Three lactoproteins （α-Sl-casein, β-lactoglobulin, and β-casein） promotors were cloned, sequenced and compared relative luciferase expression. The results showed that the promotor activity of bovine α-S1-casein ...Three lactoproteins （α-Sl-casein, β-lactoglobulin, and β-casein） promotors were cloned, sequenced and compared relative luciferase expression. The results showed that the promotor activity of bovine α-S1-casein gene was the best, and would be used to produce pharmaceutically and medically important proteins in the mammary gland of transgenic animals and also for the construction of an inducible eukaryotic expression vector.展开更多
Polar promotors have been proven effective in catalyzing the polysulfide(PS)reduction reaction(PSRR)process in lithium-sulfur(Li-S)batteries.However,the promotor surface tends to be poisoned due to the accumulation of...Polar promotors have been proven effective in catalyzing the polysulfide(PS)reduction reaction(PSRR)process in lithium-sulfur(Li-S)batteries.However,the promotor surface tends to be poisoned due to the accumulation of insoluble discharging products of lithium disulfide(Li_(2)S_(2))and lithium sulfide(Li_(2)S)during Li-S battery operation.Herein,we investigate the detailed PSRR mechanism on the surface of manganese sulfides(MnS)as a representative promoter by performing in-situ Raman mapping measurements.The catalytic ability of MnS enables thorough electrochemical reduction of PSs to Li_(2)S_(2) and Li_(2)S on the MnS surface.The generated Li_(2)S_(2) and Li_(2)S then adsorb the dissolved PSs via chemical reactions among sulfur species during the subsequent PSRR process.This phenomenon mitigates promotor poisoning and continuously improves the reversible capacity.Consequently,the assembled Li-S cell demonstrates excellent electrochemical performance after introducing a conductive interlayer containing a thin piece of carbon nanotube film and MnS promotors.展开更多
Three genetic mechanisms activate oncogenes in human neoplasms: 1) mutations, 2) gene amplification, and 3) chromosome rearrangements. These mechanisms result in either an alteration of protooncogene structure or an i...Three genetic mechanisms activate oncogenes in human neoplasms: 1) mutations, 2) gene amplification, and 3) chromosome rearrangements. These mechanisms result in either an alteration of protooncogene structure or an increase in protooncogene expression. The role of epigenetic aberrancies in carcinogenesis has been described earlier however to clinicians, the biological implications of epigenetic therapies to prevent cancer and the mechanisms involved have been a mystery. Furthermore, there is no biomarker suggested to track the carcinogenesis steps long before cancer develops, and this has caused a significant lack of proactive and preventive measures to be taken as all recommendations in preventive oncology are either deficiently and blindly made or through screening methods which are too late in the game. Here we explored a very different approach by applying our deepest understanding of epigenetics and carcinogenesis and even further we developed a framework where our clinical findings could translate to the research and vice versa by generating advanced and novel hypotheses on “how we get cancer”, by exploring the relation between the host and the tumor cells in a way no one had perceived before. The role of specific cancer stem cell pathways is dissected and how to inhibit each of these initiators using multitargeted epigenetic therapies and off-label medications are explained. We should admit that without considering this sophisticated amazing biological network, cancer will remain an unsolved challenge. Further, we were able to solve this unsolved puzzle by bridging the gap from a hypothetical point of view/hypothesis to possibilities that explain the clinical findings we had observed, and conclude that such an approach can completely change the way practitioners are treating cancer.展开更多
基金Supported by the Innovation Team Project of Northeast Agricultural University (CXT005-1-2)
文摘Three lactoproteins （α-Sl-casein, β-lactoglobulin, and β-casein） promotors were cloned, sequenced and compared relative luciferase expression. The results showed that the promotor activity of bovine α-S1-casein gene was the best, and would be used to produce pharmaceutically and medically important proteins in the mammary gland of transgenic animals and also for the construction of an inducible eukaryotic expression vector.
基金supported by the National Basic Research Program of China(2019YFA0705702)the National Natural Science Foundation of China(51872158).H.T.Liu acknowledges funding from the National Natural Science Foundation of China(No.11734013,11874089).
文摘Polar promotors have been proven effective in catalyzing the polysulfide(PS)reduction reaction(PSRR)process in lithium-sulfur(Li-S)batteries.However,the promotor surface tends to be poisoned due to the accumulation of insoluble discharging products of lithium disulfide(Li_(2)S_(2))and lithium sulfide(Li_(2)S)during Li-S battery operation.Herein,we investigate the detailed PSRR mechanism on the surface of manganese sulfides(MnS)as a representative promoter by performing in-situ Raman mapping measurements.The catalytic ability of MnS enables thorough electrochemical reduction of PSs to Li_(2)S_(2) and Li_(2)S on the MnS surface.The generated Li_(2)S_(2) and Li_(2)S then adsorb the dissolved PSs via chemical reactions among sulfur species during the subsequent PSRR process.This phenomenon mitigates promotor poisoning and continuously improves the reversible capacity.Consequently,the assembled Li-S cell demonstrates excellent electrochemical performance after introducing a conductive interlayer containing a thin piece of carbon nanotube film and MnS promotors.
文摘Three genetic mechanisms activate oncogenes in human neoplasms: 1) mutations, 2) gene amplification, and 3) chromosome rearrangements. These mechanisms result in either an alteration of protooncogene structure or an increase in protooncogene expression. The role of epigenetic aberrancies in carcinogenesis has been described earlier however to clinicians, the biological implications of epigenetic therapies to prevent cancer and the mechanisms involved have been a mystery. Furthermore, there is no biomarker suggested to track the carcinogenesis steps long before cancer develops, and this has caused a significant lack of proactive and preventive measures to be taken as all recommendations in preventive oncology are either deficiently and blindly made or through screening methods which are too late in the game. Here we explored a very different approach by applying our deepest understanding of epigenetics and carcinogenesis and even further we developed a framework where our clinical findings could translate to the research and vice versa by generating advanced and novel hypotheses on “how we get cancer”, by exploring the relation between the host and the tumor cells in a way no one had perceived before. The role of specific cancer stem cell pathways is dissected and how to inhibit each of these initiators using multitargeted epigenetic therapies and off-label medications are explained. We should admit that without considering this sophisticated amazing biological network, cancer will remain an unsolved challenge. Further, we were able to solve this unsolved puzzle by bridging the gap from a hypothetical point of view/hypothesis to possibilities that explain the clinical findings we had observed, and conclude that such an approach can completely change the way practitioners are treating cancer.
