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      • An Improvement on Assimilation of Satellite-derived Sea Surface Temperature for NEMOVAR with the use of MODIS data

        Mo-Rang Huh 부경대학교 2013 국내박사

        RANK : 247358

        SST is important in coupling the ocean and atmosphere through exchanges of heat, momentum, moisture, and gases. SST data plays a major role as a bottom boundary condition in numerical weather prediction (NWP) systems. Although in-situ measurements are considered to be true values, they have temporal and spatial constraints. A crucial issue is how to implement satellite-derived SST data as boundary conditions for ocean models as well as NWP models. The operational administrations and organizations have conducted the system for real time global SST products. But, the retrieving high quality and operational ocean initial SST data is still challenging subject. The objective of this thesis is to implement satellite-derived SST measurements into an ocean data assimilation system to improve the ocean-state forecasts. The Global Ocean Data Assimilation Experiment High-Resolution SST Pilot Project (GHRSST-PP) is a well-organized system providing the near-operational high-resolution satellite SST GHRSST Level 2 Pre-processed data used in this thesis. Advanced Along-track Scanning Radiometer, Advanced Microwave Scanning Radiometer-EOS, Advanced High-Resolution Radiometer, and Moderate Resolution Imaging Spectrometer (MODIS) data are collected and assimilated on the NEMOVAR ocean data assimilation system. The selected datasets have different characteristics and can yield a good effect when used together. According to the hindcast results, most SST satellite data are well processed. Their RMSEs are less than 0.76°C globally in all seasons (summer, autumn, and winter). However, the RMSEs for SST data from all instruments other than MODIS are approximately 0.5°C globally, even in the summer. Improving the impact of MODIS on the global dataset will require additional statistics or a quality control (QC) method. A multiple assimilation method based on a variational quality control (VarQC) is proposed. The impacts of additional QC predict that RMSEs will be reduced to less than 40% (average, maximum is 57.45% in Agulhas Return region in June). This type of approach has the advantage of using the scheme itself for quality control. This method can advance the application of satellite data to assimilation systems. Incidentally, sensitivities to spatial density of GHRSST are acceptable in that the resolution of the satellite-derived SST is close to the model grid rather than denser than the model grid.

      • Vascular smooth muscle cell-specific TXNIP deficiency ameliorates vascular calcification

        Ae-rang, Hwang 영남대학교 대학원 2023 국내박사

        RANK : 247358

        혈관석회화는 주로 신장질환 환자에서 발생하며 흡연, 고령, 당뇨병, 고혈압, 폐경기, 골다공증 등의 위험인자를 가진 환자에서 유병률이 더 높다. 이전 연구에서는 산화스트레스와 염증 반응이 혈관 석회화 발생에 관여한다고 제시된 바 있다. Thioredoxin-interacting protein(TXNIP)은 활성산소 생성 및 염증복합체(inflammasome) 활성화에 대한 양성 조절인자로 알려져 있지만 그럼에도 불구하고 혈관석회화 발생에 있어서 TXNIP의 역할은 알려져 있지 않았다. 본 연구의 목적은 세포 및 질환동물모델을 이용하여 혈관석회화 조절에 있어 TXNIP의 잠재적인 역할을 제시하는 것이다. 5/6 신장절제 마우스 모델과 사람의 신장경화증 및 당뇨병과 같은 석회화 유발 대사 질환에서 TXNIP유전자 발현의 증가를 확인하였고, 일차 평활근세포 및 비타민 D3(1,25(OH)2D3)에 의한 혈관 석회화 마우스 모델에서 TXNIP 발현 및 칼슘 축적 정도가 증가된 것을 확인하였다. 대조적으로 TXNIP 발현 및 혈관 석회화는 TXNIP WT 대조군 생쥐에 비해 TXNIP SMCKO 생쥐에서 유의하게 감소되었다. 비타민 D3 및 무기 인산염 유도로 인한 혈관평활근세포에서 TXNIP의 역할은 TXNIP WT 대조군 생쥐에 비해 TXNIP smcKO 생쥐에서 칼슘침착, alkaline phosphatase 활성을 억제시켰다. 또한 활성산소 생성, 염증복합체 활성화를 억제하였으며 혈관평활근세포 분화 마커, 골아세포 마커의 발현이 TXNIP smcKO 생쥐에서 현저히 감소되었다. 더 나아가 TXNIP 과발현은 일차 혈관평활근세포에서 골아세포 관련 유전자의 발현 및 미토콘드리아 유래 산화스트레스의 생성을 촉진하였으며 TXNIP 결손은 미토콘드리아 기능을 회복하였으며 석회화를 약화시켰다. 이러한 결과는 평활근세포에서 TXNIP의 유도가 혈관석회화 유발에 중요한 요인임을 나타내며 산화 스트레스와 염증 반응의 중요한 매개체로 알려진 TXNIP을 표적으로 하는 것은 혈관석회화를 조절하는 효과적인 전략이 될 수 있음을 시사한다. Vascular calcification mainly occurs in patients with kidney disease, and the prevalence is higher in patients with risk factors such as smoking, old age, diabetes mellitus, high blood pressure, menopause, and osteoporosis. Oxidative stress and inflammatory responses are known to participate in the development of vascular calcification. Although thioredoxin interacting protein (TXNIP) is known as a positive regulator for reactive oxygen species (ROS) generation and inflammasome activation, its role in the development of vascular calcification has not been reported. This study aimed to identify the role of TXNIP in regulating vascular calcification in vitro and in vivo. In human and 5/6 nephrectomy mice model, metabolic risk factors, such as nephropathy and diabetes increased TXNIP gene expression. In addition, in this study, primary smooth muscle cell and vitamin D3 induced calcification mouse models were used to find that administering vitamin D3 (1,25(OH)2D3) increased the protein levels of TXNIP and calcium accumulation in the vascular smooth muscle layer compared to those in the vehicle control. In contrast, TXNIP expression and vascular calcification induced by vitamin D3 were significantly reduced in the TXNIP SMCKO mice compared to that in littermate control mice. Thus, the data suggest that TXNIP is responsible for the development of vascular calcification in vivo. To verify the role of TXNIP in smooth muscle cells, primary mouse vascular smooth muscle cells from TXNIP SMCKO mice were subjected to vitamin D3 and inorganic phosphate–induced calcification in vitro. ROS generation, inflammasome activation, calcium deposition, alkaline phosphatase activity, osteoblast–like differentiation markers, and calcification were significantly inhibited in vascular smooth muscle cells from TXNIP SMCKO mice compared to those in littermate control mice. Moreover, the overexpression of TXNIP promoted the expression of calcification–related genes in primary smooth muscle cells and mitochondria–derived oxidative stress in TXNIP WT mice, inducing osteogenic differentiation of vascular smooth muscle cells. In contrast, TXNIP knockdown mice showed reduced calcification and restoration of the mitochondrial function. These results indicate that smooth muscle cell-dependent TXNIP induction is crucial for vascular calcification. Taken together, targeting TXNIP, which is known as an important mediator of oxidative stress and inflammatory response, is an effective strategy for regulating vascular calcification and will provide an opportunity to develop therapeutic agents for vascular calcification.

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