The pursuit of alternative fuel generation technologies has gained momentum due to the diminishing reserves of fossil fuels and global warming from increased CO_(2)emission.Among the proposed methods,the hydrogenation...The pursuit of alternative fuel generation technologies has gained momentum due to the diminishing reserves of fossil fuels and global warming from increased CO_(2)emission.Among the proposed methods,the hydrogenation of CO_(2)to produce marketable carbon-based products like methanol and ethanol is a practical approach that offers great potential to reduce CO_(2)emissions.Although significant volumes of methanol are currently produced from CO_(2),developing highly efficient and stable catalysts is crucial for further enhancing conversion and selectivity,thereby reducing process costs.An in-depth examination of the differences and similarities in the reaction pathways for methanol and ethanol production highlights the key factors that drive C-C coupling.Identifying these factors guides us toward developing more effective catalysts for ethanol synthesis.In this paper,we explore how different catalysts,through the production of various intermediates,can initiate the synthesis of methanol or ethanol.The catalytic mechanisms proposed by spectroscopic techniques and theoretical calculations,including operando X-ray methods,FTIR analysis,and DFT calculations,are summarized and presented.The following discussion explores the structural properties and composition of catalysts that influence C-C coupling and optimize the conversion rate of CO_(2)into ethanol.Lastly,the review examines recent catalysts employed for selective methanol and ethanol production,focusing on single-atom catalysts.展开更多
We used the ocean reanalysis dataset SODA 2.2.4 to investigate the relationship between the interior branch of subtropical-tropical cells(STCs)in the Pacific Ocean and El Nino-Southern Oscillation(ENSO)over interdecad...We used the ocean reanalysis dataset SODA 2.2.4 to investigate the relationship between the interior branch of subtropical-tropical cells(STCs)in the Pacific Ocean and El Nino-Southern Oscillation(ENSO)over interdecadal timescales between 1930 and 2010,as well as the possible mechanisms involved.Interior transport within the upper pycnocline layers of STCs(InSTC)along 9°S(InSTC9s)shows a significant correlation of 0.54 with ENSO over the study period.However,there is an interdecadal shift in the relationship between InSTC along 9°N(InSTC9n)and ENSO.The correlation coefficient between InSTC9n and ENSO is not statistically significant between 1930 and 1965(PD1),but is as high as 0.68(significant at the 95% confidence level)between 1965 and 2010(PD2).Composite and regression analysis suggests that this shift may be caused by the relationship between InSTC 9 n and the tropical wind field.During PD1,InSTC9n was driven primarily by the local wind field outside equatorial region,with a relatively weak response to the equatorial wind related to ENSO.In contrast,during PD2,the wind field associated with InSTC 9 n showed a similar spatial distribution to that of ENSO within the equatorial region,indicating a close relationship between InSTC9n and ENSO.The wind stress curl associated with ENSO drives the anomalous InSTC9n in off-equatorial regions,whose signal can propagate westward in the form of Rossby wave and modulate the thermal structure of the tropical Pacific,favoring the development of ENSO.The possible connection between the Atlantic Multidecadal Oscillation(AMO)and interdecadal changes in the ENSO-InSTC9n relationship was also examined.There is a significant connection between the AMO and the interdecadal change in the relationship between ENSO and InSTC9n;however,the associated mechanism remains to be explored in future studies.展开更多
Postoperative cognitive dysfunction is a seve re complication of the central nervous system that occurs after anesthesia and surgery,and has received attention for its high incidence and effect on the quality of life ...Postoperative cognitive dysfunction is a seve re complication of the central nervous system that occurs after anesthesia and surgery,and has received attention for its high incidence and effect on the quality of life of patients.To date,there are no viable treatment options for postoperative cognitive dysfunction.The identification of postoperative cognitive dysfunction hub genes could provide new research directions and therapeutic targets for future research.To identify the signaling mechanisms contributing to postoperative cognitive dysfunction,we first conducted Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses of the Gene Expression Omnibus GSE95426 dataset,which consists of mRNAs and long non-coding RNAs differentially expressed in mouse hippocampus3 days after tibial fracture.The dataset was enriched in genes associated with the biological process"regulation of immune cells,"of which Chill was identified as a hub gene.Therefore,we investigated the contribution of chitinase-3-like protein 1 protein expression changes to postoperative cognitive dysfunction in the mouse model of tibial fractu re surgery.Mice were intraperitoneally injected with vehicle or recombinant chitinase-3-like protein 124 hours post-surgery,and the injection groups were compared with untreated control mice for learning and memory capacities using the Y-maze and fear conditioning tests.In addition,protein expression levels of proinflammatory factors(interleukin-1βand inducible nitric oxide synthase),M2-type macrophage markers(CD206 and arginase-1),and cognition-related proteins(brain-derived neurotropic factor and phosphorylated NMDA receptor subunit NR2B)were measured in hippocampus by western blotting.Treatment with recombinant chitinase-3-like protein 1 prevented surgery-induced cognitive impairment,downregulated interleukin-1βand nducible nitric oxide synthase expression,and upregulated CD206,arginase-1,pNR2B,and brain-derived neurotropic factor expression compared with vehicle treatment.Intraperitoneal administration of the specific ERK inhibitor PD98059 diminished the effects of recombinant chitinase-3-like protein 1.Collectively,our findings suggest that recombinant chitinase-3-like protein 1 ameliorates surgery-induced cognitive decline by attenuating neuroinflammation via M2 microglial polarization in the hippocampus.Therefore,recombinant chitinase-3-like protein1 may have therapeutic potential fo r postoperative cognitive dysfunction.展开更多
基金the Canadian NRCan OERD Energy Innovation Programthe Natural Sciences and Engineering Research Council of Canada,and the Carbon Solution Program for their financial support.
文摘The pursuit of alternative fuel generation technologies has gained momentum due to the diminishing reserves of fossil fuels and global warming from increased CO_(2)emission.Among the proposed methods,the hydrogenation of CO_(2)to produce marketable carbon-based products like methanol and ethanol is a practical approach that offers great potential to reduce CO_(2)emissions.Although significant volumes of methanol are currently produced from CO_(2),developing highly efficient and stable catalysts is crucial for further enhancing conversion and selectivity,thereby reducing process costs.An in-depth examination of the differences and similarities in the reaction pathways for methanol and ethanol production highlights the key factors that drive C-C coupling.Identifying these factors guides us toward developing more effective catalysts for ethanol synthesis.In this paper,we explore how different catalysts,through the production of various intermediates,can initiate the synthesis of methanol or ethanol.The catalytic mechanisms proposed by spectroscopic techniques and theoretical calculations,including operando X-ray methods,FTIR analysis,and DFT calculations,are summarized and presented.The following discussion explores the structural properties and composition of catalysts that influence C-C coupling and optimize the conversion rate of CO_(2)into ethanol.Lastly,the review examines recent catalysts employed for selective methanol and ethanol production,focusing on single-atom catalysts.
基金Supported by the National Natural Science Foundation of China(No.41976027)the Laoshan Laboratory(No.LSKJ202201601)。
文摘We used the ocean reanalysis dataset SODA 2.2.4 to investigate the relationship between the interior branch of subtropical-tropical cells(STCs)in the Pacific Ocean and El Nino-Southern Oscillation(ENSO)over interdecadal timescales between 1930 and 2010,as well as the possible mechanisms involved.Interior transport within the upper pycnocline layers of STCs(InSTC)along 9°S(InSTC9s)shows a significant correlation of 0.54 with ENSO over the study period.However,there is an interdecadal shift in the relationship between InSTC along 9°N(InSTC9n)and ENSO.The correlation coefficient between InSTC9n and ENSO is not statistically significant between 1930 and 1965(PD1),but is as high as 0.68(significant at the 95% confidence level)between 1965 and 2010(PD2).Composite and regression analysis suggests that this shift may be caused by the relationship between InSTC 9 n and the tropical wind field.During PD1,InSTC9n was driven primarily by the local wind field outside equatorial region,with a relatively weak response to the equatorial wind related to ENSO.In contrast,during PD2,the wind field associated with InSTC 9 n showed a similar spatial distribution to that of ENSO within the equatorial region,indicating a close relationship between InSTC9n and ENSO.The wind stress curl associated with ENSO drives the anomalous InSTC9n in off-equatorial regions,whose signal can propagate westward in the form of Rossby wave and modulate the thermal structure of the tropical Pacific,favoring the development of ENSO.The possible connection between the Atlantic Multidecadal Oscillation(AMO)and interdecadal changes in the ENSO-InSTC9n relationship was also examined.There is a significant connection between the AMO and the interdecadal change in the relationship between ENSO and InSTC9n;however,the associated mechanism remains to be explored in future studies.
基金supported by the National Natural Science Foundation of China,Nos.81730033,82171193(to XG)the Key Talent Project for Strengthening Health during the 13^(th)Five-Year Plan Period,No.ZDRCA2016069(to XG)+1 种基金the National Key R&D Program of China,No.2018YFC2001901(to XG)Jiangsu Provincial Medical Key Discipline,No.ZDXK202232(to XG)。
文摘Postoperative cognitive dysfunction is a seve re complication of the central nervous system that occurs after anesthesia and surgery,and has received attention for its high incidence and effect on the quality of life of patients.To date,there are no viable treatment options for postoperative cognitive dysfunction.The identification of postoperative cognitive dysfunction hub genes could provide new research directions and therapeutic targets for future research.To identify the signaling mechanisms contributing to postoperative cognitive dysfunction,we first conducted Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses of the Gene Expression Omnibus GSE95426 dataset,which consists of mRNAs and long non-coding RNAs differentially expressed in mouse hippocampus3 days after tibial fracture.The dataset was enriched in genes associated with the biological process"regulation of immune cells,"of which Chill was identified as a hub gene.Therefore,we investigated the contribution of chitinase-3-like protein 1 protein expression changes to postoperative cognitive dysfunction in the mouse model of tibial fractu re surgery.Mice were intraperitoneally injected with vehicle or recombinant chitinase-3-like protein 124 hours post-surgery,and the injection groups were compared with untreated control mice for learning and memory capacities using the Y-maze and fear conditioning tests.In addition,protein expression levels of proinflammatory factors(interleukin-1βand inducible nitric oxide synthase),M2-type macrophage markers(CD206 and arginase-1),and cognition-related proteins(brain-derived neurotropic factor and phosphorylated NMDA receptor subunit NR2B)were measured in hippocampus by western blotting.Treatment with recombinant chitinase-3-like protein 1 prevented surgery-induced cognitive impairment,downregulated interleukin-1βand nducible nitric oxide synthase expression,and upregulated CD206,arginase-1,pNR2B,and brain-derived neurotropic factor expression compared with vehicle treatment.Intraperitoneal administration of the specific ERK inhibitor PD98059 diminished the effects of recombinant chitinase-3-like protein 1.Collectively,our findings suggest that recombinant chitinase-3-like protein 1 ameliorates surgery-induced cognitive decline by attenuating neuroinflammation via M2 microglial polarization in the hippocampus.Therefore,recombinant chitinase-3-like protein1 may have therapeutic potential fo r postoperative cognitive dysfunction.
