The efficient pyrolysis and conversion of organic matter in organic-rich shale,as well as the effective recovery of pyrolysis shale oil and gas,play a vital role in alleviating energy pressure.The state of carbon diox...The efficient pyrolysis and conversion of organic matter in organic-rich shale,as well as the effective recovery of pyrolysis shale oil and gas,play a vital role in alleviating energy pressure.The state of carbon dioxide(CO_(2))in the pyrolysis environment of shale reservoirs is the supercritical state.Its unique supercritical fluid properties not only effectively heat organic matter,displace pyrolysis products and change shale pore structure,but also achieve carbon storage to a certain extent.Shale samples were made into powder and three sizes of cores,and nitrogen(N_(2))and supercritical carbon dioxide(ScCO_(2))pyrolysis experiments were performed at different final pyrolysis temperatures.The properties and mineral characteristics of the pyrolysis products were studied based on gas chromatography analysis,Xray diffraction tests,and mass spectrometry analysis.Besides,the pore structure characteristics at different regions of cores before and after pyrolysis were analyzed using N_(2) adsorption tests to clarify the impact of fracturing degree on the pyrolysis effect.The results indicate that the optimal pyrolysis temperature of Longkou shale is about 430℃.Compared with N_(2),the oil yield of ScCO_(2) pyrolysis is higher.The pyrolysis oil obtained by ScCO_(2) extraction has more intermediate fractions and higher relative molecular weight.The ScCO_(2) can effectively improve the pore diameter of shale and its effect is better than that of N_(2).The micropores are produced in shale after pyrolysis,and the macropores only are generated in ScCO_(2) pyrolysis environments with temperatures greater than 430℃.The pore structure has different development characteristics at different pyrolysis temperatures,which are mainly affected by the pressure holding of volatile matter and products blocking.Compared to the surface of the core,the pore development effect inside the core is better.With the decrease in core size,the pore diameter,specific surface area,and pore volume of cores all increase after pyrolysis.展开更多
The autophagy adaptor protein SQSTM1/p62 is overexpressed in breast cancer and has been identified as a metastasis-related protein.However,the mechanism by which SQSTM1/p62 contributes to breast cancer progression and...The autophagy adaptor protein SQSTM1/p62 is overexpressed in breast cancer and has been identified as a metastasis-related protein.However,the mechanism by which SQSTM1/p62 contributes to breast cancer progression and tumor microenvironment remains unclear.This study revealed that silencing SQSTM1/p62 expression suppressed breast cancer progression via regulating cell proliferation and reshaping the tumor microenvironment(TME).Here,we found that SQSTM1/p62 was overexpressed in multiple human cancer tissue types and that was correlated with poor patient overall survival(OS)and disease-free survival(DFS).Moreover,we found that short-hairpin RNA(shRNA)-mediated knockdown of p62 expression significantly inhibited cell proliferation,migration,and invasion,and promoted cell death in vitro,as well as suppressed breast cancer growth and lung metastasis in vivo.In addition,flow cytometry analysis of splenocytes and tumor infiltrating lymphocytes(TILs)indicated that the numbers of CD8α+interferon(IFN)-γ+cells(CTLs)and CD4+IFN-γ+(Th1)cells were increased while those of CD4+IL-4+(Th2)cells,tumor-associated macrophages(TAMs)and myeloid-derived suppressor cells(MDSCs)were decreased.RT-PCR analyses showed that the gene expression of Th1/Th2 cytokines changed in the tumor microenvironment.Silencing SQSTM1/p62 suppressed tumor cell lung metastasis.Together,our results provide strong evidence that silencing tumor cell SQSTM1/p62 inhibited tumor growth and metastasis through cell cycle arrest and TME regulation.This finding provides a novel molecular therapeutic strategy for breast cancer progression and metastasis treatment.展开更多
基金supported by the National Natural Science Foundation of China (Nos.U22B6004,51974341)State Key Laboratory of Deep Oil and Gas (No.SKLDOG2024-ZYTS-14)the Fundamental Research Funds for the Central Universities (No.20CX06070A)。
文摘The efficient pyrolysis and conversion of organic matter in organic-rich shale,as well as the effective recovery of pyrolysis shale oil and gas,play a vital role in alleviating energy pressure.The state of carbon dioxide(CO_(2))in the pyrolysis environment of shale reservoirs is the supercritical state.Its unique supercritical fluid properties not only effectively heat organic matter,displace pyrolysis products and change shale pore structure,but also achieve carbon storage to a certain extent.Shale samples were made into powder and three sizes of cores,and nitrogen(N_(2))and supercritical carbon dioxide(ScCO_(2))pyrolysis experiments were performed at different final pyrolysis temperatures.The properties and mineral characteristics of the pyrolysis products were studied based on gas chromatography analysis,Xray diffraction tests,and mass spectrometry analysis.Besides,the pore structure characteristics at different regions of cores before and after pyrolysis were analyzed using N_(2) adsorption tests to clarify the impact of fracturing degree on the pyrolysis effect.The results indicate that the optimal pyrolysis temperature of Longkou shale is about 430℃.Compared with N_(2),the oil yield of ScCO_(2) pyrolysis is higher.The pyrolysis oil obtained by ScCO_(2) extraction has more intermediate fractions and higher relative molecular weight.The ScCO_(2) can effectively improve the pore diameter of shale and its effect is better than that of N_(2).The micropores are produced in shale after pyrolysis,and the macropores only are generated in ScCO_(2) pyrolysis environments with temperatures greater than 430℃.The pore structure has different development characteristics at different pyrolysis temperatures,which are mainly affected by the pressure holding of volatile matter and products blocking.Compared to the surface of the core,the pore development effect inside the core is better.With the decrease in core size,the pore diameter,specific surface area,and pore volume of cores all increase after pyrolysis.
基金supported by the CAMS Initiative for Innovative Medicine(No.2016-I2M-1-019)2017-I2M-3-022,the Fundamental Research Funds for the Central Universities of China(No.3332019162)+1 种基金the funds for IMBCAMS PhD Innovation(No.2018018001)the Foundation for Studying Abroad from the China Scholarship Council(No.201808110121,201906210477).
文摘The autophagy adaptor protein SQSTM1/p62 is overexpressed in breast cancer and has been identified as a metastasis-related protein.However,the mechanism by which SQSTM1/p62 contributes to breast cancer progression and tumor microenvironment remains unclear.This study revealed that silencing SQSTM1/p62 expression suppressed breast cancer progression via regulating cell proliferation and reshaping the tumor microenvironment(TME).Here,we found that SQSTM1/p62 was overexpressed in multiple human cancer tissue types and that was correlated with poor patient overall survival(OS)and disease-free survival(DFS).Moreover,we found that short-hairpin RNA(shRNA)-mediated knockdown of p62 expression significantly inhibited cell proliferation,migration,and invasion,and promoted cell death in vitro,as well as suppressed breast cancer growth and lung metastasis in vivo.In addition,flow cytometry analysis of splenocytes and tumor infiltrating lymphocytes(TILs)indicated that the numbers of CD8α+interferon(IFN)-γ+cells(CTLs)and CD4+IFN-γ+(Th1)cells were increased while those of CD4+IL-4+(Th2)cells,tumor-associated macrophages(TAMs)and myeloid-derived suppressor cells(MDSCs)were decreased.RT-PCR analyses showed that the gene expression of Th1/Th2 cytokines changed in the tumor microenvironment.Silencing SQSTM1/p62 suppressed tumor cell lung metastasis.Together,our results provide strong evidence that silencing tumor cell SQSTM1/p62 inhibited tumor growth and metastasis through cell cycle arrest and TME regulation.This finding provides a novel molecular therapeutic strategy for breast cancer progression and metastasis treatment.
