• 대한토목학회논문집
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• 제31권2A호
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• pp.121-127
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• 2011

콘크리트 내부에 존재하는 공극(void)의 공간적 분포는 콘크리트의 역학적, 물리적 거동에 큰 영향을 미친다. 따라서 콘크리트 재료 물성의 파악과 건정성 평가를 위해 내부에 존재하는 공극의 분포 상태를 파악하는 것은 매우 중요하다. 콘크리트에는 육안으로 보이는 재료 표면의 공극 이외에도 내부 공극이 존재한다. 본 연구에서는 경량골재 콘크리트의 공극 분포를 파악하기 위하여 micro CT(X-ray microtomography)를 활용하여 생성된 3차원 콘크리트 디지털 시편을 사용하였다. 흑백처리된 단면 이미지를 중첩하여 공극을 묘사할 수 있는 3차원 시편을 생성하였다. 공극의 분포 상태를 확률적으로 묘사하기 위하여 확률 분포 함수 two-point correlation function과 lineal-path function으로 분석하였다. 또한, 이미지 분석을 통해서 콘크리트 시편의 공극의 밀도 분포를 파악하였다. 콘크리트 내부에 있는 개별 경량 골재의 공극도 이미지 처리와 확률 분포함수를 사용하여 분석하였다. Micro CT와 3차원 이미지 분석 방법을 통하여 콘크리트 내부에 존재하는 공극의 분포 상태를 효과적으로 파악할 수 있음을 확인하였다.

• IMMUNE NETWORK
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• 제9권6호
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• pp.209-235
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• 2009

There has been an explosion of literature focusing on the role of regulatory T (Treg) cells in cancer immunity. It is becoming increasingly clear that Treg cells play an active and significant role in the progression of cancer, and have an important role in suppressing tumor-specific immunity. Thus, there is a clear rationale for developing clinical strategies to diminish their regulatory influences, with the ultimate goal of augmenting antitimor immunity. Therefore, manipulation of Treg cells represent new strategies for cancer treatment. In this Review, I will summarize and review the explosive recent studies demonstrating that Treg cells are increased in patients with malignancies and restoration of antitumor immunity in mice and humans by depletion or reduction of Treg cells. In addition, I will discuss both the prognostic value of Treg cells in tumor progression in tumor-bearing hosts and the rationale for strategies for therapeutic vaccination and immunotherapeutic targeting of Treg cells with drugs and microRNA.

• 대한전기학회:학술대회논문집
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• 대한전기학회 2003년도 학술회의 논문집 정보 및 제어부문 B
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• pp.959-961
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• 2003

In this paper, we describe implemented DMAC (Direct Memory Access Controller) architecture on Altera's $Excalibur^{TM}$ that includes industry-standard $ARM922T^{TM}$ 32-bit RISC processor core operating at 200 MHz. We implemented DMAC based on AMBA (Advanced Micro-controller Bus Architecture) AHB (Advanced Micro-performance Bus) interface. Implemented DMAC has 8-channel and can extend supportable channel count according to user application. We used round-robin method for priority selection. Implemented DMAC supports data transfer between Memory-to-Memory, Memory-to-Peripheral and Peripheral-to-Memory. The max transfer count is 1024 per a time and it can support byte, half-word and word transfer according to AHB protocol (HSIZE signals). We implemented with VHDL and functional verification using $ModelSim^{TM}$. Then, we synthesized using $LeonardoSpectrum^{TM}$ with Altera $Excalibur^{TM}$ library. We did FPGA P&R and targeting using $Quartus^{TM}$. We can use implemented DMAC module at any system that needs high speed and broad bandwidth data transfers.

• Molecules and Cells
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• 제37권3호
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• pp.196-201
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• 2014

Pulmonary arterial hypertension (PAH) is a progressive disease characterized by the vascular remodeling of the pulmonary arterioles, including formation of plexiform and concentric lesions comprised of proliferative vascular cells. Clinically, PAH leads to increased pulmonary arterial pressure and subsequent right ventricular failure. Existing therapies have improved the outcome but mortality still remains exceedingly high. There is emerging evidence that the seven-transmembrane G-protein coupled receptor APJ and its cognate endogenous ligand apelin are important in the maintenance of pulmonary vascular homeostasis through the targeting of critical mediators, such as Kr$\ddot{u}$ppel-like factor 2 (KLF2), endothelial nitric oxide synthase (eNOS), and microRNAs (miRNAs). Disruption of this pathway plays a major part in the pathogenesis of PAH. Given its role in the maintenance of pulmonary vascular homeostasis, the apelin-APJ pathway is a potential target for PAH therapy. This review highlights the current state in the understanding of the apelin-APJ axis related to PAH and discusses the therapeutic potential of this signaling pathway as a novel paradigm of PAH therapy.

• BMB Reports
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• 제47권6호
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• pp.311-317
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• 2014

microRNAs (miRNAs) are a class of small, non-coding RNAs that play critical posttranscriptional regulatory roles typically through targeting of the 3'-untranslated region of messenger RNA (mRNA). Mature miRNAs are known to be involved in global cellular processes, such as differentiation, proliferation, apoptosis, and organogenesis, due to their capacity to target multiple mRNAs. Thus, imbalances in the expression and/or activity of miRNAs are involved in the pathogenesis of numerous diseases, including pulmonary arterial hypertension (PAH). PAH is a progressive disease characterized by vascular remodeling due to excessive proliferation of pulmonary artery endothelial cells (PAECs) and pulmonary artery smooth muscle cells (PASMCs). Recently, studies have evaluated the roles of miRNAs involved in the pathogenesis of PAH in these pulmonary vascular cells. This review provides an overview of recent discoveries on the role of miRNAs in the pathogenesis of PAH and discusses the potential for miRNAs as therapeutic targets and biomarkers of PAH.

• 전기전자학회논문지
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• 제1권1호
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• pp.1-10
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• 1997

It is well-known that rectangular bulk-Si sensors prepared by etch or epi etch-stop micromachining technology are already in practical use today, but the conventional bulk-Si sensor shows some drawbacks such as large chip size and limited applications as silicon sensor device is to be miniaturized. We consider a circular-shape SOI(Silicon-On-Insulator) micro-cavity technology to facilitate multiple sensors on very small chip, to make device easier to package than conventional sensor like pressure sensor and to provide very high over-pressure capability. This paper demonstrates the cross-functional results for stress analyses(targeting $5{\mu}m$ deflection and 100MPa stress as maximum at various applicable pressure ranges), for finding permissible diaphragm dimension by output sensitivity, and piezoresistive sensor theory from two-type SOI structures where the double SOI structure shows the most feasible deflection and small stress at various ambient pressures. Those results can be compared with the ones of circular-shape bulk-Si based sensor$^{[17]}. The SOI micro-cavity formed the sensors is promising to integrate with calibration, gain stage and controller unit plus high current/high voltage CMOS drivers onto monolithic chip.

• Molecules and Cells
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• 제42권2호
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• pp.175-182
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• 2019

microRNAs regulate a diverse spectrum of cancer biology, including tumorigenesis, metastasis, stemness, and drug resistance. To investigate miRNA-mediated regulation of drug resistance, we characterized the resistant cell lines to 5-fluorouracil by inducing stable expression of miRNAs using lenti-miRNA library. Here, we demonstrate miR-551a as a novel factor regulating cell survival after 5-FU treatment. miR-551a-expressing cells (Hep3B-lenti-miR-551a) were resistant to 5-FU-induced cell death, and after 5-FU treatment, and showed significant increases in cell viability, cell survival, and sphere formation. It was further shown that myocyte-specific factor 2C is the direct target of miR-551a. Our results suggest that miR-551a plays a novel function in regulating 5-FU-induced cell death, and targeting miR-551a might be helpful to sensitize cells to anti-cancer drugs.

• Asian Pacific Journal of Cancer Prevention
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• 제16권12호
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• pp.4937-4944
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• 2015

MicroRNAs (miRNAs) are emerging as critical regulators in carcinogenesis and tumor progression. Recently, miR-99a has been reported as a tumor suppressor gene in various human cancers, but its functions in the context of anaplastic thyroid cancer (ATC) remain unknown. In this study, we reported that miR-99a was commonly downregulated in ATC tissue specimens and cell lines with important functional consequences. Overexpression of miR-99a not only dramatically reduced ATC cell viability by inducing cell apoptosis and accumulation of cells at G1 phase, but also inhibited tumorigenicity in vivo. We then screened and identified a novel miR-99a target, mammalian target of rapamycin (mTOR), and it was further confirmed by luciferase assay. Up-regulation of miR-99a would markedly reduce the expression of mTOR and its downstream phosphorylated proteins (p-4E-BP1 and p-S6K1). Similar to restoring miR-99a expression, mTOR down-regulation suppressed cell viability and increased cell apoptosis, whereas restoration of mTOR expression significantly reversed the miR-99a antitumor activity and the inhibition of mTOR/p-4E-BP1/p-S6K1 signal pathway profile. In clinical specimens and cell lines, mTOR was commonly overexpressed and its protein levels were statistically inversely correlated with miR-99a expression. Taken together, our results demonstrated for the first time that miR-99a functions as a tumor suppressor and plays an important role in inhibiting the tumorigenesis through targeting the mTOR/p-4E-BP1/p-S6K1 pathway in ATC cells. Given these, miR-99a may serve as a novel prognostic/diagnostic and therapeutic target for treating ATC.

• BMB Reports
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• 제53권4호
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• pp.223-228
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• 2020

Dysregulation of histone deacetylase 6 (HDAC6) can lead to the pathologic states and result in the development of various diseases including cancers and inflammatory diseases. The objective of this study was to elucidate the regulatory role of microRNA-22 (miR-22) in HDAC6-mediated expression of pro-inflammatory cytokines in lipopolysaccharide (LPS)-stimulated macrophages. LPS stimulation induced HDAC6 expression, but suppressed miR-22 expression in macrophages, suggesting possible correlation between HDAC6 and miR-22. Luciferase reporter assays revealed that 3'UTR of HDAC6 was a bona fide target site of miR-22. Transfection of miR-22 mimic significantly inhibited LPS-induced HDAC6 expression, while miR-22 inhibitor further increased LPS-induced HDAC6 expression. LPS-induced activation of NF-κB and AP-1 was inhibited by miR-22 mimic, but further increased by miR-22 inhibitor. LPS-induced expression of pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6 was inhibited by miR-22 mimic, but further increased by miR-22 inhibitor. Taken together, these data provide evidence that miR-22 can downregulate LPS-induced expression of pro-inflammatory cytokines via suppression of NF-κB and AP-1 axis by targeting HDAC6 in macrophages.

• IMMUNE NETWORK
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• 제16권1호
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• pp.61-74
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• 2016

Dendritic cells (DCs) are professional antigen-presenting cells that sample their environment and present antigens to naïve T lymphocytes for the subsequent antigen-specific immune responses. DCs exist in a range of distinct subpopulations including plasmacytoid DCs (pDCs) and classical DCs (cDCs), with the latter consisting of the cDC1 and cDC2 lineages. Although the roles of DC-specific transcription factors across the DC subsets have become understood, the posttranscriptional mechanisms that regulate DC development are yet to be elucidated. MicroRNAs (miRNAs) are pivotal posttranscriptional regulators of gene expression in a myriad of biological processes, but their contribution to the immune system is just beginning to surface. In this study, our in-house probe collection was screened to identify miRNAs possibly involved in DC development and function by targeting the transcripts of relevant mouse transcription factors. Examination of DC subsets from the culture of mouse bone marrow with Flt3 ligand identified high expression of miR-124 which was able to target the transcript of TCF4, a transcription factor critical for the development and homeostasis of pDCs. Further expression profiling of mouse DC subsets isolated from in vitro culture as well as via ex vivo purification demonstrated that miR-124 was outstandingly expressed in CD24⁺ cDC1 cells compared to in pDCs and CD172α⁺ cDC2 cells. These results imply that miR-124 is likely involved in the processes of DC subset development by posttranscriptional regulation of a transcription factor(s).