The magnetic properties and Kondo effect in Ce3TiBi5 with a quasi-one-dimensional structure were investigated using in situ high-pressure resistivity measurements up to 48 GPa.At ambient pressure,Ce_(3)TiBi_(5) underg...The magnetic properties and Kondo effect in Ce3TiBi5 with a quasi-one-dimensional structure were investigated using in situ high-pressure resistivity measurements up to 48 GPa.At ambient pressure,Ce_(3)TiBi_(5) undergoes an antiferromagnetic(AFM)transition at T_(N)∼5 K.Under high pressures within 8.9 GPa,we find that Kondo scattering contributes differently to the high-temperature resistance,R(T),depending on the applied current direction,demonstrating a significantly anisotropic Kondo effect.The complete P–T phase diagram has been constructed,in which the pressure dependence of T_(N) exhibits a dome-like shape.The AFM order remains robust under pressure,even when the coherence temperature T^(*) far exceeds 300 K.We attribute the observed anisotropic Kondo effect and the robust AFM to the underlying anisotropy in electronic hybridization under high pressure.展开更多
Global brain ischemia and neurological deficit are consequences of cardiac arrest that lead to high mortality.Despite advancements in resuscitation science,our limited understanding of the cellular and molecular mecha...Global brain ischemia and neurological deficit are consequences of cardiac arrest that lead to high mortality.Despite advancements in resuscitation science,our limited understanding of the cellular and molecular mechanisms underlying post-cardiac arrest brain injury have hindered the development of effective neuroprotective strategies.Previous studies primarily focused on neuronal death,potentially overlooking the contributions of non-neuronal cells and intercellular communication to the pathophysiology of cardiac arrest-induced brain injury.To address these gaps,we hypothesized that single-cell transcriptomic analysis could uncover previously unidentified cellular subpopulations,altered cell communication networks,and novel molecular mechanisms involved in post-cardiac arrest brain injury.In this study,we performed a single-cell transcriptomic analysis of the hippocampus from pigs with ventricular fibrillation-induced cardiac arrest at 6 and 24 hours following the return of spontaneous circulation,and from sham control pigs.Sequencing results revealed changes in the proportions of different cell types,suggesting post-arrest disruption in the blood-brain barrier and infiltration of neutrophils.These results were validated through western blotting,quantitative reverse transcription-polymerase chain reaction,and immunofluorescence staining.We also identified and validated a unique subcluster of activated microglia with high expression of S100A8,which increased over time following cardiac arrest.This subcluster simultaneously exhibited significant M1/M2 polarization and expressed key functional genes related to chemokines and interleukins.Additionally,we revealed the post-cardiac arrest dysfunction of oligodendrocytes and the differentiation of oligodendrocyte precursor cells into oligodendrocytes.Cell communication analysis identified enhanced post-cardiac arrest communication between neutrophils and microglia that was mediated by neutrophil-derived resistin,driving pro-inflammatory microglial polarization.Our findings provide a comprehensive single-cell map of the post-cardiac arrest hippocampus,offering potential novel targets for neuroprotection and repair following cardiac arrest.展开更多
文摘硫酸软骨素A(chondroitin sulfate A,CSA)是关节软骨修复中不可或缺的重要成分。CSA由软骨素4-O-磺基转移酶-1(chondroitin 4-O-sulfotransferase-1,C4ST-1)催化软骨素中N-乙酰氨基半乳糖胺(N-acetylgalactosamine,GalNAc)4号位羟基磺酸化合成。然而,由于C4ST-1酶活性较低,其催化能力受限,进而阻碍了CSA的工业化生产进程。为此,该研究旨在通过结合重组菌构建和培养基优化提升C4ST-1酶活性。首先在筛选确定了以毕赤酵母GS115为底盘细胞的基础上,进一步优化了以OST1-α分泌信号肽和SUMO Pro 3促溶标签的组合方式进行C4ST-1分泌表达,经摇瓶发酵C4ST-1最高酶活性为1889.2 U/L。鉴于前期研究发现无机盐对C4ST-1酶活性的抑制以及现有培养基成本较高问题,该研究通过优化培养基组分,发现不添加昂贵成分酵母无氨基氮源(yeast nitrogen base without amino acids,YNB)时,C4ST-1酶活性较原培养基提高68.4%。此外,结合碳源、其他氮源以及生物素的筛选与优化使C4ST-1酶活性进一步提高。最终,在5L发酵罐补料分批发酵72 h时,获得最高酶活性为5040.7 U/L。该研究不仅为CSA规模化生产奠定了基础,也将为其他糖胺聚糖(如肝素、硫酸皮肤素)合成所需的磺基转移酶发酵生产提供借鉴。
基金supported by the National Key Research and Development Program of Chinathe National Natural Science Foundation of China (Grant Nos.2024YFA1408000,12474097,and2023YFA1406001)+2 种基金the Guangdong Provincial Quantum Science Strategic Initiative (Grant No.GDZX2201001)the Center for Computational Science and Engineering at Southern University of Science and Technology,the Major Science and Technology Infrastructure Project of Material Genome Big-science Facilities Platform supported by Municipal Development and Reform Commission of Shenzhen(for J.L.Z.and Y.L.)the Chinese funding sources applied via HPSTAR。
文摘The magnetic properties and Kondo effect in Ce3TiBi5 with a quasi-one-dimensional structure were investigated using in situ high-pressure resistivity measurements up to 48 GPa.At ambient pressure,Ce_(3)TiBi_(5) undergoes an antiferromagnetic(AFM)transition at T_(N)∼5 K.Under high pressures within 8.9 GPa,we find that Kondo scattering contributes differently to the high-temperature resistance,R(T),depending on the applied current direction,demonstrating a significantly anisotropic Kondo effect.The complete P–T phase diagram has been constructed,in which the pressure dependence of T_(N) exhibits a dome-like shape.The AFM order remains robust under pressure,even when the coherence temperature T^(*) far exceeds 300 K.We attribute the observed anisotropic Kondo effect and the robust AFM to the underlying anisotropy in electronic hybridization under high pressure.
基金supported by the National Science Foundation of China,Nos.82325031(to FX),82030059(to YC),82102290(to YG),U23A20485(to YC)Noncommunicable Chronic Diseases-National Science and Technology Major Project,No.2023ZD0505504(to FX),2023ZD0505500(to YC)the Key R&D Program of Shandong Province,No.2022ZLGX03(to YC).
文摘Global brain ischemia and neurological deficit are consequences of cardiac arrest that lead to high mortality.Despite advancements in resuscitation science,our limited understanding of the cellular and molecular mechanisms underlying post-cardiac arrest brain injury have hindered the development of effective neuroprotective strategies.Previous studies primarily focused on neuronal death,potentially overlooking the contributions of non-neuronal cells and intercellular communication to the pathophysiology of cardiac arrest-induced brain injury.To address these gaps,we hypothesized that single-cell transcriptomic analysis could uncover previously unidentified cellular subpopulations,altered cell communication networks,and novel molecular mechanisms involved in post-cardiac arrest brain injury.In this study,we performed a single-cell transcriptomic analysis of the hippocampus from pigs with ventricular fibrillation-induced cardiac arrest at 6 and 24 hours following the return of spontaneous circulation,and from sham control pigs.Sequencing results revealed changes in the proportions of different cell types,suggesting post-arrest disruption in the blood-brain barrier and infiltration of neutrophils.These results were validated through western blotting,quantitative reverse transcription-polymerase chain reaction,and immunofluorescence staining.We also identified and validated a unique subcluster of activated microglia with high expression of S100A8,which increased over time following cardiac arrest.This subcluster simultaneously exhibited significant M1/M2 polarization and expressed key functional genes related to chemokines and interleukins.Additionally,we revealed the post-cardiac arrest dysfunction of oligodendrocytes and the differentiation of oligodendrocyte precursor cells into oligodendrocytes.Cell communication analysis identified enhanced post-cardiac arrest communication between neutrophils and microglia that was mediated by neutrophil-derived resistin,driving pro-inflammatory microglial polarization.Our findings provide a comprehensive single-cell map of the post-cardiac arrest hippocampus,offering potential novel targets for neuroprotection and repair following cardiac arrest.
