• Korean Journal of Remote Sensing
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• v.39 no.2
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• pp.207-221
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• 2023

This study suggests deep neural network models for estimating air temperature with Level 1B (L1B) datasets of GEO-KOMPSAT-2A (GK-2A). The temperature at 1.5 m above the ground impact not only daily life but also weather warnings such as cold and heat waves. There are many studies to assume the air temperature from the land surface temperature (LST) retrieved from satellites because the air temperature has a strong relationship with the LST. However, an algorithm of the LST, Level 2 output of GK-2A, works only clear sky pixels. To overcome the cloud effects, we apply a deep neural network (DNN) model to assume the air temperature with L1B calibrated for radiometric and geometrics from raw satellite data and compare the model with a linear regression model between LST and air temperature. The root mean square errors (RMSE) of the air temperature for model outputs are used to evaluate the model. The number of 95 in-situ air temperature data was 2,496,634 and the ratio of datasets paired with LST and L1B show 42.1% and 98.4%. The training years are 2020 and 2021 and 2022 is used to validate. The DNN model is designed with an input layer taking 16 channels and four hidden fully connected layers to assume an air temperature. As a result of the model using 16 bands of L1B, the DNN with RMSE 2.22℃ showed great performance than the baseline model with RMSE 3.55℃ on clear sky conditions and the total RMSE including overcast samples was 3.33℃. It is suggested that the DNN is able to overcome cloud effects. However, it showed different characteristics in seasonal and hourly analysis and needed to append solar information as inputs to make a general DNN model because the summer and winter seasons showed a low coefficient of determinations with high standard deviations.

• Tuberculosis and Respiratory Diseases
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• v.44 no.4
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• pp.871-888
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• 1997

Background : It is now thought that the earliest manifestation of idiopathic pulmonary fibrosis is alveolitis, that is, an accumulation of inflammatory and immune effector cells within alveolar walls and spaces. Inflammatory cells including alveolar macrophages and resident normal pulmonary tissue cells participate through the release of many variable mediators such as inflammatory growth factors and cytokines, which contribute to tissue damage and finally cause chronic pulmonary inflammation and fibrosis. This study was performed to investigate the source and distribution pattern of transforming growth factor-${\beta}_1$(TGF-${\beta}_1$), platelet derived growth factor(PDGF), basic fibroblast growth factor(bFGF), interleukin 1(IL-1), interleukin 6(IL-6), tumor necrosis factor-$\alpha$ (TNF-$\alpha$) and the role of these mediators on bleomycin(BLM)-induced pulmonary injury and fibrosis in rats. Method : Wistar rats were divided into three groups(control group, BLM treated group, BLM and vitamine E treated group). Animals were sacrificed periodically at 1, 2, 3, 4, 5, 7, 14, 21, 28 days after saline or BLM administration. The effects were compared to the results of bronchoalveolar lavage fluid analysis, light microscopic findings, immunohistochemical stains for six different mediators(TGF-${\beta}_1$, PDGF, bFGF, IL-1, IL-6 and TNF-$\alpha$) and mRNA in situ hybridization for TGF-${\beta}_1$. Results : IL-1 and IL-6 are maximally expressed at postbleomycin 1~7th day which are mainly produced by neutrophils and bronchiolar epithelium. It is thought that they induce recruitment of inflammatory cells at the injury site. The expression of IL-1 and IL-6 at the bronchiolar epithelium within 7th day is an indirect evidence of contribution of bronchiolar epithelial cells to promote and maintain the inflammatory and immune responses adjacent to the airways. TNF-$\alpha$ is mainly produced by neutrophils and bronchiolar epithelial cells during 1~5th day, alveolar macrophages during 7~28th day. At the earlier period, TNF-$\alpha$ causes recruitment of inflammatory cells at the injury site and later stimulates pulmonary fibrosis. The main secreting cells of TGF-${\beta}_1$ are alveolar macrophages and bronchiolar epithelium and the target is pulmonary fibroblasts and extracellular matrix. TGF-${\beta}_1$ and PDGF stimulate proliferation of pulmonary fibroblasts and TGF-${\beta}_1$ and bFGF incite the fibroblasts to produce extracellular matrix. The vitamine E and BLM treated group shows few positive cells(p<0.05). Conclusion : After endothelial and epithelial injury, the neutrophils and bronchiolar epithelium secrete IL-1, IL-6, TNF-$\alpha$ which induce infiltration of many neutrophils. It is thought that variable enzymes and $O_2$ radicals released by these neutrophils cause destruction of normal lung architecture and progression of pulmonary fibrosis. At the 7~28th day, TGF-${\beta}_1$, PDGF, bFGF, TNF-$\alpha$ secreted by alveolar macrophages sting pulmonary fibroblasts into proliferating with increased production of extracellular matrix and finally, they make progression of pulmonary fibrosis. TNF-$\alpha$ compares quite important with TGF-${\beta}_1$ to cause pulmonary fibrosis. Vitamine E seems to decrease the extent of BLM induced pulmonary fibrosis.