• 한국과학교육학회지
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• 제31권8호
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• pp.1145-1157
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• 2011

본 연구의 목적은 초등 과학영재 수업에서 나타나는 언어적 상호작용의 특징을 살펴보고 현장에서 언어적 상호작용 전략을 수립하는데 도움을 주고자 하는 것이다. 이를 위해 지역 교육지원청 영재교육원 수업 3곳의 총 27차시 수업에 참여하여 녹화하였으며, 전사 및 코딩의 과정을 거쳐 분석하였다. 분석에 사용된 분석틀은 Sinclair와 Coulthard(1975)의 이론에 근거한 정민수 등(2007)의 분석틀에서 교사 피드백 부분을 김영순(2010)의 분석틀로 일부 수정한 언어적 상호작용 분석틀이었다. 분석 후 분석결과 확인 및 언어적 상호작용에 대한 인식을 알아보고자 수업자와의 설문조사를 실시하였다. 연구 결과, 초등 과학영재 수업에서 가장 많이 나타난 IRF 패턴 유형은 관리적 질문-단답형 응답 유형이었다. 이러한 결과의 원인을 수업 외적인 측면으로 인식하고 있었다. 또한 수업 사례를 통해 과학영재의 창의적 사고를 이끌어 내는데 효과적인 몇 가지 패턴 유형을 확인하였는데, 이를 통하여 언어적 상호작용 전략은 막연히 개방적 질문, 지연적 피드백을 따로 구분하여 각각 좋다는 인식보다 학습 내용의 난이도 및 학생의 수준 등을 고려하여 상황에 적합한 패턴 전략으로 적용되어야 한다는 것을 알 수 있었다. 교사 3명은 평소 초등 과학영재 수업에서의 언어적 상호작용 전략에 대하여 막연히 편안한 분위기, 개방적 질문과 지연적 피드백 정도로 인식하거나 전략이 아예 없는 것으로 나타났다. 앞으로 초등과학영재 담당 교사들의 언어적 상호작용 전략에 대한 연수 등 다양한 전문성 향상 기회가 마련되어야할 것으로 사료된다.

• Journal of Ginseng Research
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• 제41권1호
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• pp.43-51
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• 2017

Background: BIOGF1K, a compound K-rich fraction prepared from the root of Panax ginseng, is widely used for cosmetic purposes in Korea. We investigated the functional mechanisms of the anti-inflammatory and antioxidative activities of BIOGF1K by discovering target enzymes through various molecular studies. Methods: We explored the inhibitory mechanisms of BIOGF1K using lipopolysaccharide-mediated inflammatory responses, reporter gene assays involving overexpression of toll-like receptor adaptor molecules, and immunoblotting analysis. We used the 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay to measure the antioxidative activity. We cotransfected adaptor molecules, including the myeloid differentiation primary response gene 88 (MyD88) and Toll/interleukin-receptor domain containing adaptor molecule-inducing interferon-${\beta}$ (TRIF), to measure the activation of nuclear factor (NF)-${\kappa}B$ and interferon regulatory factor 3 (IRF3). Results: BIOGF1K suppressed lipopolysaccharide-triggered NO release in macrophages as well as DPPH-induced electron-donating activity. It also blocked lipopolysaccharide-induced mRNA levels of interferon-${\beta}$ and inducible nitric oxide synthase. Moreover, BIOGF1K diminished the translocation and activation of IRF3 and NF-${\kappa}B$ (p50 and p65). This extract inhibited the upregulation of NF-${\kappa}B$-linked luciferase activity provoked by phorbal-12-myristate-13 acetate as well as MyD88, TRIF, and inhibitor of ${\kappa}B$ ($I{\kappa}B{\alpha}$) kinase ($IKK{\beta}$), and IRF3-mediated luciferase activity induced by TRIF and TANK-binding kinase 1 (TBK1). Finally, BIOGF1K downregulated the NF-${\kappa}B$ pathway by blocking $IKK{\beta}$ and the IRF3 pathway by inhibiting TBK1, according to reporter gene assays, immunoblotting analysis, and an AKT/$IKK{\beta}$/TBK1 overexpression strategy. Conclusion: Overall, our data suggest that the suppression of $IKK{\beta}$ and TBK1, which mediate transcriptional regulation of NF-${\kappa}B$ and IRF3, respectively, may contribute to the broad-spectrum inhibitory activity of BIOGF1K.

• Journal of Animal Science and Technology
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• 제62권3호
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• pp.385-395
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• 2020

Polyinosinic:polycytidylic acid (poly[I:C]) can stimulate Toll-like receptor 3 (TLR3) signaling pathways. In this study, DF-1 cells were treated with poly(I:C) at various concentrations and time points to examine the comparative expression patterns of innate immune response genes. The viability of DF-1 cells decreased from 77.41% to 38.68% when cells were treated different dose of poly(I:C) from 0.1 ㎍/mL to 100 ㎍/mL for 24 h respectively. The expressions of TLR3, TLR4, TLR7, TLR15, TLR21, IL1B, and IL10 were increased in dose- and time-dependent manners by poly(I:C) treatment. On the contrary, the expression patterns of interferon regulatory factors 7 (IRF7), Jun proto-oncogene, AP-1 transcription factor subunit (JUN), Nuclear Factor Kappa B Subunit 1 (NF-κB1), and IL8L2 were varied; IRF7 and IL8L2 were increasingly expressed whereas the expressions of JUN and NF-κB1 were decreased in a dose-dependent manner after they were early induced. In time-dependent analysis, IRF7 expression was significantly upregulated from 3 h to 24 h, whereas JUN and NF-κB1 expressions settled down from 6 h to 24 h after poly(I:C) treatment although they were induced at early time from 1 h to 3 h. Poly(I:C) treatment rapidly increased the expression of IL8L2 from 3 h to 6 h with a plateau at 6 h and then the expression of IL8L2 was dramatically decreased until 24 h after poly(I:C) treatment although the expression level was still higher than the non-treated control. These results may provide the basis for understanding host response to viral infection and its mimicry system in chickens.

• Parasites, Hosts and Diseases
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• 제62권1호
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• pp.30-41
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• 2024

The dense granule protein of Toxoplasma gondii, inhibitor of signal transducer and activator of transcription 1 (IST) is an inhibitor of signal transducer and activator of transcription 1 (STAT1) transcriptional activity that binds to STAT1 and regulates the expression of inflammatory molecules in host cells. A sterile inflammatory liver injury in pathological acute liver failures occurs when excessive innate immune function, such as the massive release of IFN-γ and TNF-α, is activated without infection. In relation to inflammatory liver injury, we hypothesized that Toxoplasma gondii inhibitor of STAT1 transcription (TgIST) can inhibit the inflammatory response induced by activating the STAT1/IRF-1 mechanism in liver inflammation. This study used IFN-γ and TNF-α as inflammatory inducers at the cellular level of murine hepatocytes (Hepa-1c1c7) to determine whether TgIST inhibits the STAT1/IRF-1 axis. In stable cells transfected with TgIST, STAT1 expression decreased with a decrease in interferon regulatory factor (IRF)-1 levels. Furthermore, STAT1 inhibition of TgIST resulted in lower levels of NF-κB and COX2, as well as significantly lower levels of class II transactivator (CIITA), iNOS, and chemokines (CLXCL9/10/11). TgIST also significantly reduced the expression of hepatocyte proapoptotic markers (Caspase3/8/9, P53, and BAX), which are linked to sterile inflammatory liver injury. TgIST also reduced the expression of adhesion (ICAM-1 and VCAM-1) and infiltration markers of programmed death-ligand 1 (PD-L1) induced by hepatocyte and tissue damage. TgIST restored the cell apoptosis induced by IFN-γ/TNF-α stimulation. These results suggest that TgIST can inhibit STAT1-mediated inflammatory and apoptotic responses in hepatocytes stimulated with proinflammatory cytokines.

• 대한임상검사과학회지
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• 제36권1호
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• pp.27-32
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• 2004

Bone marrow transplantation(BMT) is widely used as curative means of various malignant and nonmalignant hematologic disorders, and early and accurate determination of engraftment is very important for critical management decisions. Reticulocyte counts performed by automated flow cytometric methods is a good indicator of erythropoietic activity and its evaluation has been proposed as an early predictor of bone marrow regeneration. Some reports highlighted the usefulness of the percentage of highly fluorescent reticulocytes and the sum of highly and medium fluorescent reticulocytes(immature reticulocyte fraction, IRF). In Asan Medical Center, the criteria for engraftment following BMT or PBSCT was defined as the first day of a 3-day trend of absolute neutrophil count(ANC)${\geq}500/uL$ and platelet count${\geq}30{\times}10^3/uL$. In 1999, Grotto et al proposed an indidator of bone marrow recovery as the first day on which the IRF was twice the minimum value after bone marrow transplantation. To compare the both criterias, we got consecutive datas of immature reticulocyte fraction, absolute neutrophil count(ANC), WBC count, platelet count and reticulocyte count by XE-2100 automated hematology analyzer(Sysmex Co. Japan) from 33 patients daily after BMT. When compared to standard neutrophil engraftment(10-30 days, $16.2{\pm}4.6days$), IRF engraftment (5-21 days, $11.0{\pm}3.9days$) occured significantly earlier in 87.9% of patients(P<0.05). The mean engraftment day for WBC count(11-29 days, $16.4{\pm}4.3days$) was similar to ANC, but platelet count and reticulocyte count revealed more delayed data (10-49 days, $19.1{\pm}7.4days$ vs 17-64 days, $31.4{\pm}14.1days$). In conclusion, our results confirm that an increase in the immature reticulocyte population is the earliest sign of the hematopoietic recovery after BMT and that automated reticulocyte quantification including immature fraction may be integrated into clinical protocols to evaluate bone marrow reconstitution.

• Molecular & Cellular Toxicology
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• 제5권3호
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• pp.187-192
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• 2009

Toll-like receptors (TLRs) play an important role in host defense by sensing invading microbial pathogens. The stimulation of TLRs by microbial components triggers the activation of the myeloid differential factor 88 (MyD88)- and toll-interleukin-1 receptor domain-containing adapter inducing interferon-$\beta$ (TRIF)-dependent downstream signaling pathways. TLR/MyD88 signaling pathway induces the activation of nuclear factor-kappa B (NF-${\kappa}B$) and the expression of inflammatory cytokine genes, including tumor necrosis factor-alpha, interleukin (IL)-6, IL-12, and IL-$1{\beta}$. On the other hand, TLR/TRIF signaling pathway induces the delayed-activation of NF-${\kappa}B$ and interferon regulatory factor 3 (IRF3), and the expression of type I interferons (IFNs) and IFN-inducible genes. The divalent heavy metal cadmium (Cd) is clearly toxic to most mammalian organ systems, especially the immune system. Yet, the underlying toxic mechanism(s) remain unclear. Cd inhibits the MyD88-dependent pathway by ceasing the activity of inhibitor-${\kappa}B$ kinase. However, it is not known whether Cd inhibits the TRIF-dependent pathway. Presently, Cd inhibited NF-${\kappa}B$ and IRF3 activation induced by lipopolysaccharide (LPS) and polyinosinic-polycytidylic acid. Cd inhibited LPS-induced IRF3 phosphorylation and IFN-inducible genes such as interferon inducible protein-10 and regulated on activation normal T-cell expressed and secreted (RANTES). These results suggest that Cd can modulate TRIF-dependent signaling pathways of TLRs.

• The Journal of Asian Finance, Economics and Business
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• 제8권5호
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• pp.913-921
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• 2021

The objective of the study is to investigate the impact of the COVID-19 pandemic on Saudi Arabia stock market. The study relied on the data of the daily closing stock market price index Tadawul All Share Index (TASI), and the number of daily cases infected with COVID-19 during the period from March 15, 2020, to August 10, 2020. The study employs the Vector Auto-Regressive (VAR) model, the Impulse Response Function (IRF) and Autoregressive Conditional Heteroscedasticity (ARCH) models. The results of the correlation matrix and the Impulse Response Function (IRF) show that stock market returns responded negatively to the growth in COVID-19 infected cases during the pandemic. The results of ARCH model confirmed the negative impact of COVID-19 pandemic on KSA stock market returns. The results also showed that the negative market reaction was strong during the early days of the COVID-19 pandemic. The study concluded that stock market in KSA responded quickly to the COVID-19 pandemic; the response varies over time according to the stage of the pandemic. However, the Saudi government's response time and size of the stimulus package have played an important role in alleviating the impacts of the COVID-19 pandemic on Saudi Arabia Stock Market.

• 한국항공우주학회지
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• 제43권5호
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• pp.466-471
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• 2015

본 논문에서는 광역 관측을 위하여 새롭게 제안되고 있는 TOPS SAR 운용기법에 대한 모드 설계 및 성능 분석을 수행하였다. TOPS 모드는 기존 ScanSAR 모드의 단점인 scalloping을 개선하기 위하여 새롭게 제안된 모드로서, SAR 진행방향으로 안테나 빔을 조향하면서 영상 데이터를 획득하는 새로운 SAR 영상 획득 기술이다. 본 논문에서는 TOPS 모드에 대한 기술적 운용 개념을 소개하고, SAR 운용 변수를 추출하기 위한 모드 설계 결과를 제시한다. 또한 설계된 모드 변수를 이용하여 SAR 주요 성능인 IRF, NESZ, 및 DTAR을 분석하여 제시한다.

• 한국지하수토양환경학회:학술대회논문집
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• 한국지하수토양환경학회 2001년도 추계학술발표회
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• pp.92-96
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• 2001

Although the problem of seawater intrusion at the coastal aquifer was recognized before over one hundred years at the coastal aquifer, much groundwater keep on being salinitized by several reasons such as groundwater exhaustion, coastalline change, and human activities. The horizontal and vertical electrical soundings and geostatistical methods were used to define the local characteristics of saltwater intrusion and to estimate the saltwater interface in the southeastern area of the Pusan City. The 24 points of the Schlumberger vertical electrical soundings(VES) to loom depth and the 2 lines of dipole-dipole horizontal soundings are peformed. The resistivity data have lognormal distributions. The horizontal extents of saline water intrusion were estimated from the inversion of horizontal prospecting data. Lognormal ordinary kriging is used in A-A' resistivity profiles on May and July because the data have stationary models in semivariograms. Lognormal IRF-k kriging is used for the isopleth maps using vertical resistivity data. The 10 ohm-m resistivity line on the isopleth maps of 21m, 30m, 50m, and 70m depth using resisitivity data measured in July is sifted to the east, cpomparing that of the isopleth maps measured in May. The kriged vertical and horizontal resistivity isopleth maps suggested that the geostatistical methods can be used to define the variation of earth resistivity distribution at the saltwater interface.

• BMB Reports
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• 제35권6호
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• pp.583-589
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• 2002

The signal transducer and activator of transcription (STAT)1 is a cytoplasmic-transcription factor that is phosphorylated by Janus kinases (Jak) in response to interferon $\gamma$ (IFN-$\gamma$). The phosphorylated STAT1 translocates to the nucleus, where it turns on specific sets of IFN-$\gamma$-inducible genes, such as the interferon regulatory factor (IRF)-1. We show here that gamma irradiation reduces the IFN-$\gamma$ mRNA expression. The inhibition of the STAT1 phosphorylation and the IRF-1 expression by gamma irradiation was also observed. In contrast, the mRNA levels of IL-5 and transcription factor GATA-3 were slightly induced by gamma irradiation when compared to the non-irradiated sample. Furthermore, we detected the inhibition of cell-mediated immunity by gamma irradiation in the allogenic-mixed lymphocytes' reaction (MLR). These results postulate that gamma irradiation induces the polarized-Th2 response and interferes with STAT1 signals, thereby causing the immunosuppression of the Th1 response.