RESUMO
Geological bodies are important sources of greenhouse gas (GHG) emissions. Organic-rich oil shale in sedimentary basins is a good gas source rock, the GHG in which will be released into the atmosphere during crushing to affect climate change. Quantitative calculations of GHG emissions during oil shale crushing were carried out on oil shales from the Yaojie (YJ) and Fushun (FS) mining areas in China. Organic geochemistry, X-ray diffraction, and pore structure analysis experiments, as well as the relationship between storage time and GHG emissions, were analyzed to investigate the main controlling factors of GHG release in different types of oil shales. The results showed that the CH4 and CO2 released from the YJ oil shale were 0.002-0.145 mL/g and 0.011-0.054 mL/g, respectively; the CH4 and CO2 released from the FS oil shale were 0.0001-0.0008 mL/g and 0.002-0.045 mL/g, respectively. Residual CH4 release was closely related to total organic carbon (TOC) and maturity: the CH4 released from the organic-rich and mature YJ oil shale was much higher than that of the FS oil shale, which is relatively organic-lean and immature. The control factors of the released CO2 vary in different regions: CO2 released from the YJ oil shale was somewhat affected by the TOC, while that released from the FS oil shale was mainly controlled by carbonate minerals and their contributing pores. The results of pore structure and organic maceral analyses indicated that both organic and inorganic pores of the YJ oil shale are occupied by asphaltenes, forming a key gas preservation mechanism of residual CH4 and CO2 as solutes dissolved in asphaltenes. In addition, CO2 has a greater absorptive capacity than CH4 and is therefore more difficult to release during the same crushing time. As oil shale is stored for longer periods, residual CH4 will be preferentially released to the atmosphere, while residual CO2 will be released in large quantities during crushing.
RESUMO
Greenhouse gas (GHG) emissions from oil and gas exploration and development are major contributors to emission inventories in oil and natural gas (ONG) systems. For the developing countries, including China, studies of this aspect of the industry, being at an early stage, lack a unified method of calculation, and this leads to varied projections of national emissions. In this paper, progress is reported on direct measurement of CH4 and CO2 emissions along the oil and gas value chain, for four oil and gas fields. An improved calculation method (classification calculation method), which considers the production status of each type of oil and gas field in China, is proposed for the first time in this study. Based on in situ measurement, it is used to estimate the national CH4 and CO2 emissions from the process of petroleum exploration and development. The results showed that CH4 and CO2 emissions in 2013 were 73.29×104 and 20.32×104tonnes, respectively (in CO2 equivalent: 1559.36×104tonnes). Compared with the results (731.52×104tonnes of CH4, 1031.55×104tonnes of CO2, 16,393.48×104tonnes of CO2 equivalent) in 2013 determined by the Tier 1 method of the Intergovernmental Panel on Climate Change (IPCC), the carbon emissions from field measurement method were much lower than that of IPCC method, which indicated that carbon emissions of ONG systems in China were severely overrated by IPCC. Hence, the GHG emission results reported herein could fundamentally improve the knowledge and understanding of GHG emissions from ONG exploration and development in China.
RESUMO
Here, we explored the expression of S100A4 in esophageal squamous cell cancer (ESCC) tissues and investigated its role in hypoxia-induced invasion and metastasis in ESCC cell lines EC-1 and EC-9706. Immunohistochemistry analysis demonstrated that S100A4 was overexpressed in human ESCC tissues especially in ESCC tissues with deep invasion and lymph node metastasis. Hypoxia-induced S100A4 overexpression was observed in EC-1 and EC-9706 cells, in which it was associated with invasion and metastasis. Furthermore, we used EC-1 and EC-9706 cells again to upregulate or knockdown the expression S100A4 to investigate the mechanism role of S100A4 in hypoxia-induced invasion and metastasis in ESCC cells. And the results showed that S100A4 played an important role in promoting the invasion and metastasis of EC-1 and EC-9706 cells under hypoxia. Therefore, S100A4 overexpression might be an important mechanism by which hypoxia induced invasion and metastasis, and S100A4 could also be a potential target for the treatment of ESCC.