A new process, NOx reduction with recycling flue gas and modifying coke breeze, was proposed. The effects of modified coke breeze and recycled flue gas on NOx reduction were investigated by sinter pot tests. The resul...A new process, NOx reduction with recycling flue gas and modifying coke breeze, was proposed. The effects of modified coke breeze and recycled flue gas on NOx reduction were investigated by sinter pot tests. The results show that the NOx reduction rate is over 10wt% in the sintering of modified coke breeze, the effects of the additives on NOx reduction are: CeO2〉CaO〉K2CO3. The NOx reduction rate increases with the amount of recycled flue gas, and is 22.35wt% in the sintering with recycling 30vol% of the flue gas. When 30vol% of the flue gas is recycled into the sintering of CeO2, CaO, and K2CO3 modified coke breeze, the NOx reduction rates are 36.10wt%, 32.56wt%, and 32.17wt%, respectively.展开更多
A new process called'NOx reduction by coupling combustion with recycling flue gas(RCCRF)'was proposed to decrease NOx emission during the iron ore sintering process.The simulation test of NOx reduction was perform...A new process called'NOx reduction by coupling combustion with recycling flue gas(RCCRF)'was proposed to decrease NOx emission during the iron ore sintering process.The simulation test of NOx reduction was performed over sintered ore and in the process of coke combustion.Experimentally,NOx reduction was also carried out by sintering pot test.For sintered ore,the amount of NOx emission is reduced by 15wt%-25wt% at 400-550oC using 2.0vol% H2 or 2.0vol% CO,or reduced by 10wt%-30wt% at 560-720oC using 0.15vol% NH3.NOx reduction is around 10wt% by coupling combustion of pyrolysis gas and coke,or around 16wt% by recycling flue gas into coke combustion.By RCCRF,the maximum NOx reduction ratio is about 23wt% in coke combustion experiment and over 40wt% in sintering pot test.展开更多
In order to get the catalytic mechanism of CeO2 on graphite and coal at 400℃, the morphologies of coal, graphite, and CeO2 before and after combustion were analyzed through X-ray photoelectron spectroscopy (XPS). I...In order to get the catalytic mechanism of CeO2 on graphite and coal at 400℃, the morphologies of coal, graphite, and CeO2 before and after combustion were analyzed through X-ray photoelectron spectroscopy (XPS). It is found that the particle size of coal is mostly between 11.727 and 64.79 μm, while the particle size of CeO2 is between 1.937 and 11.79 μm. The agglomeration of coal and CeO2 can be seen by scanning electron microscopy (SEM) after reaction. XPS results show that with the addition of CeO2, the intensity of binding energy gets stronger, but there is no energy peak transition. Comparing the character of coal with and without the addition of CeO2, it can be seen that the C C bond fractures first at 400℃, while the C-H energy-band takes electrons at the same time to be far away from the Fermi level, and the O 2s, O 2p, and C sp hybrid orbitals are all excited. Adding CeO2 can enhance the activity of the whole coal. In addition, through XPS analysis, combined with the oxygen transfer theory and the electron transfer theory, the catalytic mechanism of CeO2 for pulverized coal combustion could be obtained.展开更多
PTPN11,which encodes tyrosine phosphatase Shp2,is a critical gene mediating cellular responses to hormones and cytokines.Against original prediction as tumor suppressor for tyrosine phosphatases,PTPN11 was first ident...PTPN11,which encodes tyrosine phosphatase Shp2,is a critical gene mediating cellular responses to hormones and cytokines.Against original prediction as tumor suppressor for tyrosine phosphatases,PTPN11 was first identified as a proto-oncogene because activating mutations of this gene are associated with leukemogenesis.However,most recent experimental data suggest PTPN11/Shp2 acting as a tumor suppressor in hepatocarcinogenesis.This review focuses on the tumor-promoting or suppressing roles of the gene PTPN11/Shp2 in different cell types.展开更多
The transition from spermatogonia to spermatocytes and the initiation of meiosis are key steps in spermatogenesis and are precisely regulated by a plethora of proteins.However,the underlying molecular mechanism remain...The transition from spermatogonia to spermatocytes and the initiation of meiosis are key steps in spermatogenesis and are precisely regulated by a plethora of proteins.However,the underlying molecular mechanism remains largely unknown.Here,we report that Src homology domain tyrosine phosphatase 2(Shp2;encoded by the protein tyrosine phosphatase,nonreceptor type 11[Ptpn11]gene)is abundant in spermatogonia but markedly decreases in meiotic spermatocytes.Conditional knockout of Shp2 in spermatogonia in mice using stimulated by retinoic acid gene 8(Stra8)-cre enhanced spermatogonial differentiation and disturbed the meiotic process.Depletion of Shp2 in spermatogonia caused many meiotic spermatocytes to die;moreover,the surviving spermatocytes reached the leptotene stage early at postnatal day 9(PN9)and the pachytene stage at PN11-13.In preleptotene spermatocytes,Shp2 deletion disrupted the expression of meiotic genes,such as disrupted meiotic cDNA 1(Dmc1),DNA repair recombinase rad51(Rad51),and structural maintenance of chromosome 3(Smc3),and these deficiencies interrupted spermatocyte meiosis.In GC-1 cells cultured in vitro,Shp2 knockdown suppressed the retinoic acid(RA)-induced phosphorylation of extracellular-regulated protein kinase(Erk)and protein kinase B(Akt/PKB)and the expression of target genes such as synaptonemal complex protein 3(Sycp3)and Dmc1.Together,these data suggest that Shp2 plays a crucial role in spermatogenesis by governing the transition from spermatogonia to spermatocytes and by mediating meiotic progression through regulating gene transcription,thus providing a potential treatment target for male infertility.展开更多
Fatty liver disease is a serious health problem worldwide and is the most common cause for chronic liver disease and metabolic disorders.The major challenge in the prevention and intervention of this disease is the in...Fatty liver disease is a serious health problem worldwide and is the most common cause for chronic liver disease and metabolic disorders.The major challenge in the prevention and intervention of this disease is the incomplete understanding of the underlying mechanism and thus lack of potent therapeutic targets due to multifaceted and interdependent disease factors.In this study,we investigated the role of a signaling adaptor protein,GRB2-associated-binding protein 2(Gab2),in fatty liver using an animal disease model.Gab2 expression in hepatocytes responded to various disease factor stimulations,and Gab2 knockout mice exhibited resistance to fat-induced obesity,fat-or alcohol-stimulated hepatic steatosis,as well as methionine and choline deficiency-induced steatohepatitis.Concordantly,the forced expression or knockdown of Gab2 enhanced or diminished oleic acid(OA)-or ethanol-induced lipid production in hepatocytes in vitro,respectively.During lipid accumulation in hepatocytes,both fat and alcohol induced the recruitment of PI3K or Socs3 by Gab2 and the activation of their downstream signaling proteins AKT,ERK,and Stat3.Therefore,Gab2 may be a disease-associated protein that is induced by pathogenic factors to amplify and coordinate multifactor-induced signals to govern disease development in the liver.Our research provides a novel potential target for the prevention and intervention of fatty liver disease.展开更多
Obesity is associated with the higher risk of breast cancer in postmenopausal women.The leptin signaling pathway is recognized to primarily regulate energy balance and associated with breast cancer.Furthermore,the est...Obesity is associated with the higher risk of breast cancer in postmenopausal women.The leptin signaling pathway is recognized to primarily regulate energy balance and associated with breast cancer.Furthermore,the estrogen signaling pathway plays a critical role in breast carcinogenesis.In this review,we discuss how obesity is linked to breast cancer via cross-talk of leptin and estrogen pathways.展开更多
基金the National Natural Science Foundation of China (No.50574085)the Knowledge Innovation Program of the Chinese Academy of Sciences (No.O82809)
文摘A new process, NOx reduction with recycling flue gas and modifying coke breeze, was proposed. The effects of modified coke breeze and recycled flue gas on NOx reduction were investigated by sinter pot tests. The results show that the NOx reduction rate is over 10wt% in the sintering of modified coke breeze, the effects of the additives on NOx reduction are: CeO2〉CaO〉K2CO3. The NOx reduction rate increases with the amount of recycled flue gas, and is 22.35wt% in the sintering with recycling 30vol% of the flue gas. When 30vol% of the flue gas is recycled into the sintering of CeO2, CaO, and K2CO3 modified coke breeze, the NOx reduction rates are 36.10wt%, 32.56wt%, and 32.17wt%, respectively.
基金supported by the National Natural Science Foundation of China (No.50574085)
文摘A new process called'NOx reduction by coupling combustion with recycling flue gas(RCCRF)'was proposed to decrease NOx emission during the iron ore sintering process.The simulation test of NOx reduction was performed over sintered ore and in the process of coke combustion.Experimentally,NOx reduction was also carried out by sintering pot test.For sintered ore,the amount of NOx emission is reduced by 15wt%-25wt% at 400-550oC using 2.0vol% H2 or 2.0vol% CO,or reduced by 10wt%-30wt% at 560-720oC using 0.15vol% NH3.NOx reduction is around 10wt% by coupling combustion of pyrolysis gas and coke,or around 16wt% by recycling flue gas into coke combustion.By RCCRF,the maximum NOx reduction ratio is about 23wt% in coke combustion experiment and over 40wt% in sintering pot test.
文摘In order to get the catalytic mechanism of CeO2 on graphite and coal at 400℃, the morphologies of coal, graphite, and CeO2 before and after combustion were analyzed through X-ray photoelectron spectroscopy (XPS). It is found that the particle size of coal is mostly between 11.727 and 64.79 μm, while the particle size of CeO2 is between 1.937 and 11.79 μm. The agglomeration of coal and CeO2 can be seen by scanning electron microscopy (SEM) after reaction. XPS results show that with the addition of CeO2, the intensity of binding energy gets stronger, but there is no energy peak transition. Comparing the character of coal with and without the addition of CeO2, it can be seen that the C C bond fractures first at 400℃, while the C-H energy-band takes electrons at the same time to be far away from the Fermi level, and the O 2s, O 2p, and C sp hybrid orbitals are all excited. Adding CeO2 can enhance the activity of the whole coal. In addition, through XPS analysis, combined with the oxygen transfer theory and the electron transfer theory, the catalytic mechanism of CeO2 for pulverized coal combustion could be obtained.
基金funded by NIH grants R01DK075916 and R01HL096125supported by Chinese National Key Project(2012ZX10002-009,011,013)+2 种基金National Natural Science Foundation of China(Grant Nos.30921006,30900770)Key Basic Science Foundation of Shanghai(10JC1418500)Project of the State Key Laboratory of Shanghai Jiaotong University(91-10-02).
文摘PTPN11,which encodes tyrosine phosphatase Shp2,is a critical gene mediating cellular responses to hormones and cytokines.Against original prediction as tumor suppressor for tyrosine phosphatases,PTPN11 was first identified as a proto-oncogene because activating mutations of this gene are associated with leukemogenesis.However,most recent experimental data suggest PTPN11/Shp2 acting as a tumor suppressor in hepatocarcinogenesis.This review focuses on the tumor-promoting or suppressing roles of the gene PTPN11/Shp2 in different cell types.
基金This work was supported by the National Key R&D Program of China(No.2018YFC1003701 and No.2017YFC1001402)the National Natural Science Foundation of China(Grant No.31171375).
文摘The transition from spermatogonia to spermatocytes and the initiation of meiosis are key steps in spermatogenesis and are precisely regulated by a plethora of proteins.However,the underlying molecular mechanism remains largely unknown.Here,we report that Src homology domain tyrosine phosphatase 2(Shp2;encoded by the protein tyrosine phosphatase,nonreceptor type 11[Ptpn11]gene)is abundant in spermatogonia but markedly decreases in meiotic spermatocytes.Conditional knockout of Shp2 in spermatogonia in mice using stimulated by retinoic acid gene 8(Stra8)-cre enhanced spermatogonial differentiation and disturbed the meiotic process.Depletion of Shp2 in spermatogonia caused many meiotic spermatocytes to die;moreover,the surviving spermatocytes reached the leptotene stage early at postnatal day 9(PN9)and the pachytene stage at PN11-13.In preleptotene spermatocytes,Shp2 deletion disrupted the expression of meiotic genes,such as disrupted meiotic cDNA 1(Dmc1),DNA repair recombinase rad51(Rad51),and structural maintenance of chromosome 3(Smc3),and these deficiencies interrupted spermatocyte meiosis.In GC-1 cells cultured in vitro,Shp2 knockdown suppressed the retinoic acid(RA)-induced phosphorylation of extracellular-regulated protein kinase(Erk)and protein kinase B(Akt/PKB)and the expression of target genes such as synaptonemal complex protein 3(Sycp3)and Dmc1.Together,these data suggest that Shp2 plays a crucial role in spermatogenesis by governing the transition from spermatogonia to spermatocytes and by mediating meiotic progression through regulating gene transcription,thus providing a potential treatment target for male infertility.
基金supported by the National Basic Research Program of China(grant no.2010CB945004 and 2013CB945503)the National Natural Science Foundation of China(grant no.30772546).
文摘Fatty liver disease is a serious health problem worldwide and is the most common cause for chronic liver disease and metabolic disorders.The major challenge in the prevention and intervention of this disease is the incomplete understanding of the underlying mechanism and thus lack of potent therapeutic targets due to multifaceted and interdependent disease factors.In this study,we investigated the role of a signaling adaptor protein,GRB2-associated-binding protein 2(Gab2),in fatty liver using an animal disease model.Gab2 expression in hepatocytes responded to various disease factor stimulations,and Gab2 knockout mice exhibited resistance to fat-induced obesity,fat-or alcohol-stimulated hepatic steatosis,as well as methionine and choline deficiency-induced steatohepatitis.Concordantly,the forced expression or knockdown of Gab2 enhanced or diminished oleic acid(OA)-or ethanol-induced lipid production in hepatocytes in vitro,respectively.During lipid accumulation in hepatocytes,both fat and alcohol induced the recruitment of PI3K or Socs3 by Gab2 and the activation of their downstream signaling proteins AKT,ERK,and Stat3.Therefore,Gab2 may be a disease-associated protein that is induced by pathogenic factors to amplify and coordinate multifactor-induced signals to govern disease development in the liver.Our research provides a novel potential target for the prevention and intervention of fatty liver disease.
基金supported by NIH grants(R01DK073945 and R01DK075916)a new concept award from DOD(W81XWH-10-1-0480).
文摘Obesity is associated with the higher risk of breast cancer in postmenopausal women.The leptin signaling pathway is recognized to primarily regulate energy balance and associated with breast cancer.Furthermore,the estrogen signaling pathway plays a critical role in breast carcinogenesis.In this review,we discuss how obesity is linked to breast cancer via cross-talk of leptin and estrogen pathways.