Inspired by the X(4140)structure reported in the J/ψφsystem by the CDF experiment in 2009,a series of searches have been carried out in theJ/ψφand J/ψK channels,leading to the claim of ten structures in the B→J...Inspired by the X(4140)structure reported in the J/ψφsystem by the CDF experiment in 2009,a series of searches have been carried out in theJ/ψφand J/ψK channels,leading to the claim of ten structures in the B→J/ψφK system.This article provides a comprehensive review of experimental developments,from the initial evidence of X(4140)at CDF to the amplitude analyses and diffractive process investigations by the LHCb experiment,as well as theoretical interpretations of these states.A triplet of J^(PC)=1++states with relatively large mass splittings[about 200MeV(natural units are adopted)]has been identified in the J/ψφsystem by LHCb.Their mass-squared values align approximately linearly with a possible radial quantum number,suggesting that the triplet may represent a radially excited family.For X(4140),the first state in the triplet,its width reported by LHCb is inconsistent with that measured by other experiments,and possible reasons for this discrepancy are discussed.A potential connection between an excess at 4.35 GeV in the J/ψφmass spectrum reported by the Belle experiment through a two-photon process and a potential spin-2 excess in the LHCb data is also investigated.In addition,potential parallels between the J/ψφand J/ψJ/ψsystems,both composed of two vector mesons,are discussed.The continued interest in,and complexity of,these systems underscore the necessity of further experimental exploration with increased statistical precision across a variety of experiments,particularly those with relatively flat efficiency across the Dalitz plot.The J/ψω,φφ,ρω,andρφsystems are mentioned,and the prospects for the J/ψγandγγsystems,are also highlighted.展开更多
T-2 toxin,an omnipresent environmental contaminant,poses a serious risk to the health of humans and animals due to its pronounced cardiotoxicity.This study aimed to elucidate the molecular mechanism of cardiac tissue ...T-2 toxin,an omnipresent environmental contaminant,poses a serious risk to the health of humans and animals due to its pronounced cardiotoxicity.This study aimed to elucidate the molecular mechanism of cardiac tissue damage by T-2 toxin.Twenty-four male Sprague-Dawley rats were orally administered T-2 toxin through gavage for 12 weeks at the dose of 0,10,and 100 nanograms per gram body weight per day(ng/(g·day)),respectively.Morphological,pathological,and ultrastructural alterations in cardiac tissue were meticulously examined.Non-targeted metabolomics analysis was employed to analyze alterations in cardiac metabolites.The expression of the Sirt3/FoxO3α/MnSOD signaling pathway and the level of oxidative stress markers were detected.The results showed that exposure to T-2 toxin elicited myocardial tissue disorders,interstitial hemorrhage,capillary dilation,and fibrotic damage.Mitochondria were markedly impaired,including swelling,fusion,matrix degradation,and membrane damage.Metabonomics analysis unveiled that T-2 toxin could cause alterations in cardiacmetabolic profiles as well as in the Sirt3/FoxO3α/MnSOD signaling pathway.T-2 toxin could inhibit the expressions of the signaling pathway and elevate the level of oxidative stress.In conclusion,the T-2 toxin probably induces cardiac fibrotic impairment by affecting amino acid and choline metabolism as well as up-regulating oxidative stress mediated by the Sirt3/FoxO3α/MnSOD signaling pathway.This study is expected to provide targets for preventing and treating T-2 toxin-induced cardiac fibrotic injury.展开更多
基金partially supported by the Natural Science Foundation of China(Grant Nos.12075123,12061141002,and 12535004)the Ministry of Science and Technology of China(Grant Nos.2023YFA1605804 and 2024YFA1610501)。
文摘Inspired by the X(4140)structure reported in the J/ψφsystem by the CDF experiment in 2009,a series of searches have been carried out in theJ/ψφand J/ψK channels,leading to the claim of ten structures in the B→J/ψφK system.This article provides a comprehensive review of experimental developments,from the initial evidence of X(4140)at CDF to the amplitude analyses and diffractive process investigations by the LHCb experiment,as well as theoretical interpretations of these states.A triplet of J^(PC)=1++states with relatively large mass splittings[about 200MeV(natural units are adopted)]has been identified in the J/ψφsystem by LHCb.Their mass-squared values align approximately linearly with a possible radial quantum number,suggesting that the triplet may represent a radially excited family.For X(4140),the first state in the triplet,its width reported by LHCb is inconsistent with that measured by other experiments,and possible reasons for this discrepancy are discussed.A potential connection between an excess at 4.35 GeV in the J/ψφmass spectrum reported by the Belle experiment through a two-photon process and a potential spin-2 excess in the LHCb data is also investigated.In addition,potential parallels between the J/ψφand J/ψJ/ψsystems,both composed of two vector mesons,are discussed.The continued interest in,and complexity of,these systems underscore the necessity of further experimental exploration with increased statistical precision across a variety of experiments,particularly those with relatively flat efficiency across the Dalitz plot.The J/ψω,φφ,ρω,andρφsystems are mentioned,and the prospects for the J/ψγandγγsystems,are also highlighted.
基金supported by the National Natural Science Foundation of China(No.81872567).
文摘T-2 toxin,an omnipresent environmental contaminant,poses a serious risk to the health of humans and animals due to its pronounced cardiotoxicity.This study aimed to elucidate the molecular mechanism of cardiac tissue damage by T-2 toxin.Twenty-four male Sprague-Dawley rats were orally administered T-2 toxin through gavage for 12 weeks at the dose of 0,10,and 100 nanograms per gram body weight per day(ng/(g·day)),respectively.Morphological,pathological,and ultrastructural alterations in cardiac tissue were meticulously examined.Non-targeted metabolomics analysis was employed to analyze alterations in cardiac metabolites.The expression of the Sirt3/FoxO3α/MnSOD signaling pathway and the level of oxidative stress markers were detected.The results showed that exposure to T-2 toxin elicited myocardial tissue disorders,interstitial hemorrhage,capillary dilation,and fibrotic damage.Mitochondria were markedly impaired,including swelling,fusion,matrix degradation,and membrane damage.Metabonomics analysis unveiled that T-2 toxin could cause alterations in cardiacmetabolic profiles as well as in the Sirt3/FoxO3α/MnSOD signaling pathway.T-2 toxin could inhibit the expressions of the signaling pathway and elevate the level of oxidative stress.In conclusion,the T-2 toxin probably induces cardiac fibrotic impairment by affecting amino acid and choline metabolism as well as up-regulating oxidative stress mediated by the Sirt3/FoxO3α/MnSOD signaling pathway.This study is expected to provide targets for preventing and treating T-2 toxin-induced cardiac fibrotic injury.
