We perform a kinetically complete measurement on the fragmentation of Coulomb explosion of 1-120 molecules in intense few-cycle linearly and circularly polarized laser fields. Both the fragmentations of 1t203＋ and H...We perform a kinetically complete measurement on the fragmentation of Coulomb explosion of 1-120 molecules in intense few-cycle linearly and circularly polarized laser fields. Both the fragmentations of 1t203＋ and H204＋ reveal the concerted pathway of dissociation. The length of the OH bond prior to the Coulomb explosion of both molecular ions is sensitive to the laser pulse duration and laser intensity. However, the bending angle of H-O-H is less sensitive to the pulse duration and laser intensity. We introduce the mechanism of charge resonance enhanced double ionization to elucidate the triple （or quadruple） dissociative ionization dynamics of H20, in which two electrons are non-adiabatically localized at the protons of the precursor ion H2O^＋ （or H2O^2＋） and are released simultaneously due to the over barrier ionization in the combined laser field and molecular ionic potential. Such charge resonance enhanced multiple ionization is not suppressed in few-cycle laser fields and elliptically polarized laser fields.展开更多
BACKGROUND Acute pancreatitis(AP)and recurring AP are serious health care problems causing excruciating pain and potentially lethal outcomes due to sepsis.The validated caerulein-(CAE)induced mouse model of acute/recu...BACKGROUND Acute pancreatitis(AP)and recurring AP are serious health care problems causing excruciating pain and potentially lethal outcomes due to sepsis.The validated caerulein-(CAE)induced mouse model of acute/recurring AP produces secondary persistent hypersensitivity and anxiety-like behavioral changes for study.AIM To determine efficacy of acetyl-L-carnitine(ALC)to reduce pain-related behaviors and brain microglial activation along the pain circuitry in CAE-pancreatitis.METHODS Pancreatitis was induced with 6 hly intraperitoneal(i.p.)injections of CAE(50μg/kg),3 d a week for 6 wk in male C57BL/6J mice.Starting in week 4,mice received either vehicle or ALC until experiment’s end.Mechanical hypersensitivity was assessed with von Frey filaments.Heat hypersensitivity was determined with the hotplate test.Anxiety-like behavior was tested in week 6 using elevated plus maze and open field tests.Microglial activation in brain was quantified histologically by immunostaining for ionized calcium-binding adaptor molecule 1(Iba1).RESULTS Mice with CAE-induced pancreatitis had significantly reduced mechanical withdrawal thresholds and heat response latencies,indicating ongoing pain.Treatment with ALC attenuated inflammation-induced hypersensitivity,but hypersensitivity due to abdominal wall injury caused by repeated intraperitoneal injections persisted.Animals with pancreatitis displayed spontaneous anxiety-like behavior in the elevated plus maze compared to controls.Treatment with ALC resulted in increased numbers of rearing activity events,but time spent in“safety”was not changed.After all the abdominal injections,pancreata were translucent if excised at experiment’s end and opaque if excised on the subsequent day,indicative of spontaneous healing.Post mortem histopathological analysis performed on pancreas sections stained with Sirius Red and Fast Green identified wide-spread fibrosis and acinar cell atrophy in sections from mice with CAE-induced pancreatitis that was not rescued by treatment with ALC.Microglial Iba1 immunostaining was significantly increased in hippocampus,thalamus(intralaminar nuclei),hypothalamus,and amygdala of mice with CAE-induced pancreatitis compared to naïve controls but unchanged in the primary somatosensory cortex compared to naïves.CONCLUSION CAE-induced pancreatitis caused increased pain-related behaviors,pancreatic fibrosis,and brain microglial changes.ALC alleviated CAE-induced mechanical and heat hypersensitivity but not abdominal wall injury-induced hypersensitivity caused by the repeated injections.展开更多
Evidence suggests that rapid changes to supporting glia may predispose individuals with spinal cord injury(SCI) to such comorbidities. Here, we interrogated the expression of astrocyte-and microglial-specific markers ...Evidence suggests that rapid changes to supporting glia may predispose individuals with spinal cord injury(SCI) to such comorbidities. Here, we interrogated the expression of astrocyte-and microglial-specific markers glial fibrillary acidic protein(GFAP) and ionized calcium binding adaptor molecule 1(Iba1) in the rat brain in the first 24 hours following SCI. Female Sprague-Dawley rats underwent thoracic laminectomy;half of the rats received a mild contusion injury at the level of the T10 vertebral body(SCI group), the other half did not(Sham group). Twenty-four hours post-surgery the amygdala, periaqueductal grey, prefrontal cortex, hypothalamus, lateral thalamus, hippocampus(dorsal and ventral) in rats were collected. GFAP and Iba1 m RNA and protein levels were measured by real-time quantitative polymerase chain reaction and Western blot. In SCI rats, GFAP m RNA and protein expression increased in the amygdala and hypothalamus. In contrast, gene and protein expression decreased in the thalamus and dorsal hippocampus. Interestingly, Iba1 transcripts and proteins were significantly diminished only in the dorsal and ventral hippocampus, where gene expression diminished. These findings demonstrate that as early as 24 hours post-SCI there are region-specific disruptions of GFAP and Iba1 transcript and protein levels in higher brain regions. All procedures were approved by the University of Technology Sydney Institutional Animal Care and Ethics Committee(UTS ACEC13-0069).展开更多
The neuroprotective effect against spinal cord ischemia/reperfusion injury in rats exerted by delayed xenon post-conditioning is stronger than that produced by immediate xenon post-conditioning. However, the mechanism...The neuroprotective effect against spinal cord ischemia/reperfusion injury in rats exerted by delayed xenon post-conditioning is stronger than that produced by immediate xenon post-conditioning. However, the mechanisms underlying this process remain unclear. Activated microglia are the main inflammatory cell type in the nervous system. The release of pro-inflammatory factors following microglial activation can lead to spinal cord damage, and inhibition of microglial activation can relieve spinal cord ischemia/reperfusion injury. To investigate how xenon regulates microglial activation and the release of inflammatory factors, a rabbit model of spinal cord ischemia/reperfusion injury was induced by balloon occlusion of the infrarenal aorta. After establishment of the model, two interventions were given： （1） immediate xenon post-conditioning—after reperfusion, inhalation of 50% xenon for 1 hour, 50% N2/50%O2 for 2 hours; （2） delayed xenon post-conditioning—after reperfusion, inhalation of 50% N2/50%O2 for 2 hours, 50% xenon for 1 hour. At 4, 8, 24, 48 and 72 hours after reperfusion, hindlimb locomotor function was scored using the Jacobs locomotor scale. At 72 hours after reperfusion, interleukin 6 and interleukin 10 levels in the spinal cord of each group were measured using western blot assays. Iba1 levels were determined using immunohistochemistry and a western blot assay. The number of normal neurons at the injury site was quantified using hematoxylin-eosin staining. At 72 hours after reperfusion, delayed xenon post-conditioning remarkably enhanced hindlimb motor function, increased the number of normal neurons at the injury site, decreased Iba1 levels, and inhibited interleukin-6 and interleukin-10 levels in the spinal cord.Immediate xenon post-conditioning did not noticeably affect the above-mentioned indexes. These findings indicate that delayed xenon post-conditioning after spinal cord injury improves the recovery of neurological function by reducing microglial activation and the release of interleukin-6 and interleukin-10.展开更多
Experimental studies have shown that exercise and human adipose-derived stem cells(ADSCs)play positive roles in spinal cord injury(SCI).However,whether ADSCs and/or exercise have a positive effect on SCI-induced neuro...Experimental studies have shown that exercise and human adipose-derived stem cells(ADSCs)play positive roles in spinal cord injury(SCI).However,whether ADSCs and/or exercise have a positive effect on SCI-induced neuropathic pain is still unclear.Thus,there is a need to explore the effects of exercise combined with administration of ADSCs on neuropathic pain after SCI.In this study,a thoracic 11(T11)SCI contusion model was established in adult C57BL/6 mice.Exercise was initiated from 7 days post-injury and continued to 28 days post-injury,and approximately 1×105 ADSCs were transplanted into the T11 spinal cord lesion site immediately after SCI.Motor function and neuropathic pain-related behaviors were assessed weekly using the Basso Mouse Scale,von Frey filament test,Hargreaves method,and cold plate test.Histological studies(Eriochrome cyanine staining and immunohistochemistry)were performed at the end of the experiment(28 days post-injury).Exercise combined with administration of ADSCs partially improved early motor function(7,14,and 21 days postinjury),mechanical allodynia,mechanical hypoalgesia,thermal hyperalgesia,and thermal hypoalgesia.Administration of ADSCs reduced white and gray matter loss at the lesion site.In addition,fewer microglia and astrocytes(as identified by expression of ionized calcium-binding adapter molecule 1 and glial fibrillary acidic protein,respectively)were present in the lumbar dorsal horn in the SCI+ADSCs and SCI+exercise+ADSCs groups compared with the sham group.Our findings suggest that exercise combined with administration of ADSCs is beneficial for the early recovery of motor function and could partially ameliorate SCIinduced neuropathic pain.展开更多
Quantum coherence in quantum optics is an essential part of optical information processing and light manipulation.Alkali metal vapors,despite the numerous shortcomings,are traditionally used in quantum optics as a wor...Quantum coherence in quantum optics is an essential part of optical information processing and light manipulation.Alkali metal vapors,despite the numerous shortcomings,are traditionally used in quantum optics as a working medium due to convenient near-infrared excitation,strong dipole transitions and long-lived coherence.Here,we proposed and experimentally demonstrated photon retention and subsequent re-emittance with the quantum coherence in a system of coherently excited molecular nitrogen ions(N_(2)^(+))which are produced using a strong 800 nm femtosecond laser pulse.Such photon retention,facilitated by quantum coherence,keeps releasing directly-unmeasurable coherent photons for tens of picoseconds,but is able to be read out by a time-delayed femtosecond pulse centered at 1580 nm via two-photon resonant absorption,resulting in a strong radiation at 329.3 nm.We reveal a pivotal role of the excited-state population to transmit such extremely weak re-emitted photons in this system.This new finding unveils the nature of the coherent quantum control in N_(2)^(+)for the potential platform for optical information storage in the remote atmosphere,and facilitates further exploration of fundamental interactions in the quantum optical platform with strong-field ionized molecules.展开更多
基金Supported by the National Basic Research Program of China under Grant No 2013CB922403the National Natural Science Foundation of China under Grant Nos 11125416,11434002,11121091 and 11134001
文摘We perform a kinetically complete measurement on the fragmentation of Coulomb explosion of 1-120 molecules in intense few-cycle linearly and circularly polarized laser fields. Both the fragmentations of 1t203＋ and H204＋ reveal the concerted pathway of dissociation. The length of the OH bond prior to the Coulomb explosion of both molecular ions is sensitive to the laser pulse duration and laser intensity. However, the bending angle of H-O-H is less sensitive to the pulse duration and laser intensity. We introduce the mechanism of charge resonance enhanced double ionization to elucidate the triple （or quadruple） dissociative ionization dynamics of H20, in which two electrons are non-adiabatically localized at the protons of the precursor ion H2O^＋ （or H2O^2＋） and are released simultaneously due to the over barrier ionization in the combined laser field and molecular ionic potential. Such charge resonance enhanced multiple ionization is not suppressed in few-cycle laser fields and elliptically polarized laser fields.
基金United States Department of Veterans Affairs,VA Merit Grant,No.BX002695United States National Institute of Health,No.R01AG055359,No.R01GM126181 and No.R01NS39041-15.
文摘BACKGROUND Acute pancreatitis(AP)and recurring AP are serious health care problems causing excruciating pain and potentially lethal outcomes due to sepsis.The validated caerulein-(CAE)induced mouse model of acute/recurring AP produces secondary persistent hypersensitivity and anxiety-like behavioral changes for study.AIM To determine efficacy of acetyl-L-carnitine(ALC)to reduce pain-related behaviors and brain microglial activation along the pain circuitry in CAE-pancreatitis.METHODS Pancreatitis was induced with 6 hly intraperitoneal(i.p.)injections of CAE(50μg/kg),3 d a week for 6 wk in male C57BL/6J mice.Starting in week 4,mice received either vehicle or ALC until experiment’s end.Mechanical hypersensitivity was assessed with von Frey filaments.Heat hypersensitivity was determined with the hotplate test.Anxiety-like behavior was tested in week 6 using elevated plus maze and open field tests.Microglial activation in brain was quantified histologically by immunostaining for ionized calcium-binding adaptor molecule 1(Iba1).RESULTS Mice with CAE-induced pancreatitis had significantly reduced mechanical withdrawal thresholds and heat response latencies,indicating ongoing pain.Treatment with ALC attenuated inflammation-induced hypersensitivity,but hypersensitivity due to abdominal wall injury caused by repeated intraperitoneal injections persisted.Animals with pancreatitis displayed spontaneous anxiety-like behavior in the elevated plus maze compared to controls.Treatment with ALC resulted in increased numbers of rearing activity events,but time spent in“safety”was not changed.After all the abdominal injections,pancreata were translucent if excised at experiment’s end and opaque if excised on the subsequent day,indicative of spontaneous healing.Post mortem histopathological analysis performed on pancreas sections stained with Sirius Red and Fast Green identified wide-spread fibrosis and acinar cell atrophy in sections from mice with CAE-induced pancreatitis that was not rescued by treatment with ALC.Microglial Iba1 immunostaining was significantly increased in hippocampus,thalamus(intralaminar nuclei),hypothalamus,and amygdala of mice with CAE-induced pancreatitis compared to naïve controls but unchanged in the primary somatosensory cortex compared to naïves.CONCLUSION CAE-induced pancreatitis caused increased pain-related behaviors,pancreatic fibrosis,and brain microglial changes.ALC alleviated CAE-induced mechanical and heat hypersensitivity but not abdominal wall injury-induced hypersensitivity caused by the repeated injections.
基金The University of Technology Sydney(UTS)Start-up Research Grant 2018 funded this study(to AC)。
文摘Evidence suggests that rapid changes to supporting glia may predispose individuals with spinal cord injury(SCI) to such comorbidities. Here, we interrogated the expression of astrocyte-and microglial-specific markers glial fibrillary acidic protein(GFAP) and ionized calcium binding adaptor molecule 1(Iba1) in the rat brain in the first 24 hours following SCI. Female Sprague-Dawley rats underwent thoracic laminectomy;half of the rats received a mild contusion injury at the level of the T10 vertebral body(SCI group), the other half did not(Sham group). Twenty-four hours post-surgery the amygdala, periaqueductal grey, prefrontal cortex, hypothalamus, lateral thalamus, hippocampus(dorsal and ventral) in rats were collected. GFAP and Iba1 m RNA and protein levels were measured by real-time quantitative polymerase chain reaction and Western blot. In SCI rats, GFAP m RNA and protein expression increased in the amygdala and hypothalamus. In contrast, gene and protein expression decreased in the thalamus and dorsal hippocampus. Interestingly, Iba1 transcripts and proteins were significantly diminished only in the dorsal and ventral hippocampus, where gene expression diminished. These findings demonstrate that as early as 24 hours post-SCI there are region-specific disruptions of GFAP and Iba1 transcript and protein levels in higher brain regions. All procedures were approved by the University of Technology Sydney Institutional Animal Care and Ethics Committee(UTS ACEC13-0069).
基金supported by the National Natural Science Foundation of China,No.81271387the Research Special Fund of Public Welfare and Health Department of China,No.201402009a grant form the National Key Technology R&D Program in China,No.Z141107002514031
文摘The neuroprotective effect against spinal cord ischemia/reperfusion injury in rats exerted by delayed xenon post-conditioning is stronger than that produced by immediate xenon post-conditioning. However, the mechanisms underlying this process remain unclear. Activated microglia are the main inflammatory cell type in the nervous system. The release of pro-inflammatory factors following microglial activation can lead to spinal cord damage, and inhibition of microglial activation can relieve spinal cord ischemia/reperfusion injury. To investigate how xenon regulates microglial activation and the release of inflammatory factors, a rabbit model of spinal cord ischemia/reperfusion injury was induced by balloon occlusion of the infrarenal aorta. After establishment of the model, two interventions were given： （1） immediate xenon post-conditioning—after reperfusion, inhalation of 50% xenon for 1 hour, 50% N2/50%O2 for 2 hours; （2） delayed xenon post-conditioning—after reperfusion, inhalation of 50% N2/50%O2 for 2 hours, 50% xenon for 1 hour. At 4, 8, 24, 48 and 72 hours after reperfusion, hindlimb locomotor function was scored using the Jacobs locomotor scale. At 72 hours after reperfusion, interleukin 6 and interleukin 10 levels in the spinal cord of each group were measured using western blot assays. Iba1 levels were determined using immunohistochemistry and a western blot assay. The number of normal neurons at the injury site was quantified using hematoxylin-eosin staining. At 72 hours after reperfusion, delayed xenon post-conditioning remarkably enhanced hindlimb motor function, increased the number of normal neurons at the injury site, decreased Iba1 levels, and inhibited interleukin-6 and interleukin-10 levels in the spinal cord.Immediate xenon post-conditioning did not noticeably affect the above-mentioned indexes. These findings indicate that delayed xenon post-conditioning after spinal cord injury improves the recovery of neurological function by reducing microglial activation and the release of interleukin-6 and interleukin-10.
基金supported in part by the National Natural Science Foundation of China,Nos.81971151(to YW),82201360(to XC),82102583(to LW),and 82202739(to GPM)China Postdoctoral Science Foundation,Nos.YJ20210208 and 2022M713592+2 种基金Guangdong Basic and Applied Basic Research Foundation,China,No.2021A1515110188(to XC)the Natural Science Foundation of Guangdong Province,China,No.2020A1515010306(to LW)the Science and Technology Program of Guangzhou,China,No.202102020040(to LW)。
文摘Experimental studies have shown that exercise and human adipose-derived stem cells(ADSCs)play positive roles in spinal cord injury(SCI).However,whether ADSCs and/or exercise have a positive effect on SCI-induced neuropathic pain is still unclear.Thus,there is a need to explore the effects of exercise combined with administration of ADSCs on neuropathic pain after SCI.In this study,a thoracic 11(T11)SCI contusion model was established in adult C57BL/6 mice.Exercise was initiated from 7 days post-injury and continued to 28 days post-injury,and approximately 1×105 ADSCs were transplanted into the T11 spinal cord lesion site immediately after SCI.Motor function and neuropathic pain-related behaviors were assessed weekly using the Basso Mouse Scale,von Frey filament test,Hargreaves method,and cold plate test.Histological studies(Eriochrome cyanine staining and immunohistochemistry)were performed at the end of the experiment(28 days post-injury).Exercise combined with administration of ADSCs partially improved early motor function(7,14,and 21 days postinjury),mechanical allodynia,mechanical hypoalgesia,thermal hyperalgesia,and thermal hypoalgesia.Administration of ADSCs reduced white and gray matter loss at the lesion site.In addition,fewer microglia and astrocytes(as identified by expression of ionized calcium-binding adapter molecule 1 and glial fibrillary acidic protein,respectively)were present in the lumbar dorsal horn in the SCI+ADSCs and SCI+exercise+ADSCs groups compared with the sham group.Our findings suggest that exercise combined with administration of ADSCs is beneficial for the early recovery of motor function and could partially ameliorate SCIinduced neuropathic pain.
基金the National Natural Science Foundation of China(11822410,12034013,11734009,and 11974245)the National Key R&D Program of China(2017YFA0303701 and 2019YFA0705000)+10 种基金the Shanghai Municipal Science and Technology Major Project(2019SHZDZX01)the Program of Shanghai Academic Research Leader(20XD1424200)the Natural Science Foundation of Shanghai(19ZR1475700)the Strategic Priority Research Program of Chinese Academy of Sciences(XDB16030300)the Key Research Program of Frontier Sciences of Chinese Academy of Sciences(QYZDJ-SSW-SLH010)the Youth Innovation Promotion Association of Chinese Academy of Sciences(2018284)NSF(ECCS-1509268,and CMMI-1826078)AFOSR(FA9550-20-1-0366)partially supported by the Fundamental Research Funds for the Central Universitiesthe support from the Program for Professor of Special Appointment(Eastern Scholar)at Shanghai Institutions of Higher Learningthe support from Shandong Quancheng Scholarship(00242019024)。
文摘Quantum coherence in quantum optics is an essential part of optical information processing and light manipulation.Alkali metal vapors,despite the numerous shortcomings,are traditionally used in quantum optics as a working medium due to convenient near-infrared excitation,strong dipole transitions and long-lived coherence.Here,we proposed and experimentally demonstrated photon retention and subsequent re-emittance with the quantum coherence in a system of coherently excited molecular nitrogen ions(N_(2)^(+))which are produced using a strong 800 nm femtosecond laser pulse.Such photon retention,facilitated by quantum coherence,keeps releasing directly-unmeasurable coherent photons for tens of picoseconds,but is able to be read out by a time-delayed femtosecond pulse centered at 1580 nm via two-photon resonant absorption,resulting in a strong radiation at 329.3 nm.We reveal a pivotal role of the excited-state population to transmit such extremely weak re-emitted photons in this system.This new finding unveils the nature of the coherent quantum control in N_(2)^(+)for the potential platform for optical information storage in the remote atmosphere,and facilitates further exploration of fundamental interactions in the quantum optical platform with strong-field ionized molecules.
