hh, Notch, and JAK/STAT Signaling Molecules in Mouse Embryonic Stem Cells

        Rho Jeung-Yon,Bae Gab-Yong,Chae Jung-Il,Yu Kweon,Koo Deog-Bon,Lee Kyung-Kwang,Han Yong-Mahn The Korean Society of Animal Reproduction 2006 Reproductive & developmental biology Vol.30 No.2

        Major characteristics of embryonic stem cells (ESCs) are sustaining of sternness and pluripotency by self-renewal. In this report, transcriptional profiles of the molecules in the developmentally important signaling pathways including Wnt, BMP4, $TGF-\beta$, RTK, Hh, Notch, and JAK/STAT signaling pathways were investigated to understand the self-renewal of mouse ESCs (mESCs), J1 line, and compared with the NIH3T3 cell line and mouse embryonic fibroblast (MEF) cells as controls. In the Wnt signaling pathway, the expression of Wnt3 was seen widely in mESCs, suggesting that the ligand may be an important regulator for self-renewal in mESCs. In the Hh signaling pathway, the expression of Gli and N-myc were observed extensively in mESCs, whereas the expression levels of in a Shh was low, suggesting that intracellular molecules may be essential for the self-renewal of mESCs. IGF-I, IGF-II, IGF-IR and IGF-IIR of RTK signaling showed a lower expression in mESCs, these molecules related to embryo development may be restrained in mESCs. The expression levels of the Delta and HESS in Notch signaling were enriched in mESCs. The expression of the molecules related to BMP and JAK-STAT signaling pathways were similar or at a slightly lower level in mESCs compared to those in MEF and NIH3T3 cells. It is suggested that the observed differences in gene expression profiles among the signaling pathways may contribute to the self-renewal and differentiation of mESCs in a signaling-specific manner.

      • KCI등재

        Alteration of Expression of Ca²+ Signaling Proteins and Adaptation of Ca²+ Signaling in SERCA2+/- Mouse Parotid Acini

        최종훈,조해,홍정희,이승일,신동민 연세대학교의과대학 2008 Yonsei medical journal Vol.49 No.2

        Purpose: The sarco/endoplasmic reticulum Ca²+-ATPase (SERCA), encoded by ATP2A2, is an essential component for G-protein coupled receptor (GPCR)-dependent Ca²+ signaling. However, whether the changes in Ca²+ signaling and Ca²+ signaling proteins in parotid acinar cells are affected by a partial loss of SERCA2 are not known. Materials and Methods: In SERCA2+/- mouse parotid gland acinar cells, Ca²+ signaling, expression levels of Ca²+ signaling proteins, and amylase secretion were investigated. Results: SERCA2+/- mice showed decreased SERCA2 expression and an upregulation of the plasma membrane Ca²+ ATPase. A partial loss of SERCA2 changed the expression level of 1, 4, 5-tris-inositolphosphate receptors (IP3Rs), but the localization and activities of IP3Rs were not altered. In SERCA2+/- mice, muscarinic stimulation resulted in greater amylase release, and the expression of synaptotagmin was increased compared to wild type mice. Conclusion: These results suggest that a partial loss of SERCA2 affects the expression and activity of Ca²+ signaling proteins in the parotid gland acini, however, overall Ca²+ signaling is unchanged.

      • KCI등재

        A 6Gb/s Transceiver Design with Phase-Difference Modulation Signaling for Multi-drop DRAM Interface

        한창윤,서재영,김병섭 한국과학기술원 반도체설계교육센터 2022 IDEC Journal of Integrated Circuits and Systems Vol.8 No.3

        In this paper, we designed the phase-difference modulation (PDM) transceiver for the application of PDM signaling in the multi-drop DRAM interface. Because PDM signaling reduced the effect of the reflected signal by positioning the reflected signal between the clock edges, In addition, PDM transceiver did not increase the hardware cost because it does not demand DFE and FFE circuits. With PDM signaling, we implemented the two amplifiers, which make the design complexity of the clock recovery circuit simple: the clock recovery circuit is a simple interpolator. The proposed PDM transceiver was fabricated in 65 nm CMOS technology and verified the performance by simulations. To verify the performance of the PDM signaling, we compared the simulated 6 Gb/s eye diagram in the multi-drop channel with the NRZ signaling. The simulated vertical and horizontal eye sizes in PDM signaling were increased to 60.5 mV and 63.7 ps, respectively; but the simulated eye was closed in NRZ signaling. Therefore, with PDM signaling, the multi-drop memory interfaces with high capacity are feasible without increasing the power and hardware cost.

      • KCI등재

        Naringenin alleviates bone cancer pain in rats via down-regulating spinal P2X7R /PI3K/AKT signaling: involving suppression in spinal inflammation

        Song Jian-Gang,Liu Lv 대한독성 유전단백체 학회 2021 Molecular & cellular toxicology Vol.17 No.4

        Background Bone cancer pain (BCP) seriously affects patient’s quality of life, which remains a difficult clinical problem, lacking effective drugs for treating it. The inflammation in the spinal cord involves the pathogenesis of BCP. The inhibition of spinal phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway or spinal P2X7 receptor (P2X7R) has previously been shown to alleviate BCP. Naringenin (NAR) has analgesic role and anti-inflammatory property. Objective The present study investigated the protection of NAR against BCP and explored whether the inhibition of spinal inflammation and the blockade of spinal P2X7R/PI3K/AKT signaling involved in this protection. Result NAR significantly alleviated mechanical allodynia (the increase of paw withdrawal threshold in Von Frey test) and thermal hyperalgesia (the increase of paw withdrawal latency in Hargreaves test) in BCP rats. Additionally, NAR inhibited inflammatory cytokines (the reduced levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) were measured using Elisa assay) and down-regulated P2X7R/PI3K/AKT signaling (the decreased P2X7R expression, the reduced ratios of phosphorylated (p)-PI3K/PI3K and p-AKT/AKT, which were detected Western blot) in the spinal cord of BCP rats. Conclusion NAR alleviated BCP through inhibiting inflammatory cytokines and down-regulating P2X7R/PI3K/AKT signaling in the spinal cord of rats. These findings revealed that NAR, as an effective agent against BCP, may provide an effective approach in the management of bone cancer patients. Background Bone cancer pain (BCP) seriously affects patient’s quality of life, which remains a difficult clinical problem, lacking effective drugs for treating it. The inflammation in the spinal cord involves the pathogenesis of BCP. The inhibition of spinal phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway or spinal P2X7 receptor (P2X7R) has previously been shown to alleviate BCP. Naringenin (NAR) has analgesic role and anti-inflammatory property. Objective The present study investigated the protection of NAR against BCP and explored whether the inhibition of spinal inflammation and the blockade of spinal P2X7R/PI3K/AKT signaling involved in this protection. Result NAR significantly alleviated mechanical allodynia (the increase of paw withdrawal threshold in Von Frey test) and thermal hyperalgesia (the increase of paw withdrawal latency in Hargreaves test) in BCP rats. Additionally, NAR inhibited inflammatory cytokines (the reduced levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) were measured using Elisa assay) and down-regulated P2X7R/PI3K/AKT signaling (the decreased P2X7R expression, the reduced ratios of phosphorylated (p)-PI3K/PI3K and p-AKT/AKT, which were detected Western blot) in the spinal cord of BCP rats. Conclusion NAR alleviated BCP through inhibiting inflammatory cytokines and down-regulating P2X7R/PI3K/AKT signaling in the spinal cord of rats. These findings revealed that NAR, as an effective agent against BCP, may provide an effective approach in the management of bone cancer patients.

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