FCS-like zinc finger(FLZ)gene family members are C2-C2 zinc finger proteins that take part in seed dormancy,resistance to Myzus persicae 1,sucrose signaling and abiotic stresse tolerance.However,their functions,especi...FCS-like zinc finger(FLZ)gene family members are C2-C2 zinc finger proteins that take part in seed dormancy,resistance to Myzus persicae 1,sucrose signaling and abiotic stresse tolerance.However,their functions,especially the molecular mechanism through which FLZs function,are not well understood.In this study,we characterized 120FLZs in wheat and revealed the function and mechanism of TaFLZ54D increasing salt stress tolerance in transgenic wheat.Expression analysis demonstrated that TaFLZ54D can be induced by NaCl treatment and it had the highest expression level under NaCl treatment among the 120 FLZs.Over-expression of TaFLZ54D increased wheat salt stress tolerance and the transgenic plants had higher levels of superoxide dismutase(SOD)and peroxidase(POD)activities and soluble sugar content,but a lower Na^(+)/K^(+)ratio and malondialdehyde(MDA)content than the wild type(WT)plants.Potassium ion transmembrane transporters and serine/threonine kinase inhibitor proteins showed differential expression between Ta FLZ54D transgenic wheat and the WT.Yeast two hybrid and luciferase complementation assays revealed that TaSGT1 and TaPP2C are the proteins that interact directly with TaFLZ54D.In summary,TaFLZ54D enhances salt stress tolerance through interaction with TaSGT1 and TaPP2C to reduce Na^(+)absorption and mitigate oxidative stress.The interaction between TaFLZ54D and TaSGT1,as well as TaPP2C indicated a link between salt stress tolerance of TaFLZ54D and the ubiquitin-mediated degradation of negative regulatory proteins.展开更多
OBJECTIVES Parkinson disease(PD)is the second most common neurodegener⁃ative disease,but none of the current treatments for PD could halt the progress of the disease due to the limited understanding of the pathogenesi...OBJECTIVES Parkinson disease(PD)is the second most common neurodegener⁃ative disease,but none of the current treatments for PD could halt the progress of the disease due to the limited understanding of the pathogenesis.Increasing evidence proves that the close com⁃munication between the brain and the gastroin⁃testinal system is influenced by gut microbiota in PD pathogenesis,known as microbiota-gut-brain axis.However,the explicit mechanisms of micro⁃biota dysbiosis in PD development have not been well elucidated yet.FLZ,a novel squamosamide derivative,has been proved to be effective in many PD models and is undergoing the phaseⅠclinical trial to treat PD in China.The aims of our study are to assess the neuroprotective effects of FLZ treatment on PD and to further explore the underlying microbiota-related mechanisms of PD by using FLZ as a tool.METHODS Chronic administration of rotenone(30 mg·kg-1 per day)was utilized to induce a mouse model to mimic the pathological process of PD.Behavioral tests and gastrointestinal function tests were conduct⁃ed to evaluate the PD symptoms.Gut microbiota alterations were analyzed by 16s rRNA sequenc⁃ing.The intestinal permeability and blood-brain barrier structures were assessed by various methods.The pro-inflammatory cytokines and LPS levels in the colon,serum,and brain were detected by ELISA.Furthermore,the levels of in⁃flammation and TLR4/MyD88/NF-κB pathway in the substantia nigra(SN)and colon were mea⁃sured.RESULTS Behavioral tests and gastroin⁃testinal function tests found that rotenone-in⁃duced mice showed gastrointestinal dysfunctions(week 3)prior to the motor deficits(week 4).However,FLZ treatment significantly alleviated these PD symptoms.16S rRNA sequencing illus⁃trated that PD-related microbiota alterations in⁃duced by rotenone were reversed by FLZ treatment at various taxa levels.Especially,we identified an increased genus Akkermansia in the Rotenone group(P=0.0006),which could be reversed by FLZ administration(P=0.0070).By reducing microbiota dysbiosis,qPCR results showed that FLZ treatment suppressed intestinal inflammation of rotenone-challenged mice.After⁃wards,transmission electron microscopy(TEM),in vivo FITC permeability assay,bacterial translocation assay,and Western blotting togeth⁃er suggested that FLZ treatment attenuated the intestinal barrier destruction induced by rote⁃none.Subsequently,ELISA results showed that FLZ administration inhibited the leakage of pro-inflammatory cytokines(TNF-α,IL-1β,and IL-6)and LPS into the serum,suggesting the atten⁃uation of systemic inflammation.Then,several experiments including TEM analysis found that FLZ treatment restored blood-brain barrier struc⁃ture.Consequently,the immunofluorescence staining demonstrated that neuroinflammation(increased Iba-1+and GFAP+cells)and dopami⁃nergic neuronal death(reduced TH+cells)in the SN caused by rotenone were remarkably attenu⁃ated.Further mechanistic research proved that the anti-inflammatory effects of FLZ administra⁃tion were mediated through the TLR4/MyD88/NF-κB pathway both in the SN and colon.CONCLU⁃SION FLZ treatment ameliorates microbiota dys⁃biosis to protect the PD model via inhibiting TLR4 pathway,which contributes to one of the underlying mechanisms beneath its neuroprotec⁃tive effects.Our research also supports the importance of microbiota-gut-brain axis in PD pathogenesis,suggesting its potential role as a novel therapeutic target for PD treatment.展开更多
Increasing evidence shows that the early lesions of Parkinson's disease(PD)originate from gut,and correction of microbiota dysbiosis is a promising therapy for PD.FLZ is a neuroprotective agent on PD,which has bee...Increasing evidence shows that the early lesions of Parkinson's disease(PD)originate from gut,and correction of microbiota dysbiosis is a promising therapy for PD.FLZ is a neuroprotective agent on PD,which has been validated capable of alleviating microbiota dysbiosis in PD mice.However,the detailed mechanisms still need elucidated.Through metabolomics and 16S rRNA analysis,we identified glycoursodeoxycholic acid(GUDCA)was the most affected differential microbial metabolite by FLZ treatment,which was specially and negatively regulated by Clostridium innocuum,a differential microbiota with the strongest correlation to GUDCA production,through inhibiting bile salt hydrolase(BSH)enzyme.The protection of GUDCA on colon and brain were also clarified in PD models,showing that it could activate Nrf2 pathway,further validating that FLZ protected dopaminergic neurons through promoting GUDCA production.Our study uncovered that FLZ improved PD through microbiota-gut-brain axis,and also gave insights into modulation of microbial metabolites may serve as an important strategy for treating PD.展开更多
Parkinson’s disease(PD)is the second most common neurodegenerative disease,but none of the current treatments for PD can halt the progress of the disease due to the limited understanding of the pathogenesis.In PD dev...Parkinson’s disease(PD)is the second most common neurodegenerative disease,but none of the current treatments for PD can halt the progress of the disease due to the limited understanding of the pathogenesis.In PD development,the communication between the brain and the gastrointestinal system influenced by gut microbiota is known as microbiota-gut-brain axis.However,the explicit mechanisms of microbiota dysbiosis in PD development have not been well elucidated yet.FLZ,a novel squamosamide derivative,has been proved to be effective in many PD models and is undergoing the phase I clinical trial to treat PD in China.Moreover,our previous pharmacokinetic study revealed that gut microbiota could regulate the absorption of FLZ in vivo.The aims of our study were to assess the protective effects of FLZ treatment on PD and to further explore the underlying microbiota-related mechanisms of PD by using FLZ as a tool.In the current study,chronic oral administration of rotenone was utilized to induce a mouse model to mimic the pathological process of PD.Here we revealed that FLZ treatment alleviated gastrointestinal dysfunctions,motor symptoms,and dopaminergic neuron death in rotenone-challenged mice.16 S rRNA sequencing found that PD-related microbiota alterations induced by rotenone were reversed by FLZ treatment.Remarkably,FLZ administration attenuated intestinal inflammation and gut barrier destruction,which subsequently inhibited systemic inflammation.Eventually,FLZ treatment restored blood-brain barrier structure and suppressed neuroinflammation by inhibiting the activation of astrocytes and microglia in the substantia nigra(SN).Further mechanistic research demonstrated that FLZ treatment suppressed the TLR4/MyD88/NF-κB pathway both in the SN and colon.Collectively,FLZ treatment ameliorates microbiota dysbiosis to protect the PD model via inhibiting TLR4 pathway,which contributes to one of the underlying mechanisms beneath its neuroprotective effects.Our research also supports the importance of microbiota-gut-brain axis in PD pathogenesis,suggesting its potential role as a novel therapeutic target for PD treatment.展开更多
The gut microbiota plays an important role in regulating the pharmacokinetics and pharmacodynamics of many drugs.FLZ,a novel squamosamide derivative,has been shown to have neuroprotective effects on experimental Parki...The gut microbiota plays an important role in regulating the pharmacokinetics and pharmacodynamics of many drugs.FLZ,a novel squamosamide derivative,has been shown to have neuroprotective effects on experimental Parkinson’s disease(PD)models.FLZ is under phase I clinical trial now,while the underlying mechanisms contributing to the absorption of FLZ are still not fully elucidated.Due to the main metabolite of FLZ was abundant in feces but rare in urine and bile of mice,we focused on the gut microbiota to address how FLZ was metabolized and absorbed.In vitro studies revealed that FLZ could be exclusively metabolized to its major metabolite M1 by the lanosterol 14 alpha-demethylase(CYP51)in the gut microbiota,but was almost not metabolized by any other metabolism-related organs,such as liver,kidney,and small intestine.M1 was quickly absorbed into the blood and then remethylated to FLZ by catechol O-methyltransferase(COMT).Notably,dysbacteriosis reduced the therapeutic efficacy of FLZ on the PD mouse model by inhibiting its absorption.The results show that the gut microbiota mediate the absorption of FLZ through a FLZ-M1-FLZ circulation.Our research elucidates the vital role of the gut microbiota in the absorption of FLZ and provides a theoretical basis for clinical pharmacokinetic studies and clinical application of FLZ in the treatment of PD.展开更多
The bZIP transcription factor ABSCISIC ACID INSENSITIVE5(ABI5)is a master regulator of seed germination and post-germinative growth in response to abscisic acid(ABA),but the detailed molecularmechanism by which it rep...The bZIP transcription factor ABSCISIC ACID INSENSITIVE5(ABI5)is a master regulator of seed germination and post-germinative growth in response to abscisic acid(ABA),but the detailed molecularmechanism by which it represses plant growth remains unclear.In this study,we used proximity labeling to map the neighboring proteome of ABI5 and identified FCS-LIKE ZINC FINGER PROTEIN 13(FLZ13)as a novel ABI5 interaction partner.Phenotypic analysis of flz13 mutants and FLZ13-overexpressing lines demonstrated that FLZ13 acts as a positive regulator of ABA signaling.Transcriptomic analysis revealed that both FLZ13 and ABI5 downregulate the expression of ABA-repressed and growth-related genes involved in chlorophyll biosynthesis,photosynthesis,and cell wall organization,thereby repressing seed germination and seedling establishment in response to ABA.Further genetic analysis showed that FLZ13 and ABI5 function together to regulate seed germination.Collectively,our findings reveal a previously uncharacterized transcriptional regulatorymechanismby which ABA mediates inhibition of seed germination and seedling establishment.展开更多
Friedberg, Lee and Zhao (FLZ) proposed a method for effectively evaluating the eigenenergies and eigen wavefunctions of quantum systems. In this work, we study several special cases to investigate applicability of the...Friedberg, Lee and Zhao (FLZ) proposed a method for effectively evaluating the eigenenergies and eigen wavefunctions of quantum systems. In this work, we study several special cases to investigate applicability of the method.Concretely, we calculate the ground-state eigenenergy of the Hellmann potential as well as the Cornell potential, and also evaluate the energies of the systems where linear term is added to the Coulomb as a perturbation. The results obtained in this method have a surprising agreement with the traditional method or the numerical results. Since the results in this method have obvious analyticity compared to that in other methods, and because of the simplicity for calculations this method can be applied to solving the Schrodinger equation and provides us a better understanding of the physical essence of the concerned systems. But meanwhile applications of the FLZ method are restricted at present, especially for certain potential forms, but due to its obvious advantages, it should be further developed.展开更多
The new method proposed recently by Friedberg, Lee, and Zhao is extended to obtain an analytic expansion for the ground-state wavefunction of a time-dependent strong-coupling Schroedinger equation. Two different types...The new method proposed recently by Friedberg, Lee, and Zhao is extended to obtain an analytic expansion for the ground-state wavefunction of a time-dependent strong-coupling Schroedinger equation. Two different types of the time-dependent harmonic oscillators are considered as examples for application of the time-dependent expansion. It is show that the time-dependent strong-coupling expansion is applicable to the time-dependent harmonic oscillators with a slowly varying time-dependent parameter.展开更多
基金supported by the National Natural Science Foundation of China(31871622)the Key R&D Program of Shandong Province,China(2022LZG001)。
文摘FCS-like zinc finger(FLZ)gene family members are C2-C2 zinc finger proteins that take part in seed dormancy,resistance to Myzus persicae 1,sucrose signaling and abiotic stresse tolerance.However,their functions,especially the molecular mechanism through which FLZs function,are not well understood.In this study,we characterized 120FLZs in wheat and revealed the function and mechanism of TaFLZ54D increasing salt stress tolerance in transgenic wheat.Expression analysis demonstrated that TaFLZ54D can be induced by NaCl treatment and it had the highest expression level under NaCl treatment among the 120 FLZs.Over-expression of TaFLZ54D increased wheat salt stress tolerance and the transgenic plants had higher levels of superoxide dismutase(SOD)and peroxidase(POD)activities and soluble sugar content,but a lower Na^(+)/K^(+)ratio and malondialdehyde(MDA)content than the wild type(WT)plants.Potassium ion transmembrane transporters and serine/threonine kinase inhibitor proteins showed differential expression between Ta FLZ54D transgenic wheat and the WT.Yeast two hybrid and luciferase complementation assays revealed that TaSGT1 and TaPP2C are the proteins that interact directly with TaFLZ54D.In summary,TaFLZ54D enhances salt stress tolerance through interaction with TaSGT1 and TaPP2C to reduce Na^(+)absorption and mitigate oxidative stress.The interaction between TaFLZ54D and TaSGT1,as well as TaPP2C indicated a link between salt stress tolerance of TaFLZ54D and the ubiquitin-mediated degradation of negative regulatory proteins.
文摘OBJECTIVES Parkinson disease(PD)is the second most common neurodegener⁃ative disease,but none of the current treatments for PD could halt the progress of the disease due to the limited understanding of the pathogenesis.Increasing evidence proves that the close com⁃munication between the brain and the gastroin⁃testinal system is influenced by gut microbiota in PD pathogenesis,known as microbiota-gut-brain axis.However,the explicit mechanisms of micro⁃biota dysbiosis in PD development have not been well elucidated yet.FLZ,a novel squamosamide derivative,has been proved to be effective in many PD models and is undergoing the phaseⅠclinical trial to treat PD in China.The aims of our study are to assess the neuroprotective effects of FLZ treatment on PD and to further explore the underlying microbiota-related mechanisms of PD by using FLZ as a tool.METHODS Chronic administration of rotenone(30 mg·kg-1 per day)was utilized to induce a mouse model to mimic the pathological process of PD.Behavioral tests and gastrointestinal function tests were conduct⁃ed to evaluate the PD symptoms.Gut microbiota alterations were analyzed by 16s rRNA sequenc⁃ing.The intestinal permeability and blood-brain barrier structures were assessed by various methods.The pro-inflammatory cytokines and LPS levels in the colon,serum,and brain were detected by ELISA.Furthermore,the levels of in⁃flammation and TLR4/MyD88/NF-κB pathway in the substantia nigra(SN)and colon were mea⁃sured.RESULTS Behavioral tests and gastroin⁃testinal function tests found that rotenone-in⁃duced mice showed gastrointestinal dysfunctions(week 3)prior to the motor deficits(week 4).However,FLZ treatment significantly alleviated these PD symptoms.16S rRNA sequencing illus⁃trated that PD-related microbiota alterations in⁃duced by rotenone were reversed by FLZ treatment at various taxa levels.Especially,we identified an increased genus Akkermansia in the Rotenone group(P=0.0006),which could be reversed by FLZ administration(P=0.0070).By reducing microbiota dysbiosis,qPCR results showed that FLZ treatment suppressed intestinal inflammation of rotenone-challenged mice.After⁃wards,transmission electron microscopy(TEM),in vivo FITC permeability assay,bacterial translocation assay,and Western blotting togeth⁃er suggested that FLZ treatment attenuated the intestinal barrier destruction induced by rote⁃none.Subsequently,ELISA results showed that FLZ administration inhibited the leakage of pro-inflammatory cytokines(TNF-α,IL-1β,and IL-6)and LPS into the serum,suggesting the atten⁃uation of systemic inflammation.Then,several experiments including TEM analysis found that FLZ treatment restored blood-brain barrier struc⁃ture.Consequently,the immunofluorescence staining demonstrated that neuroinflammation(increased Iba-1+and GFAP+cells)and dopami⁃nergic neuronal death(reduced TH+cells)in the SN caused by rotenone were remarkably attenu⁃ated.Further mechanistic research proved that the anti-inflammatory effects of FLZ administra⁃tion were mediated through the TLR4/MyD88/NF-κB pathway both in the SN and colon.CONCLU⁃SION FLZ treatment ameliorates microbiota dys⁃biosis to protect the PD model via inhibiting TLR4 pathway,which contributes to one of the underlying mechanisms beneath its neuroprotec⁃tive effects.Our research also supports the importance of microbiota-gut-brain axis in PD pathogenesis,suggesting its potential role as a novel therapeutic target for PD treatment.
基金supported by The National Key Research and Development Program of China(grant No.2023YFC3502800)the CAMS Innovation Found for Medical Sciences(No.2022-I2M-2-001,China).
文摘Increasing evidence shows that the early lesions of Parkinson's disease(PD)originate from gut,and correction of microbiota dysbiosis is a promising therapy for PD.FLZ is a neuroprotective agent on PD,which has been validated capable of alleviating microbiota dysbiosis in PD mice.However,the detailed mechanisms still need elucidated.Through metabolomics and 16S rRNA analysis,we identified glycoursodeoxycholic acid(GUDCA)was the most affected differential microbial metabolite by FLZ treatment,which was specially and negatively regulated by Clostridium innocuum,a differential microbiota with the strongest correlation to GUDCA production,through inhibiting bile salt hydrolase(BSH)enzyme.The protection of GUDCA on colon and brain were also clarified in PD models,showing that it could activate Nrf2 pathway,further validating that FLZ protected dopaminergic neurons through promoting GUDCA production.Our study uncovered that FLZ improved PD through microbiota-gut-brain axis,and also gave insights into modulation of microbial metabolites may serve as an important strategy for treating PD.
基金supported by grants from National Sciences Foundation of China(81773718,81630097,and 81773589)The National Key Research and Development Program of China(Grant No.SQ2018YFA090025-04)+3 种基金CAMS Innovation Fund for Medical Sciences(No.2016-I2M-3e011,China)The Drug Innovation Major Project(2018ZX09711001-003-020,2018ZX09711001-003-005,and 2018ZX09711001-008-005,China)CAMS The Fundamental Research Funds for the Central Universities(2018RC350002,China)CAMS&PUMC Innovation Fund for Graduate(No.2019-1007-23,China)
文摘Parkinson’s disease(PD)is the second most common neurodegenerative disease,but none of the current treatments for PD can halt the progress of the disease due to the limited understanding of the pathogenesis.In PD development,the communication between the brain and the gastrointestinal system influenced by gut microbiota is known as microbiota-gut-brain axis.However,the explicit mechanisms of microbiota dysbiosis in PD development have not been well elucidated yet.FLZ,a novel squamosamide derivative,has been proved to be effective in many PD models and is undergoing the phase I clinical trial to treat PD in China.Moreover,our previous pharmacokinetic study revealed that gut microbiota could regulate the absorption of FLZ in vivo.The aims of our study were to assess the protective effects of FLZ treatment on PD and to further explore the underlying microbiota-related mechanisms of PD by using FLZ as a tool.In the current study,chronic oral administration of rotenone was utilized to induce a mouse model to mimic the pathological process of PD.Here we revealed that FLZ treatment alleviated gastrointestinal dysfunctions,motor symptoms,and dopaminergic neuron death in rotenone-challenged mice.16 S rRNA sequencing found that PD-related microbiota alterations induced by rotenone were reversed by FLZ treatment.Remarkably,FLZ administration attenuated intestinal inflammation and gut barrier destruction,which subsequently inhibited systemic inflammation.Eventually,FLZ treatment restored blood-brain barrier structure and suppressed neuroinflammation by inhibiting the activation of astrocytes and microglia in the substantia nigra(SN).Further mechanistic research demonstrated that FLZ treatment suppressed the TLR4/MyD88/NF-κB pathway both in the SN and colon.Collectively,FLZ treatment ameliorates microbiota dysbiosis to protect the PD model via inhibiting TLR4 pathway,which contributes to one of the underlying mechanisms beneath its neuroprotective effects.Our research also supports the importance of microbiota-gut-brain axis in PD pathogenesis,suggesting its potential role as a novel therapeutic target for PD treatment.
基金supported by grants from National Sciences Foundation of China(81773718,81630097,and 81773589)The National Key Research and Development Program of China(Grant No.SQ2018YFA090025-04)+2 种基金CAMS Innovation Fund for Medical Sciences(No.2016-I2M-3-011,China)The Drug Innovation Major Project(2018ZX09711001-003-020,2018ZX09711001003-005,and 2018ZX09711001-008-005,China)CAMS The Fundamental Research Funds for the Central Universities(2018RC350002,China)。
文摘The gut microbiota plays an important role in regulating the pharmacokinetics and pharmacodynamics of many drugs.FLZ,a novel squamosamide derivative,has been shown to have neuroprotective effects on experimental Parkinson’s disease(PD)models.FLZ is under phase I clinical trial now,while the underlying mechanisms contributing to the absorption of FLZ are still not fully elucidated.Due to the main metabolite of FLZ was abundant in feces but rare in urine and bile of mice,we focused on the gut microbiota to address how FLZ was metabolized and absorbed.In vitro studies revealed that FLZ could be exclusively metabolized to its major metabolite M1 by the lanosterol 14 alpha-demethylase(CYP51)in the gut microbiota,but was almost not metabolized by any other metabolism-related organs,such as liver,kidney,and small intestine.M1 was quickly absorbed into the blood and then remethylated to FLZ by catechol O-methyltransferase(COMT).Notably,dysbacteriosis reduced the therapeutic efficacy of FLZ on the PD mouse model by inhibiting its absorption.The results show that the gut microbiota mediate the absorption of FLZ through a FLZ-M1-FLZ circulation.Our research elucidates the vital role of the gut microbiota in the absorption of FLZ and provides a theoretical basis for clinical pharmacokinetic studies and clinical application of FLZ in the treatment of PD.
基金supported by grants from the Open Competition Program of Top Ten Critical Priorities of Agricultural Science and Technology Innovation for the 14th Five-Year Plan of Guangdong Province(2022SDZG05)the National Natural Science Foundation of China(32270291,32061160467,31870171)to C.G.+7 种基金the Youth Innovation Promotion Association,Chinese Academy of Sciences(2023364)the Guangdong Basic and Applied Basic Research Foundation(2022A1515012319)the Guangzhou Basic and Applied Basic Research Foundation(2023A04J0094)to C.Y.the Sub-Project of Chinese Academy of Sciences Pilot Project(XDA24030502)the Guangdong Provincial Special Fund for Modern Agriculture Industry Technology InnovationTeams(2020KJ148)to Y.W.the National Natural Science Foundation of China(32170362),the Guangdong Natural Science Funds for Distinguished Young Scholars(2022B1515020026)the Youth Innovation Promotion Association,Chinese Academy of Sciences(Y2021094)the Fund of South China Botanical Garden,Chinese Academy of Sciences(QNXM-02)to M.L.
文摘The bZIP transcription factor ABSCISIC ACID INSENSITIVE5(ABI5)is a master regulator of seed germination and post-germinative growth in response to abscisic acid(ABA),but the detailed molecularmechanism by which it represses plant growth remains unclear.In this study,we used proximity labeling to map the neighboring proteome of ABI5 and identified FCS-LIKE ZINC FINGER PROTEIN 13(FLZ13)as a novel ABI5 interaction partner.Phenotypic analysis of flz13 mutants and FLZ13-overexpressing lines demonstrated that FLZ13 acts as a positive regulator of ABA signaling.Transcriptomic analysis revealed that both FLZ13 and ABI5 downregulate the expression of ABA-repressed and growth-related genes involved in chlorophyll biosynthesis,photosynthesis,and cell wall organization,thereby repressing seed germination and seedling establishment in response to ABA.Further genetic analysis showed that FLZ13 and ABI5 function together to regulate seed germination.Collectively,our findings reveal a previously uncharacterized transcriptional regulatorymechanismby which ABA mediates inhibition of seed germination and seedling establishment.
文摘Friedberg, Lee and Zhao (FLZ) proposed a method for effectively evaluating the eigenenergies and eigen wavefunctions of quantum systems. In this work, we study several special cases to investigate applicability of the method.Concretely, we calculate the ground-state eigenenergy of the Hellmann potential as well as the Cornell potential, and also evaluate the energies of the systems where linear term is added to the Coulomb as a perturbation. The results obtained in this method have a surprising agreement with the traditional method or the numerical results. Since the results in this method have obvious analyticity compared to that in other methods, and because of the simplicity for calculations this method can be applied to solving the Schrodinger equation and provides us a better understanding of the physical essence of the concerned systems. But meanwhile applications of the FLZ method are restricted at present, especially for certain potential forms, but due to its obvious advantages, it should be further developed.
基金Supported by the National Natural Science Foundation of China under Grant No.10905019the Program for Changjiang Scholars and Innovative Research Team in University(PCSIRT,No.IRT0964)the Construct Program of the National Key Discipline
文摘The new method proposed recently by Friedberg, Lee, and Zhao is extended to obtain an analytic expansion for the ground-state wavefunction of a time-dependent strong-coupling Schroedinger equation. Two different types of the time-dependent harmonic oscillators are considered as examples for application of the time-dependent expansion. It is show that the time-dependent strong-coupling expansion is applicable to the time-dependent harmonic oscillators with a slowly varying time-dependent parameter.
